Atlas of diabetic foot

Atlas of the Diabetic Foot

Atlas of the Diabetic Foot. N. Katsilambros, E. Dounis, P. Tsapogas and N. Tentolouris

Copyright © 2003 John Wiley & Sons, Ltd. ISBN: 0-471-48673-6

Atlas of the Diabetic Foot

Professor Nicholas Katsilambros, MDDirector of the 1st Department of Propaedeutic Medicine and the Diabetic Centre

Athens University Medical School

Laiko General Hospital

Athens, Greece

Eleftherios Dounis, MD, FACSDirector of the Orthopedic Department


Athens, Greece

Panagiotis Tsapogas, MDSenior Registrar in Internal Medicine and Diabetes

Laiko General Hosptial

Athens, Greece

Nicholas Tentolouris, MDSenior Registrar in Internal Medicine and Diabetes


Athens, Greece

Copyright 2003 John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester,West Sussex PO19 8SQ, England

Telephone (+44) 1243 779777

Email (for orders and customer service enquiries): [email protected]

Visit our Home Page on www.wileyeurope.com or www.wiley.com

All Rights Reserved. No part of this publication may be reproduced, stored in a retrieval system ortransmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning or

otherwise, except under the terms of the Copyright, Designs and Patents Act 1988 or under the terms ofa licence issued by the Copyright Licensing Agency Ltd, 90 Tottenham Court Road, London W1T 4LP,

UK, without the permission in writing of the Publisher. Requests to the Publisher should be addressedto the Permissions Department, John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West

Sussex PO19 8SQ, England, or emailed to [email protected], or faxed to (+44) 1243 770620.

This publication is designed to provide accurate and authoritative information in regard to the subject

matter covered. It is sold on the understanding that the Publisher is not engaged in renderingprofessional services. If professional advice or other expert assistance is required, the services of a

competent professional should be sought.

Other Wiley Editorial Offices

John Wiley & Sons Inc., 111 River Street, Hoboken, NJ 07030, USA

Jossey-Bass, 989 Market Street, San Francisco, CA 94103-1741, USA

Wiley-VCH Verlag GmbH, Boschstr. 12, D-69469 Weinheim, Germany

John Wiley & Sons Australia Ltd, 33 Park Road, Milton, Queensland 4064, Australia

John Wiley & Sons (Asia) Pte Ltd, 2 Clementi Loop #02-01, Jin Xing Distripark,

Singapore 129809

John Wiley & Sons Canada Ltd, 22 Worcester Road, Etobicoke, Ontario, Canada M9W 1L1

Wiley also publishes its books in a variety of electronic formats. Some content that appears in printmay not be available in electronic books.

British Library Cataloguing in Publication Data

A catalogue record for this book is available from the British Library

ISBN 0-471-486736

Typeset in 10/12pt Times by Laserwords Private Limited, Chennai, India

Printed and bound in ItalyThis book is printed on acid-free paper responsibly manufactured from sustainable forestry

in which at least two trees are planted for each one used for paper production.

Contents

Preface vii

Acknowledgments ix

Chapter I Who is the Patient at Risk for Foot Ulceration? 1

Chapter II Classification, Prevention and Treatment of Foot Ulcers 23

Chapter III Anatomical Risk Factors for Diabetic Foot Ulceration 41

Chapter IV Some Uncommon Conditions 73

Chapter V Neuropathic Ulcers at Various Sites 85

Chapter VI Neuro-Ischemic Ulcers at Various Sites 105

Chapter VII Gangrene 125

Chapter VIII Infections 151

Chapter IX Neuro-Osteoarthropathy. The Charcot Foot 185

Appendix 1 Anatomy of the Foot 213

Appendix 2 Manufacturers of Preventive and Therapeutic Footwear 217

Index 221

Preface

Diabetes mellitus is a common disease all over the world and its frequency is steadilyincreasing. The availability of a wide variety of treatment options results in improvementor even normalization of hyperglycemia as well as of the accompanying metabolicdisorders. However people with diabetes continue to suffer from the complications ofthe disease.

Diabetic foot-related problems occur frequently and may have serious consequences.Amputations at different anatomical levels are the most serious of them.

The present Atlas represents a systematic description of the many different foot lesions,which are often seen in diabetic patients. Each figure corresponds to a case treated in ourDiabetes Centre at the Athens University Medical School. Our patients are evaluated andtreated in collaboration with the Orthopedic Department as well as with other specialistsdepending upon individual needs. A short text, which follows each illustration, describesthe history of the patient, the physical signs observed, the approach to treatment, and isfollowed by a short comment.

It is hoped that this Atlas will be of assistance, as a reference guide and a teachinginstrument, not only to diabetologists and surgeons, but also to all doctors involved inthe treatment of diabetic patients. This book may help them not only to recognize and totreat the diabetic foot lesions, but also to prevent them.

On behalf of the authorsN. Katsilambros

Acknowledgments

The authors of this Atlas would like to express their thanks and gratitude to EliasBastounis, Professor of Surgery and Christos Liapis, Associate Professor, both of whomare vascular surgeons, as well as to Othon Papadopoulos, Assistant Professor, who is aplastic surgeon and to all the academics in the University of Athens for their help withcertain cases in which they are specialists. The help of Constantine Revenas, radiologistand Associate Director in Laiko General Hospital, in the field of ultrasonography is alsogratefully acknowledged.

The authors would also like to express their sincere gratitude to nurse Georgia Markou,who is indispensable to the Outpatient Diabetic Foot Clinic, for her meticulous attentionto the efficient functioning of the clinic and to the upkeep of patient records.

Thanks are also due the numerous doctors who have assisted the Outpatient DiabeticFoot Clinic either as specialists in infectious diseases or orthopedics or as scholars in thefield of diabetes and the diabetic foot.

Chapter IWHO IS THE PATIENT AT RISKFOR FOOT ULCERATION?

� INTRODUCTION

� WHICH PATIENTS ARE AT RISK

FOR FOOT ULCERATION?

� DIABETIC NEUROPATHY

� PERIPHERAL VASCULAR DISEASE

� BIBLIOGRAPHY



Who is the Patient at Risk for Foot Ulceration? 3

INTRODUCTION

The prevalence of foot ulceration in thegeneral diabetic population is 4–10%, beinglower (1.5–3.5%) in young and highest(5–10%) in older patients. The lifetime riskfor foot ulcers in diabetic patients is about15%. The major adverse outcome of footulceration is amputation. Data from severalstudies have documented that foot ulcersprecede approximately 85% of all ampu-tations performed in patients with diabetes.Risk of ulceration and amputation increases2- to 4-fold with both age and duration ofdiabetes. According to one report, preva-lence of amputations in diabetic patientsis 1.6% in the age range 18–44 years,3.4% among those aged 45–64 years, and3.6% in patients older than 65 years. Inci-dence of lower extremity amputations inthe United States was 9.8 per 1000 patientswith diabetes in 1996, increasing by 26%from 1990, despite efforts to reduce theserates. Data from other countries confirmthe increase of amputation rates worldwide.This may be due to aging of the diabeticpopulation, and better reporting. As the dia-betic population increases, more amputa-tions are expected in the future.

Foot ulceration and amputation affect thequality of life for patients and create aneconomic burden for both the patient andthe health care system. Therefore, effortsto identify the patient who is at risk forfoot ulceration, prevention and appropriatetreatment must, of necessity, become amajor priority for healthcare providers.

WHICH PATIENTS AREAT RISK FOR FOOT

ULCERATION?

Risk factors for foot ulceration are asfollows.

• History of previous foot ulceration oramputation

• Peripheral neuropathy• Peripheral vascular disease• Trauma (poor footwear, walking bare-

foot, objects inside the shoes)• Foot deformities (prominent metatarsal

heads, claw tow, hammer toe, pes cavus,nail deformities, deformities related toprevious trauma and surgery, bony prom-inences, etc.)

• Callus formation• Neuro-osteoarthropathy• Limited joint mobility• Long duration of diabetes• Poor diabetes control

In addition to these well-recognized riskfactors for foot ulceration, several — butnot all — studies have shown that footulcers are more common in male patients.In addition, social factors including lowsocial status, poor access to healthcareservices, poor education and a solitarylifestyle have all been associated withfoot ulceration. Another important factorfor foot ulceration is poor compliance bythe patient with medical instructions andneglecting to follow procedures. Edemamay impair blood supply to the foot, par-ticularly in patients with peripheral vascu-lar disease. Inhibition of sweating (anhidro-sis) — due to peripheral neuropathy — maycause dry skin and fissures. Dry skintogether with limited joint mobility andhigh plantar pressures contribute to callusformation.

Peripheral neuropathy and vascular dis-ease alone do not cause foot ulceration. Itis the combination of the factors mentionedabove, that act together in the vast majorityof cases. Trauma from either the patient’sshoes or from external causes, and loss ofprotective sensation and peripheral vasculardisease are among the major contributorsto foot ulceration. Diabetic neuropathy is

4 Atlas of the Diabetic Foot

the common denominator in almost 90% ofdiabetic foot ulcers. Trauma initially causesminor injuries, which are not perceived bythe patient with loss of protective sensa-tion. As the patient continues his activi-ties, a small injury enlarges and may becomplicated by infection. The pathway tofoot ulceration in diabetes is depicted inFigure 1.1.

DIABETIC NEUROPATHY

Diabetic neuropathy is defined — accordingto the International Consensus Group onNeuropathy — as ‘the presence of symp-toms and/or signs of peripheral nerve dys-function in people with diabetes, afterexclusion of other causes’. The prevalence

of peripheral neuropathy in diabetes is23–42% and is higher (50–60%) amongolder type 2 diabetic patients. It should bementioned that the prevalence of symp-tomatic peripheral neuropathy (burning sen-sation, pins and needles or allodynia in thefeet, shooting, sharp and stabbing pain ormuscle cramps at the legs) is only 15–20%and the majority of the patients with neu-ropathy are free of symptoms. Often, thefirst sign of peripheral neuropathy is a neu-ropathic ulcer. Other patients have neuro-pathic pain and on examination are foundto have severe loss of sensation. This com-bination is described as ‘painful-painlesslegs’ and these patients are at increased riskfor foot ulceration.

All patients with diabetes should be ex-amined annually for peripheral neuropathy,

Figure 1.1 Pathways to foot ulceration in diabetic patients. (From Boulton AJM. The pathwayto ulceration: Aetiopathogenesis. In Boulton AJM, Connor H, Cavanagh PR (Eds), The Foot inDiabetes (3rd edn). Chichester: Wiley, 2000; 61–72, with permission)


so that those at risk for ulceration can beidentified. The tests for peripheral neuropa-thy are many and some of them are quitesophisticated, and are undertaken only inspecialist centers. However, the tests thatare used to characterize the patient with lossof protective sensation are simple, fast andeasily carried out at the outpatient clinic.These tests are as follows.

1. Questioning the patient to ascertain whe-ther symptoms of peripheral neuropathy,as described above, are present. Typi-cally neuropathic symptoms are worseduring the night and may wake thepatient, who finds relief on walking.

2. Loss of sensation of (a) pain (using adisposable pin; this test is carried outonly when the skin is intact), (b) lighttouch (using a cotton wisp), and (c) tem-perature (using two metal rods, one ata temperature of 4 ◦C and the other at40 ◦C) on the dorsum of the feet. Typ-ically, in diabetic peripheral neuropa-thy the sensory deficit is pronouncedat the periphery of the extremities (ina ‘glove and stocking distribution’). Azone of hypoesthesia is found betweenthe area of loss of sensation and amore central area of normal sensation.Achilles tendon reflexes may be reducedor absent. Wasting of small musclesof the feet results in toe deformities(claw, hammer, curly toes) and promi-nent metatarsal heads. Vibration percep-tion is tested using a 128-Hz tuning forkon the dorsal side of the distal phalanxof the great toes (Figure 1.2). A tun-ing fork should be placed perpendicu-lar to the foot at a constant pressure.During examination the patient is pre-vented from seeing where the examinerhas placed the tuning fork. Examinationis repeated twice and there is at leastone ‘sham’ application in which the tun-ing fork is not vibrating. The patient has

Figure 1.2 Examination of vibration percep-tion by the use of tuning fork

normal sensation when his reactions arecorrect in two out of three tests, but is atrisk for ulceration when they are incor-rect in two out of the three tests.

3. Pressure perception is tested with Sem-mes–Weinstein monofilaments. Manystudies have shown that inability to per-ceive pressure is related to a several-foldincrease in the risk for foot ulceration.The filaments are available in large setswith varying levels of force required tobend them. Diabetic neuropathy can bedetected using the 5.07 monofilament(this filament bends with the application


Figure 1.3 Semmes–Weinstein (5.07) monofilament examination

of a 10-g force). Monofilament shouldbe applied perpendicular to the skin sur-face and with sufficient force so thatit bends or buckles (Figure 1.3). Totalduration of skin contact of the fila-ment should be approximately 2 s. Dur-ing examination the patient is preventedfrom seeing if and where the examinerapplies the filament. The patient is askedto say whether he can feel the pres-sure applied (yes/no) and in which foot(right/left foot). Examination is repeatedtwice at the same site and there is atleast one ‘sham’ application, in which nofilament is applied (a total of three ques-tions per site). The patient has normalprotective sensation when the correctanswer is given for two out of the threetests and is at risk for ulceration whenthey are not. The International Consen-sus on the Diabetic Foot suggested threesites to be tested on both feet: the plan-tar aspect of the great toe, the first andthe fifth metatarsal heads. The filamentmust be applied at the perimeter and notat an ulcer site, callus, scar or site ofnecrotic tissue.

4. Determination of vibration perceptionthresholds using a biothesiometer or aneurothesiometer. Vibration perceptionthreshold is measured at the tip of thegreat toes with the vibrating head of thedevice balanced under its own weight(Figure 1.4). The vibrating stimulus isincreased until the patient feels it, thestimulus is then withdrawn and the testrepeated. This test is usually carriedout three times at each site and themean value is calculated. Several studieshave shown that a vibration perceptionthreshold over 25 V is associated witha 4- to 7-fold increase in risk for footulceration.

PERIPHERAL VASCULARDISEASE

ASSESSMENT OF THEVASCULAR STATUS IN

PATIENTS WITH DIABETES

The prevalence of peripheral vascular dis-ease in diabetic patients is 15–30%. The


Figure 1.4 Examination of vibration perception by the use of a biothesiometer

disease progresses with both duration ofdiabetes and age. A diagnostic work-upof the peripheral extremities is based onclinical examination (history of intermittentclaudication, rest pain, walking distance,palpation of leg pulses, and measurement ofankle brachial index). Co-existence of neu-ropathy in diabetic patients might reducethe pain of intermittent claudication or evenischemic rest pain. Palpation of feet pulsesremains the cornerstone of screening forperipheral vascular disease. The absence oftwo or more pulses on both feet is diagnos-tic of peripheral vascular disease. Based onthe results of clinical examination, a deci-sion must be made as to whether the doctorwill proceed with more sophisticated meth-ods of examination of the lower extremitiesin order to determine the exact level anddegree of the arterial obstruction.

Fontaine Clinical Staging

Fontaine clinical staging of peripheral arte-rial disease includes four stages:

Stage I is asymptomatic; patients may com-plain of numbness or that their legs geteasily tired, but they do not seek medicalhelp. Usually the superficial femoral arteryis stenosed at the level of the Hunterianduct; lateral circulation of the deep femoralartery is adequate for the needs of the limb.

Stage II in which patients suffer from inter-mittent claudication; they are subclassifiedas Stage IIa, if they can walk without symp-toms for more than 250 m; or Stage IIb, ifthey have to stop earlier. If patients feelpain in the leg, it is usually due to occlusionof the femoral artery, while an occlusion ofthe iliac artery causes pain in the thigh.

Stage III patients suffer from rest pain ofthe limb, which may become constant andvery intense, usually during the night; thepain is often resistant to analgesics. Theprognosis is not good; half of these patientswill have an amputation within the next5 years.

Stage IV patients have gangrene. Minortrauma, ulcers or paronychias may evolve


into gangrene when stage III peripheralartery disease is present. The patient feelspain at rest unless diabetic neuropathy isalso present.

Noninvasive Vascular Testing

Calculation of the Ankle Brachial Index(ABI). The ankle brachial index (ankle armindex) is widely used and can easily bemeasured in the outpatient clinic. Measure-ments are made with the use of a pocket-size continuous-wave Doppler probe oper-ating at 4 or 10 MHz. The brachial systolicpressure on both sides is determined first.Then the ankle systolic pressure on eachside is determined with the Doppler probeby applying a blood pressure cuff aroundthe ankle, just above the malleolus. Anklepressure is measured at both posterior tib-ial (behind the medial malleolus) and dorsalpedal arteries. No pressure is applied on theprobe. Pressures are determined at a beam-vessel angle of approximately 60◦. Aftermeasuring the systolic pressures, the high-est ankle pressure is divided by the highestbrachial pressure; this ratio is called theankle brachial index (ABI). Occasionally,no audible signal can be obtained from thefoot arteries. In these cases, a careful searchoften reveals a peroneal collateral signalanteriorly, next to the lateral malleolus.Normally, systolic ankle pressure exceedssystolic arm pressure by 12–24 mmHg.The normal value of the ABI is 1 to 1.2.A level of less than 0.9 is usually takenas indicative of occlusive arterial disease.An ankle systolic pressure of <50 mmHgor an ABI <0.3 in the presence of restpain or tissue damage denotes critical limbischemia. The equivalent toe systolic pres-sure is 30 mmHg or less.

A change of >0.15 in the ABI duringfollow-up suggests significant narrowingand it is an indication for further study with

angiography. A spontaneous rise in the ABIis usually attributable to the development ofcollateral circulation.

Medial calcification, which is very com-mon in diabetes (Figure 1.5), renders theunderlying arteries incompressible, result-ing in spuriously high ABI values (morethan 1.2). In these cases, the severity ofarterial occlusive disease can be assessedby toe pressure measurements. Other causesof inaccurately high ABI values include toohigh positioning of the upper body, chronicvenous insufficiency and significant ankleedema. Spurious low ABI values can resultfrom the rapid deflation of the cuff, exces-sive probe pressure, and an insufficient restperiod.

Despite these limitations, the ankle bra-chial index is a useful screening tool forthe assessment of presence and sever-ity of peripheral vascular disease and itremains the basic examination suggested byan international panel on the assessmentof peripheral vascular disease in diabetes(see below).

Toe Pressures. Toe pressures are measuredby a pneumatic cuff with a diameter which

Figure 1.5 Extensive calcification of the pos-terior tibial artery


is about 1.2 times that of the digit, wrappedaround the proximal phalanx, with a flowsensor (usually a photoplethysmograph)located distally (Figure 1.6). In addition,toe pressures can also be measured using adigital strain gauge. Normal toe pressuresaverage 24–40 mmHg or less comparedto ankle pressure. Rest pain, skin lesions,or both are present in approximately 50%of limbs with toe pressures ≤30 mmHg,and in a much lower proportion of patientswith toe pressures above this level. Toepressures do not differ between patientswith and without diabetes. Spuriously high

toe pressures due to arterial calcificationseldom occur at the toe level. For this rea-son, toe pressure determination is valuablein diabetic patients when an ankle pressureis abnormally high.

Transcutaneous Oximetry. Transcutane-ous oximetry (measurement of transcuta-neous oxygen pressure, TcPO2) is usedfor the assessment of severe peripheralvascular disease. It is usually measured atthe dorsum of the feet with the patientin the supine position (Figure 1.7). Withincreasing age, the TcPO2 tends to decrease,

Figure 1.6 Toe and ankle pressure measurement

Figure 1.7 Transcutaneous oximetry


paralleling a similar decline in arterialPO2. Normal subjects have values of 40to 70 mmHg. In general, a resting TcPO2

greater than 55 mmHg may be consid-ered normal, regardless of age. Patientswith anemia may also have lower val-ues. Patients with rest pain or gangrenehave values between 0 and 30 mmHg.In diabetes, TcPO2 is lower than in age-matched arteriopathic patients. A TcPO2

<40 mmHg is associated with failure ofwound healing, while an increase afterangioplasty or bypass surgery predicts suc-cess of the intervention. Because the resultsare not affected by arterial calcification, thismethod is particularly valuable for evaluat-ing diabetic vascular disease.

Segmental Pressures Measurement. Ab-normal blood pressure values found byany of the above methods indicate thatarterial occlusive disease is present, butthey do not identify the specific segmentsinvolved. Further diagnostic informationcan be obtained by measuring pressure gra-dients in the legs. However, only rarelydo these measurements need to be madewhen the ABI is normal. To determinesegmental pressure in the legs, pressurecuffs 10–12 cm wide are applied aroundthe thigh at the groin level, above theknee, below the knee and at the ankle level(Figure 1.8). By listening with a Dopplerprobe over the pedal arteries (posterior tib-ial or dorsal pedal), the pressure at thelevel of the inflated cuff can be mea-sured. A pressure index can be obtained bydividing the segmental systolic pressure bythe brachial pressure. The pressure indexshould be equal to 1.0 or slightly higher.Normal pressure index at the high thighlevel is 1.3. The pressure gradient betweenany two adjacent levels in the normal legis <20–30 mmHg. Gradients >30 mmHgsuggest that a significant stenosis is present

Figure 1.8 Normal segmental pressures. Thepressure gradient between any two adjacent lev-els in the normal leg is less than 20–30 mmHg.Gradients greater than 30 mmHg suggest thata significant stenosis is present at the interven-ing arterial segment. When the gradient exceeds40 mmHg the artery is occluded

at the intervening arterial segment. Whenthe gradient exceeds 40 mmHg the arteryis occluded.

It should be taken into account thatpatients with severe stenosis at a proximallevel (e.g. aortoiliac disease) may have spu-riously normal pressure gradients betweenhigh thigh and low thigh in the presence ofsevere superficial femoral artery stenosis.


In addition, obstructions below the kneemay not be diagnosed, unless the stenosis issufficiently severe to involve all three tibialarteries.

Segmental Plethysmography. Plethysmo-graphy is a useful technique for the assess-ment of peripheral arteries. There areseveral types of plethysmographs (air, mer-cury, indium–gallium and strain gaugeplethysmographs) and all measure the sameparameter: the momentary change in thevolume of the soft tissues when a pulsewave fills the arteries of the area of theleg which is being examined. Photoplethys-mography measures blood concentration inthe cutaneous microcirculation by detect-ing the reflection of the applied infraredlight. Air plethysmographs are the standardinstruments for segmental plethysmogra-phy. Pressure cuffs are applied at differentlevels of the leg as in segmental pressuremeasurement. A plethysmograph recordsthe change in volume as a wave, whichreflects the intra-arterial changes. The nor-mal segmental volume pulse contour ischaracterized by a steep, almost vertical

upstroke, a sharp systolic peak, and a downslope that bows towards baseline duringdiastole. In the middle of the down slopethere is a prominent dicrotic wave. Dis-tal to a stenosis, the upslope is less steep,the peak becomes rounded, the down slopebows away from the baseline, and thedicrotic wave disappears. Examples of var-ious degree of arterial stenosis are shownin Figure 1.9. A plethysmography record isnot affected by the presence of arterial cal-cification; for this reason it is a valuablemethod for the assessment of peripheralvascular disease in diabetes.

Ultrasonography. Arterial ultrasound ex-amination has become very popular inrecent years. It is a simple, low cost andvalid method for determination of the siteand degree of obstructive lesions, and ofthe patency of a vessel after revasculariza-tion. The site of an arterial stenosis canbe identified by serial placements of theDoppler probe along the extremities. How-ever, there is no justification for its use asa routine screening procedure. The exactsite of arterial disease is located by the

Figure 1.9 Plethysmography pulse volume waveforms associated with different degrees ofperipheral vascular disease


Figure 1.10 Qualitative analysis of spectralwaveforms proximal to the site of the probe.(A) Normal. (B) Mild arterial stenosis causingturbulence during systole. (C and D) Loss ofreverse flow due to more severe stenosis. (Eand F) As the degree of stenosis increases, therate of acceleration of the upstroke decreases,the peak becomes rounded (E) and the wavebecomes continuous and less pulsatile (F–H).Completely damped waveforms (F–H) in thepedal arteries are compatible with multilevelvessel disease and indicate the presence ofblood flow due to the development of collateralcirculation

use of duplex scanning. Duplex scannersuse the combination of real time B-modeultrasound imaging of the arterial wall,together with pulsed Doppler imaging andexamine flow patterns in a defined area

within the artery lumen. Pulsed Dopplerimaging produces spectral analysis of thepulse wave which delineates the completespectrum of frequencies (that is, bloodflow velocities) found in the arterial wave-form during a single cardiac cycle. Tis-sues are displayed in varying shades ofgray (duplex) on the screen. The additionof color frequency mapping (color duplexor triplex) makes identification of arterialstenosis easier and allows a better descrip-tion of the atheromatous plaques on thearterial wall. A normal spectrum shows atypical triphasic flow pattern, consisting ofa steep systolic upstroke, a systolic peak,a reverse flow component in early diastoleand a pre-systolic zero flow (Figure 1.10).A clear spectral window under the sys-tolic peak is a normal finding, signalingthe absence of slow turbulent flow compo-nents. If a stenosis is present the windowbecomes occluded. The degree of steno-sis can be quantified by analyzing thespectral waveform, and by determining thepeak systolic velocity ratio (PSV ratio). Ingeneral, a cross-sectional reduction of atleast 30% must be present to produce adetectable spectral change. The flow veloc-ities may vary, but peak systolic veloci-ties in the arteries above knee are about50–100 cm/s, while below knee they areapproximately 50 cm/s.

Qualitative analysis of the waveform.Inspecting the contour of the spectral wave-form is of considerable diagnostic value.

Table 1.1 Peak systolic velocity ratio (PSVratio) for the determination of the degree ofstenosis

PSV ratioReduction in

cross-sectional area

<2.5 0–49%>2.5 50–74%>5.5 75–99%


Atherosclerotic disease proximal to the site

of the probe produces a subtle change

in the contour of the systolic peak or in

the early deceleration phase (Figure 1.10).

With increasing proximal stenosis, the

reverse flow component is damped and thendisappears entirely.

Quantitative analysis of the waveform.The most widely used criterion for

Table 1.2 Criteria for lower limb arterial stenosis in spectral analysis

Percentagestenosis

Pre-stenoticspectrum

Intra-stenoticspectrum

Spectrum justpast the stenosis

0–50% Normal:— Triphasic or biphasic— Narrow frequency band— Clear spectral window

Increase in PSV(by <100% and/or<180 cm/s)

No significantturbulence

Possible flow reversal

51–75% Normal Increase in PSV(by >100% and/or>180 cm/s)

Flow reversalPossible slightturbulence

76–99% Normal or slightly reducedvelocity

Increase in PSV(by >250% and/or>180 cm/s)

Significant turbulenceComplete occlusionof spectral window

Figure 1.11 Normal triphasic spectral waveform from the right superficial femoral artery. Notethe narrow, steep increase and decrease of the waveform. Peak systolic velocity is 79.1 cm/s (normalpeak systolic velocities in the arteries above knee are 50–100 cm/s). (Courtesy of C. Revenas)


diagnosis of peripheral arterial stenosis isthe peak systolic velocity ratio. This ratioexpresses the relationship of the intra-stenotic peak systolic velocity to the lowestpost-stenotic or pre-stenotic peak systolicvelocity. The PSV ratio allows estimationof the degree of a stenosis without distor-tion by a second stenosis located at a moredistal or a proximal site (Table 1.1). Othercriteria used for the estimation of arterialstenosis are presented in Table 1.2.

Duplex ultrasonography has a sensitivityof 80% and specificity above 90% fordetecting femoral and popliteal stenosiscompared with angiography, but it is lessreliable for the assessment of the severity ofstenosis in the tibial and peroneal arteries.

Normal and abnormal spectral waveformrecordings are shown in Figures 1.11–1.18.

Other Methods. Modern methods for theassessment of peripheral arteries includehelical or spiral computed tomography (CT)and magnetic resonance angiography. Spi-ral CT has the ability to generate three-dimensional images and is most useful inthe evaluation of large arteries (e.g. tho-racic or abdominal aorta). Disadvantagesinclude intravascular administration of iod-inated contrast material and the inabilityto assess small vessel disease. Magneticresonance angiography (MRA) is mainlyused for examining the cerebral vessels andthe carotid arteries. Recent data suggestthat this method might replace angiogra-phy as a primary imaging examination for

Figure 1.12 Normal triphasic spectral waveform from the right posterior tibial artery. At the topof the figure the duplex scan of the artery is seen. Peak systolic velocity is 49 cm/s. (Courtesy ofC. Revenas)


Figure 1.13 In the left upper panel a significant stenosis (STEN) of the left superficial femoralartery with collateral circulation development (COL) is shown. Note (left lower panel) the triphasicspectral waveform in the collateral vessel and that the peak systolic velocity is 78 cm/s, which istoo high for such a vessel. In the area of the femoral artery stenosis, the peak systolic velocityis high (193 cm/s) and the waveform is triphasic, but blood flow during diastole is low, as seenfrom the short duration of the reverse flow (right lower panel). Adjacent to the spectral waveform,a color duplex scan of the artery with the stenosis is shown. These findings suggest the presenceof stenosis of approximately 50–80%. In the upper right panel a dynamic Doppler recording isshown, which gives a clearer image of the collateral vessels. (Courtesy of C. Revenas)

Figure 1.14 Biphasic spectral waveforms obtained from the left superficial femoral artery. Thespectral window is widened and is filled in, although not completely. Peak systolic velocity is low(51.4 cm/s). These findings indicate the presence of significant proximal stenosis at one or multiplelevels. (Courtesy of C. Revenas)


Figure 1.15 The spectral waveform from the right anterior tibial artery in an area of stenosis isseen in the upper left panel. Peak systolic velocity is high (69.7 cm/s) — peak systolic velocitiesin the arteries below knee are normally ∼50 cm/s — and there is mild widening of the spectrumduring both systole and diastole. This record corresponds to a stenosis of about 30%. The spectralwaveform from the left superficial femoral artery is shown in the lower left panel. There is mildspectral widening, and loss of pre-systolic flow. The color duplex image of the right tibial arteriesis shown in the right upper panel. A duplex scan of the left posterior tibial artery is shown in thelower right panel. (Courtesy of C. Revenas)

peripheral vascular disease. Angiographymay be reserved for percutaneous interven-tions and in cases of equivocal findingsonly. In addition, an MRA is a simple, non-toxic and relatively inexpensive method.

An International Meeting on the Assess-ment of Peripheral Vascular Disease inDiabetes was held in 1993 and made thefollowing recommendations for the detec-tion and follow-up of peripheral vasculardisease.

• All adults (age ≥ 18 years) with diabetesshould be asked whether they sufferfrom intermittent claudication. Presence

of claudication is an indication for anklebrachial index (ABI) determination onan annual basis. If the ABI is less than0.9, the patient needs intensive manage-ment of cardiovascular risk factors. Allpatients with lifestyle-limiting claudica-tion should be referred for specialist vas-cular assessment. Intensive managementof cardiovascular risk factors includesreduction of lipid levels, smoking ces-sation, control of blood pressure, weightand glucose levels and the use of aspirinas in coronary heart disease.

• All adults (age ≥ 18 years) with diabetesshould be examined annually for signs of


Figure 1.16 Near normal spectral waveforms obtained from the right common (upper panel) andright superficial (lower panel) femoral arteries. The peak systolic velocity is reduced slightly; thewaveform is triphasic and there is minimal widening of the spectral window. These findings suggestthe presence of a mild proximal stenosis. (Courtesy of C. Revenas)


Figure 1.17 Upper left panel: a biphasic waveform of the left posterior tibial artery at ankle level.The peak systolic velocity is reduced (27.4 cm/s) and there is widening of the spectral windowduring systole, while velocity is high during diastole. The artery diameter is normal as seen ina color duplex image on the left of the spectral waveform. These findings suggest the presenceof a proximal stenosis of about 40%. Right upper panel: the same artery at another site after astenosis. The low peak systolic velocity (14.5 cm/s), biphasic waveform, and spectral wideningduring systole, as well as the high velocity during diastole are notable features. These findingssuggest the presence of a proximal stenosis of more than 50%. Left lower panel: duplex scan of theleft anterior tibial artery from the same patient and the recorded spectral waveform. An even lowerpeak systolic velocity (12.1 cm/s), significant widening of the systolic spectral window and highdiastolic velocity are shown. The diameter of the artery is normal (lower right panel). The abovefindings signify the presence of a proximal stenosis of about 50–60%. (Courtesy of C. Revenas)

critical limb ischemia (gangrene, ulcer,skin changes, or ischemic rest pain). Ifsuch signs are present, the patient shouldbe referred for specialist vascular assess-ment. In addition, intensive managementof co-existent cardiovascular risk factorsshould be initiated.

• Palpation of the dorsalis pedis and pos-terior tibial artery as well as ausculta-tion for femoral artery bruits should be

performed on an annual basis for alladults with diabetes. If one pedal arteryis absent or diminished or if bruits areaudible, ABI determinations should becarried out annually. If the ABI valueis below 0.9, intensive management ofco-existent cardiovascular risk factorsshould be initiated.

• Patients for whom ABI monitoring isrecommended: (a) all those with type 1


Figure 1.18 Lower panel: complete obstruction of the right superficial femoral artery (RSFA) atthe canal of Hunter. A collateral vessel (COL) is seen proximal to the stenosis. Distal to the site ofthe obstruction there is blood flow in the superficial femoral artery from collateral vessels. Upperpanel: the spectral waveform obtained from the collateral vessel shown in the lower panel of thefigure. The waveform is biphasic, both peak systolic and diastolic velocities are high and there iswidening of the systolic spectral window. The waveform obtained from the right superficial femoralartery distal to the site of the complete obstruction is shown. Notice the low peak systolic and thehigh diastolic velocity. This waveform is called tardus pardus. This type of spectral waveform issimilar to that obtained from the venous circulation, and signifies blood flow in an artery resultingfrom the development of collateral circulation. As more collateral vessels fill the artery, the spectralwaveform may be triphasic, but the peak systolic velocity will be reduced. (Courtesy of C. Revenas)


diabetes older than 35 years, or who havehad diabetes for over 20 years at base-line; (b) all patients older than 40 yearsat baseline with type 2 diabetes; (c) anydiabetic patient who has newly detecteddiminished pulses, femoral bruits, or afoot ulcer; (d) any diabetic patient withleg pain of unknown etiology.

• Based on the results of the ABI, the fol-lowing recommendations are suggested:

� If the ABI is above 0.9, measurementshould be repeated every 2–3 years.

� If the ABI is 0.50–0.89, measure-ment should be repeated within 3months and intensive management ofco-existent cardiovascular risk factorsshould be initiated.

� If the ABI is below 0.5, the patientshould be referred for specialist vascu-lar assessment and intensive manage-ment of co-existent cardiovascular riskfactors should be initiated.

• If an incompressible artery with an anklepressure above 300 mmHg or an anklepressure 75 mmHg above arm pressureis found, these measurements should berepeated in 3 months. If still present,these patients should be referred for vas-cular assessment and intensive manage-ment of co-existent cardiovascular riskfactors should be undertaken.

Invasive VascularTesting — Arteriography

Arteriography remains the definitive diag-nostic procedure before any form of sur-gical intervention. It should not be usedas a diagnostic procedure to establish thepresence of arterial disease. Contrast mater-ial may exaggerate any preexisting renaldisease and for this reason the contrastmaterial used should be limited as muchas possible. In addition, the InternationalMeeting on the Assessment of Peripheral

Vascular Disease in Diabetes strongly rec-ommended that in diabetic patients arteriog-raphy should be carried out before any deci-sion regarding an amputation is made, inorder to assess the exact status of the vascu-lar tree, particularly when the ankle brachialindex and toe systolic pressure indicate thatarterial disease is present.

Keywords: Etiopathogenesis of footulceration; diabetic neuropathy, diagnosis;symptoms of peripheral neuropathy; vibra-tion perception threshold; Semmes–Weins-tein monofilaments; assessment of vascularstatus; ankle brachial index; medial arterialcalcification; toe pressure; transcutaneousoximetry; segmental pressures measure-ment; segmental plethysmography; ultra-sonography; duplex; triplex; waveforms,quantitative analysis; waveforms, qualita-tive analysis; peak systolic velocity ratio;spiral computed tomography; magnetic res-onance angiography; invasive vascular test-ing; angiography; Fontaine stage

BIBLIOGRAPHY

1. The International Working Group on theDiabetic Foot. International Consensus onthe Diabetic Foot. Amsterdam, The Nether-lands, 1999.

2. Boulton AJM, Greis FA, Jervell JA. Guide-lines for the diagnosis and outpatient man-agement of diabetic peripheral neuropathy.Diabet Med 1998; 15: 508–514.

3. Boulton AJM. The pathway to ulceration:Aetiopathogenesis. In Boulton AJM, Con-nor H, Cavanagh PR (Eds), The Foot in Dia-betes (3rd edn). Chichester: Wiley, 2000;61–72.

4. Veves A, Uccioli L, Manes C, VanAcker K, Komninou H, Philippides P, Kat-silambros N, De Leeuw I, Menzinger G,Boulton AJ. Comparison of risk factors forfoot problems in diabetic patients attendingteaching outpatient clinics in four different


European states. Diabet Med 1994; 11:709–713.

5. Ziegler RE, Summer DS. Physiologicassessment of peripheral arterial occlusivedisease. In Rutherford RB (Ed.), VascularSurgery (5th edn). Philadelphia: Saunders,2000; 140–165.

6. Katsilambros N, Hatzakis A, Perdikaris G,Pefanis A, Papazachos G, Papadoyannis D,Balas P. Peripheral occlusive arterial dis-ease in longstanding diabetes mellitus. Apopulation study. Int Angiol 1989; 8: 36–40.

7. Kasilambros NL, Tsapogas PC, ArvanitisMP, Tritos NA, Alexiou ZP, Rigas KL. Risk

factors for lower extremity arterial diseasein non-insulin-dependent diabetic persons.Diabet Med 1996; 13: 243–246.

8. Donnelly R, Hinwood D, London NJM.Non-invasive methods of arterial and ven-ous assessment. In Donnelly R, LondonNJM (Eds), ABC of Arterial and VenousDisease. London: BMJ Books, 2000; 1–4.

9. Orchard TJ, Strandness DE. Assessment ofperipheral vascular disease in diabetes. Dia-betes Care 1993; 16: 1199–1209.

10. Veves A, Giurini JM, LoGerfo FW. TheDiabetic Foot: Medical and Surgical Man-agement. Totowa, NJ: Humana Press, 2002.

Chapter IICLASSIFICATION, PREVENTIONAND TREATMENT OF FOOT ULCERS

� CLASSIFICATION SYSTEMS

� CLINICAL PRESENTATION OF NEUROPATHIC,ISCHEMIC AND NEURO-ISCHEMIC ULCERS

� PREVENTION OF FOOT ULCERS

� METHODS FOR OFFLOADING PRESSURE

ON THE FOOT

� DRESSINGS

� NEW TREATMENTS

� BIBLIOGRAPHY



Classification, Prevention and Treatment of Foot Ulcers 25

CLASSIFICATION SYSTEMS

• The Meggitt–Wagner classification is themost well-known and validated systemfor foot ulcers, and is shown in Table 2.1.The advantages and disadvantages ofthis classification system are described inTable 2.2.

• ‘The University of Texas classifica-tion system for diabetic foot wounds’,

Table 2.1 Meggitt–Wagner classification offoot ulcers

Grade Description of the ulcer

Grade 0 Pre- or post-ulcerative lesioncompletely epithelialized

Grade 1 Superficial, full thickness ulcerlimited to the dermis, notextending to the subcutis

Grade 2 Ulcer of the skin extendingthrough the subcutis withexposed tendon or bone andwithout osteomyelitis orabscess formation

Grade 3 Deep ulcers with osteomyelitisor abscess formation

Grade 4 Localized gangrene of the toesor the forefoot

Grade 5 Foot with extensive gangrene

Table 2.2 Advantages and disadvantages ofthe Meggitt–Wagner classification system

Advantages

• It is simple to use and has beenvalidated in a number of studies

• Higher grades are directly related toincreased risk for lower limb amputation

• It provides a guide for planningtreatment

• It is considered the gold-standard,against which other systems should bevalidated

Disadvantages

• Although the presence of infection andischemia are related to poor outcome,ischemia in patients classified intogrades 1–3 and infection in grade 1, 2and 4 patients is not taken into account

• The location of the ulcer is not described

• Patient-related factors (poor foot care,emotional upset, denial) and footdeformities are not evaluated

(Table 2.3) has recently been proposedand validated by the University of Texas.This system evaluates both depth of theulcer — as in Meggitt–Wagner classifi-cation system — and presence of infec-tion and ischemia. Uncomplicated ulcersare classified as stage A, infected ulcersas stage B, ulcers with ischemia as

Table 2.3 ‘The University of Texas classification system for diabetic foot wounds’

Grade

Stage 0 1 2 3

A Pre- orpost-ulcerativelesioncompletelyepithelialized

Superficial wound notinvolving tendon,capsule or bone

Woundpenetrating totendon orcapsule

Wound penetrating tobone or joint

B With infection With infection With infection With infection

C With ischemia With ischemia With ischemia With ischemia

D With infectionand ischemia

With infection andischemia

With infectionand ischemia

With infection andischemia


Table 2.4 Advantages and disadvantages of‘The University of Texas classification system’

Advantages

• It is simple to use and more descriptive

• It has been evaluated and shown topredict more accurately the outcome ofan ulcer (healing or amputation) than theMeggitt–Wagner classification.

• Cases with infection and/or ischemia aretaken into account in this system

• It provides a guide for planningtreatment

Disadvantages

• Patient-related factors (poor foot care,emotional upset, denial) and footdeformities are not evaluated

• The location of the ulcer is not described

stage C and ulcers with both infectionand ischemia as stage D. Grades 1 and2 are similar to the Meggitt–Wagnerclassification. Grade 3 ulcers are ulcerspenetrating the bone or joint. Thehigher the grade, and the stage of anulcer, the greater the risk for non-healing or amputation. The advantagesand disadvantages of ‘The Univer-sity of Texas classification system’ aredescribed in Table 2.4.In addition to these two classificationsystems, other systems have been pro-posed:

• Edmonds and Foster have proposed asimpler classification. According to thissystem, based on clinical tests and deter-mination of the ankle brachial pressureindex, foot ulcers are classified into neu-ropathic and neuro-ischemic.

• Brodsky suggested the ‘depth-ischemia’classification, which is a modificationof the Meggitt–Wagner classification.According to this proposal, ulcers areclassified into four subgroups (A, notischemic; B, ischemic without gangrene;C, partial gangrene of the foot; and

D, complete foot gangrene) with grades0–3 (similar to the Meggitt–Wagnerclassification).

• Macfarlane and Jeffcoate proposed theS(AD)SAD classification for diabeticfoot ulcers. According to this system,ulcers are classified on the basis ofsize (area and depth), presence ofsepsis, arteriopathy, and denervation.This system awaits clinical validation.

Any valid classification system of footulcers should facilitate appropriate treat-ment, simplify monitoring of healing prog-ress and serve as a communication codeacross specialties in standardized terms.Despite its disadvantages, the ‘Universityof Texas classification system’ offers manyadvantages over the Meggitt–Wagner sys-tem and is the most appropriate systemdevised to date. In addition, inclusion ina classification system of other parameterssuch as location of the ulcer, foot deformi-ties and other factors which may be relatedto the outcome of an ulcer, makes the sys-tem more complex and cumbersome. ‘TheUniversity of Texas classification system’ isexpected to be widely adopted in the future.

CLINICAL PRESENTATIONOF NEUROPATHIC,

ISCHEMIC ANDNEURO-ISCHEMIC ULCERS

• Neuropathy is present in about 85–90%of foot ulcers in patients with diabetes.

• Ischemia is a major factor in 38–52% ofcases of foot ulcers.

NEUROPATHIC ULCERS(FIGURES 2.1–2.3)

• Develop at areas of high plantar pres-sures (metatarsal heads, plantar aspect of


Figure 2.1 Typical neuropathic ulcer with cal-lus formation on the first metatarsal head beforedebridement

Figure 2.2 Neuropathic ulcer on the first meta-tarsal head with healthy granulating tissue onits bed

Figure 2.3 Neuropathic ulcer on the first meta-tarsal head with healthy granulating tissue on itsbed and callus formation

the great toe, heel or over bony promi-nences in a Charcot-type foot).

• Are painless, unless they are complicatedby infection.

• There is callus formation at the bordersof the ulcer.

• Its base is red, with a healthy granularappearance.

• On examination evidence of peripheralneuropathy (hypoesthesia or completeloss of sensation of light touch, pain,temperature, and vibration, absence ofAchilles tendon reflexes, abnormal vibra-tion perception threshold, often above25 V, loss of sensation in response to5.07 monofilaments, atrophy of the smallmuscles of the feet, dry skin and dis-tended dorsal foot veins) is present.However, the pattern of sensory loss mayvary considerably from patient to patient.


Figure 2.4 Ischemic ulcer underthe heel in a patient with severeperipheral vascular disease

• The foot has normal temperature or maybe warm.

• Peripheral pulses are present and theankle brachial pressure index is normalor above 1.3.

ISCHEMIC ULCERS(FIGURES 2.4–2.8)

• Develop on the borders or the dorsal as-pect of the feet and toes or between toes.

• They are usually painful.

Figure 2.5 Ischemic ulcer on the dorsum ofthe second toe in a patient with critical limbischemia. Case discussed in Chapter 7

Figure 2.6 Dry gangrene of the fifth right toe.Redness, and edema, which are typical signs ofinfection involving the forefoot, are present

• There is usually redness at the borders ofthe ulcer.

• Its base is yellowish or necrotic (black).• There is a history of intermittent claudi-

cation.• On examination indications of peripheral

vascular disease (skin is cool, pale orcyanosed, shiny and thin, with loss ofhair, and onychodystrophy; peripheralpulses are absent or weak; the anklebrachial index is <0.9) are present.

• Non-invasive vascular testing (dup-lex or triplex ultrasound examination,


Figure 2.7 Ischemic ulcer after sharpdebridement of the gangrene shown inFigure 2.6

Figure 2.8 Ischemic ulcer on the tip of thethird right toe, with necrotic center

segmental pressures measurement, ple-thysmography), and angiography confirmperipheral vascular disease.

• There are no findings of peripheral neu-ropathy.

MIXED ETIOLOGY ULCERS(NEURO-ISCHEMIC ULCERS)

(FIGURES 2.9 AND 2.10)

Neuro-ischemic ulcers have a mixed etiol-ogy, i.e. neuropathy and ischemia, and amixed appearance.

PREVENTION OF FOOTULCERS

Based on the results of clinical examina-tion, and/or laboratory testing and imagingstudies, every patient with diabetes maybe classified on the basis of the risk forfoot problems (Table 2.5). This classifica-tion helps as a guide for patient manage-ment. Patients with active foot ulcers arenot included in this classification.

Inappropriate footwear is a major causeof ulceration. The aim of providing spe-cial shoes and insoles (preventive footwear) to diabetic patients at risk for footulceration, is to reduce peak plantar pres-sure over areas ‘at risk’, and to protecttheir feet against injuries from friction.Although there is limited scientific informa-tion about shoe selection, recommendationscan be made in this regard, based on risk


Figure 2.9 Neuro-ischemic ulcer on heel. Thiswas a painless ulcer due to severe diabeticperipheral neuropathy. Another neuro-ischemiculcer is seen under the first metatarsal head.Claw toes and lateral plantar cracks on themidfoot are also evident

Table 2.5 Classification of categories of dia-betic patients based on the risk for ulceration

Risk category

0 Protective sensation is intact; the patientmay have foot deformity

1 Loss of protective sensation

2 Loss of protective sensation and highplantar pressure, or callosities, orhistory of foot ulcer

3 Loss of protective sensation and history ofulcer, and severe foot or toe deformityand/or limited joint mobility; significantperipheral vascular disease

(Modified from Chantelau E. Footwear for the high-risk patient. In Boulton AJM, Connor H, CavanaghPR (Eds), The Foot in Diabetes (3rd edn). Chichester:Wiley, 2000; 131–142, with permission).

stratification studies. Shoes for the patientat risk for ulceration should have certaincharacteristics. High heel shoes are com-pletely inappropriate, as they shift bodyweight towards the forefoot, and increasepressure under the metatarsal heads. Pa-tients with toe deformities need shoes withsufficient room in the toe box to prevent

Figure 2.10 Neuro-ischemic ulcer in the medial aspect of the right first metatarsal head withfibrous tissue and necrosis on its bed


friction and pressure on the dorsum ofthe toes.

A recent study from the UK estimatedthat providing preventive footwear for 700patients at risk for foot ulceration per year(with an average total cost of ¤179,000),would only need to prevent two below-knee amputations per year in order to becost-effective, since the total cost of anamputation procedure is about ¤88,000.

Foot deformity is defined according tothe ‘International Consensus on the Dia-betic Foot’ as ‘the presence of structuralabnormalities of the foot such as pres-ence of hammer toes, claw toes, halluxvalgus, prominent metatarsal heads, statusafter neuro-osteoarthropathy, amputationsor other foot surgery’. Additional foot defor-mities which can also lead to foot ulcerationare described in other chapters of this book.

RISK CATEGORY 0

Patients in this category are characterizedby preserved protective sensation and nor-mal blood supply to their feet. These pat-ients should have their feet examined onan annual basis, as asymptomatic nerve orvascular damage may develop. There is noneed for special footwear. Patients shouldbe instructed to choose shoes of proper styleand fit, which pose no risk to their feetshould they develop loss of sensation orinadequate blood supply to the feet. Ath-letic footwear is a good choice.

RISK CATEGORY 1

Correct foot care should be explained to allpatients classified in categories 1–3, andthese patients should be examined in theoutpatient diabetes clinic every 4 months.Loss of protective sensation should be‘replaced’ by increased awareness of situ-ations which threaten the foot. Patients in

category 1 are at twice the risk of devel-oping foot ulcers than those in category0. Particular care should be taken whenthese patients buy new shoes. Patients withloss of protective sensation tend to selectshoes which are too small because they aremore able to feel a tight shoe. Shoes shouldnot be too loose either. The inside of theshoe should be 1–2 cm longer than the footitself. The internal width should be equal tothe width of the foot at the metatarsopha-langeal joints. The fitting must be carriedout with the patient in the standing positionand preferably at the end of the day.

All patients with loss of protective sen-sation should have soft, shock-absorbingstock insoles in all shoes they wear. Suchinsoles are usually made of open cellurethane foam, microcellular rubber orpolyethylene foam (plastazote). Accordingto the design of the insole and the mate-rial used, peak plantar pressure reductionduring walking may range from 5 to 40%.As insoles may take up considerable spaceinside the shoe, care should be taken toallow sufficient room for the dorsum of thefoot (by the use of extra depth stock shoes)otherwise ulceration may develop in thisarea. Many materials used in footwear losetheir effectiveness in a relatively short time,depending on the patient’s degree of activ-ity. Therefore, regular replacement of theinsoles is necessary at least three times ayear. Shoes should also be changed at leastonce a year. Some specifically designedsocks (padded socks) may be also be used,since these reduce peak plantar pressuresduring walking by up to 30%.

EDUCATING PATIENTSIN APPROPRIATE FOOT CARE

Education of patients who are at riskof developing foot ulceration is the cor-nerstone of disease management. Patients


should fully understand the risks posed bythe loss of protective sensation or an inad-equate blood supply to their feet. Educa-tion of the patient at risk may reduce theincidence of foot ulcers and subsequentlyamputations.

The patient at risk for foot ulcerationshould:

• Inspect his or her feet every day, includ-ing areas between toes. Inspection ofthe sole may be accomplished usinga mirror.

• Let someone else inspect his or her feetin cases where the patient is unable todo it.

• Avoid walking barefoot any time, in- oroutdoors.

• Avoid wearing shoes without socks, evenfor short periods.

• Buy shoes of the correct size.• Avoid wearing new shoes for more than

1 h per day; feet should be inspectedafter taking off new shoes; in the case offoot irritation the patient should informthe healthcare provider.

• Change shoes at noon, and, if possible,again in the evening; this prevents highpressures remaining on the same area ofthe foot for a prolonged period.

• Inspect and palpate the inside of his orher shoes before wearing them.

• Wash his or her feet every day, takingcare to dry them, especially the webspaces.

• Avoid putting his or her feet onto heaters.• Test the water temperature before bathing

using his or her elbow; the temperatureof the water should be less than 37 ◦C.

• Avoid the use of chemical agents orplasters and razors for the removal ofcorns and calluses; they must be treatedby a health care provider.

• Cut the nails straight across.• Wear socks with seams inside out, or pre-

ferably without any seams at all.

• Use lubricating oils or creams for dryskin, but not between toes.

• Inspect his or her feet after prolongedwalking.

• Notify his or her healthcare providerat once, if a blister, cut, scratch, sore,redness or black area develops, or if anydischarge appears on socks.

RISK CATEGORY 2

Patients in this category do not usuallyneed custom-made shoes. The use ofappropriate insoles, which reduce peakplantar pressures under specific areas, isusually enough; these are inserted incommercially available extra-depth shoes.Insoles must be custom-molded and shock-absorbing. The idea is to redistribute plantarpressures by the use of such insoles, that is,to decrease the load from regions ‘at-risk’to ‘safe’ regions. In addition, insoles reduceshear stress since total contact minimizesthe horizontal and vertical foot movement.These insoles have two or three layersand are made of materials of differentdensity. A thin layer of the materialwith the lowest density (the most potentshock-absorbing material, usually cross-linked polyethylene foams) is placed at thefoot–insole interface; the firmest material(acrylic plastics, thermoplastic polymersor cork) is placed at the shoe–insoleinterface. A soft, shock-absorbing, durablematerial (closed cell neoprene, rubberor urethane polymer) is placed betweenthem (Figures 2.11 and 2.12). Appropriateinsoles for the patient at risk for ulcerationshould have a minimum thickness of6.25 mm. Patients at high risk requirethicker (12.5 mm) insoles.

RISK CATEGORY 3

These patients need the greatest help to re-main free of foot ulceration. Patients in this


Figure 2.11 Upper side of a three-layer cus-tom-made insole used to offload pressure onthe forefoot. The upper layer is composedof cross-linked polyethylene foam, the mid-dle layer of polyurethane, and the lower layerof cork

category are 12–36 times more likely todevelop foot ulcers than patients in cate-gory 0. Severe foot deformities and limitedmobility of the foot joints are associatedwith high plantar pressures.

Limited joint mobility is defined as a lim-itation in dorsiflexion of the first metatar-sophalangeal joint of more than 50◦ whenthe patient is seated (hallux rigidus).

Patients with severe peripheral vasculardisease are also included in this category.Inadequate circulation makes the thin skinvulnerable to ulceration.

In addition to custom-molded insoles,custom-made and extra depth-shoes are

often necessary. Patients with recurrent footulcerations, or an active lifestyle, often needmodifications of the outsole. In the rockerstyle shoe the rigid outsole rotates over aridge (fulcrum) as the patient walks; thisridge is located 1 cm behind the metatarsalheads (see Figure 5.2). The rocker outsoleallows the shoe to ‘rock’ forward duringpropulsion before the metatarsophalangealjoints are allowed to flex, thereby reducingthe pressure applied to the forefoot. In aroller style shoe the contour of the outsoleis a continuous curve without the ridge usedin the rocker style. During walking, as theperson lifts the heel, the shoe rolls forwardon the curved outsole. This prevents thepressure from remaining in one region.Rocker style shoes are more effective inreducing forefoot plantar pressure than theroller style shoes.

METHODS FOROFFLOADING PRESSURE

ON THE FOOT

The mainstay in the management of anactive plantar foot ulcer is the effectiveoffloading of the ulcer area. Once an ulcer is

Figure 2.12 Lower side of insole illustrated in Figure 2.11


present, it will not heal unless the mechani-cal load on it is removed. Among the meth-ods used for this purpose are complete bedrest, crutch-assisted gait, wheelchair, andprosthetics. However, these methods areimpractical for the majority of patients touse for a period of several weeks while theulcer heals. Common approaches for reduc-ing the load on the ulcerated area includethe use of a total-contact cast or othercommercially-available casts, and therapeu-tic footwear.

TOTAL-CONTACT CAST

A total-contact cast (Figure 2.13) is a plas-ter of Paris cast, which extends from kneeto toes. This is the method of choice for thetreatment of grades 1 and 2 (according tothe Meggitt–Wagner classification) diabeticfoot ulcers which are located on the forefoot

Figure 2.13 Total-contact cast

and midfoot; the cast reduces peak plantarpressures in these areas by almost 40–80%,but is less effective with ulcers located onthe hindfoot. In one study, the use of atotal-contact cast resulted in almost 90% ofplantar ulcers healing within an average of6–7 weeks. This method permits walkingwhile uniformly decreasing the pressure onthe sole of the foot.

The ulcerated area should be debridedand covered with a thin dry dressing. Atotal-contact cast is applied with the patientin the prone position and the foot and anklein a neutral position (i.e. with the footflexed at a 90◦-angle to the ankle). A layerof fiberglass tape is usually applied overthe plaster, to strengthen the cast and allowearly ambulation. A small rubber rockeris added for walking. A plywood board isinserted between the rubber rocker and thecast in order to minimize the possibility ofthe sole of the cast becoming cracked. Thecast should be changed every 3–7 days.The use of a total-contact cast is contraindi-cated when infection or gangrene (Meg-gitt–Wagner stages 3–5) is present. Skinatrophy and an ankle brachial index below0.4 are considered to be relative contraindi-cations to the use of a total-contact cast.Although a total-contact cast permits walk-ing, patients are instructed to minimize theiractivity in order to reduce the pressure ontheir soles. Instability and the risk of fallsare disadvantages of this cast. Both in- andoutdoor compliance is another advantage,especially for the non-compliant patient,since this cast is not easily removed.

OTHER COMMERCIALLY-AVAILABLE CASTS

Removable Cast Walkers

Prefabricated walkers function on a similarprinciple to the total-contact cast and


are removable, commercially available,lightweight casts (see Figure 9.11). Theyare not designed to provide total contact,and the addition of inflatable or adjustablepads reduces movement of the limb withinthe cast. A custom-molded removableinsole is adjusted to reduce plantar pressure.Use of removable cast walkers allowsinspection and dressing of the woundon a daily basis. They may be used inpatients with infected and ischemic ulcers.In addition, patients can bathe and sleepmore comfortably. The rocker shape ofthe outsole reduces further pressure onthe forefoot while standing and walking.In addition, these casts are ideal forclinics, which do not have personnel withexperience in plastering.

Scotch-Cast Boot

This is a lightweight, well-padded fiber-glass cast, extending from just below thetoes to the ankle, and it is worn with acast sandal (Figure 2.14). It may be fab-ricated as a removable or non-removablecast. With appropriate modifications of thepads, the scotch-cast boot reduces pressureon any region of the sole when needed.Removable scotch-cast boots can be used incases of both ischemic and infected ulcers,since drainage and wound dressings are eas-ily applied. As with the total-contact cast,experience in plastering is required.

PRESSURE RELIEF SHOES(THERAPEUTIC FOOTWEAR)

These are temporary shoes which allowsome level of ambulation, while at thesame time offloading pressure on the ulcer-ated area. These shoes are easy to use andare of low cost and since they enable thepatient to walk quite normally, they lead

Figure 2.14 Scotch-cast boot

to a better quality of life. A rigid rockersole is incorporated in order to reduce theweight-bearing load in the forefoot by upto 40% during walking. The appropriatechoice of insole may reduce plantar pres-sure by an additional 20%. Half shoes(see Figure 3.36) are indicated for ulcerslocated on the forefoot (almost 90% of dia-betic foot ulcers are located in this area).They offload pressure on the entire forefoot,while increasing pressure on the midfootand heel, permitting the patient to engagein limited walking activities. Instability isa problem, and the patient needs to usecrutches. With the use of half shoes themean time to ulcer healing was reportedto be 7–10 weeks in two studies. Patientsare instructed to walk on their heel andavoid forefoot contact with the ground atthe end of the stance phase. A sole lift


Figure 2.15 Shoe terms

on the opposite shoe may be necessary toequalize the limb length. These shoes areeasily removed for dressing changes.

Heel-free shoes (see Figure 5.18) reducepeak plantar pressure on the heel bytransferring pressures to the midfoot andforefoot. They have the same advantagesand disadvantages as half shoes. Bothhalf and heel-free shoes are commerciallyavailable.

Ulcers located on midfoot (mainly overbony prominences due to neuro-osteoarth-ropathy) are best treated with the use ofcustomized insoles with windows under theulcerated area.

Shoe terms are shown in Figure 2.15.

DRESSINGS

The characteristics required for optimalwound dressings have been described asfollows. They should

• be free from particulate or toxic conta-minants

• remove excess exudates and toxic com-ponents

• maintain a moist environment at thewound/dressing interface

• be impermeable to microorganisms, thusprotecting against secondary infection

• allow gaseous exchange• be easily removal without trauma• be transparent, or changed frequently,

thus allowing monitoring of the wound• be acceptable to the patient, conformable

and occupy a minimum of space inthe shoe

• be cost-effective• be available in hospitals and community

health care centers

There is a broad spectrum of wounddressing materials currently available. Theirparticular properties and indications aredescribed in Table 2.6 and the advantagesand disadvantages of the available types ofdressings are described in Table 2.7.

NEW TREATMENTS

HYPERBARIC OXYGEN

There have been no controlled trials com-paring the use of hyperbaric oxygen therapy


Table 2.6 Properties, and indications of available dressings

Typeof

dressingNecrosis/

sloughGangre-

nous InfectionLow

exudateHigh

exudate

Flatwound

with lowexudate

Flatwound

with highexudates

Cavitywithoutsinus

Cavitywithsinustract

Dry + + + +Enzymatic

debrider+

Films + +Foams + + + +Hydrogels + + +Hydrocolloids + + +Alginates + + Alginate Alginate Alginate

rope rope rope

Table 2.7 Advantages and disadvantages of available types of dressings

Type ofdressing Advantages Disadvantages

Traditionaldressings(gauze andabsorbentcellulose)

Cheap and widely available. Appropriatefor gangrenous lesions

Adhere to the wound bed and may causebleeding on removal. Provide littleprotection against bacterialcontamination

Films Semi-permeable. Form bacterial barrier.Durable. Require changing every 4–5days. Cheap

Useful on flat or superficial wounds only.Some patients are allergic to theadhesive in the dressing

Foams Appropriate for ulcers with highproduction of exudates. Providethermal insulation. Easily conformable.May be used to fill cavities withoutsinus tracts

Variability in absorbency of differentfoams. Limited published data

Hydrogels Effective, versatile and easy to apply.Very selective, with no damage tosurrounding skin. Safe process, usingthe body’s own defense mechanisms.Promote autolysis and healing.Decrease risk of infection. Useful inremoving slough from wounds. Maybe used to fill cavities with sinus tracts

Effect difficult to quantify. Not aseffective and rapid as surgicaldebridement. Not appropriate forneuro-ischemic ulcers, which produceminimal exudates. Wound must bemonitored closely for signs of infection

Hydrocolloids Safe and selective, using the body’s owndefense mechanisms. Good for necroticlesions, with light to moderateexudates. May be used to fill cavitieswithout sinus tracts. Can be easily usedwith a shoe. Adhesive surface preventsslippage. Do not require daily dressingchanges. Cost-effective

Their occlusive and opaque natureprevents daily observation of thewound. Wound must be monitoredclosely for signs of infection. Maypromote anaerobic growth and mask asecondary infection

(continued overleaf )


Table 2.7 (continued )

Type ofdressing Advantages Disadvantages

Alginates Useful as absorbents of exudates. Goodfor infected ulcers. Some productshave hemostatic properties

Not appropriate for neuro-ischemiculcers, which produce minimalexudates. Some researchers think theymay traumatize the wound bed andpredispose to infections. May dry outand form a plug within the wound bed.Requires painstaking removal with theuse of large amounts of saline

Enzymaticdebriders

Good for any wound with a large amountof necrotic debris, and for escharformation. Promote autolysis and fasthealing. Decrease maceration of theskin, and risk of infection

Costly. Must be applied carefully only tothe necrotic tissue. May require aspecific secondary dressing. Irritationand discomfort may occur

Medicateddressings

Data based on animal models and cellcultures only

in the treatment of neuropathic ulcers. Atthe present time it is only used to treatpatients with severe foot infections whichhave not responded to other treatments.Hyperbaric oxygen is particularly effectivein patients with foot ischemia.

FACTORS ACCELERATINGWOUND HEALING

Platelet-Derived Growth Factor-β

Platelet-derived growth factor-β (PDGF-β, becaplermin, Regranex, Janssen-Cilag)has been developed as a topical, effectiveand safe therapy for the treatment of dia-betic foot ulcers and has also been foundto be effective and safe as local therapyfor the treatment of non-infected diabeticfoot ulcers. It is applied as a gel on theulcer surface once daily by the patient,while the ulcer is debrided on a weeklybasis. A dose of 100 µg/g has been demon-strated to be the most effective. Comparedto standard treatment, more ulcers treatedwith becaplermin heal completely and in a

shorter time. The maximum time requiredto achieve has been reported as 20 weeks.

Dermagraf

Dermagraf (Smith & Nephew) is a bio-engineered ‘human dermis’ designed toreplace the patient’s own damaged dermis.It is applied to the ulcerated area on aweekly basis. Preliminary results show thatit is an effective and safe treatment. Accord-ing to a controlled trial, 50% of diabeticfoot ulcers healed within 8 weeks whentreated with Dermagraf, compared to 8%of ulcers treated with standard methods.Dermagraf should be stored at −70 ◦C andmust be thawed, rinsed and cut to the sizeof the ulcer prior to implantation. As withbecaplermin, the presence of infection is acontraindication to its use.

Graftskin

Graftskin (Apligraf, Novartis) consists ofan epidermal layer formed by human ker-atinocytes and a dermal layer, composed


of human fibroblasts derived from neonatalforeskin in a bovine collagen matrix. Stud-ies have shown that treatment with Apligrafresulted in a higher percentage of diabeticfoot ulcers healing completely and in ashorter time (56% of the ulcers healed in65 days), compared to placebo (39% of theulcers healed in 90 days). Apligraf has beenshown to be safe and, in addition, its usewas found to lead to a reduction in the inci-dence of osteomyelitis and amputations.

Granulocyte-Colony StimulatingFactor (GCSF)

Subcutaneous administration of GCSF oncedaily for 1 week in patients with infectedfoot ulcers resulted in a faster resolution ofthe infection, earlier eradication of bacte-rial pathogens isolated from wound swabs,shorter duration of i.v. antibiotic admin-istration and shorter duration of hospitalstay in a double-blind placebo-controlledstudy. Larger controlled studies are neededto evaluate the efficacy and safety of GCSFin the treatment of the infected foot ulcers.

Hyaff

Hyaff (Convatec, Bristol–Myers–Squ-ibb) is a semi-synthetic ester of hyaluronicacid. Serum or wound exudates, when incontact with Hyaff, form a moist environ-ment which promotes granulation and heal-ing. So far it has been used in the treat-ment of neuropathic ulcers with promisingresults.

Keywords: Classification of foot ulcers;Meggitt–Wagner classification of footulcers; ‘The University of Texas classifi-cation system for diabetic foot wounds’;neuro-ischemic ulcers, characteristics; isch-emic ulcers, characteristics; neuropathic

ulcers, characteristics; prevention of footulcers; risk category for foot ulcers; edu-cation in foot care; insoles; limited jointmobility; methods for offloading pressureon the foot; total-contact cast; manufac-tured casts; removable cast walkers; scotch-cast boot; therapeutic footwear; heel-freeshoes; half shoes; shoe terms; hyperbaricoxygen; platelet-derived growth factor-β;Dermagraf; Graftskin; Apligraf; granu-locyte-colony stimulating factor; Hyaff;dressings; dressings, advantages and dis-advantages

BIBLIOGRAPHY

1. Meggitt B. Surgical management of thediabetic foot. Br J Hosp Med 1976; 16:227–232.

2. Wagner FW. The dysvascular foot: a systemfor diagnosis and treatment. Foot Ankle1981; 2: 64.

3. Lavery LA, Armstrong DG, Harkless LB.Classification of diabetic foot wounds.J Foot Ankle Surg 1996; 35: 528–531.

4. Armstrong DG, Lavery LA, Harkless LB.Validation of a diabetic wound classificationsystem. Diabetes Care 1998; 21: 855–861.

5. Consensus development conference on dia-betic foot wound care. Diabetes Care 1999;22: 1354–1360.

6. Young MJ. Classification of ulcers and itsrelevance to management. In Boulton AJM,Connor H, Cavanagh PR (Eds), The Footin Diabetes (3rd edn). Chichester: Wiley,2000; 61–72.

7. Edmonds ME, Foster AVM. Classificationand management of neuropathic and neu-roischaemic ulcers. In Boulton AJM, Con-nor H, Cavanagh PR (Eds), The Foot inDiabetes (2nd edn). Chichester: Wiley,1994; 109–120.

8. Brodsky JW. The diabetic foot. In BowkerJH, Pfeifer MA (Eds), Levin and O’Neal’sThe Diabetic Foot (6th edn). St Louis:Mosby, 2001; 273–282.

9. Macfarlane RF, Jeffcoate WJ. Classificationof foot ulcers: The S(SAD)SAD system.Diabetic Foot 1999; 2: 123–131.


10. Shaw JE, Boulton JE. The pathogenesis ofdiabetic foot problems. Diabetes 1997;46(Suppl. 2): S58–S61.

11. Edmonts ME, Bates M, Doxford M,Gough A, Foster A. New treatments inulcer healing and wound infection. Dia-betes Metab Res Rev 2000; 16(Suppl. 1):S51–S54.

12. Dinh T, Pham H, Veves A. Emerging treat-ments in diabetic wound care. Wounds2002; 14: 2–10.

13. Veves A, Falanga V, Armstrong DG,Sabolinski ML. Graftskin, a human skin

equivalent, is effective in the managementof noninfected neuropathic diabetic footulcers. Diabetes Care 2001; 24: 290–295.

14. Jones V. Selecting a dressing for the dia-betic foot: factors to consider. Diabetic Foot1998; 1: 48–52.

15. Harding KG, Jones V, Price P. Topicaltreatment: which dressing to choose. Dia-betes Metab Res Rev 2000; 16(Suppl. 1):S47–S50.

Chapter IIIANATOMICAL RISK FACTORSFOR DIABETIC FOOT ULCERATION

� PES PLANUS

� PES PLANUS DEFORMITY — BUNIONETTE

� PES CAVUS

� BUNIONETTE (TAILOR’S BUNION)

� CLAW TOES

� CLAW AND CURLY TOE DEFORMITIES

� VARUS DEFORMITY OF TOES

� HELOMA DURUM, BUNION, BURSITIS, CLAW TOE

� HELOMA MOLLE

� HALLUX VALGUS WITH OVERRIDING TOE

� CONVEX TRIANGULAR FOOT (HALLUX VALGUS

AND QUINTUS VARGUS)

� HALLUX VALGUS, OVERRIDING TOE,CLAW TOES, EDEMA

� ONYCHOMYCOSIS: HALLUX VALGUS

AND HAMMER TOE DEFORMITY

� MALLET TOE

� PROMINENT METATARSAL HEADS

AND CLAW TOES




� POSTOPERATIVE HALLUX VALGUS AFTER SECOND

TOE REMOVAL

� FIRST RAY AMPUTATION

� CALLUS UNDER BONE PROMINENCE

� CALLUS OVER PROMINENT METATARSAL HEADS

� HEMORRHAGIC CALLUS

� ULCER UNDER A CALLUS AREA

� ULCER UNDER HALLUX

� HEEL CRACKS

� BILATERAL CHOPART DISARTICULATION

� NEUROPATHIC ULCER

� INGROWN NAILS (ONYCHOCRYPTOSIS)

Anatomical Risk Factors for Diabetic Foot Ulceration 43

PES PLANUS (FLAT FOOT)

A 73-year-old female patient with type 2diabetes diagnosed at the age of 55 yearsand treated with insulin since the age of65 years, attended the diabetic foot clinicbecause of a small superficial painful ulcerover her medial malleolus. The patientcomplained of dysesthesias (she had a coldor warm sensation in her feet), and she hadhypertension for which she had been treatedwith enalapril since the age of 55 years.The ulcer was noticed 4 weeks previouslyand had been caused by an external minortrauma.

On examination, bilateral pes planuswith minor hyperkeratosis over the firstmetatarsal head was found (Figure 3.1).The ankle brachial index, peripheral pulses,vibration perception threshold, and monofil-ament (5.07) sensation were all normal. Theulcer was debrided on a weekly basis, andit healed in 4 weeks.

Pes planus (or flat foot) is characterizedby diminished longitudinal and transverseconcavities of the foot. Diminished plan-tar transverse concavity is associated with

an increase in frontal transverse convex-ity of the tarsometatarsal joint line (Lis-franc joint line) and divergence of the fivemetatarsal bones. The load transfer is dis-placed to the medial border of the mid-tarsal region. However, there is evidencethat flat feet protect against loading of themetatarsal heads, although they are poorshock absorbers. Pes planus may causebunionette formation and plantar heel spurpain, but other foot problems are uncom-mon. Foot orthotics and arch supports donot alter the osseous relationships and areineffective in many patients. Surgical treat-ment is rarely indicated in adults.

Keywords: Pes planus; malleoli ulcer;infection

PES PLANUS DEFOR-MITY — BUNIONETTE

A 74-year-old male patient with type 2diabetes diagnosed at the age of 61 yearsattended the outpatient diabetic foot clinicfor chiropody treatment. On examination,he was found to have mild callus formation

Figure 3.1 Pes planus


at the plantar and the lateral area of thefifth metatarsal head (Figures 3.2 and 3.3).Bilateral pes planus (flat foot) deformityof his feet and a bony prominence at thelateral aspect of the fifth metatarsal head(a bunionette or tailor’s bunion) were alsofound (see Figure 3.2). Blackening of thenail of the hallux was due to a subungualhematoma. Pedal pulses were palpable andthe patient had severe peripheral neuropa-thy. The patient had the callus removed andwas instructed in appropriate foot care. Inaddition, he was advised to wear suitableshoes with a wide toe box.

Pes planus or flat foot is the commonestfoot deformity (prevalence is about 20%

in the adult population) and its prevalenceincreases with the age. The majority offlat feet are considered to be variationsof normal. People with this deformity areable to walk as comfortably as people withnormal arches (see also Figure 3.1).

Keywords: Pes planus; flat foot; bunionette

PES CAVUS

A 64-year-old female patient with type 2diabetes diagnosed at the age of 62 yearswas referred to the outpatient diabetic foot

Figure 3.2 Pes planus with bunionette. Plantar aspect

Figure 3.3 Pes planus with bunionette. Dorsal aspect


Figure 3.4 Pes cavus

clinic for foot care. She had been treatedwith insulin for the last 4 years. The patienthad a history of hypertension. No diabeticcomplications were mentioned.

On examination, peripheral pulses werebounding. She had severe peripheral neu-ropathy (no sensation of pain, light touch,temperature, vibration or 5.07 monofila-ments) and dry skin. A high plantar archdue to pes cavus was noted, which wasmore apparent in the standing position.Mild hallux valgus, clawing of the toes, andcallus formation over the inner aspect of thefirst metatarsal heads as well as at the tipof the second toe and the second metatarsalhead bilaterally were observed (Figure 3.4).The patient had the callus removed, and thenails cut and she was educated in foot care.Suitable shoes and insoles were prescribedand she was advised to attend the foot clinicon a monthly basis for chiropody treatment.

Pes cavus is a deformity not necessarilyrelated to diabetes. Indeed, the patientmentioned that her foot shape had beenthe same before the diagnosis of diabetesand her mother probably had the samedeformity.

Normally the inner edge of the mid-foot is raised off the floor forming an arch,which extends between the first metatarsaland the calcaneus. When the arch of thefoot is higher than normal (pes cavus)claw toes often develop. In cavus foot theforefoot, and especially the first ray, isdrawn downwards and an abnormal dis-tribution of plantar pressure upon stand-ing and walking leads to callus formationunder the metatarsal heads. Cavus feet tendto be stiffer than normal; some patientsmay be prone to ankle strains. Patientsshould be advised to wear appropriate shoes(extra depth and broad at the toe box) and


Figure 3.5 Bunionette with claw toes

orthotic, shock-absorbing insoles. Surgeryfor the correction of the abnormality israrely recommended.

Keywords: Pes cavus

BUNIONETTE (TAILOR’SBUNION)

A 54-year-old female diabetic patient atten-ded the outpatient diabetic foot clinic forregular chiropody treatment. She had severediabetic neuropathy with reduced sensationof light touch, vibration, pain, temperatureand 5.07 monofilaments. Peripheral pulseswere normal. Muscle atrophy of the feet,claw toes, mild hallux valgus, varus defor-mity of the lesser toes, and an exostosisof the lateral part of the fifth metatarsalhead (bunionette, Figure 3.5) were present.Another exostosis was noted at the tuberos-ity of the fifth metatarsal bone. Appropriate

shoes with a high and broad toe box wereprescribed, and the patient was educated incorrect foot care.

Bunionette, or tailor’s bunion, is oftenassociated with varus deformity of thelesser toes. Ulceration over a bunionettemay occur in a patient who has no feel-ing of pain, and an infection of the ulcermay spread to the bursa and the underly-ing bone.

Keywords: Bunionette

CLAW TOES

A 56-year-old male patient with type 2diabetes diagnosed at the age of 44 yearsattended the outpatient diabetes clinic. Hehad been treated with insulin since theage of 53 years, with excellent results(HBA1c: 6.7%). He had background dia-betic retinopathy.


Figure 3.6 Muscle atrophy with claw toes and hallux valgus

On examination, the patient had severediabetic neuropathy with complete loss ofsensation of pain, light touch and tempera-ture; his vibration perception threshold was40 V on both feet; Achilles tendon reflexeswere absent. Peripheral pulses were nor-mal and the ankle brachial index was 1.2bilaterally. Temperature of the feet was nor-mal; the skin was dry, with normal hair andnails, while mild vein distension was noted.Severe atrophy of the intrinsic foot muscles(lumbrical and interossei) — due to motorneuropathy — resulted in an imbalance ofthe foot muscles, and cocked-up toes (clawtoes) (Figure 3.6). Such an appearance isso typical, that the diagnosis of peripheralneuropathy can be made by inspection ofthe feet alone.

A claw toe, the most common defor-mity in diabetic patients, consists of dor-siflexion of the metatarsophalangeal joint,while the proximal interphalangeal and dis-tal interphalangeal joints are in plantar flex-ion (Figure 3.7). Shifting of the fat padsunderneath the metatarsal heads to the frontleaves the metatarsal heads exposed; highplantar pressures develop under metatarsalheads. This patient did not have problemswith his feet. He was educated in appropri-ate foot care and instructed to wear suitablefootwear with a toe box large enough toaccommodate the deformity.

Figure 3.7 Claw toe

Keywords: Muscle atrophy; peripheralneuropathy; claw toes

CLAW AND CURLY TOEDEFORMITIES

A 68-year-old female patient with type 2diabetes attended the outpatient diabetesclinic for her usual follow-up. On exami-nation, she had severe diabetic neuropathyand palpable peripheral pulses. Claw toedeformity of her left second and third toeswas noticed, as well as a curly fourth toe(Figure 3.8). Subungual hemorrhage andingrown hallux nail, and hemorrhagic cal-luses of the second and third toes were alsopresent. A hammer deformity was seen onthe second toe of her right foot. Protective


Figure 3.8 Curly fourth toe with inwardmalrotation. Claw toes

footwear was prescribed and the patient waseducated in foot care.

A curly toe consists of neutral position orplantar flexion of the metatarsophalangealjoint, and plantar flexion of the proximalinterphalangeal and distal interphalangealjoints, by more than 5◦ each (Figures 3.9and 3.10). Inward or outward rotation maybe present. Curly toes may be either fixedor flexible.

Keywords: Claw toe; curly toe; ham-mer toe

VARUS DEFORMITYOF TOES

In varus deformity of toes the third, fourthand fifth toes drift medially. The nails of

Figure 3.9 Curly fourth toe

Figure 3.10 Curly fourth toe. Note inwardmalrotation

the toes may cause superficial ulcers on theadjacent toes. This patient was a 60-year-old female with type 2 diabetes diagnosedat the age of 51 years. She had severediabetic neuropathy; peripheral pulses werenormal, and she had never had a foot ulcer.In addition to varus deformity, clawing ofher toes was present (Figure 3.11). Varusdeformity often co-exists with bunionette.

Keywords: Varus deformity of toes

HELOMA DURUM, BUNION,BURSITIS, CLAW TOE

A 67-year-old male patient with type 2 dia-betes attended the outpatient diabetic foot


Figure 3.11 Varus and claw toes deformity

clinic because he had developed painlesshyperkeratosis on the dorsum of his toes.

He had severe peripheral sensorimotorneuropathy; peripheral pulses were normal.Significant muscle atrophy was seen onthe dorsum of his feet (Figure 3.12). Mildhallux valgus and claw toes deformity werealso present. As a result of a bunion (seebelow) due to hallux valgus deformity, ared and swollen bursa developed at themedial aspect of both first metatarsal heads,caused by pressure and friction exerted onthese areas by his shoes. Painless cornswere also present on the dorsum of the toes.Such corns — called heloma durum or hardcorns — are a result of pressure and frictionon the deformed toes caused by wearinglow toe box shoes. Suitable shoes (with abroad and high toe box) were prescribed inorder to accommodate the deformity. Thepatient did well; heloma durum and bursitisdid not relapse.

A bunion is a bony prominence thatdevelops on the inner side of the foot, nearthe base of the first toe. An infected ulcer

Figure 3.12 Heloma durum, bunion, bursitisand claw toe

over a bunion or a heloma durum maylead to infection spreading into a joint orthe bone.

Keywords: Heloma durum; bunion; bursi-tis; claw toe

HELOMA MOLLE

A 54-year-old male patient with type 2diabetes diagnosed at the age of 48 yearsattended the outpatient diabetic foot clinicfor callus removal. He had severe dia-betic neuropathy (loss of sensation of pain,light touch, temperature, vibration and 5.07monofilaments), and he complained of mildpain on his left little toe.

On examination, a painful corn was seenat the medial aspect of his left little toe(Figure 3.13).

Corns are circular hyperkeratotic areaswhich may be soft or hard. They have a pol-ished or translucent center and may becomepainful due to persistent pressure and fric-tion. Soft corns develop in the interdigital


Figure 3.13 Heloma molle

spaces; these are known as heloma molle,and they are caused by pressure and fric-tion from the adjacent toe bones. This typeof corn often has a soft consistency (incontrast to a heloma durum) due to mois-ture retention in the interdigital space. Thecommonest location of a heloma molle isthe lateral side of the fourth toe, caused bypressure and friction on the adjacent headof the proximal phalanx of the fifth toe, butit may also occur in the other interdigitalspaces. Osteoarthritic changes of the distalinterphalangeal joints often cause helomamolle. Kissing heloma molles result whenthe ends of the phalanges are too wide.Tight shoes aggravate the problem. Thiscondition is especially common in women

who wear high-heel shoes, which shift thebody’s weight to the front of the foot,squeezing the toes into a narrow, taperingtoe box.

Heloma molle, like heloma durum maycause discomfort, and it may be compli-cated by infection. The patient is advised towear wide shoes or shoes with a high toebox. Surgical removal of small portions ofthe bones or the exostoses that are involvedin the pathogenesis of the heloma molle isthe permanent treatment.

Keywords: Corns; heloma molle; helomadurum

HALLUX VALGUS WITHOVERRIDING TOE

A 69-year-old female patient with type 2diabetes diagnosed at the age of 55 yearsand treated with antidiabetic tablets wasreferred to the outpatient diabetic foot clinicbecause of a recurrent ulcer over her firstleft metatarsal head. The patient had nomacroangiopathic complications; peripheralneuropathy was found on examination.

Hallux valgus with fixed varus deformityand clawing of second toe in supraductuswas noticed, together with callus formation

Figure 3.14 Hallux valgus with overriding toe


under her first metatarsal head and ulcera-tion of its medial aspect (Figure 3.14).

Hallux valgus and the associated varusposture of the first metatarsal bone causevarious deformities of the other toes, suchas varus, clawing and valgus formation. Thelong and short extensor tendons of all thetoes shrink like bowstrings, causing sublux-ation of the phalangeal bases. Contracturesof tendons and joint capsules result in fixa-tion of the deformity. Due to the deformityof the third and fourth toes the heads of thethree central metatarsal bones become low-ered, resulting in their exposure and callusformation. In more severe cases of halluxvalgus, the line of load is displaced progres-sively towards the medial side of the foot,and the longitudinal arch becomes lower,leading to pes planovalgus.

Keywords: Overriding toe; hallux valgus

CONVEX TRIANGULARFOOT (HALLUX VALGUS

AND QUINTUS VARUS)

A 48-year-old female diabetic patient withtype 2 diabetes diagnosed 6 months before

her first visit, and treated with sulfonylurea,was referred to the outpatient diabetic footclinic because of an ulcer on her right foot.

The diabetes had been adequately con-trolled but the patient was already exhibit-ing signs of diabetic complications, suchas background retinopathy and neuropathy.On examination, she had a right convextriangular foot, with an ulcer under thehead of the fifth metatarsal head followingcallus formation at this site (Figure 3.15).She had symptomatic diabetic neuropathy,exemplified by a burning sensation in thefeet, which was especially exacerbated atnight; peripheral pulses were palpable andthe ankle brachial index was 1.0 bilaterally.Small muscle atrophy of the feet was noted,as well as dry skin and loss of feeling ofa 5.07 monofilament; vibration perceptionthreshold was 30 V.

A plain X-ray showed a convex triangu-lar foot deformity (Figure 3.16). This defor-mity is characterized by convergence offirst and fifth toes, and claw deformitiesof the central three toes. The first and fifthmetatarsals are short and diverge. Both lon-gitudinal and transverse plantar concavitiesare accentuated, and the second and thirdmetatarsals are fixed in excessive equinus

Figure 3.15 Neuropathic ulcer under fifth metatarsal head


Figure 3.16 Plain radiograph of a con-vex triangular foot

from this level. Cavus feet balance on theheel and the central part of the metatarsalpaddle. This deformity may cause highpressures over the metatarsal paddle dur-ing walking.

Debridement was performed and appro-priate footwear and insoles were prescribed(Figure 3.17). A suitable insole relievedpressure strain from the sole of the patient’sfoot by redistributing pressures. High plan-tar pressures can be seen on the graph pro-duced by insole pressure sensors (Parotecsystem, Germany) (Figure 3.18), when thepatient used her own shoes (Panel A), andafter the prescribed insole and shoe wereused (Panel B); pressures applied to the soleof the patient’s foot during heel strike, mid-support and push-off phase of walking with

the patient’s original shoe (left graph), andwith the custom-made insole (right graph)are shown in Panel C.

After 6 weeks the ulcer heeled com-pletely (Figure 3.19).

Keywords: Convex triangular foot; halluxvalgus; quintus varus

HALLUX VALGUS,OVERRIDING TOE, CLAW

TOES, EDEMA

A 68-year-old female patient with type 2diabetes diagnosed at the age of 45 yearsattended the outpatient diabetic foot clinic


Figure 3.17 Extra-depth shoes and cus-tom insoles

for routine chiropody treatment. She wasbeing treated with insulin. The patienthad hypertension, advanced backgroundretinopathy which had been treated withlaser in both eyes, and diabetic nephropa-thy (urine protein: 2.6 g/24 h). On exami-nation, she had severe diabetic neuropathyand gross ankle edema due to nephropathy.Peripheral pulses were normal and the anklebrachial index was 1.1 on both feet. Mildhallux valgus, claw toes, overriding of thesecond to the third toe and lateral drip of thetoes were observed (Figures 3.20 and 3.21).Callus formation at the inner aspect of thefirst and on the second metatarsal headswas noted. Fat pads on the first, second andthird metatarsal heads were displaced dis-tally to the base of the proximal phalangesdue to clawing of the toes. A superficialpainful infected ulcer at the dorsum of thesecond toe was also present, due to over-riding and clawing of the toes. Debridementof the callus was carried out. The patientwas put on clindamycin for 2 weeks. Treat-ment with frusemide 40 mg daily was alsocommenced to reduce edema. Extra depth

shoes and orthotic insoles were prescribedin order to reduce the pressure on the plan-tar area and the friction from the shoes onthe deformed toes.

The correct shoes and orthotic insolesare often enough to reduce the risk for footulceration in the majority of the patientswith foot deformities and loss of pro-tective sensation. In addition, edema hasa detrimental effect on the foot at risk,as it reduces local blood supply and hasbeen associated with increased risk forulceration. Therefore, reduction of ankleedema is recommended for patients at riskfor ulceration.

Beyond diabetic nephropathy, other cau-ses of ankle edema in diabetes include heartfailure and diabetic neuropathy. Edema dueto neuropathy is not rare. This form ofedema results from sympathetic denerva-tion, which leads to loss of the vasomotorreflex upon standing, arteriovenous shunt-ing and increased capillary pressure. Neu-ropathic edema responds to the admin-istration of the sympathomimetic agentephedrine.


Figure 3.18 In-shoe plantar pressure measure-ments (A) when the patient used her own shoes;and (B) after wearing the prescribed insole andshoe. (C) Pressures on the sole of the patient’sfoot during walking in her own shoes (graph onleft), and when wearing the custom-made insole(graph on right)

Keywords: Hallux valgus; toe overriding;claw toes; edema

ONYCHOMYCOSIS;HALLUX VALGUS AND

HAMMER TOE DEFORMITY

A 68-year-old female patient with dia-betes diagnosed at the age of 50 years and

Figure 3.19 The neuropathic ulcer shown inFigure 3.15 after it had healed following6 weeks of treatment

treated with insulin, was referred to theoutpatient diabetic foot clinic because offoot deformities and recurrent superficialtoe ulcers.

The patient had findings of periph-eral neuropathy. Peripheral pulses werepalpable. No other diabetic complicationswere present.

Onychomycosis was noticed and con-firmed by direct microscopic examinationof nail specimens. The skin on her feet wasdry; hallux valgus and hammer toe defor-mity of her second left toe were observed.Tiny superficial ulcers on the dorsum of hersecond and third toes due to shear pres-sure were present, as well as a small ulceron the inner aspect of her great toe, and


Figure 3.20 Hallux valgus, over-riding toe, claw toes and edema

a hemorrhagic callus on the tip of the leftgreat toe (Figures 3.22 and 3.23).

Mild hallux valgus and hammer toedeformity on the right second and third toeswas apparent, with a superficial ulcer onthe dorsum of the second toe (Figure 3.24).Hammer toe is a complex deformity con-sisting of contraction (hyperflexion) of theproximal interphalangeal joint, while themetatarsophalangeal joint is either dorsi-flexed or in the neutral position. The distalinterphalangeal joint may be in the neu-tral position, hyperextended or in plantarflexion (Figure 3.25). Hammer toe may beflexible or rigid.

Overriding toe deformity often occursin the second and the fifth toes. Thecause of the overriding fifth toe is mainly

congenital, while a second overriding toe isacquired and multifactorial. Elongation andlaxity of the plantar synovium bursa of themetatarsal joint result in dorsal subluxationof the affected joint. The second toe lacksplantar interossei muscles, therefore lum-brical muscles predominate, causing dor-siflexion of the toe. Subluxation of themetatarsophalangeal joint results in shrink-age of the dorsal synovium bursa and thedorsal interossei muscles. Further atrophyof the intrinsic muscles contributes to thedevelopment of the deformity which maybe fixed or flexible.

Debridement of the calluses and instruc-tion in foot care was provided to thispatient, and shoes with a high toe box andshock absorbing insoles were prescribed.


Figure 3.21 Hallux valgus, overriding toe, claw toes and edema. Plantar aspect of the footillustrated in Figure 3.20

Keywords: Onychomycosis; hallux valgus;hammer toe deformity

MALLET TOE

A mallet toe consists of plantar flexion ofthe distal interphalangeal, and neutral posi-tion of metatarsophalangeal and proximalinterphalangeal joints (Figure 3.26).

Toe deformities (hammer, claw, curly,mallet toe and overriding of toes) areunknown in non-shoe wearing populations.Their incidence varies from 2 to 20%, andincreases with age. Women are affectedfour to five times more often than men.

Most people have no underlying disease,although neuromuscular diseases and in-flammatory arthropathies may be accompa-nied by such toe deformities.

Toe deformities are more common inpeople with diabetes, due to muscle atrophyand limited joint mobility. Deformities suchas those described above, when presentin a patient with loss of sensation dueto diabetic neuropathy, pose a risk forthe development of neuropathic ulcers, asprominences are susceptible to skin-on-shoe friction. Patients are instructed tocheck their feet every day. Shoes with ahigh toe box protect the deformed toes fromulceration.


Figure 3.22 Hallux valgus, toe overriding andonychomycosis

Figure 3.24 Mild hallux valgus and hammertoe deformity on the right second and third toes,with a superficial ulcer on the dorsum of thesecond toe. Right foot of the patient whose feetare shown in Figures 3.22 and 3.23

Figure 3.23 Hammer toe deformity of the second, third and fourth toes, hemorrhagic callus andonychomycosis. Anterolateral view of the foot shown in Figure 3.22


Figure 3.25 Hammer toe

Figure 3.26 Mallet toe

Keywords: Mallet toe; toe deformities

PROMINENT METATARSALHEADS AND CLAW TOES

A 65-year-old male patient with longstand-ing type 2 diabetes attended the outpatient

diabetic foot clinic for callus removal andtreatment of ulcers on the tip of his secondand fifth right toes (Figure 3.27).

On examination, he had bounding pedalpulses, and severe peripheral neuropathy.Metatarsal heads were prominent, and clawtoes were present.

Claw toe deformities may cause promi-nence of metatarsal heads with subsequent


Figure 3.27 Prominent metatarsal heads and claw toes

callus formation and ulceration. Ulcers maydevelop at the tips of the claw toes, sincethey are abnormally exposed to pressureduring walking.

Protective footwear (high toe box andorthotic insoles) was provided to thispatient.

Keywords: Claw toes; prominent metatar-sal heads

POSTOPERATIVE HALLUXVALGUS AFTER SECOND

TOE REMOVAL

A 55-year-old female patient with type 2diabetes diagnosed at the age of 40 years,treated with insulin, and erratic glycemiccontrol, visited the diabetic foot clinicbecause of recurrent callus formation. She

had background retinopathy, hypertension,and severe peripheral neuropathy, and ahistory of amputation of her left secondtoe 3 years previously due to osteomyelitisafter a perforated ulcer.

After removal of her second toe, herleft great toe gradually dislocated to a val-gus posture, underriding the adjacent (third)toe (Figure 3.28). Gross callus formationdeveloped at the medioplantar aspect of thefirst metatarsal head, which caused con-stant discomfort during walking and danc-ing (Figure 3.29). Callus was also noticedover the third metatarsal head.

At the outpatient clinic the callositywas removed and a full thickness ulcerrevealed. More callus built up quickly asa result of the very active lifestyle of thepatient and her refusal to wear appropriatefootwear, she therefore had to attend theclinic every week.

A plain X-ray showed disarticulationof the left second toe, dislocation of the


Figure 3.28 Hallux valgus and toe overriding after second toe disarticulation

Figure 3.29 Gross callus formation on the first and third metatarsal heads after second toedisarticulation


metatarsophalangeal joint of the great toe,medial pronation of the first metatarsalhead, and hallux valgus deformity withrotation, together with dislocation of thesesamoids, and arthritis; necrosis of thehead of the third metatarsal bone was alsoevident (Figure 3.30).

She was referred to the orthopedicdepartment where her second metatarsalwas removed. The hallux valgus deformitywas corrected by arthrodesis of the metatar-sophalangeal joint.

After the operation there was no signif-icant callus development within the next3 months (Figure 3.31).

Keywords: Hallux valgus; prophylacticsurgery; second ray amputation

FIRST RAY AMPUTATION

A 72-year-old male patient with type 2 dia-betes diagnosed at the age of 56 years and

Figure 3.30 X-ray image of the foot illustrated in Figures 3.28 and 3.29. Disarticulation of theleft second toe, dislocation of the metatarsophalangeal joint of the great toe, medial pronation ofthe first metatarsal head, and hallux valgus deformity with rotation, together with dislocation at thesesamoids and arthritis; necrosis of the head of the third metatarsal bone is also evident


Figure 3.31 Photograph of the footshown in Figures 3.28–3.30 3 monthsafter arthrodesis of the first metatar-sophalangeal joint and second ray am-putation. Note the absence of signifi-cant callus formation

treated with sulfonylurea and metformin,attended the outpatient diabetic foot clinicbecause of a deep, infected neuropathiculcer under the first metatarsal head. Hisdiabetes control was acceptable (HBA1c:7.6%). He had a history of hypertension anddyslipidemia and was being treated witha combination of angiotensin convertingenzyme inhibitor with diuretic and simva-statin. He had neuropathic pain in his feet.He described the pain as a burning sensa-tion which worsened at night. On examina-tion, an ulcer 3 × 3 cm in size and 1.5 cmin depth surrounded by callus formationwas seen on the left first metatarsal head.Its base was sloughy. Second left clawtoe deformity was also observed. Pedalpulses were palpable, the ankle brachialindex was 1.0; the patient had findingsof severe peripheral neuropathy (loss ofsensation of light touch, pain, tempera-ture, vibration, and 5.07 monofilaments; the

vibration perception threshold was 35 V onboth feet).

A plain radiograph revealed osteomyeli-tis of the first metatarsal head extend-ing to the base of the proximal pha-lanx of the great toe. Cultures of thebase of the ulcer revealed the presenceof Staphylococcus aureus and Escherichiacoli. Based on the results of the swab cul-ture he was given amoxicillin and clavu-lanic acid for 2 weeks. After this timea first ray amputation under local anes-thesia was carried out. A culture of thebone was negative for pathogens but patho-logic examination of the resected boneshowed findings of chronic osteomyelitis(granulated fibrous tissue with a predom-inance of plasma cells and lymphocytesand involucrum formation at the perios-teum). The postoperative period was freefrom complications and the wound healedwell in 2 weeks (Figure 3.32). Antibiotics


Figure 3.32 First ray amputation due to osteomyelitis

were discontinued 7 days after the opera-tion and he was put on imipramine for theneuropathic pain.

Removal of the great toe results in dys-function of the foot during both stanceand propulsion. This disability is relatedto the length of the removed metatarsalshaft. Most surgeons preserve the longestmetatarsal shaft possible. The base of theproximal phalanx should be preserved,in order to keep the attachment of theshort flexor of hallux intact, thus keep-ing sesamoids in place and maintainingthe windlass mechanism. This mechanismprotects the first metatarsal head fromoverloading during the propulsion phaseof gait. In the case of an obligatoryremoval of hallux — due to osteomyelitis ofthe proximal phalanx — the surgeon shouldpreserve all uninvolved portions of the

metatarsal, except the avascular sesamoidsand their fibrocartilaginous plate. A hal-lux disarticulation at the metatarsopha-langeal joint exposes the head of the thirdmetatarsal to abnormally high pressure dur-ing stance, and may displace the second toemedially.

Keywords: First ray amputation; histology;chronic osteomyelitis

CALLUS UNDER BONEPROMINENCE

A 72-year-old male patient with type 2 dia-betes attended the outpatient diabetes clinicfor his usual follow-up. His diabetes controlwas fair with glibenclamide. He was free


Figure 3.33 Callus over prominence of metatarsal head

from retinopathy or nephropathy, but hehad severe diabetic neuropathy. On exami-nation a callus was present under the headof his right third metatarsal, which causedminor discomfort (Figure 3.33). Anotherbony prominence was evident on the outeraspect of his fifth metatarsal, without cal-lus formation. Claw toes, onychomycosisand dry skin were also present. The calluswas removed, and a tiny superficial ulcerrevealed. The patient was prescribed extradepth shoes with orthotic insoles (preven-tive footwear). Hydrating cream was usedto prevent skin cracking.

Keywords: Callus; claw toes; dry skin

CALLUS OVER PROMINENTMETATARSAL HEADS

A 70-year-old female patient who had type2 diabetes since the age of 50 years andwas being treated with insulin, attendedthe foot clinic for chiropody treatment. Shehad a history of ischemic heart disease(myocardial infarction and stroke), periph-eral vascular disease treated with low dose


of aspirin; and proliferative retinopathy.She complained of numbness in both feetand a deep aching pain in her calves andpainful heel cracks.

On examination, peripheral pulses wereabsent and her ankle brachial index was 0.8on the left and 0.7 on the right. The vibra-tion perception threshold was 30 V in bothfeet. Achilles tendon reflexes were absent,and pain, temperature, light touch andvibration sensation were severely dimin-ished. Pes cavus and hallux valgus werepresent on both feet (most prominent onthe left), together with an obvious promi-nence of her metatarsal heads and callusformation. The fat pads of her metatarsalheads were translocated towards the toes.The skin on her feet was dry (Figure 3.34).The calluses were debrided on a regularbasis, and appropriate footwear was pre-scribed. Heel cracks (see Figure 4.6) per-sisted despite debridement.

Calluses develop in areas of high pres-sure in the feet as a physiological reactionof the skin in response to loading. A callusadds further pressure to the underlying tis-sues functioning as a foreign body under thefoot. Prospective studies have shown thatregular removal of calluses reduces the riskof foot ulceration.

Keywords: Prominent metatarsal heads;callus

HEMORRHAGIC CALLUS

A 64-year-old male patient with type 2diabetes diagnosed at the age of 47 yearsattended the outpatient diabetic foot clinicbecause of an ulcer under his right foot.

On examination, a painless ulcer sur-rounded by a hemorrhagic callus wasseen under the third metatarsal head(Figure 3.35). Claw toe deformity, a curly

Figure 3.35 A neuropathic ulcer under a hem-orrhagic callus

Figure 3.34 Callus over prominenceon metatarsal heads. Pes cavus and hal-lux valgus


fourth toe, and a heloma molle in the fourthinterdigital space were also observed. Thepatient had bounding peripheral pulses andsevere peripheral neuropathy. After sharpdebridement of his callus, an ulcer ofdimensions 2.0 × 1.5 cm and depth 1 cmwas revealed. Plantar fascia was exposed.A plain radiograph excluded osteomyelitis.The patient was instructed in foot care.Offloading of the ulcer area was achievedby the use of an ‘almost half’ shoe(Figure 3.36) and a total-contact orthoticinsole, with a window under the ulcer area.These shoes cause instability, so the patientwas instructed to use a crutch. The ulcerhealed completely in 8 weeks.

The cause of the ulcer in this patient washigh plantar pressure under his prominentmetatarsal heads (Figure 3.37). After theulcer had healed, protective footwear (extradepth shoes and custom-made insoles) wasprescribed in order to reduce the peakpressure on the third metatarsal head. Norelapse of the ulcer occurred in the subse-quent months.

Keywords: Hemorrhagic callus; half shoes;protective footwear

Figure 3.36 Therapeutic half shoe for thetreatment of forefoot ulcers

ULCER UNDER A CALLUSAREA

A 70-year-old male patient with longstand-ing type 2 diabetes attended the outpa-tient diabetic foot clinic for callus removalon his right foot. On examination, a neu-ropathic ulcer surrounded by callus wasnoticed under his fourth metatarsal head(Figure 3.38). He had normal peripheralpulses and severe peripheral neuropathy.Claw toes, varus deformity of the foot andprominent metatarsal heads on his right foot

Figure 3.37 Peak plantar pressures recorded with a pedobarograph


were observed. Discoloration of the skinon the lower tibia due to venous insuffi-ciency was also evident. The callus wasdebrided. Shoes and insoles similar to thoseshown in Figure 3.36 were prescribed untilthe ulcer healed. The cause of the ulcer inthis patient was the callus resulting fromhigh plantar pressures. High peak pressuresare present in almost all cases where thereare prominent metatarsal heads due to clawtoe deformity. Prevention of callus forma-tion is necessary to avoid recurrence of theulcer. Protective footwear was prescribedafter the ulcer had healed.

Keywords: High plantar pressure; cal-lus, prominent metatarsal heads; varus de-formity

Figure 3.38 A neuropathic ulcer under a callus

ULCER UNDER HALLUX

A 70-year-old male patient with longstand-ing type 2 diabetes treated with insulinand sulfonylurea, attended the outpatientdiabetic foot clinic because of a hemor-rhagic callus under the phalangophalangealjoint of the right hallux (Figure 3.39).He had ischemic heart disease, hyperten-sion, peripheral vascular disease, back-ground retinopathy and microalbuminuria.The patient had severe diabetic neuropa-thy; the ankle brachial index was 0.7. Afterhis callus was debrided a clean neuro-ischemic ulcer was revealed. A plain radio-graph excluded osteomyelitis. Therapeu-tic footwear was prescribed and the ulcerhealed in 6 weeks.

The forefoot is the usual site for ulcer-ation. In one series, ulcers of the fore-foot accounted for 93% of all foot ulcers.Almost 20% of the ulcers developed underthe hallux, 22% over the metatarsal heads,26% on the tips of the toes and 16% on thedorsum of the toes. Ulcer under the hal-lux is associated with rigid hallux and highpeak pressures on this area.

Keywords: Hemorrhagic callus; prevalenceof foot ulceration

HEEL CRACKS

Painful heel cracks due to dry skin werenoted in the patient whose feet are shownin Figure 3.34 (Figure 3.40).

Dry skin in diabetic patients is causedby sympathetic cholinergic denervation ofthe sweat glands in their feet. Patients withdry foot skin often develop reactive hyper-hydrosis of the upper body. Heel cracks


Figure 3.39 Hemorrhagic callus under the hallux

Figure 3.40 Heel cracks

may become infected and may lead to deepulcers with calcaneous involvement if leftuntreated. The crack resists healing, despitethe correct foot care. Heel cracks are aggra-vated by microvascular disease and neu-ropathy, and resist healing, despite adequatefoot care. Local application of hydratingcreams — avoiding the areas between thetoes — is the treatment which is usuallyrecommended.

Keywords: Dry skin; heel cracks

BILATERAL CHOPARTDISARTICULATION

A 73-year-old male patient with type 2diabetes diagnosed at the age of 61 yearsattended the outpatient diabetes foot clinicfor a chronic ulcer under his left par-tially amputated foot. He had had bilateralmid-tarsal (Chopart) disarticulations (on theright foot at the age of 66 years and onthe left foot at the age of 68 years) because


of infected foot ulcers under the metatarsalheads complicated by osteomyelitis.

On examination, his feet pulses werepalpable, but the patient had severe periph-eral neuropathy. A full thickness neuro-pathic ulcer, which developed 2 monthsafter the amputation, was evident on theplantar area of the left foot (Figure 3.41).The patient had never used any ankle pros-thesis or orthosis, but instead used crutchesand shoes with a firm outsole and a softmolded insert. The ulcer healed for a periodof only 2 months, when the patient washospitalized because of a hip fracture.

Chopart disarticulation is performedthrough the talonavicular and calcaneocu-boid joints, preserving the hindfoot only(talus and calcaneus). As no muscles attachto the talus, all active dorsiflexion of theremaining short foot is lost. However,dorsiflexion can be restored, by reattachingthe anterior tibial tendon to the neck of thetalus. Chopart disarticulation preserves thenormal length of the leg and the patientcan undertake limited walking without aprosthesis. Reasonable walking is possibleby the use of an intimately fitting fixed-ankle prosthesis or orthosis placed into ashoe with a rigid rocker bottom.

In the present case, walking withoutcrutches was not possible even if an appro-priate prosthesis was used because of thebilateral Chopart disarticulation. However,the use of a prosthesis and offloading thepressure on the ulcerated area with suitableinsoles helped to heal the ulcer. In addition,the patient’s severe instability, which wasthe cause of the hip fracture, was reduced.

Any type of amputation alters the biome-chanics of the foot and is considered tobe a risk factor both for a recurrence offoot ulceration and for a new amputation.Several studies have shown that previousamputations account for 30–50% of newamputations on the same or the contralat-eral foot within the following 5 years.

Keywords: Neuropathic ulcer; mid-tarsaldisarticulation; Chopart disarticulation

NEUROPATHIC ULCER

An ostensibly small neuropathic ulcersurrounded by callus formation waspresent under the fourth metatarsal head

Figure 3.41 Full thickness neuropathic ulcer in a patient with Chopart disarticulation


Figure 3.42 A neuropathic ulcer under callus formation in a patient with fourth toe disarticulation

(Figure 3.42) of a patient with severediabetic neuropathy. A history of fourth toedisarticulation at the metatarsophalangealjoint was reported to have occurred 2 yearspreviously because of osteomyelitis in theproximal phalanx. Claw second and thirdtoe, quintus varus (due to fourth toedisarticulation), dry skin and heel crackswere also present. The real size of the ulcerwas 1.5 × 1.5 × 1.0 cm post-debridement.The little toe diverged medially and the

third toe laterally. Therapeutic footwearwas prescribed and the ulcer healed in2 months.

A fourth ray amputation may lead tobetter functional and cosmetic results. Soleincisions pose a risk for ulceration; there-fore incisions are carried out on the dorsumor the side of the foot. Scar tissue whichhas healed over an ulcer may predisposeto new ulceration in a similar manner tocallus formation.


Figure 3.43 Onychocryptosis (ingrown nail) of both halluxes. Note brown nail discolorationprobably caused by chronic infection with Candida albicans. Second, third, and fourth left clawtoe deformity

Keywords: Fourth toe disarticulation; neu-ropathic ulcer

INGROWN NAILS(ONYCHOCRYPTOSIS)

An ingrown toenail is a common condi-tion usually affecting the hallux. A sectionof a nail curves into the adjacent fleshand becomes embedded in the soft tissue(Figure 3.43). Peeling the nail at the edge ortrimming it down at the corners is the mostcommon cause. In addition to congenitalor traumatic reasons, ingrown nails may becaused by tight shoes or socks which press

on the sides of the nail making it curve intothe skin.

An ingrown nail predisposes to localinfection (paronychia) as it provides anentry point for pathogens; therefore itshould be treated as soon as it is rec-ognized. Nails should be trimmed in astraight line.

Infection with Candida albicans is an-other cause of chronic paronychia, espe-cially when patients’ feet are exposed tomoisture for long periods. The nail is usu-ally affected and becomes ridged, deformedand brown.

Keywords: Onychocryptosis; ingrown nail

Chapter IVSOME UNCOMMON CONDITIONS

� ONYCHOGRYPOSIS

� PALMOPLANTAR KERATODERMA

� CALCIUM PYROPHOSPHATE DIHYDRATE (CPPD)DEPOSITION DISEASE

� HYPERKERATOTIC ECZEMA

� NECROBIOSIS LIPOIDICA

� SQUAMOUS CELL CARCINOMA

� DERMATOFIBROSARCOMA PROTUBERANS



Some Uncommon Conditions 75

ONYCHOGRYPOSIS

A 75-year-old male patient with type 2 dia-betes diagnosed at the age of 64 years wasreferred to the foot clinic for foot care. Hewas a psychiatric patient treated on an out-patient basis. The patient had findings ofperipheral neuropathy with loss of sensationof pain, light touch, vibration and tempera-ture. Peripheral pulses were palpable. Clawtoes and extreme onychogryposis was noted(Figure 4.1). His nails were cut using a spe-cial nail trimmer. Instruction in foot carewas given; extra depth shoes were providedin order to accommodate the deformity. Hevisited the clinic on a monthly basis and hadhis nails cut without any other foot prob-lems.

Onychogryposis is caused by chronicrepetitive trauma particularly to the nailson the great toe. The nails may be grosslythickened, hard and very elongated (Fig-ure 4.2 shows this condition in another pat-ient). They may be elevated from the nailbed, curved inwards or turned sideways.

The deformed nail can press against anothertoe causing ulcerations. When the patientdoes not wear shoes, the deformed toenailoften grows vertically. When socks or shoesare being worn, the deformed toenails tendto develop in such a way as to accommo-date the clothing.

Keywords: Onychogryposis

PALMOPLANTARKERATODERMA

A 64-year-old male patient with type 2diabetes diagnosed at the age of 55 yearsattended the foot clinic for foot care andinstruction in the management of his condi-tion, palmoplantar keratoderma. On exam-ination diffuse thickening of the palmarand plantar skin, together with hyperker-atosis was noted (Figure 4.3). Nail deformi-ties were also observed. He had findings ofperipheral neuropathy, while the peripheralarteries were palpable.

Figure 4.1 Onychogryposis


Figure 4.2 Onychogryposis

Figure 4.3 Palmoplantar keratoderma

The patient was instructed in appropri-ate foot care. Local debridement with ker-atolytics was prescribed. Protection fromfriction with soft insoles may be helpful inthis condition.

Palmoplantar keratoderma is an autoso-mal-dominant trait characterized by diffuse,

thickened hyperkeratosis of the palms ofthe hands and soles of the feet. Thehyperkeratosis may be so thick that theskin may crack, especially in dry, coldweather. Infection with Tinea pedis fre-quently occurs as the fissures provide aportal of entry for the fungus. The nails on


the hands and toes may be dystrophic andbecome infected with fungus.

Keywords: Palmoplantar keratoderma

CALCIUMPYROPHOSPHATE

DIHYDRATE (CPPD)DEPOSITION DISEASE

A 74-year-old female with type 2 diabetesdiagnosed at the age of 68 years and treatedwith sulfonylurea with acceptable diabetescontrol, was referred to the outpatient dia-betic foot clinic for possible osteomyelitisof her fifth left toe. She had intense painat this site when resting and walking. Thepain started after the patient had worn atight pair of shoes for a few hours.

On examination, redness, edema, andcallus formation were noted at the outeraspect of the left fifth toe (Figure 4.4). Shehad findings of diabetic neuropathy (no

sensation of vibration, no Achilles tendonreflexes, but she could feel pinpricks; vibra-tion perception threshold was 45 V on bothfeet). Peripheral pulses were palpable.

Debridement of the callus revealed acheesy material emanating from the baseof a superficial ulcer. A culture of thismaterial did not reveal any microorgan-isms. A plain radiograph showed radio-dense deposits at the articular bursae of thedistal interphalangeal joint; no osteomyeli-tis was apparent (Figure 4.5). Examinationof this material with compensated polar-ized light microscopy showed rhomboid-shaped and weakly positive birefringentcrystals, which is typical of CPPD depo-sition disease.

The patient was advised to rest. Shevisited the foot clinic on a weekly basisfor callus debridement. The ulcer healedcompletely in 3 weeks.

CPPD deposition disease (or pseudo-gout) of the foot joints may pose a problemwith diagnosis when the location is atyp-ical. The knee is the most frequent jointaffected by pseudo-gout, followed by the

Figure 4.4 Painful inflammatory lesion of the fifth toe, due to calcium pyrophosphate dihydratedeposition disease


Figure 4.5 Radio-dense deposits at the articular bursae of the distal interphalangeal joint of thefifth toe due to calcium pyrophosphate dihydrate deposition disease

wrist, shoulder, ankle, elbow and hands,although every joint can be affected. Treat-ment includes rest, aspiration of the jointfluids, and systemic use of non-steroidalanti-inflammatory medication.

Keywords: Pseudo-gout; calcium pyro-phosphate dihydrate deposition disease;CPPD deposition disease

HYPERKERATOTICECZEMA

A 65-year-old male patient with longstand-ing diabetes visited the outpatient diabeticfoot clinic for a chronic pruritic lesion ofhis left foot.

On examination, he had severe diabeticneuropathy and peripheral pulses were pal-pable. A hyperkeratotic lesion with denseyellowish scales over a red skin patch wasobserved on the plantaro-lateral aspect ofhis left foot (Figure 4.6). The scales werefirmly adherent on the epidermis, and not

easily debrided. Dry skin on the heel wasalso present.

The patient was referred to the derma-tology department for treatment.

This situation occurs on the palms of thehands and soles of the feet, almost exclu-sively in men. It may result from irritationor allergy, although the cause is usuallyunknown. Topical moisturizers containinglactic acid or urea are applied after soak-ing the affected area for 20 min. Topicalcoal tar preparations may be applied dailyunder occlusion if severe lichenification ispresent. Per os antihistaminic medication,or low-dose corticosteroids may be of somehelp for short periods.

Keywords: Hyperkeratotic eczema

NECROBIOSIS LIPOIDICA

A 50-year-old lady with type 1 diabetesdiagnosed at the age of 38 years, visitedthe outpatient clinic for control of her


Figure 4.6 Hyperkeratotic eczema. Hyperkeratotic lesion with dense yellowish scales over a redskin patch. The scales are firmly adhered to the epidermis and not easily debrided with a blade.Dry skin on the heel

diabetes (HbA1c: 7.0–7.9%) on a regularbasis. She was free of micro- or macro-angiopathy. Two years after her diabeteswas diagnosed, the patient noticed a fewsmall, red, irregular, violaceous papuleson the dorsum of her feet. These papulesslowly enlarged, coalesced and becamescaly, irregular plaques, with minimal cen-tral atrophy, and an advancing red border(Figure 4.7). New lesions appeared on herleft ankle and right leg. Apart from causingcosmetic problems, the lesions were asymp-tomatic.

A biopsy of these lesions showed necro-biosis lipoidica (formerly ‘necrobiosis lipoi-dica diabeticorum’), an unusual disorder ofunknown mechanism, strongly associatedwith diabetes mellitus but also found insubjects with normal or abnormal glucosetolerance.

Typically, such lesions occur on theanterior shin of both lower legs, but theyalso may be located on the arms, handsor head. They may precede the diag-nosis of diabetes, and sometimes they

Figure 4.7 Necrobiosis lipoidica. Scaly, irreg-ular plaques, with minimal central atrophy andan advancing red border


are pruritic, dysesthetic or painful. Theyulcerate — usually after a trauma (shown inFigures 4.8 and 4.9 in other patients) — inapproximately 35% of the cases, but do notusually lead to infection.

Histological examination of the lesionsshows necrobiosis, which provides the focifor ‘hyalinized’ collagen bundles (Fig-ure 4.10), fibrosis, histiocyte infiltration(Figure 4.11) and granulomata (Fig-ure 4.12). Capillary walls become thick-ened (Figure 4.10).

Topical application of corticosteroidsmay have fair results against progression of

Figure 4.8 Ulcerated lesions associated withnecrobiosis lipoidica. Note a not ulcerated lesionover the epiphysis of the fibula

Figure 4.9 Infected ulcerated lesions associ-ated with necrobiosis lipoidica

Figure 4.10 Histological findings in samplestaken from the patient with necrobiosis lipoidicashown in Figure 4.7. A, foci of ‘hyalinized’ col-lagen bundles (necrobiosis), fibrosis, and histi-ocyte infiltration. Thickened capillary walls areevident (arrow). H&E stain, ×100

the lesions. Various other agents have beentried, such as aspirin or pentoxyphyllin,with mixed results.

Keywords: Necrobiosis lipoidica


Figure 4.11 Histological findings in samplestaken from the patient with necrobiosis lipoidicashown in Figure 4.7. Foci of ‘hyalinized’ colla-gen bundles (necrobiosis), fibrosis and histiocyteinfiltration can be seen. H&E stain, ×100

SQUAMOUS CELLCARCINOMA

Squamous cell carcinoma (SCC) developedon a neglected burn scar in a 48-year-olddiabetic male patient. SCC is the secondmost common skin cancer after basal cellcarcinoma. It arises from the dermis andit is most common in areas exposed tothe sun. It is an aggressive and invasive

Figure 4.12 Histological findings in samplestaken from the patient with necrobiosis lipoidicashown in Figure 4.7. Note the presence of agranuloma (arrow). H&E stain, ×100

cancer; it may penetrate underlying tissues,and it metastasizes in distant tissues, lymphnodes, and organs. Presentations vary andfor this reason the neoplasm is difficult todiagnose. Pink, red or tan plaques, ulcers(Figure 4.13) or erosions and scaling maybe apparent. Secondary SCC arises in areasof old scars, especially burn scars, chronicnon-healing wounds and radiation lesions(Marjolin’s ulcers). Plastic surgeons useda free latissimus dorsi musculocutaneousflap to repair the defect, after extensive

Figure 4.13 Squamous cell carcinoma presented as an ulcer on the lateral aspect of the foot of adiabetic patient. The design of the excision and the recipient vessels are indicated. (Courtesy of O.Papadopoulos)


Figure 4.14 Free latissimus dorsi musculo-cutaneous flap used to repair the defect, afterextensive excision of a squamous cell carcinoma.Patient whose foot is shown in Figure 4.13.(Courtesy of O. Papadopoulos)

removal of the cancer, within a healthyborder (Figure 4.14).

Keywords: Squamous cell carcinoma

DERMATOFIBROSARCOMAPROTUBERANS

Recurrent dermatofibrosarcoma protuber-ans (DFSP) was diagnosed in a 71-year-old

male diabetic patient. DFSP is an uncom-mon aggressive soft tissue sarcoma of lowmalignant potential, arising in the der-mis of young to middle-aged adults andit is slightly more frequent in men thanwomen (57 versus 43%). It is most com-monly located on the trunk and proxi-mal extremities. Initially it presents as anasymptomatic bluish, red or flesh-colorednodule with a diameter of a few millimeters

Figure 4.16 A free latissimus dorsi musculo-cutaneous flap was used to repair the defect,after extensive excision of a dermatofibrosar-coma protuberans of heel. Patient of Figure 4.15.(Courtesy of O. Papadopoulos)

Figure 4.15 Ulceration of recurrent dermatofibrosarcoma protuberans of the heel of a diabeticpatient. The design of the excision and the recipient vessels are indicated. (Courtesy of O.Papadopoulos)


to >20 cm located on top of plaque-likelesions, or as superficial ulceration of someof these nodules. It infiltrates the surround-ing tissues and, if untreated, it may ulcer-ate (Figure 4.15). It may recur after surgi-cal excision and lead to metastases. Moh’smicrographic surgery, using wide marginresection, is the mainstay of treatment.

Plastic surgeons used a free latissimusdorsi musculocutaneous flap to repair thedefect, after wide removal of the cancer(Figure 4.16).

Keywords: Dermatofibrosarcoma protu-berans

Chapter VNEUROPATHIC ULCERSAT VARIOUS SITES

� NEUROPATHIC ULCER OVER PROMINENT FIRST

METATARSAL HEAD

� NEUROPATHIC ULCER OVER PROMINENT

METATARSAL HEADS

� NEUROPATHIC ULCER OVER A COLLAPSED

MIDFOOT

� NEUROPATHIC ULCER UNDER FOURTH

METATARSAL HEAD

� NEUROPATHIC ULCERS UNDER PROMINENT

METATARSAL HEADS

� ULCERS OVER A CHARCOT FOOT

� A NEUROPATHIC ULCER UNDER THE HEEL

� BURNS ON TOES AND FOREFOOT

� CHRONIC NEUROPATHIC ULCER COMPLICATED

BY OSTEOMYELITIS

� ON THE TOES

� ON THE MIDFOOT

� ON THE HEEL



Neuropathic Ulcers at Various Sites 87

NEUROPATHIC ULCEROVER PROMINENT FIRST

METATARSAL HEAD

A 54-year-old male patient with type 2diabetes diagnosed at the age of 45 yearswas referred to the outpatient diabetic footclinic because he had developed an ulceron the plantar area of his left foot. He wastreated with antidiabetic tablets and dia-betes control was good (HBA1c: 7.1%). Onexamination he had a full thickness ulceron the head of the first metatarsal in anarea where there was gross callus formation(Figure 5.1). No signs of infection wereobserved. He had findings of diabetic neu-ropathy (no sensation of pain, light touch,temperature or vibration). Vibration per-ception threshold was 45 V on the rightand >50 V on the left foot. His peripheral

pulses were palpable and the ankle brachialpressure index was 1.2 bilaterally.

The patient did not have a previous his-tory of problems with his feet. He deniedany pain or trauma. He was aware of thepresence of the ulcer, after he had seen dis-charge on his socks and the insole of hisshoes. Debridement of the ulcer was car-ried out and the patient was advised to resthis feet; therapeutic footwear was also pre-scribed (Figure 5.2). This patient attendedthe diabetic foot clinic on a weekly basisand he changed the dressings every day.The ulcer healed completely in 10 weeks.

This is a typical neuropathic ulcer. Suchulcers are painless — unless they becomeinfected — and develop in patients withneuropathy under areas of high-pressureloading. A callus forms at points of highrepetitive pressure on the sole of the foot

Figure 5.1 Neuropathic ulcer on the first metatarsal head


Figure 5.2 Therapeutic footwear prescribed for the patient whose foot is shown in Figure 5.1.Among the most commonly used therapeutic footwear is the rocker style shoe. Notice that the apex(ridge) of the rocker sole is located behind the metatarsal heads

and is a powerful predictor of ulcera-tion. Such areas are the metatarsal headsand the plantar aspect of the great toe.Callus formation on the heel is not verycommon. In addition, calluses can developover areas of bony prominences at othersites in the case of foot deformities (clawand hammer toes, toe overriding, neuro-osteoarthropathy). Even though the etiol-ogy of callus formation has not been deter-mined, the fact that a callus acts as a for-eign body in the shoe and contributes tohigh plantar pressure is well known. It istherefore recommended that callus forma-tion should be prevented and when a callusis present, it should be removed regularly.Appropriate footwear is thought to preventcallus formation and the efficacy of thismeasure will be reflected by the proportionof patients wearing the correct footwearwho develop ulcers. Hemorrhage into a cal-lus is known as a ‘pre-ulcer’ and it shouldbe treated as an ulcer.

Keywords: Neuropathic foot ulcer

NEUROPATHIC ULCEROVER PROMINENT

METATARSAL HEADS

A 53-year-old female patient who had hadtype 2 diabetes since the age of 41 yearsand was being treated with insulin, wasreferred to the outpatient foot clinic becauseof a chronic foot ulcer. She had back-ground retinopathy, cataract, hypertensionand ischemic heart disease. The patientcomplained of numbness and a sensationof pins and needles in her feet, which wors-ened during the night.

On examination she was found to havea full thickness ulcer under her second andthird prominent metatarsal heads and clawtoes (Figure 5.3). The patient had severeperipheral neuropathy (no sensation of light


Figure 5.3 Neuropathic ulcer overprominent metatarsal heads

touch, pin prick, temperature, 5.07 monofil-ament, absence of Achilles tendon reflexes;and a vibration perception threshold over50 V). Peripheral pulses were palpable andthe ankle brachial pressure index was 1.1bilaterally.

The patient reported having a cal-lus — probably due to high peak plantarpressures at the site of the callus — forthe past 2 years, which she treated withpumice stone. Six months before her firstvisit, she noticed that the callus was harderand its base had become purple; when shedecided to remove it using a blade, anulcer developed, which she then treatedwith local antiseptics.

Debridement of the ulcer was carried outon a weekly basis.

Healthy granulating tissue was presentat the base of this clean ulcer, togetherwith mild callus formation at the border.The patient was advised to take prolongedbed rest and the ulcer healed completely in6 weeks. Appropriate preventive footwearand orthotic insoles were prescribed inorder to prevent the formation of anew ulcer.

This patient erroneously thought thatpain in her feet was proof of a healthyperipheral nerve system. The combinationof painful neuropathic symptoms and at thesame time, complete absence of sensation


(a ‘painful–painless foot’) is a quite com-mon feature of neuropathic diabetes.

Keywords: Neuropathic ulcer; granulatingtissue

NEUROPATHIC ULCEROVER A COLLAPSED

MIDFOOT

A typical neuropathic ulcer under a bonyprominence in a patient with midfootcollapse due to neuro-osteoarthropathy isshown in Figure 5.4. Callus formation ispresent at the margins of the ulcer, while

Figure 5.4 Neuropathic ulcer over a bonyprominence in a patient with neuro-osteoarth-ropathy

its base is clean, covered by healthy gra-nulating tissue.

Therapeutic footwear was prescribed(extra depth shoes with an orthotic insoleand a window under the ulcerated area)and the patient was advised to minimize hisactivities. The ulcer healed in 3 months.

Ulcers in patients with midfoot collapserecur very often. Prevention of new ulcersover the same bony prominence is achievedby prophylactic surgery (osteotomy of theprominent bone). Preservation of plantarligaments is essential, since their extensiveresection may cause progression of therocker bottom deformity.

Keywords: Neuropathic ulcer; bony promi-nence; prophylactic osteotomy

NEUROPATHIC ULCERUNDER FOURTH

METATARSAL HEAD

A 74-year-old female patient with type 2diabetes diagnosed at the age of 62 years,was referred to the outpatient diabetic footclinic because of callus formation on herright sole. She was being treated withinsulin and had a history of hypertensionand ischemic heart disease.

On examination she was found to havesevere peripheral neuropathy and normalperipheral pulses. In addition, significantmuscle atrophy of her feet, claw toesand a hemorrhagic callus on the fourthmetatarsal head of her right foot were found(Figure 5.5). An impressive finding was thepalpation of her metatarsal heads just belowthe skin as the fat pads had been displacedanteriorly. After callus removal a super-ficial ulcer was revealed (Figure 5.6). Ananteroposterior radiograph showed diffuse


Figure 5.5 Hemorrhagic callus under thefourth metatarsal head. Claw toes and prominentmetatarsal heads are also present

Figure 5.6 A neuropathic ulcer in the samepatient whose foot is shown in Figure 5.5

demineralization of the foot and signifi-cant widening with periosteal reaction atthe metatarsal heads (Figures 5.7 and 5.8).The patient was advised to rest. Extra depth

Figure 5.7 Diffuse osteopenia and significantwidening with periosteal reaction on the meta-tarsal heads can be seen in this X-ray of the footshown in Figure 5.5

shoes and orthotic insoles were prescribedin order to accommodate her deformed toesand relieve the load under the metatarsalheads. Post-debridement in-shoe pressureswhen she used her own shoes showed asignificant load under her metatarsal heads(Figure 5.9 Panel A). The maximum pres-sure in this area was 282 kPa; however,after insertion of an orthotic insole themaximum in-shoe pressure was reduced to155 kPa (Figure 5.9 Panel B). The ulcerhealed in 8 weeks.

Reduced thickness of the fat pad is asso-ciated with high plantar pressures. Althoughsome authors have suggested that thresh-old pressures of 500–1000 kPa may leadto the development of foot ulceration whenwalking barefoot, it seems that each patienthas an individual threshold. In the presentcase the maximum pressure was obviouslybelow this threshold. However, high plantar


Figure 5.8 Significant widening with periosteal reaction of the first three metatarsal heads (samepatient whose foot is shown in Figures 5.5–5.7)

Figure 5.9 Plantar pressures before (A) andafter (B) orthotic insoles in the patient whosefoot is shown in Figures 5.5–5.7

pressures alone do not cause foot ulcera-tion; a combination of different risk factors(mentioned in Chapter 1) is necessary forthe development of ulceration.

Demineralization of the foot bones isnot common, but when this occurs it sig-nifies an adequate circulation, which is aprerequisite for bone resorption. Localized,mature periosteal reaction and demineral-ization involving metatarsal heads is com-mon in diabetic patients with neuropathy. Itsetiology is poorly understood. Focal oste-olysis of phalanges, metatarsal heads, andother single foot bones, as well as stress frac-tures of the metatarsal heads can also be seenin neuropathic patients. Bone resorption atthe phalanges may be so extensive that a partor even a whole phalanx may be resorbed.Metatarsal resorption usually starts from themetaphysis and extends to the epiphysissparing the diaphysis. Bones which havebecome demineralized may have a pencil-like appearance.

Keywords: Neuropathic ulcer; plantar pres-sures, periosteal reaction


NEUROPATHIC ULCERSUNDER PROMINENT

METATARSAL HEADS

This 32-year-old type 1 female diabeticpatient, diagnosed at the age of 16 years,attended the outpatient diabetic foot clinicfor chronic neuropathic ulcers of her feet.She was treated with intensive insulin treat-ment. The patient had a renal transplantat the age of 30 years, because of end-stage renal failure due to diabetes, andshe had laser treatment on both eyes atthe age of 28 years. Soon after her trans-plantation she noticed a bulla under herlast three left metatarsal heads which read-ily ruptured and a superficial ulcer devel-oped. She also reported an ulcer of 2 years’duration under the third metatarsal headof her right foot. She had never beeninstructed in foot care and had never worn

Figure 5.10 Neuropathic ulcers under promi-nent metatarsal heads and on the midsole. Clawtoes and dry skin are also apparent

the correct footwear. She had two smallchildren and had not been taking good careof her feet. The patient was being treatedwith erythropoietin injections, cyclosporin,methylprednisolone, mycofenolate mofetiland furosemide.

On examination she was found to havebounding pedal pulses, and severe dia-betic neuropathy. The vibration perceptionthreshold was above 50 V in both feetbilaterally.

A non-infected neuropathic ulcer wasnoted under her left third, fourth and fifthmetatarsal heads. Its dimensions were 3.5 ×4 × 0.4 cm, and it was surrounded by cal-lus. A smaller neuropathic ulcer was alsoobserved under her midsole (Figure 5.10).Claw toe deformity of her lesser toes, dryskin and desquamation of the tip of herthird toe were also present. Under her

Figure 5.11 Neuropathic ulcer surrounded bycallus. Claw toe. Right foot of patient whose leftfoot is shown in Figure 5.10


Figure 5.12 Original in-shoe peak plantar pres-sures on the left (upper panel) and right foot(lower panel) of the patient whose feet areillustrated in Figures 5.10 and 5.11

Figure 5.13 Healing neuropathic ulcers in thepatient whose feet are shown in Figures 5.10–5.11. Note bunionette deformity at the right foot

right third metatarsal head a neuropathiculcer was noted in an area of gross callusformation, in addition to claw toe defor-mity (Figure 5.11). A callus was presentunder her right fifth metatarsal head overa bunionette deformity. Mild callus forma-tion was observed on the heels of bothfeet. Onychomycosis affecting all toes wasalso present (discussed in Chapter 8, seeFigure 8.7).

A plain radiograph did not reveal osteo-myelitis. Sharp debridement was performedand therapeutic half shoes were prescribed.In-shoe peak pressure measurement showedhigh pressures under both heels, metatarsalheads, and halluxes when the patient wore

Figure 5.14 Effect of orthotic insoles and cor-rect footwear on in-shoe peak plantar pressureson the left (upper panel) and right foot (lowerpanel) in the patient whose feet are illustrated inFigures 5.10–5.11


her own shoes (Figure 5.12). She hadstandard treatment on a weekly basis andthe ulcers began to heal slowly. Six monthsafter her first visit, an ulcer developedunder her left third metatarsal head anda callus under her right fifth metatarsalhead (Figure 5.13). New shoes were pre-scribed with orthotic insoles: the in-shoepeak pressures were reduced from 33.3to 16.83 N/cm2 under her right, and from37.42 to 20.13 N/cm2 under her left foot(Figure 5.14).

The patient continued visiting the out-patient foot clinic almost every week, and6 months after her first visit her ulcers hadhealed.

Keywords: Neuropathic ulcer; peak plan-tar pressures

ULCERS OVER A CHARCOTFOOT

The following two figures (before andafter debridement) show the left foot ofa male patient of 62 years of age withtype 2 diabetes diagnosed at the age of48 years and treated with insulin. A smokersince the age of 18 years, the patienthad had an ulcer on the plantar aspectof his left hallux which was complicatedby osteomyelitis and led to amputation3 years previously. One year before hisfirst visit to the foot clinic the patientdeveloped an ulcer on the lateral aspect ofhis left foot which resulted in osteomyelitisand surgical debridement of the metatarsalbone. After a femoral-popliteal bypass graftin his left foot, the patient developedneuro-osteoarthropathy. He presented tothe outpatient clinic with two painlessulcers under his first and third metatarsalheads surrounded by hemorrhagic calluses.

Hyperkeratosis under his fifth metatarsalhead and a scar at the site of the surgicaldebridement were noted (Figure 5.15).

The graft was functioning well and thepatient had no claudication. Debridementof the ulcer under his fourth metatarsalexposed the bone (Figure 5.16). Cultureswere obtained from the sloughy base of theulcer — a positive sign of infection — andthe patient was treated with an empiri-cal combination of cotrimoxazole and clin-damycin. The patient did not attend follow-up, therefore no X-ray or any further studiesare available.

Charcot foot typically does not developin patients with peripheral vascular dis-ease since increased blood supply to thebone is needed for the osseous tissue to beovermetabolized. Autonomic sympatheticneuropathy leads to bone arteriovenous

Figure 5.15 Hallux disarticulation at the meta-tarsophalangeal joint, callus under first and fifthmetatarsal heads, and deep infected neuropathiculcer under the third metatarsal head. Claw toes


Figure 5.16 Foot shown in Fig-ure 5.15 after sharp debridement.Note bone exposure at the base ofthe ulcer under the third metatarsalhead

shunting, hypervascularity and demineral-ization. Some cases are reported to occurafter bypass surgery of the arteries.

Exposure of the bone denotes osteomy-elitis and it should be treated accordingly.

Keywords: Neuropathic ulcers; Charcotfoot; osteomyelitis; amputation

A NEUROPATHIC ULCERUNDER THE HEEL

A 51-year-old female patient with type2 diabetes since the age of 38 years and

treated with insulin, was referred to theoutpatient diabetic foot clinic because ofa chronic non-healing ulcer under herright heel. She had good diabetes control(HBA1c: 7.2%). Four months before herfirst visit she noticed a painless blister onthe right heel caused by a small stone inher shoe; the blister ruptured and since thepatient did not feel any pain she did not giveher foot any attention. Some discharge waspresent on her socks, but it was the patient’sdaughter who saw a superficial ulcer on theright heel. The patient visited a primarycare clinic and was advised to clean theulcer with povidone iodide and apply cleandressings every day. A 2-week course of


antibiotics was prescribed. She continuedher daily activities and after 4 months theulcer was still active.

On examination the patient was foundto have severe diabetic neuropathy withloss of sensation of pain, temperature, lighttouch and vibration. The vibration per-ception threshold was 36 V on both feet.Peripheral pulses were normal and the anklebrachial index was 1.2 and 1.1 in the rightand left foot respectively. A full thick-ness ulcer with a sloughy base was notedon the right heel (Figure 5.17). No othersigns of infection were present. An X-raydid not show involvement of the calca-neus. Cultures from the base of the ulcerrevealed Staphylococcus aureus. She wastreated with amoxicillin–clavulanic acidfor 2 weeks and the ulcer was debridedon a weekly basis; dressings were changeddaily. Meanwhile she was advised to restand heel-free shoes to offload pressure

Figure 5.17 Deep heel neuropathic ulcer withinfected sloughy bed caused by trauma

from the ulcerated area were prescribed(Figure 5.18). After 6 months the ulcer hadhealed completely (Figure 5.19).

Bedridden patients develop heel ulcersor gangrene quite frequently (20–30%),

Figure 5.18 Commercially available heel-freeshoes for the treatment of hindfoot ulcers

Figure 5.19 Hindfoot shown in Figure 5.17after the ulcer has completely healed


Figure 5.20 Neuropathic heel ulcer caused by shoe seam

usually on the posterolateral aspect. Exces-sive walking in new shoes can causeblister formation on the posterior aspectof the heel in patients with neuropathy.Shoe seams may also cause ulcers on theheel (Figure 5.20). Therefore shoes andsocks without seams are prescribed topatients with loss of protective sensation.Heel ulceration is difficult in managementsince debridement in this area precludesfunctional weight bearing. Major amputa-tions are often necessary when heel ulcersare infected.

Keywords: Neuropathic ulcer; heel

BURNS ON TOESAND FOREFOOT

A 55-year-old male patient with type 2diabetes since the age of 43 years attendedthe outpatient diabetic foot clinic due toulcers on his feet. His diabetes was poorlycontrolled with sulfonylureas and he hada history of a disarticulated left great toe

at the metatarsophalangeal joint due toosteomyelitis.

On examination the patient was febrile;peripheral pulses were palpable, the anklebrachial index was 1.2; the vibration per-ception threshold was over 50 V in bothfeet; temperature, light touch and pinpricksensation were absent as were the Achillestendon reflexes. Blood pressure was nor-mal; no other diabetic complications werefound. HbA1c was 11.0%. There was aperforating dirty ulcer on the outer aspectof his right foot. A large amount of cal-lus had built up around the plantar ori-fice (Figures 5.21 and 5.22). The patientreported edema of the forefoot which hadrecently subsided as was evident from thescaling of the skin. Callus formation wasalso observed over the second, third andfifth metatarsal heads of the left foot.The patient was empirically treated withciprofloxacin.

Debridement of the callus was car-ried out. Cultures revealed Staphylococcusaureus and Escherichia coli. Osteomyelitisof the fifth metatarsal head was evident on aplain radiograph (Figure 5.23). The patient


Figure 5.21 Perforating, infected neuropathic ulcer under the fifth metatarsal head. Scaling is dueto edema that has subsided

Figure 5.22 Right foot: neuropathic ulcer shown in Figure 5.21. Left foot: hallux disarticulation,medial displacement of second toe with claw deformity; callus formation under second, third andfifth metatarsal heads


Figure 5.23 Plain radiograph of theright foot of the patient whose foot isshown in Figure 5.21. Osteomyelitis ofthe fifth metatarsal head and the proxi-mal phalanx of the fifth toe, subluxationof the metatarsophalangeal joint, cal-cification of the digital artery betweenthe first two metatarsals and osteoarthri-tis of the first distal phalangophalangealjoint of the hallux are all apparent

continued ciprofloxacin treatment; cotri-moxazole was added for almost 6 monthsand the ulcer gradually healed (Figure 5.24)with the help of therapeutic shoes.

Instruction in appropriate foot care wasprovided. The patient visited the outpa-tient clinic erratically; callus formation onthe site of the healed ulcer was removedevery 3 months; he refused strict glycemiccontrol as he was afraid that episodes ofhypoglycemia would jeopardize his posi-tion at work. He used intermediate-actinginsulin at bedtime and sulfonylureas duringthe day. His HbA1c remained at 9.0% dur-ing the following year. Preventive footwearwas not accepted.

The patient attended the clinic 2 yearslater because of multiple burns over the

tips of his toes and superficial ulcers overthe fifth metatarsal heads of both feet(Figure 5.25). He had put his feet in frontof the fire in order to dry out his wet socks.No pain was felt. Although the patient wasaware of the burns he continued his activi-ties for a week before this visit.

Full thickness burns were present overthe tips of all toes. Blisters over theright fifth metatarsal head and the leftfourth and fifth toes were removed andulcers had developed since the patientwas still working regularly, despite med-ical advice to the contrary (Figure 5.26).Calluses formed around the new plantarulcers. Amoxicillin–clavulanic acid treat-ment was initiated and the patient attendedthe diabetic foot clinic on a weekly basis.


Figure 5.24 The ulcer shown in Fig-ure 5.21 after it has almost completelyhealed

Figure 5.25 Thermal injury sus-tained by the patient whose feet areillustrated in Figure 5.22


Figure 5.26 Neuropathic ulcers under the fifthmetatarsal heads and progression of thermalinjury in the patient whose feet are shown inFigures 5.21–5.25. The patient did not complywith doctors’ instructions

All ulcers healed within 2 months exceptthe one on the right great toe, which wascomplicated by osteomyelitis and acute soft

tissue infection. Five months after the burnhis right hallux had to be disarticulated.

The patient still refused preventive shoesand 4 months after this second amputa-tion new ulcers developed under the fifthmetatarsal heads bilaterally (Figure 5.27).

Keywords: Thermal injury; osteomyelitis

CHRONIC NEUROPATHICULCER COMPLICATED

BY OSTEOMYELITIS

A 55-year-old male patient with type 2diabetes diagnosed at the age of 50 yearswas referred to the outpatient diabetic footclinic because of a chronic neuropathiculcer on his right foot. He had a historyof hypertension, background retinopathy inboth eyes and diabetic nephropathy (urineprotein 1.5 g/24 h). He had been treatedwith sulfonylurea but had discontinued

Figure 5.27 Right hallux disarticula-tion at the metatarsophalangeal jointand recurrence of ulcers under the fifthmetatarsal heads (patient whose feet areshown in Figures 5.21–5.26)


the treatment 1 year before his first visit,when overt nephropathy developed. He hadexcellent diabetes control (HBA1c: 6.4%).

On examination his feet pulses werebounding (ankle pressure index 1.2 bilater-ally); he had severe peripheral neuropathy:no sensation of pain, light touch, vibra-tion or temperature; the vibration percep-tion threshold was 48 V on the left andabove 50 V on the right foot. A full thick-ness clear neuropathic ulcer surrounded bycallus was observed under the right firstmetatarsal head, with dimensions of 3 ×3 × 0.5 cm (Figure 5.28). Mild claw defor-mities of the toes and displacement of themetatarsal fat pads to the base of the prox-imal phalanges due to muscle atrophy werealso noted.

Sharp debridement was carried out andspecial extra depth shoes with an orthoticinsole were prescribed. Care was taken tooffload pressure from the ulcerated area.

Figure 5.28 Neuropathic ulcer under promi-nent first metatarsal head. Healthy granulatingtissue can be seen at the base of the ulcer

The patient was advised to limit his dailyactivities and he attended the diabetesfoot clinic on a weekly basis. The sizeof the ulcer was reduced by half within4 weeks. Two weeks later, after a profes-sional trip, the patient visited the clinicagain. His ulcer was infected and a largeamount of callus had formed around it. Hisright hallux had a ‘sausage-like’ appear-ance and signs of infection were observed(redness and edema). A culture from thebase of the ulcer revealed the presenceof Staphylococcus aureus and Enterobactercloacae post-debridement. A radiograph atthat time showed mild erosion of the firstmetatarsal head.

The patient was given treatment withcotrimoxazole and clindamycin. The radio-graph was repeated 2 weeks later andextensive erosion of the first metatarsalhead was revealed (Figure 5.29). Acuteosteomyelitis was diagnosed. The patientcontinued with the antibiotics for 12 weeksand had regular chiropody treatment on aweekly basis. The ulcer healed completelyin 20 weeks (Figure 5.30).

Treatment of acute osteomyelitis shouldbe based on bone cultures when pos-sible, and should be continued for6–12 weeks. The commonest pathogen of

Figure 5.29 Erosion of first metatarsal headwith periosteal reaction due to osteomyelitis(patient whose ulcer is shown in Figure 5.28)


Figure 5.30 Healed ulcer of the patient whosefeet are shown in Figures 5.28–5.29. Note thescar over the ulcerated area and callus formationat the tip of the second toe due to claw deformity

acute osteomyelitis in patients with footulcers is Staphylococcus aureus (60–90%).Other pathogens include Staphylococ-cus epidermidis, Escherichia coli, Pseu-domonas aeruginosa, and other Enterobac-ter spp. More than one pathogen is oftenisolated. In order to achieve therapeutic lev-els of antibiotics in the bone it is prefer-able to administer antibiotics intravenously

for the first 2 weeks. However, oral antibi-otics with good bioavailability (fluoro-quinolones, clindamycin) may be adequatefor therapy. Treatment regimens for staphy-lococcal osteomyelitis are as follows:

• Clindamycin 600 mg × 3 orally or 600mg × 3 i.v.

• Fucidic acid 500 mg × 3 orally or 500mg × 3 in a 500-ml solution deliveredslowly i.v. (over 4–6 h)

• Cotrimoxazole 960 mg × 2 orally or i.v.• Ciprofloxacin 750 mg × 2 orally, or 400

mg × 3 i.v.• Rifampicin 900 mg × 1 orally or i.v.• Teicoplanin 600 mg × 1 orally or i.m.

or i.v.• Vancomycin 500 mg × 4 i.v. or 1 g ×

2 i.v.

Fluoroquinolones, teicoplanin and van-comycin should be prescribed for methi-cillin-resistant staphylococcus only. Fluoro-quinolones in particular, should always becombined with another anti-staphylococcaldrug in the first month of treatment, sinceit is likely that a resistant strain will prevailin the infection.

Keywords: Acute osteomyelitis; treatment

Chapter VINEURO-ISCHEMIC ULCERSAT VARIOUS SITES

� UNDER HALLUX

� NEURO-ISCHEMIC ULCER WITH OSTEOMYELITIS

UNDER THE HALLUX

� ON THE DORSUM OF THE FOOT

� INTERDIGITAL

� AT MEDIAL SIDE OF THE FOOT

� ON FIRST METATARSAL

� ON MIDSOLE AND HEEL

� ON FOREFOOT

� NEURO-ISCHEMIC ULCER ON THE HALLUX

WITH OSTEOMYELITIS

� ON THE DORSUM OF CLAW TOES

� OVER THE FIFTH METATARSAL HEAD



Neuro-Ischemic Ulcers at Various Sites 107

NEURO-ISCHEMIC ULCERUNDER HALLUX

A 68-year-old obese male patient withtype 2 diabetes diagnosed at the age of46 years visited the outpatient diabetic footclinic because of two chronic ulcers onhis right hallux. He was treated with acombination of sulfonylurea during the dayand a mixture of 20% rapid acting–80%intermediate acting insulin before dinner;he also had dislipidemia which was beingtreated with simvastatin.

On examination, he had severe diabeticneuropathy (no sensation of light touch,pin prick, temperature, 5.07 monofilament,absence of Achilles tendon reflexes and avibration perception threshold over 50 V).

Figure 6.1 Infected full thickness neuro-isch-emic ulcers under the right hallux with edemaand superficial ulceration at the tip and asubungual hematoma caused by inappropriatefootwear

Peripheral pulses were palpable, but theankle brachial index was 0.7 bilaterally.

Two painful full thickness neuro-isch-emic ulcers with sloughy bed were seenunder his right hallux; edema and super-ficial ulceration at the tip of his hallux,and subungual hematomata of the first twotoes were also present (Figure 6.1). Therewas no X-ray evidence of osteomyelitis.Sharp debridement was carried out andhe was treated empirically with amoxi-cillin–clavulanic acid. No pathogen wasisolated on swab cultures, probably dueto the use of local antiseptics. Offload-ing of pressure was successful with thehelp of appropriate therapeutic footwear(see Figure 3.36) and the ulcer began toheal smoothly (Figure 6.2); 3 months afterthe initial visit it had healed completely(Figure 6.3).

Keywords: Neuro-ischemic ulcer

NEURO-ISCHEMIC ULCERWITH OSTEOMYELITIS

UNDER THE HALLUX

A 67-year-old man who had type 2 diabetessince the age of 44 years and was beingtreated with insulin, visited the diabeticfoot clinic because of an ulcer on his lefthallux. He had acceptable diabetes control.He had proliferative retinopathy which hadbeen treated with laser, and intermittentclaudication at 400 m. He had smoked for27 years.

Twenty days before his visit, he hadworn a new pair of shoes and driven hiscar for a long distance. The following daya blister developed on his left great toe.Within a day the area became edematousand black.

On examination the patient was foundto have a deep, foul-smelling ulcer with


Figure 6.2 Healing of the ulcers shown in Figure 6.1

Figure 6.3 Hallux ulcers shown in Figures 6.1 and 6.2 after they have fully healed

gangrenous areas and a purulent dischargeover the medial and dorsal aspect of his leftgreat toe (Figure 6.4).

Peripheral pulses were weak and theankle brachial index was 0.8. The patientcould not feel pain, temperature, lighttouch, or a 5.07 monofilament. The vibra-tion perception threshold was 40 and 45 Vat the tips of the left and right great toerespectively.

Sharp debridement was carried out re-vealing the underlying bone. An X-rayshowed osteomyelitis of the distal pha-lanx (Figure 6.5). The patient was treatedempirically with ciprofloxacin and clin-damycin as a swab culture from the baseof the ulcer had revealed Staphylococcusaureus. Despite local foot care and the sys-temic antibiotics, the ulcer was still activeand osteomyelitis spread locally affecting


Figure 6.4 Deep tissue infected neuro-ischemic ulcer with necrotic areas on the left hallux

Figure 6.5 Plain radiograph of thefoot illustrated in Figure 6.4, showingosteomyelitis involving proximal inter-phalangeal joint and adjacent phalan-ges of the left hallux

the proximal phalanx. Three months afterhis first visit the patient’s left great toewas amputated (Figure 6.6). Antimicrobialtreatment was continued for 2 weeks afterthe amputation.

The consequences of hallux disarticula-tion at the metatarsophalangeal joints havebeen discussed previously (see Figure 3.32).

Keywords: Neuro-ischemic ulcer; osteo-myelitis; amputation

NEURO-ISCHEMIC ULCERON THE DORSUM

OF THE FOOT

A large (3.5 × 2.0 cm) painless neuro-ischemic ulcer developed on the right footof a 68-year-old male patient with type2 diabetes which had been diagnosed atthe age of 61 years. Peripheral pulses were


Figure 6.6 Disarticulation at the metatarso-phalangeal joint of left hallux of the patientwhose foot is shown in Figures 6.4 and 6.5

weak and the ankle brachial index was0.6. At the base of the ulcer the fascia ofthe dorsum of the forefoot was exposed(Figure 6.7). There were no signs of infec-tion. A subungual hematoma of the halluxand an ulcer which was healing on the sec-ond toe were noted in addition to significantankle edema. The ulcer was a result of fric-tion between the foot and the forepart of thepatient’s narrow shoe upper (vamp) follow-ing the rupture of a large blister.

Therapeutic footwear was prescribed(Figure 6.8) and the ulcer healed within2 months.

Appropriate footwear was prescribedsubsequently in an attempt to avoid recur-rence of the ulcer (preventive footwear).Such footwear is made of soft, self-mold-able material without any seams, and hasextra depth in order to accommodate an

Figure 6.7 A large neuro-ischemiculcer with exposed fascia on the dor-sum of the forefoot. There is a subun-gual hematoma of the hallux and a healingulcer on the second toe in addition to sig-nificant ankle edema

Figure 6.8 Therapeutic footwear forulcers on the dorsum of the forefoot


appropriate insole and the forefoot deformi-ties (Figure 6.9). Skin injuries due to shoefriction are thus avoided; this is essentialfor patients whose skin is thin and fragiledue to arterial disease.

Keywords: Foot; dorsum; neuro-ischemiculcer

INTERDIGITALNEURO-ISCHEMIC ULCER

A neuro-ischemic ulcer on the lateral aspect

of the fourth toe (Figure 6.10) was causedby pressure from the patient’s little toe.Shoes with narrow toe boxes are oftenthe cause of such ulcers. Mild callusformation — due to pressure of the adja-cent toes — was seen around the ulcer.The patient suffered mild discomfort. Asilicone-ring (Figure 6.11) was used tokeep the third and fourth toes apart untilthe ulcer healed. The patient was instructedin foot care and the correct footwear wasalso prescribed.

Keywords: Interdigital neuro-ischemiculcer

Figure 6.9 Preventive footwear andshock-absorbing insole for patients at riskfor ulceration. The shoe upper is made ofsoft self-moldable material without seams.A high toe box facilitates insertion ofthe insole

Figure 6.10 Interdigital neuro-ischemic ulceration caused by tight shoes


Figure 6.11 Silicone ring used to keep adjacent toes apart

NEURO-ISCHEMIC ULCERSON THE MEDIAL SIDE

OF THE FOOT

A 51-year-old obese male patient whohad type 2 diabetes since the age of34 years and was currently being treatedwith glimepiride, visited the outpatient dia-betic foot clinic. During the past 12 monthshis diabetes control varied (HbA1c:7.5–9.0%). The patient had hypertensionwhich was being treated with quinapriland furosemide; he was a smoker untilthe age of 49 years and was currentlybeing treated with inhalations of ipra-tropium bromide and oral theophylline forthe management of chronic obstructive pul-monary disease. Painful leg and foot neu-ropathy was treated with carbamazepine,with fair results. A vascular surgeon had

prescribed low dose aspirin and buflomedil.Background retinopathy (hemorrhages andsoft exudates) and nephropathy were alsodiagnosed.

Moderate pes planus was noted (Fig-ure 6.12). Reflexes of both knees andAchilles tendons were absent, and therewas decreased deep and superficial sen-sation (light touch, cold and warm sen-sation, monofilament, pin-prick sensationand vibration perception threshold). Thepatient also suffered from venous insuffi-ciency, mild ankle edema and skin atrophy.Hematocrit, 35.5%; creatinine, 1.3 mg/dl(114.9 µmol/L); urine protein, 1100 mg/24 h; normal plasma lipid profile; BMI,32 kg/m2. A 4-cm aneurysm of the abdomi-nal aorta was found by ultrasound scan. Theankle brachial index was 1.4 due to calcifi-cation of the posterior tibial and the dorsalpedal arteries. A triplex of the leg arteries


Figure 6.12 Neuro-ischemic ulcers on the hindfoot

revealed significant diffuse stenoses mainlyof the arteries in the left leg.

The patient had two painful superficialulcers on the medial aspect of his rightfoot due to trauma from his footwear,which he first noticed 3 months earlier.He used topical povidone iodide with noimprovement.

The ulcers were clean without signs ofinfection. A mild callus had formed asa result of shoe friction. At the clinicthe ulcers were debrided on a weeklybasis and dressed with standard gaugewith 15% saline. They healed completelyin 1 month. Povidone iodide was dis-continued as it impairs wound healing.Instruction in appropriate foot care andfoot hygiene was provided, and suitablefootwear was prescribed.

Neuro-ischemic ulcers comprise almost40% of all diabetic foot ulcers. Ischemiculcers develop at sites which are notstressed by high pressure, such as the lat-eral, medial or dorsal aspect of the footand are usually painful. Intervention with

vascular surgery (bypass grafting or percu-taneous transluminal angioplasty) is usuallyneeded in order to restore the blood supplyto the periphery.

Keywords: Peripheral vascular disease;neuro-ischemic foot ulcers; pes planus

NEURO-ISCHEMIC ULCERON THE FIRST

METATARSAL WITHOSTEOMYELITIS

An ostensibly small, painless neuro-isch-emic ulcer on the medial-plantar area ofthe first metatarsal head with callus forma-tion and purulent discharge was the reasonfor this patient’s visit (Figure 6.13). Clawdeformity of lesser toes was present. Afterdebridement, a 1.5 × 1.0 × 1.0 cm ulcerwas revealed. A plain radiograph showedosteomyelitis of the first metatarsal head.Staphylococcus aureus was isolated from


Figure 6.13 An ostensibly small neuro-ischemic ulcer complicated by osteomyelitis. Clawdeformity of lesser toes is also apparent

the discharge and the patient was treatedwith clindamycin for 6 months, with a goodoutcome.

Keywords: Neuro-ischemic ulcer; osteo-myelitis

NEURO-ISCHEMIC ULCERSON THE MIDSOLE

AND HEEL

After surgical debridement this diabeticpatient suffered from two painful neuro-ischemic ulcers on the right midsole andthe medial aspect of the heel (Figures 6.14and 6.15). Cellulitis around the plantarulcer was observed. Pedal pulses wereweak and the ankle brachial index was0.7. The ulcers resulted from ruptured blis-ters which had developed after prolongedwalking in new shoes. Initially the ulcerswere painless due to peripheral neuropathy,

and the patient continued his activities.An angiogram showed mild atheromatousdisease at the iliac and common femoralartery, severe stenosis in the middle of theright superficial femoral artery and a lesserdegree of stenosis in the popliteal arteries.Balloon angioplasty of the right superfi-cial femoral artery was carried out and anintravascular stent was inserted. Use of awheelchair to offload pressure, adequate useof various antibiotics and a revasculariza-tion procedure resulted in complete healingof the ulcers.

Keywords: Neuro-ischemic ulcers

NEURO-ISCHEMIC ULCERON THE FOREFOOT WITH

OSTEOMYELITIS

A 64-year-old male patient with type 2 dia-betes that had been diagnosed at the age


Figure 6.14 The deep neuro-ischemic ulcer with surrounding cellulitis on the right sole resultedfrom ruptured blisters which developed after prolonged walking in new shoes

Figure 6.15 Heel ulcer in the patient whose foot is shown in Figure 6.14. The yellowishappearance of the bed of the ulcer is indicative of ischemia


of 55 years, was referred to the outpatientdiabetic foot clinic because of an infectedchronic ulcer on his left foot. The patienthad a history of heart failure, ischemic heartdisease and stage II peripheral vascular dis-ease (intermittent claudication) according tothe Fontaine classification (see Chapter 1).He also reported burning pain and numb-ness in his feet which worsened during thenight. Three months earlier, after a longwalk, the patient noticed the appearance ofa small ulcer under his left first metatarsalhead. He did not ask for medical help atthat time since he felt no pain. A yellowishdischarge was present on his socks and theinsole of the left shoe.

On examination, an infected, foul-smell-ing ulcer was observed under his secondmetatarsal head, extending into the secondweb space (Figure 6.16). Another ulcer sur-rounded by callus was also noted underthe first metatarsal head. Peripheral pulseswere weak on both feet. He had find-ings of severe diabetic neuropathy. Afterdebridement a purulent discharge emanatedfrom the deeper tissues of the dorsumof the foot. A plain radiograph did notreveal osteomyelitis. A culture of the pusrevealed Staphylocccus aureus. The patientwas afebrile, but he was admitted to thehospital and treated with i.v. administra-tion of amoxicillin–clavulanic acid. Twoweeks after his admission osteomyelitis atthe proximal phalanx of the second toewas diagnosed. The patient sustained a sec-ond toe disarticulation at the metatarsopha-langeal joint. The wound healed well, andthe infection subsided completely.

Several relapses of foot ulceration oc-curred in the following years. The patientattended the foot clinic erratically anddid not wear appropriate footwear. Twoyears after his amputation a new neuro-ischemic ulcer developed on the midsole(Figure 6.17) caused by a worn-out insole.

Figure 6.16 An infected neuro-ischemic ulcersoaked in profound discharge, on the plan-tar area between the first and the second leftmetatarsal heads extending into the second webspace. A second ulcer surrounded by callus isalso seen under the first metatarsal head

A new neuro-ischemic ulcer under his firstmetatarsal head was also present. There wascallus formation below his disarticulatedsecond toe.

Refusal to wear suitable footwear is amajor problem in patients at risk for footulcers. Although there is evidence to sug-gest that the correct footwear reduces theincidence of foot ulcers, and many health-care systems cover 70–100% of the costof preventive footwear (shoes and insoles),only 20% of patients wear appropriatefootwear on a regular basis. Effective edu-cation may increase this rate. In addition,the recurrence of ulcers after initial heal-ing is also common. A recurrent ulcer is


Figure 6.17 The same patient whose foot isillustrated in Figure 6.16, two years after sec-ond toe disarticulation. A neuro-ischemic ulcercaused by a worn-out insole is seen on mid-sole. A recurrent neuro-ischemic ulcer is presentunder the first metatarsal head. A callus hasformed below the disarticulated second toe

defined as any tissue breakdown at the samesite as the initial ulcer occurring during the30 days following the initial healing. Anynew ulcer that occurs at the same site within30 days of healing is considered to be partof the original episode. An ulcer at a differ-ent site is considered to be a new episodeindependent of the time of its development.New ulcers develop at the same or differentsites in a foot with prior foot ulceration inabout 50% over 2–5 years. Thus the heal-ing of an ulcer is just the first step in themanagement of the patient at risk. Appro-priate education, prescription of the correct

footwear and reduction — if possible — ofthe risk factors for foot ulceration (cor-rection of foot deformities, regular callusremoval, improvement in vascular supply tothe feet), may reduce the risk for recurrenceof foot problems in patients with diabetes.

Keywords: Neuro-ischemic ulcer; recur-rent ulcers; compliance with suitablefootwear

NEURO-ISCHEMIC ULCERON THE HALLUX WITH

OSTEOMYELITIS

A 76-year-old female patient with type 2diabetes diagnosed at the age of 62 years,attended the outpatient diabetic foot clinicfor a chronic ulcer on the right hallux. Shehad a history of ischemic heart disease andperipheral vascular disease.

On examination she had findings ofperipheral neuropathy. Pedal pulses wereweak on both feet. The patient had apainful neuro-ischemic ulcer with dimen-sions 1.0 × 1.0 × 0.4 cm and a sloughybase on the medial aspect of the right hal-lux caused by a tight shoe (Figure 6.18).A plain radiograph revealed osteomyeli-tis involving the condyle of the proxi-mal phalanx of the hallux (Figure 6.19).The ankle brachial index was 0.6. Duplexultrasonography of the arteries of the legsrevealed multilevel bilateral atheroscleroticdisease in her superficial femoral arter-ies and severe stenosis in the arteries ofher left tibia. The pedal arteries were notinvolved. The patient underwent a femoro-popliteal and a popliteal-peripheral bypass.Since sharp debridement of the ulcer wastoo painful, a dextranomer was appliedfor mechanical debridement on a dailybasis. A swab culture and a culture of


Figure 6.18 Neuro-ischemic ulcer with a sloughy base on the medial aspect of the right hallux

Figure 6.19 Osteomyelitis of the condyle in the proximal phalanx of the hallux of the foot shownin Figure 6.18


the sequestrum seen in a plain radiographrevealed Pseudomonas aeruginosa and thepatient was treated with ciprofloxacin. Withlocal wound care and antibiotic treatmentthe ulcer healed completely in 12 weeks(Figure 6.20). She continued with antibiotictreatment for a total of 6 months.

Inadequate blood supply prevents heal-ing of foot ulcers especially when they arecomplicated by osteomyelitis.

Debridement of an ulcer is the corner-stone of the management of active, acuteor chronic wounds. The aim of debride-ment is to remove fibrin (white, yellow orgreen tissue seen on the bed of an ulcer)and necrotic tissue (black tissue) and to pro-duce a clean, well vascularized wound bed.Types of debridement are as follows:

• Sharp surgical (using scalpels), the goldstandard for wound preparation, removesboth necrotic tissue and microorganisms

• Mechanical (using wet-to-dry dressings,hydrotherapy, wound irrigation and dex-tranomers)

• Enzymatic (using chemical enzymes suchas collagenase, papain or trypsin in acream or ointment base)

• Autolytic debridement (using in vivoenzymes which self-digest devitalizedtissue such as hydrocolloids, hydrogels,and transparent films)

Callus formation at the borders of neu-ropathic ulcers should be removed. Themajority of patients with severe diabeticneuropathy feel no pain, therefore exten-sive sharp debridement or even opera-tions on the feet can be performed with-out anesthesia.

The use of enzymatic debridement isincreasing. Chronic wounds are enzymati-cally debrided in elderly patients when reg-ular, sharp debridement is not possible, e.g.if the necrotic zone is thin; in ulcers withsinuses; and as an additional procedure tosharp debridement. Combination of colla-genase with hygrogels or alginates seemsto have synergistic effects.

Autolytic debridement uses the body’sown enzyme and moisture to re-hydrate,soften and finally liquefy hard eschar andslough. It is selective, as only the necrotictissue is liquefied, and painless to thepatient. Its main indication is non-infectedulcers with mild to moderate exudates.Autolytic debridement can be achieved withthe use of occlusive or semi-occlusivedressings which maintain the wound fluidin contact with the necrotic tissue. (For amore detailed description of the differenttypes of dressings and their indications seeChapter 2.)

The use of sterile maggots (biosur-gery, larval therapy, maggot debridement

Figure 6.20 The final stages of ulcer healing in the foot shown in Figures 6.18 and 6.19. Notethe chronic onychomycosis of the hallux with brown discoloration and thickening of the nail


Figure 6.21 Neuro-ischemic ulcers onthe dorsum of claw toes

Figure 6.22 Commercially-availablepreventive footwear with high toe boxand minimal seaming for forefoot defor-mities


therapy) is a practical and highly cost-effective alternative to conventional dress-ings or surgical intervention in the treat-ment of sloughy or necrotic wounds. Itis also a valuable tool in cases wherewounds have been infected with antibiotic-resistant pathogens.

All chronic wounds are contaminatedwith bacteria. Studies have shown that aburden of 1.0 × 106 colony-forming unitsper gram of tissue can cause signifi-cant tissue damage and impair healing.The use of cadexomer iodide decreasesmicrobial load, and is particularly use-ful in the treatment of wounds colo-nized by methicillin-resistant Staphylococ-cus aureus, Pseudomonas aeruginosa orCandida albicans.

Other local antimicrobials are also effec-tive against a wide range of commonmicroorganisms.

Keywords: Neuro-ischemic ulcer; osteo-myelitis; types of debridement

NEURO-ISCHEMIC ULCERSON THE DORSUM OF CLAW

TOES

Severe claw toe deformity, combined withperipheral diabetic neuropathy and vascu-lar disease, predisposes to ulceration of thedorsum of the toes after repetitive traumadue to irritation of the thin skin by inap-propriate shoes (Figure 6.21). The use ofextra depth shoes such as those shown inFigure 6.22, in addition to basic foot care,should be sufficient to ensure ulcer healingand prevention of recurrence, provided theulcers are not infected Non-invasive vascu-lar testing of this patient revealed multilevelstenosis of the arteries in both legs. Thepatient was referred to the vascular surgerydepartment.

Keywords: Neuro-ischemic ulcers on thedorsum of toes; preventive footwear; clawtoes

NEURO-ISCHEMIC ULCERWITH OSTEOMYELITIS

OVER THE FIFTHMETATARSAL HEAD

A 49-year-old male patient with a 4-yearhistory of type 2 diabetes being treatedwith gliclazide, and an 8-year history ofmultiple sclerosis, was admitted because ofmild fever and ulcers on his right foot.He had sustained an amputation of the lasttwo phalanges of his right fifth toe 2 yearsbefore admission.

Figure 6.23 Neuro-ischemic ulcers on theright foot over the fifth and first metatarsalheads. The last two phalanges of the fifth toehave been amputated and there is a superfi-cial ulcer on the dorsum of the second toe.Onychodystrophy is due to peripheral vascu-lar disease


On examination he had a temperature of37.9 ◦C, a pulse rate of 82 pulses per minuteand his blood pressure was 140/80 mmHg.An infected ulcer was present on the upperaspect of his foot over the base of hisamputated toe, and a second one over theplantar aspect of the fifth metatarsal head(Figure 6.23). He had hypoesthesia in bothfeet, and absence of pulses in his right legand foot. There were pulses in his left footand both femoral arteries. Achilles tendonreflexes were reduced and he had a Babin-ski sign on the right foot. His white bloodcell count was 12,200/mm3 with 74.7%neutrophils. His erythrocyte sedimentationrate was 38 mm/h. Blood glucose was188 mg/dl (10.4 mmol/l) and his HbA1c

was 7.5%. Protein was present in a urine

Figure 6.24 X-ray of the foot shown in Fig-ure 6.23. There is osteomyelitis in the fifthmetatarsal head and the distal phalanges of thefifth toe have been amputated

sample. An X-ray revealed osteomyelitis ofthe head of the fifth metatarsal, right underthe ulcerated area (Figure 6.24). The patientwas treated empirically with clotrimoxazoleand clindamycin. Strenotropomonas mal-tophilia was isolated from a swab culture

Figure 6.25 Arteriography of the patientwhose foot is shown in Figure 6.23. There issevere obstruction of the distal part of the rightfemoral and popliteal arteries; the pedal arteriesare patent and filled by collateral circulation


and netilmicin was added to the treatmentregimen after the antibiogram.

An angiogram revealed severe obstruc-tion of the lower right femoral and poplitealarteries (Figure 6.25). Vascular surgeonssuggested a femoro-tibial bypass graft afterhis general condition had been stabilizedfor several months, or in the case of an

emergency, since no gangrene was presentat the time. Pentoxyphillin and buflomedilwere prescribed. The ulcer improved after2 weeks of antibiotic treatment and localcare.

Keywords: Neuro-ischemic ulcer; angiog-raphy; osteomyelitis

Chapter VIIGANGRENE

� DRY GANGRENE OF TOES

� DRY GANGRENE WITH ISCHEMIC NECROSIS

OF THE SKIN

� DRY GANGRENE OF HEEL

� DRY GANGRENE OF ALL TOES

� WET GANGRENE AND SEPSIS

� DRY GANGRENE OF THE TOE

� STENT

� DIGITAL SUBTRACTION ANGIOGRAPHY

� WET GANGRENE OF THE TOES

� WET GANGRENE OF THE FOOT

� WET GANGRENE LEADING TO MID-TARSAL

DISARTICULATION

� EXTENSIVE WET GANGRENE OF THE FOOT

� WET GANGRENE OF THE HALLUX



Gangrene 127

DRY GANGRENEOF THE TOES

A 65-year-old male patient with type 2 dia-betes diagnosed at the age of 61 years andtreated with sulfonylurea, was admitted tothe Vascular Surgery Department. He was aheavy smoker and had a sedentary lifestyle.He had hypertension, background diabeticretinopathy and dyslipidemia (triglycerides:4 mmol/l; HDL-cholesterol: 0.67 mmol/l).His diabetes control was poor (HBA1c:8.5%). The patient complained that in theprevious 3 weeks he had experienced painwhich required analgesia when he was atrest. He had typical symptoms of intermit-tent claudication for 2 years with progres-sive worsening.

On examination, extensive dry gangrenewas found involving all the toes and witha necrotic area over the dorsum of hisleft foot (Figure 7.1). The foot arteriesand left popliteal artery could not be felt,while the femoral arteries were just pal-pable bilaterally. Pulses in the right footarteries were absent; the skin was coldand the right popliteal artery was just pal-pable. The ankle brachial index was 0.4.The patient had reduced sensation of pain,light touch and temperature. The vibrationperception threshold was 35 V on the leftand 30 V on the right foot. Critical limbischemia with dry gangrene was diagnosed;an angiogram showed extensive stenosisof the common iliac, superficial femoraland popliteal arteries of both feet. Aorto-femoral and femoro-popliteal bypass graftswere undertaken 2 days after admission,followed by mid-tarsal disarticulation (atLisfranc’s joint). The postoperative periodwas without any complications and thewound healed completely.

Gangrene is characterized by the presenceof cyanotic, anesthetic tissue associated with

or progressing to necrosis. It occurs whenthe arterial blood supply falls below mini-mal metabolic requirements. Gangrene canbe described as dry or wet. Wet gangrene isdry gangrene complicated by infection (seebelow, and Figures 7.24 and 7.25).

Dry gangrene is characterized by itshard, dry texture, usually occurring in thedistal aspects of the toes, often with a cleardemarcation between viable and necrotictissue. Once demarcation occurs, as is thecase in this patient, the involved toes maybe liable to auto-amputation. However, thisis a long (several months) and unpleasantprocess. In addition, many patients do nothave an adequate circulation to heal a distalamputation. For these reasons it is commonpractice to evaluate the arteries angiograph-ically and to carry out a bypass or a percu-taneous transluminal angioplasty with con-comitant limited distal amputation, in orderto improve the chances of wound healing.

CRITICAL LEG ISCHEMIA

Critical leg ischemia is defined — accordingto the consensus statement on critical limbischemia — as either of the following twocriteria: persistently recurring ischemic restpain, requiring regular adequate analgesiafor more than 2 weeks, with an ankle sys-tolic pressure ≤50 mmHg and/or a toe pres-sure ≤30 mmHg; or ulceration or gangreneof the foot or toes, with an ankle systolicpressure ≤50 mmHg and/or a toe pressure≤30 mmHg. In such patients it is impor-tant to differentiate neuropathic pain fromischemic rest pain (neuropathic pain typi-cally occurs or worsens at rest in the night).Measurement of the ankle brachial indexor toe pressure can easily differentiate thetwo conditions.

Keywords: Dry gangrene; critical limbischemia


Figure 7.1 Dry gangrene involving all the toes of the left foot with a necrotic area over themid-dorsum. Note the hard, dry texture and the clear demarcation between viable and necrotictissue. (Courtesy of E. Bastounis)

Gangrene 129

DRY GANGRENE WITHISCHEMIC NECROSIS

OF THE SKIN

Dry gangrene in a female patient with type2 diabetes, involving the distal parts ofthe toes of her right foot is illustrated inFigure 7.2. The pedal arteries were not pal-pable and the ankle brachial index was 0.4.A well-demarcated red area extended up tothe ankle and the lateral foot, indicatingischemic necrosis of the skin. Angiogra-phy showed the patient to have multilevelsevere atherosclerotic disease with involve-ment of the tibial and pedal arteries. Anattempt at mid-tarsal (at Lisfranc’s joint)disarticulation was unsuccessful, as it wasdiscovered during the operation that thedeep tissues were all necrotic. Finally, thepatient sustained a below-knee amputation.

Keywords: Dry gangrene

DRY GANGRENE OF HEEL

A 74-year-old female patient with long-standing type 2 diabetes was admitted tothe hospital because of a stroke. She hadpalsy of her left arm and foot. Her hos-pitalization was complicated by aspirationpneumonia, which confined the patient tobed for 2 weeks. The patient had a historyof ischemic heart disease and hypertension.Peripheral pulses were weak in both feet.On the sixth day of her hospitalization ablister with a black base developed on theposterolateral aspect of her left foot, and itevolved into an ischemic ulcer and dry gan-grene (Figure 7.3). A triplex ultrasonogramrevealed extensive severe bilateral stenosesin the superficial femoral and poplitealarteries. Revascularization was not possible

Figure 7.2 Dry gangrene of the distal areas ofthe toes of the right foot. The well-demarcatedred area extending up to the ankle and the lateralfoot indicates ischemic necrosis of the skin.(Courtesy of E. Bastounis)

due to the patient’s general condition. Aheel protector ring was applied so thatthe heel was completely suspended off thebed and sharp debridement was performed.The ulcer healed after 4 months with dailyfoot care.

Pressure ulcers are caused by constantpressure over bony heel prominences froman opposing surface such as a mattress. Thisresults in reduced blood flow in the heelwith soft tissue necrosis and consequentpressure ulcer development. These ulcersmay account for extended hospitalizationsand they are recognized as both detrimentalto an individual’s quality of life and a finan-cial burden to the healthcare system. Pres-sure ulcers of the heel are preventable bythe use of a heel protector ring (Figure 7.4)or other calf support devices (Figure 7.5).Since the calf has a large resting surface


Figure 7.3 Dry gangrene due to constant pressure under the bony heel prominence

excessive pressure is avoided. In addi-tion, revascularization should be performedimmediately in patients with heel gangrene,since such ulcers heal slowly and maybecome infected.

Keywords: Heel ulcer; dry gangrene; pres-sure ulcer; heel protective devices

Figure 7.4 Heel protector ring which keepsthe heel suspended and completely off mattress

DRY GANGRENEOF ALL TOES

Dry gangrene in a male diabetic patientinvolving all the toes is shown in Fig-ure 7.6. In this patient a bypass graft ofhis leg arteries was not possible becauseof extensive multilevel disease. The patientsustained a mid-tarsal (at the Lisfranc’sjoint) disarticulation.

Keywords: Dry gangrene; mid-tarsal dis-articulation

WET GANGRENEAND SEPSIS

A 65-year-old male patient who had type2 diabetes since the age of 45 years andwas being treated with sulfonylureas, wasbrought to the emergency clinic suffer-ing from a fever. He had left paraplegiafollowing a stroke 6 months earlier. Onemonth before admission the toes of hisleft foot became gradually very painful;

Gangrene 131

Figure 7.5 Calf support device whichprovides a larger resting surface thus off-loading pressure from the heel

Figure 7.6 Dry gangrene of all toes


Figure 7.7 A black ischemic ulcer on the dorsum of the left second toe, with edema. Note thewhitish tip of the toe due to ischemia. Fungal infection of the thickened nail of hallux with yellowishdiscoloration and subungual debris is apparent

the patient was usually calm, but occa-sionally he suffered from bouts of excru-ciating pain. A general practitioner pre-scribed cotrimoxazole, pentoxyphyllin andfentanyl patches.

On examination, the patient was febrileand his condition was critical. His secondleft toe was edematous and painful, witha black ischemic ulcer on the dorsum; thetip of the toe was white (Figure 7.7); agangrenous pressure ulcer was visible onthe left heel (Figure 7.8), due to lengthyconfinement to bed. Callosity was presentunder the right fifth metatarsal head, aswell as onychodystrophy, due to periph-eral vascular disease. No pulses were pal-pable on his left foot. Both his calves werepainful to touch. No other site of infec-tion was found. The patient was classifiedas Fontaine stage IV. Osteomyelitis was

not found on the radiographs. Swab cul-tures revealed Staphylococcus aureus andPseudomonas aeruginosa and the patientwas treated with ciprofloxacin and clin-damycin. Blood cultures were negative.On the second day the patient felt betterand became afebrile by the third day ofhospitalization.

A digital subtraction angiography, car-ried out 10 days after admission, showed80% stenosis of both iliac arteries, andalmost complete obstruction of both super-ficial femoral arteries (Figure 7.9), whilethe popliteal arteries were filled from proxi-mal collateral circulation (Figure 7.10). Theperipheral arteries had moderate atheroma-tous disease. Aorto-iliac intravascular stentswere inserted (Figure 7.11).

His second left toe was disarticulated.Surgical debridement of the heel ulcer was

Gangrene 133

Figure 7.8 Low pressure gangrenous ulcer on the left heel of the foot shown in Figure 7.7

carried out and calf supportive devicespromoted the healing process.

An infected gangrenous area of the footand particularly on a toe with bounding feetpulses is a condition that is sometimes seen.This is called ‘diabetic gangrene’ and it iscaused by a thrombosis in the toe arter-ies which is induced by toxins producedby certain bacteria (mainly staphylococciand streptococci). Plantar abscesses mayalso result in septic arteritis of the plantararch and eventually gangrene of the mid-dle toe.

Keywords: Wet gangrene; sepsis; heelulcer; digital subtraction arteriography; dia-betic gangrene

DRY GANGRENEOF THE TOE

A 52-year-old woman with type 2 diabetesmellitus diagnosed at the age of 42 yearsand being treated with sulfonylureas, wasreferred to the outpatient diabetic foot clinic


Figure 7.9 Digital subtraction ang-iography of the foot illustrated inFigures 7.7 and 7.8, showing severemultifocal stenosis of both iliac arter-ies and almost complete obstruction ofboth superficial femoral arteries

for dry gangrene of her right fourth toe. Noother diabetic complications were reported.She denied intermittent claudication.

A minor painless trauma of the affectedtoe was reported 1 week previously andthe toe became black 24 h later. Edemaand redness of the forefoot was reportedand she was treated with cotrimoxazole andclindamycin, and bed rest. Within a weekthe injury became smaller and dried out.

On examination, she had findings ofperipheral neuropathy; the pulses in herfoot arteries were diminished. The anklebrachial index was 0.5 on the right, and 0.6on the left side.

The fourth toe was gangrenous andshrunken, and a neuro-ischemic ulcer wasnoted under the head of the third metatarsal.Scaling of the skin due to edema which hadsubsided was also observed and onychodys-trophy was present (Figure 7.12). Digital

subtraction angiography revealed signifi-cant stenosis of both proximal iliac arter-ies, just after the celiac aortic bifurcation(Figure 7.13). Aortic stents were insertedat the sites of stenosis, by catheterizationwhich was carried out by an experiencedradiologist, and the foot circulation wasthus restored (Figure 7.14).

An X-ray of her left foot revealedan unknown stress fracture in the proxi-mal phalanx of her fifth toe (Figure 7.15).Osteoarthritis was also apparent in the firstand fourth metatarsophalangeal joints.

Ten days after stent insertion the fourthtoe was amputated under local anesthesia.No complications occurred postoperatively,and the wound healed completely.

Keywords: Dry gangrene; intravascularstent; stress fracture; revascularization; toeamputation

Gangrene 135

Figure 7.10 Digital subtraction angiography of the foot illustrated in Figures 7.7–7.9, showing thepopliteal arteries being supplied from extensive proximal collateral vessels. (Courtesy of C. Liapis)

STENT

A 71-year-old male patient was admittedbecause of gangrene in his left foot. Dia-betes mellitus was diagnosed on admis-sion and he was treated with low dosesof insulin. Antibiotic therapy was initiated,in addition to pentoxyphillin, prostaglandinE1 synthetic analog and phentanyl for thepain. A digital subtraction angiography wascarried out which disclosed multiple sitesof stenosis in both iliac and superficialfemoral arteries (Figure 7.16 upper panel,and Figure 7.17). A suboptimal angioplasty

was carried out on both arteries and stentswere inserted (Figure 7.16 lower panel, andFigure 7.18).

During percutaneous transluminal angio-plasty a balloon catheter is used to increasethe diameter of the lumen of the arterioscle-rotic artery. This is a quite safe and min-imally invasive technique (as compared tosurgery); it preserves saphenous veins, andreduces the length of hospital stay. How-ever, this procedure fails more often in dia-betic than in non-diabetic patients due tointimal hyperplasia.

Stents are used to treat suboptimal angio-plasty, lesions with severe dissections or


Figure 7.11 Post-stent digital subtrac-tion angiography of foot shown inFigures 7.7–7.10. (Courtesy of C. Liapis)

Figure 7.12 Dry gangrene of right fourth toe. There is a neuro-ischemic ulcer under the thirdmetatarsal head

Gangrene 137

Figure 7.13 Digital subtraction angiography of the foot shown in Figure 7.12. Severe stenosisfollowing the bifurcation of celiac aorta can be seen

significant residual stenosis after angio-plasty. The first endovascular stent app-roved for use in the iliac arteries was thePalmaz stent, a single stainless steel tube,deployed by balloon expansion. The Wall-stent, a flexible self-expanding stent whichis available in several different diametersizes, is also in use. New, covered stentsare being evaluated, with the hope thatthey may mimic surgical grafts and resistre-stenosis.

Keywords: Stents; peripheral vasculardisease; angioplasty; digital subtractionangiography

DIGITAL SUBTRACTIONANGIOGRAPHY

A 54-year-old female suffering from type 2diabetes and being treated with metformin


Figure 7.14 Post-stent digital sub-traction angiography of the foot shownin Figures 7.12 and 7.13. (Courtesy ofC. Liapis)

and insulin, was admitted to the vascularsurgery ward; she complained of worsen-ing intermittent claudication in her rightleg which had occurred over the previ-ous 2 months. As her ankle brachial indexwas very low (0.4), a digital subtractionangiography of the abdominal aorta and thearteries of the lower extremities was car-ried out.

A catheter was inserted through herright brachial artery and the tip of thecatheter was advanced into the abdominalaorta.

Advanced stenotic lesions of the abdom-inal aorta were present with partial steno-sis of the lumen. The iliac and commonfemoral arteries were patent.

Severe stenoses in the superficial femoralarteries were present, predominantly in theright vessel, with a subtotal occlusion of thedistal area of the artery (Figures 7.19 and7.20); extensive collateral vessel develop-ment was noted and both popliteal arterieswere fairly patent. There was mild athero-matous disease in the tibial arteries.

Digital subtraction angiography has re-placed film screen angiography since itprovides superior contrast resolution andthe capability of post-processing the data. Ituses less contrast and maximizes guidancefor minimally invasive therapy.

Keywords: Peripheral vascular disease;digital subtraction angiography

Gangrene 139

Figure 7.15 Plain radiograph of thefoot shown in Figures 7.12–7.14. Astress fracture of the proximal phalanxof the fifth toe and osteoarthritis inthe first and fourth metatarsophalangealjoints can be seen

WET GANGRENEOF THE TOES

A 54-year-old male patient with type 2 dia-betes diagnosed at the age of 49 years wasadmitted to the Vascular Surgery Depart-ment because of wet gangrene involving thetoes of his left foot. He had been treatedwith sulfonylurea over the previous 8 yearswhich had led to acceptable diabetes con-trol (HBA1c: 7.5%). The patient was anex-smoker. During the last 10 years he hadalso suffered from hypertension which hadbeen treated with an angiotensin convert-ing enzyme inhibitor and a diuretic. Hehad typical intermittent claudication with

pain in both calves while walking distancesof 150 m.

On examination, wet gangrene was notedon the fourth and fifth toes of his leftfoot. An infected area of ischemic necro-sis was also present on the dorsal aspectof his left third toe (Figure 7.21). Theperipheral pulses were absent and the anklebrachial pressure index was 0.4 bilater-ally; he also had findings of mild periph-eral neuropathy. The patient was in quitesevere pain, and he was treated with sys-temic analgesics and i.v. antibiotics (ticar-cillin–clavulanic acid and clindamycin).An angiogram revealed multifocal athero-matous lesions of both iliac and super-ficial femoral arteries (Figure 7.22), as


Figure 7.16 Digital subtraction angiographyshowing multiple sites of stenosis in both iliacand superficial femoral arteries (upper panel).Stent inserted in left superficial femoral artery(lower panel). (Courtesy of C. Liapis)

well as increased development of col-lateral vessels. A proximal stenosis wasnoted on both tibial and peroneal arter-ies. A femoral–popliteal bypass graft and,

eventually, a ray amputation of the last twotoes were carried out and the wound wasleft open for drainage.

Atherosclerotic lesions in diabetic pat-ients occur at sites similar to those in non-diabetics (such as sites of arterial bifur-cation), while more advanced disease iscommon in diabetic patients affecting evencollateral vessels. The pathology of theaffected arteries is similar in both diabeticsand non-diabetics. Typical atheroscleroticlesions of diabetic patients with peripheralvascular disease include diffuse multifo-cal stenosis. In addition, diabetic periph-eral vascular disease has a predilection forthe tibioperoneal arteries. All tibial arteriesmay be occluded with distal reconstitutionof a dorsal pedal or common plantar artery.Atherosclerosis begins at a younger age andprogresses more rapidly in diabetics thanin non-diabetics. While non-diabetic menare affected by peripheral vascular diseasemuch more commonly than non-diabeticwomen (men-to-women ratio 30 : 1), theincidence among diabetic men is twice thatobserved among diabetic women.

Keywords: Peripheral vascular disease;wet gangrene; digital subtraction angiog-raphy

WET GANGRENEOF THE FOOT

Gangrene complicated with infection (wetgangrene) in a patient with longstandingtype 2 diabetes. Redness and edema, dueto infection, extended up to the lower thirdof the tibia (Figure 7.23). In this patient abelow-knee amputation was necessary.

Keywords: Wet gangrene

Gangrene 141

Figure 7.17 Digital subtraction angiographyof the foot illustrated in Figure 7.16, showingmultiple sites of stenosis in right superficialfemoral artery. (Courtesy of C. Liapis)

Figure 7.18 Digital subtraction angiographyof the foot shown in Figures 7.16 and 7.17.Stent inserted in right superficial femoralartery. (Courtesy of C. Liapis)


Figure 7.19 Digital subtraction angi-ography. Severe stenoses in the rightsuperficial femoral artery with exten-sive collateral vessel development.(Courtesy of C. Liapis)

WET GANGRENE LEADINGTO MID-TARSAL

DISARTICULATION

A 70-year-old male patient who had type2 diabetes since the age of 58 years wasreferred to the outpatient diabetic foot clinicbecause of wet gangrene of his left foot. Hewas treated with insulin but his diabetescontrol was poor. He had hypertension,background diabetic retinopathy and he wasa current smoker. The patient noticed blackareas on the toes of his foot 7 days previ-ously, but he continued his daily activitiessince he felt only mild pain.

On examination, he was feverless andhis cardiac rhythm was normal. Wet gan-grene on his left midfoot and forefootand an infected necrotic ulcer on theouter aspect of the dorsum were noted(Figure 7.24). An infected ulcer was foundunder the base of his fifth toe (Figure 7.25),probably the portal of pathogens. Peripheralpulses were absent. He had findings of dia-betic neuropathy: loss of sensation of pain,light touch and vibration.

The patient was admitted to the hospitaland was treated with i.v. administrationof clindamycin plus piperacillin–clavulanicacid. Extensive surgical debridement ofthe necrotic areas was carried out. Anangiogram revealed diffuse peripheral

Gangrene 143

Figure 7.20 Digital subtraction angiographyof the foot shown in Figure 7.19. Multilevelstenoses of the left superficial femoral artery.(Courtesy of C. Liapis)

vascular disease with involvement of thepedal arteries. Seven days after admissionthe patient sustained a mid-tarsal (atLisfranc’s joint) disarticulation.

Wet gangrene is the most common causeof foot amputations in persons with dia-betes. It often occurs in patients with severeperipheral vascular disease following infec-tion. Dry gangrene may become infectedand progress to wet gangrene. Patients withdry gangrene, awaiting a surgical proce-dure, should be educated in meticulous footcare. They must be taught to inspect theirfeet daily, including the interdigital spaces,and wash them twice daily with mild soapand lukewarm water; their feet should bedried thoroughly, particular the web spaces.It is extremely important for patients toavoid wet dressings and debriding agents,as the use of these may convert localizeddry gangrene to limb-threatening wet gan-grene. The correct footwear is crucial toavoid further injury to the ischemic tissue.

Keywords: Wet gangrene; mid-tarsal disar-ticulation

EXTENSIVE WETGANGRENE OF THE FOOT

A 51-year-old male patient with type 1 dia-betes diagnosed at the age of 25 years wasadmitted to the Vascular Surgery Depart-ment because of extremely painful wet gan-grene on his right foot. The patient hadproliferative diabetic retinopathy which hadbeen treated with laser, significant loss ofhis visual acuity (3/10 in both eyes), hyper-tension and diabetic nephropathy. He hadlived in a nursing home. His diabetes con-trol was good (HBA1c: 7%). The patienthad complained of pain in his right footwhen he was at rest, 4 weeks prior to


Figure 7.21 Wet gangrene of the last two toes. An infected area of ischemic necrosis is alsoapparent on the dorsal aspect of the third toe. (Courtesy of E. Bastounis)

Figure 7.22 Digital subtraction angiographyof the foot shown in Figure 7.21. Multifocalatheromatous lesions of both iliac and superficialfemoral arteries and increased development ofcollateral vessels can be seen. This patternof arterial obstruction is considered typical indiabetes. (Courtesy of E. Bastounis)

admission; the pain worsened progressivelyand had become refractory to analgesics inthe last 2 days. He denied any trauma tohis feet. The patient had fever (38.7 ◦C)with rigors and tachycardia; his hemoglobinlevel was 10 g/l and his white blood cellcount was 16,000/l.

Figure 7.23 Wet gangrene of the right foot.Redness and edema due to infection extends asfar as the lower third of the tibia. (Courtesy ofE. Bastounis)

Gangrene 145

Figure 7.24 Wet gangrene of midfoot andforefoot in addition to an infected necroticulcer on the outer aspect of the dorsum.(Courtesy of E. Bastounis)

Figure 7.25 An infected ulcer under the base of the fifth toe of the patient whose foot is shown inFigure 7.24, probably the portal for pathogens. Gangrene of second toe and mild callus formationunder the third metatarsal head can also be seen. (Courtesy of E. Bastounis)


Figure 7.26 Wet gangrene involvingthe forefoot with cellulitis extending asfar as the right ankle. The bone andarticular surfaces of the interphalangealjoint of the fourth toe are exposed. Con-genital overriding fifth toe and ulcera-tion under the fifth metatarsal is appar-ent together with onychodystrophy andingrown nail of hallux. (Courtesy ofE. Bastounis)

On examination, he had wet gangreneinvolving the right forefoot, with cellulitisextending as far as the right ankle(Figure 7.26). The bone and articularsurfaces of the interphalangeal joint ofthe fourth toe were exposed. Rupturedblisters were observed under the right sole(Figure 7.27). The patient was treated withi.v. antibiotics (piperacillin–sulbactam plusmetronidazole) while extensive surgicaldebridement of the necrotic tissue anddrainage of the abscess cavities was carriedout. Staphylococcus aureus, Escherichiacoli and anaerobic cocci were isolatedfrom a deep tissue culture. An angiographrevealed multilevel atheromatous stenosisof his common femoral, superficial femoral,popliteal and tibial arteries.

The patient had his second and thirdtoes amputated. Extensive longitudinal inci-sions in the dorsum and the lateral footwere undertaken. Within 2 days his condi-tion worsened rapidly, and he sustained anamputation below his right knee.

Wet gangrene is characterized by a moistappearance, gross swelling and blister-ing. This is an emergency situation whichoccurs in patients with severe ischemiawho sustain an unrecognized trauma totheir toe or foot. Urgent debridement ofall affected tissues and use of antibioticsoften results in healing if sufficient viabletissue is present to maintain a functionalfoot together with adequate circulation. Ifwet gangrene involves an extensive part ofthe foot, urgent guillotine amputation at a

Gangrene 147

Figure 7.27 Sole of the foot shown in Fig-ure 7.26 with wet gangrene of the forefoot,ulceration under fifth metatarsal head and rup-tured blisters. (Courtesy of E. Bastounis)

level proximal enough to encompass thenecrosis and gross infection, may be lifesaving. At the same time a bypass surgeryor a percutaneous transluminal angioplastyshould be performed when feasible. Salinegauze dressings, changed every 8 h, workwell in open amputations. Revision to abelow-knee amputation may be considered3–5 days later.

Keywords: Wet gangrene; deep tissue in-fection; onychocryptosis; ingrown nail

WET GANGRENEOF THE HALLUX

A 72-year-old male patient with type 2 dia-betes diagnosed at the age of 60 years andbeing treated with insulin, attended the out-patient diabetic foot clinic because of painin his right hallux. His diabetes controlwas poor (HBA1c: 8.7%). He had hyper-tension and background retinopathy in botheyes. He was an ex-smoker. The patient had

Figure 7.28 Wet gangrene of the right hallux and claw toe deformity. Ischemic changes (loss ofhair, redness over toes, dystrophic nail changes) can also be seen


Figure 7.29 Triplex scan of the foot shown in Figure 7.28. Increased peak systolic velocity (PSV)of blood flow (269 cm/s) through the stenotic segment of the left common femoral artery, biphasicflow pattern and widening of the spectral window under systolic peak can be seen (normal PSV inthe common femoral artery is approximately 100 cm/s). These findings correspond to a stenosis ofthe left common femoral artery of 50–60%

Figure 7.30 Triplex scan of the foot shown in Figures 7.28 and 7.29. The spectral window in theright posterior tibial artery is biphasic, the spectrum is wide and the peak systolic velocity (PSV)is reduced (PSV at this level is expected to be about 50 cm/s). These findings denote a proximalstenosis of approximately 60%

Gangrene 149

Figure 7.31 Triplex scan of the foot shown in Figures 7.28–7.30. The spectral waveform of theright anterior tibial artery is biphasic, the spectral window is wide, the peak systolic velocity isdecreased, the velocity during diastole is increased and the downslope of the waveform is delayed.This pattern of flow is described as tardus pardus and corresponds to the presence of a proximalstenosis of 60–70%

Figure 7.32 Triplex scan of the foot shown in Figures 7.28–7.31. Examination of the left anteriortibial artery shows a monophasic waveform, indicating that a stenosis of greater than 80% is present

ischemic rest pain due to peripheral vascu-lar disease (Fontaine’s stage IV). Six daysearlier he had become aware of a worseningpain in his right hallux, the onset of whichhad been acute.

On examination, wet gangrene was notedon the right hallux; peripheral pulses wereabsent and the ankle brachial index was 0.4bilaterally. He had severe peripheral neu-ropathy (no Achilles tendon reflexes, loss of


sensation of 5.07 monofilaments and vibra-tion; the vibration perception threshold was45 V in both feet) and claw toe deformity.In addition, ischemic changes of his feetwere also noted (loss of hair, redness overtoes, dystrophic nail changes, and cold feet)(Figure 7.28).

Onychocryptosis was the cause of hisgangrene due to inappropriate nail care,resulting in paronychia and localizedischemic necrosis. The patient was treatedwith amoxicillin–clavulanic acid. A colorduplex scan (triplex) of the leg arteriesshowed mild atheromatous stenosis in hisiliac and common femoral arteries (seebelow), and severe stenosis in his rightsuperficial femoral artery. An angiogramconfirmed the ultrasound findings andrevealed a >95% stenosis in the middleof his right superficial femoral artery, withthe development of collateral circulation.The right anterior tibial artery was almostcompletely obstructed just after to thepopliteal artery trisection; the foot arterieswere patent.

The patient underwent a right aorto-popliteal and a popliteal-peripheral bypass.His recovery was good and the infectedhallux improved gradually.

Education in foot care was provided.The patient was advised to wear appropri-ate footwear.

Increased peak systolic velocity (PSV)of blood flow (269 cm/s) through the

stenotic segment of the left commonfemoral artery, a biphasic flow pattern andwidening of the spectral window under thesystolic peak were observed (Figure 7.29)(normal PSV in the common femoralartery is approximately 100 cm/s). Thesefindings correspond to a 50–60% stenosisin the left common femoral artery. Thespectral window in the right posterior tibialartery (Figure 7.30) was also biphasic, thespectrum was wide and the PSV wasreduced (PSV at this level is expectedto be about 50 cm/s) indicating that aproximal stenosis of approximately 60%was present. The waveform of the rightanterior tibial artery (Figure 7.31) wasbiphasic, the spectral window was wide,the peak systolic velocity was decreased,the velocity during diastole was increasedand the downslope of the waveform wasdelayed. This pattern of flow is describedas tardus pardus and corresponds to thepresence of a proximal stenosis of 60–70%.Examination of the left anterior tibialartery (Figure 7.32) showed a monophasicwaveform, indicating that a stenosis ofgreater than 80% was present.

Keywords: Dry gangrene; dystrophic nails;onychocryptosis; ingrown nail; triplex scan-ning; peak systolic velocity; evaluation ofarterial stenosis

Chapter VIIIINFECTIONS

� THE INFECTED FOOT ULCER

� SOFT TISSUE INFECTION UNDER CALLUS

� INFECTION UNDER CALLUS OVER FIFTH TOE

� SOFT TISSUE INFECTION

� WEB SPACE INFECTION

� ONYCHOMYCOSIS

� FUNGAL INFECTION WITH MULTIMICROBIAL

COLONIZATION

� DEEP TISSUE INFECTION AFTER

INTERPHALANGEAL MYCOSIS

� DEEP TISSUE INFECTION

� DEEP TISSUE INFECTION OF A CHARCOT FOOT

WITH A NEUROPATHIC ULCER

� OSTEOMYELITIS

� OSTEOMYELITIS OF THE HALLUX

� PHLEGMON

� INFECTED PLANTAR ULCER WITH OSTEOMYELITIS

� NEUROPATHIC ULCER WITH OSTEOMYELITIS

� OSTEOMYELITIS OF THE FIRST METATARSAL HEAD

� CHRONIC NEUROPATHIC ULCER

WITH OSTEOMYELITIS

� BONE SCINTIGRAPHY IMAGING

� OSTEOMYELITIS OF THE HEEL



Infections 153

THE INFECTED FOOTULCER

Invasion of foot tissues by microorganisms,usually accompanied by an inflammatoryresponse, may follow colonization of theskin by initially harmless bacteria, or occuras a primary event.

Diagnosing a foot ulcer infection isbased on clinical criteria. A superficialor a full-thickness ulcer, treated inade-quately, predisposes to infection, althoughcellulitis or osteomyelitis can occur with-out a break in the skin. Infected ulcersare often asymptomatic, especially if thepatient feels no pain, due to diabeticpolyneuropathy; or they may cause milddiscomfort, and produce some drainage,which eventually may become purulent andodorous. Disturbance of blood glucose con-trol may be early evidence of a localinfection.

Clinical assessment of any ulcer includesdescription of location, appearance, extent,depth, temperature, and odor. Appearanceincludes color, type and condition of tis-sue, presence of drainage, an eschar, necro-sis or surrounding callus. Infected woundsmay be purple or red, or even brown orblack, depending on the pathogen and itsetiology, and their drainage may be serous,hemorrhagic or purulent. Induration of theskin and swelling usually denotes infec-tion. Extent is measured either directly ona clear film, or by defining length andwidth of the ulcer. Depth is estimated witha sterile blunt probe, which also deter-mines underlying sinus tracts, abscessesor penetration to a bone. Temperature isestimated by the hand of the examineror measured by a dermal thermometer.Underlying infections raise skin tempera-ture. Foul odor of an ulcer may denote

infection by a specific pathogen (such asProteus, Pseudomonas, anaerobes, a mixedinfection, or fungi), or, simply a necroticprocess.

Wound infections are categorized asmild, moderate or severe. Mild infectionsare superficial infections confined to theskin and the subcutaneous fat, with mini-mal or no purulence or cellulitis. Moder-ate infections are deep and may involvefasciae, muscles, tendons, joints or bones.They may present as cellulitis of 0–2 cmin diameter, or a plantar abscess, and theymay cause systemic symptoms; they imposea certain risk of amputation. Severe infec-tion of a foot ulcer is a deep infection withmore than 2 cm of cellulitis, lymphangi-tis, gangrene, and/or necrotizing fasciitis,threatening limb loss and causing systemictoxicity. Absence of symptoms or signs ofsystemic illness does not exclude a limb-threatening infection.

Cultures for aerobic and anaerobic path-ogens and fungi assist in the managementof infection. Curettage of the base of thedebrided ulcer, culture of material collectedby surgical biopsy of deep tissue or bone,or aspiration of drainage are preferred;superficial swab cultures are not usuallyhelpful, since they often produce differentresults from cultures of deep tissues. Theyare also difficult to interpret because of thenumber of pathogens found on the surfaceof a wound and they are unsuitable foranaerobes.

Before culturing a wound, any overlyingnecrotic tissue should be removed by vigor-ous scrubbing with saline-moistened sterilegauze.

Bacteria that colonize normal skin arecoagulase-negative staphylococci, α-hemo-lytic streptococci and other gram-positiveaerobes, and corynebacteria. Staphylococ-cus aureus or β-hemolytic streptococci,


pathogens that colonize the skin of dia-betic patients, are the causative agents ofacute infections in antibiotic-naıve patients,and are nearly always the cause of cel-lulitis in non-ulcerated skin; Staphylococ-cus aureus is the most commonly recov-ered pathogen in most infections in whicha single agent is isolated. Polymicrobialcultures, with an average of five or sixorganisms, are often obtained from patientswith chronic lesions, especially when theyhave been treated with antibiotics for sometime; anaerobes, mostly Bacteroides sp. andvarious anaerobic gram-positive cocci areoften isolated from deep necroses; Pro-teus spp. and Escherichia coli predominateamong gram-negative bacilli; and Pseu-domonas is often isolated from indurated,wet wounds. In severe infections, gram-negative pathogens and anaerobes predom-inate, versus gram-positive pathogens andenterobacteriaceae, which are usually iso-lated from mild infections. Severity ofinfection does not predict the causativemicroorganism.

Colonization of skin with any bacteriumwithout concomitant infection, does notneed treatment; therefore culture resultsshould be interpreted with caution.

Mild or moderate cellulitis may betreated with dicloxacillin, first-generationcephalosporins or clindamycin. Cotrimox-azole is an alternative for treating a provenstaphylococcal infection, as well as forenterobacteriaceae.

When infection is mild and the causativepathogens and their susceptibility to antibi-otics are predictable, empirical antibiotictherapy is justified. A narrower-spectrumagent may be chosen, such as first-gen-eration cephalosporins and/or clindamycin.One to three weeks of therapy may sufficefor soft tissue infections. The more severethe infection and the higher the prevalenceof antibiotic resistance, the greater the need

for microbiological information. Second-generation oral cephalosporins, amoxicil-lin–clavulanic acid or fluoroquinolones,and clindamycin or metronidazole may beeffective oral treatment against moderateinfections, for patients who do not needhospitalization, when a mixed infection issuspected or before microbiological dataare available.

Patients with severe infections, andthose in a systemic toxic condition, shouldbe hospitalized and treated with intra-venous antibiotics, since they may beunable to swallow or tolerate oral ther-apy, in addition to which more pre-dictable levels of antibiotics in infectedtissues can be achieved with intravenousadministration. Such patients are usu-ally treated with broad-spectrum antibi-otics, before cultures and antibiogramsare available. Imipenem–cilastin, ampi-cillin–sulbactam, piperacillin–tazobactam,third-generation cephalosporins or fluo-roquinolones are usually effective; clin-damycin or metronidazole may be addedand an agent with a narrower spectrum maybe chosen later based on the antibiograms.Urgent surgical drainage or removal of deadtissues may also be needed. Arterial insuf-ficiency may compromise therapy as it pre-vents the antibiotics from reaching the siteof infection. In this case surgical revascu-larization of the limb is carried out.

Radiographic evaluation is necessarywhen osteomyelitis is suspected or forwounds of long duration. Subcutaneous gas,foreign bodies, fractures, cortical erosionsor neuro-osteoarthropathy may be seen onplain radiographs.

Keywords: Infection, clinical assessment;infection, diagnosis; cultures, curettage;infection, mild; infection, moderate; infec-tion, severe

Infections 155

SOFT TISSUE INFECTIONUNDER CALLUS AT THE

TIP OF A CLAW TOE

In the case of claw toe deformity of the sec-ond toe, callus formation and onychodys-trophy was due to exposure of the tip of thetoe to high pressure during the propulsionphase of gait.

A purulent discharge was evident afterremoval of the callus (Figure 8.1). Thepatient felt no pain or discomfort dueto severe peripheral neuropathy. No othersigns of infection were present on thetoe or the forefoot, therefore drainage ofpus was adequate, and no further treat-ment was needed. Appropriate footwearwas prescribed.

Keywords: Soft tissue infection; claw toe;onychodystrophy; subungual hemorrhage;third ray amputation

INFECTION UNDERCALLUS OVER FIFTH TOE

A 66-year-old female patient, with type2 diabetes which was diagnosed at theage of 51 years was referred to the dia-betic foot clinic for chiropody treatment.On physical examination she had severeperipheral neuropathy, and bounding pedalpulses. Superficial vein dilatation on thedorsal foot, dry skin — as a result of neu-ropathy — and hyperkeratosis over the fifthmetatarsal head were noted. Painless hyper-keratosis was seen over the dorsal aspectof the left little toe, caused by inappropri-ate footwear. After callus removal a puru-lent discharge was noticed (Figure 8.2). Acoagulase-negative Staphylococcus aureuswas isolated from the pus. A plain radio-graph was negative for bone involvement.No antibiotic was given since the pus haddrained completely. The ulcer healed within2 weeks after local treatment.

Figure 8.1 Purulent discharge was evident after removal of callus from the tip of this secondclaw toe with onychodystrophy. A third ray amputation was carried out 2 years ago. A subungualhemorrhage due to intense trimming of the nail of the fourth toe can be seen


Figure 8.2 Superficial vein dilatation can be seen on the dorsal foot along with dry skin andhyperkeratosis over the fifth metatarsal head. There was painless hyperkeratosis over the dorsalaspect of the left little toe. After callus removal purulent discharge was noted

Non-limb-threatening infections are usu-ally caused by gram-positive cocci, typi-cally Staphylococcus aureus and Strepto-coccus spp. In hospitalized patients withdiabetic foot infections, methicillin-resistantStaphylococcus aureus as well as entero-cocci are more prevalent.

Keywords: Infection; callus, claw toes

SOFT TISSUE INFECTION

A 58-year-old male patient with type 2 dia-betes, diagnosed at the age of 45 years,attended the outpatient diabetic foot clinicfor chiropody treatment on a fortnightlybasis. He had severe peripheral neuropa-thy, claw toe deformity and prominentmetatarsal heads. He mentioned mild pain

on his left midsole on finding a coin in hisshoe after prolonged walking.

On examination, he had a lax blistercontaining purulent fluid under his leftmidsole. There was extensive surroundingerythema and callus formation under thesecond metatarsal head (Figure 8.3). Theblister was removed and dressed, and thepatient was advised to use crutches andwalk on his heel. He was treated withclindamycin for 2 weeks. Debridement ofthe callus was also carried out.

The blister had developed following anunrecognized trauma to the foot. Suchinjuries are detrimental to patients with lossof sensation. The coin in the patient’s shoeput an additional load under his midsole.All patients with loss of protective sensa-tion should be instructed to inspect and feelthe inside of their shoes before they wearthem. A selection of objects collected from

Infections 157

Figure 8.3 A lax blister containing purulentfluid under the midsole with extensive surround-ing erythema. Injury caused by a coin in theshoe which was not felt by the patient. Cal-lus formation under the second metatarsal headis apparent

patients’ shoes at the outpatient diabeticfoot clinic is shown in Figure 8.4.

Diabetic bullae may also cause blisters indiabetic patients. They occur on the lowerlegs, the dorsum of the feet, hands, andforearms and less commonly, under thesoles of the feet. Diabetic bullae more oftenaffect men. They appear suddenly as tenseand usually bilateral blisters, with diametersof 0.5 to several cm; they contain clear fluidwithout any surrounding erythema and healin a few weeks without scarring. Relapsesare common.

Keywords: Trauma; in-shoe foreign ob-jects; diabetic bullae

WEB SPACE INFECTION

A 72-year-old female patient with type 2diabetes diagnosed at the age of 61 years,was referred to the outpatient diabetic footclinic because of an infection in her leftfoot. The patient had poor diabetes control(HBA1c: 8.5%), and was being treated withinsulin twice daily. She had background

Figure 8.4 Objects collected frompatients’ shoes. Loss of protectivesensation prevents patients from feel-ing injurious stimuli


diabetic retinopathy and diabetic nephropa-thy. She reported itching in the fourth inter-digital space 6 months previously, probablydue to a fungal infection.

On examination, peripheral pulses wereweak and she had severe loss of sensation.There was significant ankle edema. A full-thickness painless, infected neuro-ischemiculcer was present in the fourth web space,with exposure of the subcutaneous tissue(Figure 8.5). No signs of systemic toxic-ity were found. The ankle brachial indexwas 0.7. The ulcer was debrided anddressed. Swab cultures obtained from thebase of the ulcer revealed Staphylococ-cus aureus and Escherichia coli. A plainradiograph excluded osteomyelitis. She wastreated with amoxicillin–clavulanic acidfor 2 weeks. Oral furosemide was initi-ated in order to reduce the ankle edema.The patient had her wound dressed athome daily and attended the outpatientdiabetic foot clinic on a weekly basis.A triplex examination of the leg arteriesrevealed the presence of moderate steno-sis in the left superficial femoral and leftpopliteal arteries. No vascular surgery was

undertaken at that time as the ulcer healedprogressively.

Fungal infections develop as a resultof poor foot hygiene, hyperhidrosis, andaccumulation of moist detritus in thewebs (Figure 8.6 shows another patient).Interdigital tinea pedis is the most commonform of chronic fungal foot infection.Itching, redness, scaling, erosion andsoaking of the skin with fluid usually occur,while in the late phase the redness subsides.Trichophyton metagrophytes Trichophytonrubrum or Epidermophyton floccosum maybe found.

Topical terbinafine cream cures mostinfections caused by Dermatophyta, andshould be continued for 2 weeks aftersymptoms subside.

Superficial bacterial infections in theinterdigital spaces may cause thrombosisof the adjacent digital arteries and spreadto deeper structures through the lumbricaltendons. Furthermore, edema impedes footcirculation, especially in the presence ofperipheral vascular disease. Adequate foothygiene and treatment of the fungal infec-tion could prevent this complication.

Figure 8.5 Full-thickness, infected neuro-ischemic ulcer in the fourth web space with exposureof the subcutaneous tissue. Ankle edema due to diabetic nephropathy, and onychodystrophy canbe seen

Infections 159

Figure 8.6 Fungal infection in the interdigital space with claw toe deformity

Keywords: Web space; infection; fungusinfection; chronic tinea pedis; Trichophy-ton metagrophytes Trichophyton rubrum orEpidermophyton floccosum.

ONYCHOMYCOSIS

The patient whose feet are shown inFigures 5.12–5.16 was suffering from ony-chomycosis and the nails and nail bedswere completely destroyed by fungus asshown in Figure 8.7. Onychomycosis perse does not cause foot problems, but whenit affects the proximal nail (proximal subun-gual onychomycosis) it may cause chronicparonychia and serve as a portal for bac-teria, resulting in deep tissue infection. Itoften co-exists with mycosis of the webspaces and it may be superinfected by bac-teria, leading to deep tissue infection aswell.

This patient was treated with terbina-fine hydrochloride, both systemic (tablets250 mg once daily) and topical (cream),for 3 months and was instructed in theappropriate foot care.

Figure 8.7 Fungal infection affecting all nailsin addition to claw toes. Patient whose feet areshown in Figures 5.12–5.16

Chronic onychomycosis is classifiedinto three clinical types: distal subungualonychomycosis is the most common form.The distal edge of the nail becomes infectedand a yellow discoloration, onycholysis


and subungual debris develop. In proximalsubungual fungal infection, the secondcommonest form, Trichophyton rubrumaccumulates hyperkeratotic debris underthe nail plate and loosens the nail,eventually separating it from its bed.This fungus infects the underlying matrixand nail plate leaving the nail surfaceintact. Leuconychia mycotica, caused byTrichophyton metagrophytes, infects thenail superficially. The nail surface becomesdry, soft and friable but the nail remainsattached to its bed. In addition to thesefungi Epidermophyton floccosum may alsobe isolated from infected areas.

Itraconazole and fluconazole are alsoeffective in the treatment of chronic ony-chomycosis.

Keywords: Onychomycosis; distal subun-gual onychomycosis; proximal subungualfungal infection; leuconychia mycotica; Tri-chophyton metagrophytes, Trichophytonrubrum or Epidermophyton floccosum; ter-binafine; itraconazole; fluconazole

FUNGAL INFECTION WITHMULTIMICROBIAL

COLONIZATION

Superficial ulcers of 10 days’ duration onthe facing sides of the left first and sec-ond toe of a 70-year-old type 2 dia-betic lady with diabetic neuropathy, beforedebridement are shown in Figures 8.8 and8.9. Note soaking of the skin. An X-ray excluded osteomyelitis. Staphylococcuscoagulase-negative, Pseudomonas aerugi-nosa and enterobacteriaceae were recov-ered after swab cultures in addition to Can-dida albicans. She was treated successfullywith itraconazole for 5 weeks. The patientused a clear gauze in order to keep hertoes apart, together with local hygiene pro-cedures twice daily. Weekly debridementwas carried out and no antimicrobial agentwas needed.

Keywords: Fungal infection

Figure 8.8 Neuro-ischemic ulcers facing each other on the first and second toe with fungalinfection and soaked skin in addition to claw toes. Foot shown from the plantar aspect

Infections 161

Figure 8.9 Neuro-ischemic ulcers facing each other on first and second toe, with fungal infection.Front aspect of Figure 8.8

DEEP TISSUE INFECTIONAFTER

INTERPHALANGEALMYCOSIS

A 60-year-old female patient with type 2diabetes diagnosed at the age of 47 yearsand treated with sulfonylurea and met-formin and with poor glycemic control, wasreferred to the diabetic foot outpatient clinicbecause of a severe foot infection.

The patient had known mycosis betweenthe fourth and the fifth toes of her rightfoot. Three days before her visit she noticedredness and mild pain on the dorsum ofher toes. Her family doctor gave her cefa-clor, but she became febrile and her footbecame swollen, red and painful. No traumawas reported.

On examination, her foot was red, warmand edematous with pustules on its dorsum(Figure 8.10). The peripheral arteries werenormal on palpation and peripheral neu-ropathy was present. Pathogen entry wasprobably via the area of the mycosis.

The patient was admitted to the hospitaland treated with intravenous ciprofloxacinand clindamycin. No osteomyelitis wasfound on repeated radiographs. Extensivesurgical debridement was carried out. Deeptissue cultures revealed Staphylococcus au-reus, Escherichia coli and anaerobes. Thepatient was discharged in fair conditionafter a stay of 1 month.

Keywords: Mycosis; deep tissue infection

DEEP TISSUE INFECTION

A 50-year-old type 1 male diabetic patientwith known diabetes since the age of25 years was referred to the outpatient dia-betic foot clinic for a large infected neuro-ischemic ulcer.

The patient suffered from retinopa-thy — treated with laser — established dia-betic nephropathy, hypertension — treatedwith enalapril and furosemide — and severeneuropathy.


Figure 8.10 Deep tissue infection of the foot following web space mycosis. Redness and edemaof the whole foot with pustules on the dorsum can be seen along with claw toes

Six months before visiting a surgeon, thepatient had noticed a painless superficialulcer caused by a new pair of shoes.Hoping it would subside quickly, he did notseek a doctor’s advice and continued hisdaily activities although the ulcer becamelarger with surrounding erythema andeventually became purulent and odorous.Fever developed. A deep tissue culturerevealed Staphylococcus aureus, Klebsiellaspp. and anaerobes. Surgical debridementwas carried out, and amoxicillin–clavulanicacid treatment was initiated. After 1 monthof stabilization, with dressings beingchanged daily, the patient noticed increasedpurulent discharge and an intense foul odor.

On examination at the diabetic footclinic, the patient was febrile and weak.He had complete loss of sensation. Periph-eral pulses were palpable. Gross ankle andforefoot edema was noted and the shortextensor of the toes and anterior tibial ten-dons was exposed (Figure 8.11). The com-mon tendon sheath and subcutaneous tis-sue were necrosed. An acrid odor emanatedfrom the foot even before the bandageswere removed. A seropurulent dischargewas being emitted from deeper structures.The patient was referred back to his sur-geon; admission to the hospital and intra-venous antibiotics together with extensivedebridement followed, and due to abiding

Infections 163

Figure 8.11 Deep tissue infection of the foot with gross ankle and forefoot edema. The shortextensor of the toes and the anterior tibial tendons are exposed, while the common tendon sheathand subcutaneous tissue are necrosed

septic fever and the critical condition ofthe patient, a below-knee amputation wasundertaken 2 days later.

Keywords: Deep tissue infection; amputa-tion

DEEP TISSUE INFECTIONOF A CHARCOT FOOT

WITH A NEUROPATHICULCER

A 65-year-old female patient with type 2diabetes mellitus since the age of 40 yearsattended the diabetic foot clinic because ofa large ulcer of the sole of her left foot.She was being treated with insulin result-ing in acceptable diabetes control (HbA1c:

7.28%). She had a history of hypothy-roidism as well as a history of ulcers underher right foot at the age of 63 years, whichhad healed completely.

The present ulcer had developed aftera minor trauma to the sole of her footwhile walking barefoot during the summer.It evolved within a month together with afast progressing gross deformity of the foot.The patient complained of mild discomfortbut no pain, so she kept on using bothfeet without any means of reducing thepressure on her ulcerated foot. She wastreated with amoxicillin–clavulanic acidand clindamycin for 20 days.

On examination, her left foot was swol-len, with midfoot collapse; it was warm(2.5 ◦C temperature difference to the con-tralateral foot), and crepitus was heard onpassive movement. A large neuropathic


Figure 8.12 Neuro-osteoarthropathy. A largeneuropathic non-infected ulcer surrounded bycallus occupies the midsole

non-infected ulcer of size 8 × 7 × 0.4 cmoccupied the midsole surrounded by cal-lus (Figure 8.12). A small, full-thicknessneuropathic ulcer was present within anarea of callus formation over the rightfirst metatarsal head (Figure 8.13). The skinon both her feet was dry and the periph-eral pulses were palpable. The vibrationperception threshold was 20 V in bothfeet. Monofilament sensation was absent,as were sensations of light touch, pain andtemperature perception.

Debridement was carried out; an X-rayshowed disruption of the tarsometatarsaljoint (Lisfranc’s joint), bone absorption ofthe first and second cuneiforms and dislo-cation of the cuboid bone (Figure 8.14). Adiagnosis of acute neuro-osteoarthropathy

Figure 8.13 Right foot of the patient whoseleft foot is shown in Figure 8.12. A small,full-thickness neuropathic ulcer within an areaof callus is present over the right first metatarsalhead

was made and a single dose of 90 mg ofpamidronate was administered. The pres-ence of ulcers prevented the use of atotal-contact cast since daily changes ofdressings were needed. The patient wasinstructed to refrain from walking andto visit the diabetic foot clinic on aweekly basis. After 1 month the mid-sole ulcer was smaller compared to itsinitial size (Figure 8.15) and showed nosigns of infection. The ulcer under herright sole healed. There was no differ-ence in the temperature between the twofeet.

After an absence of 3 weeks the patientvisited the clinic with acute foot infec-tion and fever. The midsole ulcer was

Infections 165

Figure 8.14 Plain radiographs showing neuro-osteoarthropathy in the left foot of the patient whosefeet are illustrated in Figures 8.12 and 8.13. Disruption of the tarsometatarsal joint (Lisfranc’s joint),resorption of the first and second cuneiforms and midfoot collapse can be seen

Figure 8.15 Left neuro-osteoarthropathicfoot of the patient whose feet are shown inFigures 8.12–8.14. Progress of the plantarneuropathic ulcer after 1 month of chiropodytreatment. Healthy granulated tissue coversthe bed of the ulcer


Figure 8.16 Left neuro-osteoarthropathic foot of the patient whose feet are shown inFigures 8.12–8.15, 3 weeks after the photograph shown in Figure 8.15 was taken. Signs of infection(cellulitis, blisters and edema) are present

much smaller (Figure 8.16), surrounded bycellulitis, and a new infected ulcer waspresent on the lateral aspect of the hind-foot (Figure 8.17). The patient insisted thatshe had complied with the instructions,except for the last week, when she feltconfident that the ulcer had healed. Shewas admitted to the hospital and under-went extensive surgical debridement. Intra-venous antibiotics (ciprofloxacin, penicillinand clindamycin) were administered but the

high fever persisted despite treatment; theinfection spread to the lower tibia and thepatient became septic. On the 10th day ofhospitalization, the critical condition of thepatient necessitated a below-knee amputa-tion. She was discharged in good clinicalcondition after 1 week.

Keywords: Deep tissue infection; acuteneuro-osteoarthropathy; neuropathic ulcer;below-knee amputation

Infections 167

Figure 8.17 Lateral aspect of the foot shown in Figure 8.16. Infection has spread to the wholefoot and the lower tibia. The superficial ulcer on the lateral aspect of the hindfoot may have beencaused by rupture of a blister

OSTEOMYELITIS

A 69-year-old female patient with type 2diabetes diagnosed at the age of 54 yearsand treated with sulfonylurea, was referredto the outpatient diabetic foot clinic foran infection of her right second toe. Shehad background diabetic retinopathy andhypertension. She complained of numbnessand a sensation of pins and needles in herfeet at night.

On examination, she had findings ofsevere neuropathy (no feeling of lighttouch, pain, temperature, vibration or a 5.08monofilament; Achilles tendon reflexeswere absent; the vibration perception thres-hold was >50 V in both feet). Peripheralpulses were weak and the ankle brachialindex was 0.7. Dry skin and nail dystro-phies were present. A superficial ulcer witha sloughy base was seen on the dorsum of

her right second toe which was red, swollenand painful, having a sausage-like appear-ance (Figure 8.18). She did not mention anytrauma, but inspection of her shoes revealeda prominent seam inside the toe box of herright shoe.

The sausage-like appearance of a toeusually denotes osteomyelitis. Bone infec-tion was confirmed on X-ray, showingosteolysis of the first and second pha-langes. Staphylococcus aureus and Kleb-siella pneumoniae were cultured from thebase of the ulcer. The patient was treatedwith cotrimoxazole and clindamycin for2 months. She was also referred to theVascular Surgery Department for a per-cutaneous transluminal angioplasty of herright popliteal artery. After 2 months theulcer was still active and the patient hadlocal extension of osteomyelitis despitethe restoration of the circulation in theperiphery. She eventually had her second


Figure 8.18 Sausage-like toe deformity usu-ally denotes underlying osteomyelitis

ray amputated. A bone culture revealedthe presence of Staphylococcus aureus.She continued with cotrimoxazole for twomore weeks.

Keywords: Osteomyelitis; painful–pain-less feet

OSTEOMYELITIS OF THEHALLUX

A 30-year-old male patient with type 1 dia-betes diagnosed at the age of 11 years wasadmitted because of infected foot ulcers onhis right hallux. He had a mild fever anda history of proliferative diabetic retinopa-thy and microalbuminuria. Diabetes con-trol was poor (HBA1c: 9.5%). He reporteda trauma to his left foot 2 months earlierwhen an object fell on his feet while work-ing. A superficial ulcer had developed onthe dorsal aspect of his right great toe;the ulcer had become infected because thepatient felt no pain and therefore did notseek medical advice.

On examination, pedal pulses were nor-mal. Severe peripheral neuropathy wasfound and the vibration perception thresh-old was 30 V in both feet. An infected righthallux with purulent discharge, necrotic tis-sue at the tip, and cellulitis were observed(Figure 8.19). A plain radiograph showedosteomyelitis involving both distal pha-langes (Figure 8.20).

A culture of the pus revealed Pseudo-mans maltophila, Enterobacter cloacae and

Figure 8.19 Infection of the halluxwith purulent discharge, necrotic tissueat the tip and cellulitis

Infections 169

Figure 8.20 Osteolysis of the distalphalanx and condyle of the proximalphalanx due to osteomyelitis of thehallux. Plain radiograph of the footshown in Figure 8.19

anaerobes, and the patient was treated withciprofloxacin and ampicillin–sulbactam for2 weeks, based on the antibiogram. Anamputation of the right great toe was under-taken due to persistent osteomyelitis.

Keywords: Hallux; osteomyelitis; amputa-tion

PHLEGMON

A 62-year-old male diabetic patient withtype 2 diabetes diagnosed at the age of42 years and treated with sulfonylurea,

biguanide and acarbose and whose diabetescontrol was acceptable, visited the outpa-tient diabetic foot clinic due to infection ofthe sole of his right foot. He had hyperten-sion and coronary heart disease treated withmetoprolol and aspirin. He had no previoushistory of foot problems.

On examination, the patient had fever,severe diabetic neuropathy, and bound-ing pedal pulses. He had hallux valgus,claw toes, prominent metatarsal heads, ony-chodystrophy and dry skin. Callus forma-tion superimposed on a neuropathic ulcerover his third metatarsal head was present;a callus was also noted over his fifthmetatarsal head. A superficial, painless,


infected ulcer with purulent discharge waspresent under Lisfranc’s joint (Figure 8.21).This infection progressed to a phlegmon2 days after a minor shear trauma.

The patient was admitted, and intra-venous amoxicillin–clavulanate was initi-ated. A plain radiograph excluded osteo-myelitis or gas collection within the softtissues. Computerized tomography revealeda phlegmonous subcutaneous mass under

the base of the metatarsals (Figure 8.22).A sterile probe was used to detect anysinuses or abscesses, but none was found.The patient remained bedridden for 1 weekand the infection subsided. He continuedantibiotics for one more week with lim-ited mobilization and he was released fromhospital in excellent condition. Oral antibi-otics were continued for two more weeks.Preventive footwear was prescribed and the

Figure 8.21 Superficial infected ulcerwith purulent discharge under Lisfranc’sjoint. Callus formation is superimposedon neuropathic ulcer over the third meta-tarsal head with callus formation over thefifth metatarsal head. Hallux valgus, clawtoes, prominent metatarsal heads, ony-chodystrophy and dry skin can be seen

Infections 171

Figure 8.22 Computerized tomography of the feet of the patient whose right foot is shown inFigure 8.21. A phlegmonous subcutaneous mass is present under the base of the metatarsals (arrow)

patient continued to visit the outpatient dia-betic foot clinic on a regular basis.

Computerized tomography is useful inidentifying areas of phlegmon within thesoft tissues. It may provide informationabout the exact anatomic location andextent, so that aspiration or surgical drain-age can be undertaken. Magnetic resonanceimaging and ultrasound studies are alsohelpful in this respect.

Keywords: Neuropathic ulcer; computer-ized tomography; phlegmon

INFECTED PLANTARULCER WITH

OSTEOMYELITIS

A 50-year-old female diabetic patient withtype 2 diabetes diagnosed at the age of44 years and treated with sulfonylurea, wasreferred to the outpatient diabetic footclinic because of a chronic infected ulceron her left foot. The patient lived aloneand she was being treated for depression;she had good diabetes control. A minor

trauma under her left foot was reported tohave occurred 2 years previously. She hadtreated the injury with different types ofgauzes and creams, but it failed to heal.She presented to the clinic with a large,painless, infected ulcer under her left foot(Figure 8.23).

On examination, an irregular, soaked,foul-smelling ulcer with sloughy bed, andsurrounding cellulitis of 3 cm in diameterwas found; body temperature was normal.Diabetic neuropathy was diagnosed, whileperipheral pulses were normal. Signsof osteomyelitis (osteolysis of the firstmetatarsal head, and the base of proximalphalanx of the hallux, with periostealreaction) were noted on the radiograph(Figure 8.24). A post-debridement swabculture from the base of the ulcer revealedmethicillin-resistant Staphylococcus aureusand Escherichia coli. The patient wasadmitted to the hospital. The white bloodcell count was 14,700/mm3, anemia (Hb:9.8 g/dl) characteristic of chronic diseasewas found, the erythrocyte sedimenta-tion rate was 90 mm/h and the levelof C-reactive protein was 70 mg/dl. Shewas treated with 600 mg teicoplanin


Figure 8.23 A large, irregular, soaked andinfected neuropathic ulcer with sloughy bedand surrounding cellulitis of 3 cm in diameteris shown here. A minor trauma reported tohave occurred 2 years earlier was the cause ofthis ulcer

intravenously once daily and the ulcerwas debrided and dressed. The cellulitisprogressively subsided, the ulcer becameclear and healthy granulating tissue beganto cover the ulcerated area (Figure 8.25).The patient was discharged from thehospital in good clinical condition. Shecontinued treatment with intramuscularteicoplanin for three more months andattended the outpatient diabetic foot clinicon a weekly basis. Complete offloadingof pressure from the ulcerated area wasachieved by the use of a wheelchairfor most of her activities. Platelet-derived growth factor-β (becaplermin) was

Figure 8.24 Osteolysis of the first metatarsalhead and the base of proximal phalanx ofthe hallux with periosteal reaction due toosteomyelitis are shown on this plain radiographof the foot illustrated in Figure 8.23

applied once daily. The ulcer diminishedprogressively (Figure 8.26) and healed in4 months; no relapse occurred.

All patients with deep or long-standingulcers should be evaluated for osteomyeli-tis. The possibility of an ulcer being com-plicated by osteomyelitis increases whenthe diameter of the ulcer exceeds 2 cmand the depth is greater than 3 mm; thepossibility of complications becomes evenhigher when the white blood cell count, theerythrocyte sedimentation rate and the C-reactive protein levels are high.

Treatment of acute osteomyelitis in-cludes parenteral administration of antibi-otics for 2 weeks initially, and the continua-tion of oral treatment for a prolonged period(at least 6 weeks).

Infections 173

Figure 8.25 Clear ulcer with healthy granulat-ing tissue after 1 month of appropriate treat-ment in the patient whose foot is shown inFigures 8.23 and 8.24

Keywords: Neuropathic ulcer; acute osteo-myelitis; platelet-derived growth factor-β(PDGF-β, becaplermin)

NEUROPATHIC ULCERWITH OSTEOMYELITIS

A 57-year-old obese male patient with type2 diabetes diagnosed at the age of 40 yearswas referred to the outpatient diabetic footclinic because of a chronic ulcer underhis right foot. He was being treated withinsulin and metformin with acceptable dia-betes control (HBA1c: 7.8%). He had a his-tory of background retinopathy and cataractin both eyes. He reported a severe deeptissue infection 5 years earlier after a burnsustained under his right foot. At that timehe was hospitalized for about 1 month andtreated with intravenous antibiotics and sur-gical debridement.

On examination, the patient had severediabetic neuropathy with loss of sensationof pain, light touch, temperature, vibration,

Figure 8.26 Healing of the ulcer affectingthe foot shown in Figures 8.23–8.25. Thisphotograph was taken 3 months after thatshown in Figure 8.25


Figure 8.27 Full-thickness neuropathic ulcer post-debridement under a prominent fourth meta-tarsal head

Figure 8.28 Commercially-available extra depth therapeutic shoe

and 5.07 monofilaments. Achilles tendonreflexes were absent. The vibration percep-tion threshold was above 50 V bilaterally,while the peripheral pulses were normal.A scar was noted on the dorsum of hisright foot which had an overriding fourthtoe, as a result of past surgical proce-dures. A full-thickness neuropathic ulcerwas present under his fourth metatarsalhead surrounded by callus (Figure 8.27).

A bony prominence could also be feltunder the ulcerated area. A plain radio-graph did not show osteomyelitis or neuro-osteoarthropathy. Debridement of the ulcerwas carried out and extra depth therapeu-tic shoes with a flat insole were prescribed(Figure 8.28); a window was made in theinsole in order to offload pressure on theulcerated area; the ulcer began to heal well(Figure 8.29).

Infections 175

Figure 8.29 Healing of the neuropathic ulcer shown in Figure 8.27 pre-debridement

The patient kept himself very active.He returned to the clinic after 3 weeksabsence with a deeper ulcer involving thetendons (Figure 8.30). The underlying bonecould not be detected with a sterile metalprobe and a plain radiograph did not showosteomyelitis. An elevated erythrocyte sed-imentation rate (74 mm/h) and mild leuko-cytosis were found, therefore the possi-bility of osteomyelitis was high. A mag-netic resonance imaging-T1-weighted sagit-tal image of the foot was obtained, showinga phlegmonous mass starting from the skinand extending to the deeper tissues caus-ing erosion of the fourth metatarsal head(Figure 8.31). The patient was hospitalizedso that offloading pressure from the ulcer-ated area was enforced, and intravenousantibiotics were administered. Two weekslater the size of the ulcer had decreased byalmost 50%.

Several methods are used for the diag-nosis of osteomyelitis. Probe-to-bone tests(contacting the bone with a sterile metalprobe) have a sensitivity of more than90% and they are carried out at the bed-side. Plain radiographs have a sensitiv-ity of 55%, but when repeated — usually

2 weeks later — the sensitivity is higher,making this the most cost-effective diag-nostic procedure. Computerized tomogra-phy may reveal areas with subtle abnor-malities such as periosteal reactions, smallcortex erosions and soft tissue abnormal-ities. Magnetic resonance imaging has asensitivity of almost 100% and a speci-ficity of over 80% and has the poten-tial to reveal abscesses. Therefore thisis the preferred method for the diagno-sis of osteomyelitis in many centers incases where the plain radiographs do notprovide sufficient information to make aconclusive diagnosis. However, the speci-ficity of MRI decreases in the presence ofneuro-osteoarthropathy, prior bone biopsy,recent bone fracture or recent surgery.Magnification radiography is also a veryuseful method for the detection of earlyosteomyelitis and it is used to follow upthe disease.

Bone scintigraphy imaging is explainedin Figure 8.37.

Keywords: Neuropathic ulcer; magneticresonance imaging; MRI; osteomyelitis;diagnostic methods for osteomyelitis


Figure 8.30 The neuropathic ulcer shown inFigures 8.27 and 8.29 has been aggravated bythe patient’s refusal to reduce activity levelsand poor compliance with measures to offloadpressure from the affected area

OSTEOMYELITIS OF THEFIRST METATARSAL HEAD

A 74-year-old male patient with type 2diabetes attended the outpatient diabeticfoot clinic because of a chronic painlessulcer on the medial aspect of the right firstmetatarsal head (Figure 8.32). The ulcer

developed over a bunion deformity, and hadpersisted for 10 months.

On examination, the peripheral pulseswere palpable and the patient had severeperipheral neuropathy. He could not feelpain, light touch, vibration or 5.07 monofil-aments. The vibration perception thresholdwas above 50 V in both feet. After debride-ment, the underlying bone could be felt bymeans of a sterile probe. A plain radiographrevealed osteomyelitis of the first metatarsalhead and the proximal phalanx of the rightgreat toe (Figure 8.33). The patient sus-tained a first ray amputation.

Chronic osteomyelitis needs surgical re-moval of the infected bone. However,recent data suggest that prolonged treatmentwith antibiotics (for 1 or 2 years) may erad-icate chronic osteomyelitis. However, noconsensus on this issue exists at present.

Keywords: Chronic osteomyelitis; first rayamputation; neuropathic ulcer

CHRONIC NEUROPATHICULCER WITH

OSTEOMYELITIS

A 46-year-old male patient with type 1diabetes diagnosed at the age of 27 yearswas referred to the outpatient diabetes footclinic because of a chronic ulcer under hisright fifth metatarsal head. He had accept-able diabetes control (HBA1c: 7.7%), pro-liferative diabetic retinopathy treated withlaser in both eyes, but no nephropathy. Hecomplained of muscle cramps during thenight and chronic constipation interruptedby episodes of nocturnal diarrhea. Thepatient had a history of painless diabeticfoot ulceration for 3 years under his rightfoot after a burn injury. He had attended thesurgery department of a country hospital,

Infections 177

Figure 8.31 MRI image showing osteomyelitis. A magnetic resonance imaging-T1-weightedsagittal image of the foot illustrated in Figure 8.30 showing a phlegmonous mass (arrow) extendingfrom the skin into the deeper tissues and causing erosion of the fourth metatarsal head

Figure 8.32 Chronic neuropathic ulcer over a bunion deformity


Figure 8.33 Plain radiograph of the foot illustrated in Figure 8.32 showing bone resorption,periosteal reaction and destruction of metatarsophalangeal joint of the hallux due to osteomyelitis

where he had his foot dressed and severalcourses of antibiotics were prescribed. Thepatient continued to keep himself active,without any special footwear since he feltno discomfort or pain.

On examination, severe diabetic neu-ropathy was found. The peripheral pulseswere palpable and a full-thickness neuro-pathic ulcer with gross callus formation wasobserved under his right fifth metatarsalhead (Figure 8.34). Sharp debridement wascarried out and the underlying bone wasprobed with a sterile probe. A plain radio-graph revealed pseudoarthrosis of a stressfracture of the upper third of his fifthmetatarsal, bone resorption in the metatar-sophalangeal joint, and osteolytic lesions inthe fifth metatarsal epiphysis (Figures 8.35and 8.36). Post-debridement cultures fromthe base of the ulcer revealed Staphylococ-cus aureus, Proteus vulgaris and Entero-coccus spp. The patient was treated withamoxicillin–clavulanic acid 625 mg threetimes daily for 2 weeks. He was advised torest and appropriate footwear and insoleswere prescribed. A fifth ray amputation wasundertaken and antibiotics continued fortwo more weeks. A bone culture revealed

Staphylococcus aureus. The wound healedcompletely in 2 weeks.

A ray amputation consists of removal ofa toe together with its metatarsal. The unin-volved half of the fifth metatarsal shaft waspreserved, so that it retained the insertion ofthe short peroneal muscle. Ray amputationresults in narrowing of the forefoot, but thecosmetic and functional result is excellent.However, the biomechanics of the foot aredisturbed after such an operation and thisleads to the exertion of high pressure underthe metatarsal heads of the adjacent rays.

Keywords: Neuropathic ulcer; osteomyeli-tis; ray amputation

BONE SCINTIGRAPHYIMAGING

The scintigraphy findings of a patient withpossible osteomyelitis are discussed belowand the history of this patient is illustratedin Figures 9.3 to 9.5 in Chapter 9.

A plain radiograph showed findingscompatible with osteomyelitis or neuro-osteoarthropathy of the second and third

Infections 179

Figure 8.34 Full-thickness chronic neuropa-thic ulcer with gross callus formation under theright fifth metatarsal head

metatarsal heads of this female patient. Shewas referred for a technetium-99m (99Tc)phosphonate scan. Images obtained dur-ing the flow phase are shown in the leftupper panel of Figure 8.37; during thisphase a series of 3-s image acquisitionsof the site in question is obtained. Theyshowed increased radionuclide uptake bythe tarsometatarsal area of her left foot.A static blood pool image (blood poolphase) obtained 5 min later is shown inthe right upper panel. A static delayed

image (delayed phase) obtained 3 h lateris shown in the left lower panel. Allimages showed increased uptake in thesame areas. A gallium-67 citrate study per-formed on the same day (right lower panelof Figure 8.37), showed increased radionu-clide uptake at the tarsometatarsal area.Based on the results of bone scintigra-phy the patient was diagnosed as havingosteomyelitis in the tarsometatarsal area.

99Tc scintigraphy is useful in casesof questionable osteomyelitis. It has ahigh sensitivity (over 90%) but a lowspecificity (33%), particularly in the pres-ence of neuro-osteoarthropathy. Althoughincreased radionuclide uptake during theflow and pool phase is not specific tothe diagnosis of osteomyelitis (it maymean soft tissue, bone infection or both),delayed images of the 99Tc scintigraphyshowed increased blood flow to the bonesonly, thus increasing the specificity of themethod in the diagnosis of bone infection.Patients with neuro-osteoarthropathy haveincreased bone blood flow in the absenceof osteomyelitis.

Like 99Tc scintigraphy, gallium-67 cit-rate accumulates in both osteomyelitis andneuro-osteoarthropathy. This is the reasonfor its low specificity in the diagnosis ofosteomyelitis in diabetic patients. Indium-111 white blood cell imaging (111In WBCs)is expensive, time consuming, has poor spa-tial resolution and does not distinguish softtissue from bone infection.

Keywords: Scintigraphy; bone scans; diag-nosis of osteomyelitis

OSTEOMYELITIS OF THEHEEL

A 71-year-old female patient with type2 diabetes was admitted to the hospital


Figure 8.35 Anteroposterior plain radiographof patient of Figure 8.34. Osteomyelitis. Pseu-doarthrosis of a stress fracture of the upper thirdof the fifth metatarsal, bone resorption at themetatarsophalangeal joint, and osteolytic lesionsat the fifth metatarsal epiphysis

because of a severe infection of her rightfoot. She had a history of type 2 diabetesdiagnosed at the age of 51 years, diabeticnephropathy, background diabetic retinopa-thy — treated with laser — hypertensionand ischemic heart disease. She also hada history of stroke at the age of 69 years.A heel ulcer caused after the rupture of a

Figure 8.36 Lateral plain radiograph of footshown in Figures 8.34 and 8.35, focused on theosteomyelitic lesion in the fifth metatarsal. Notethat the phalanx of fifth toe continues over fourthmetatarsal head

blister under her right heel, which devel-oped after walking in tight new shoes, hadpersisted for about 1 year. The ulcer pro-gressively became deeper and larger. Thepatient reported two septic episodes withinfection at the same site, for which shewas hospitalized for prolonged periods.

On examination, her body temperaturewas 39.2 ◦C, blood pressure 90/50 mmHg,heart rate 120 beats/min and weak, andshe was anuric. Her right foot andthe tibia were warm, red and swollen.A large, foul-smelling, neuro-ischemiculcer with gross purulent discharge wasseen on the posterior surface of herright heel (Figure 8.38). The calcaneuswas exposed.

Infections 181

Figure 8.37 Increased radionuclide uptake by the tarsometatarsal bones, possibly due toosteomyelitis. Technetium-99m (99Tc) phosphonates scan: flow phase (left upper panel); bloodpool phase (right upper panel); delayed phase (left lower panel). Gallium-67 citrate study (rightlower panel)

A plain radiograph showed a largeskin defect on the posterioplantar aspectof her heel and bone resorption of theposterior calcaneus (Figure 8.39). Exten-sive calcinosis of the posterior tib-ial artery and medial plantar branchartery was also noted. After surgicaldebridement, bone and deep tissue cul-tures were obtained. Immediate supportwith i.v. fluids and antibiotic admin-istration was commenced (ciprofloxacin400 mg × 3 and clindamycin 600 mg × 3)and her situation improved within 12 h.

Tissue cultures revealed Enterococcusspp., Acinetobacter baumannii, and Pro-teus mirabilis. Based on an antibio-gram, treatment was changed to ampicil-lin–sulbactam and continued for 2 weeks.Disarticulation through the ankle joint(Syme ankle disarticulation) was not fea-sible; a healthy heel flap and the heel padis a prerequisite for this procedure so thatthe end of the stump is capable of bear-ing the patient’s weight. Two weeks afterher admission the patient sustained a below-knee amputation.


Figure 8.38 Large, neuro-ischemic ulcer with gross purulent discharge on the posterior surfaceof right heel. The calcaneus is exposed

Empirical treatment with antibiotics insevere foot infections should always includeagents against staphylococci, enterobacte-riaceae and anaerobes. In this case, twoagents with good bone bioavailability wereused since osteomyelitis was present. Ther-apeutic options in patients with severe footinfections include:

• Fluoroquinolone plus metronidazole orclindamycin. This combination is effec-tive against Staphylococcus aureus (only

methicillin-susceptible strains), entero-bacteriaceae, and anaerobes.

• β-lactam and β-lactamase inhibitor com-binations (ticarcilline–clavulanic acid,piperacillin–tazobactam). Ampicillin–sulbactam is particularly active againstEnterococcus spp. For patients who havereceived extensive antibiotic therapy,ticarcilline–clavulanic acid or pipera-cillin–tazobactam may be preferredbecause of their increased activity againstnosocomial gram-negative bacilli. Suchregimens are also effective against

Infections 183

Figure 8.39 Plain radiograph of the foot illustrated in Figure 8.38 showing a large skin defect onthe posterioplantar aspect of the heel and bone resorption of the posterior calcaneus. Calcinosis ofthe posterior tibial artery and medial plantar branch artery is also apparent

Staphylococcus aureus (only methicillinsodium-susceptible strains), Streptococ-cus spp. and most anaerobes.

• In patients who have severe penicillinallergy, combination therapy with aztre-onam and clindamycin, or a fluoro-quinolone and clindamycin is effective.

• Imipenem–cilastin or meropenem asmonotherapy.

Doctors should always consider that:• Modification of the treatment may

be necessary according to the resultsof cultures.

• Vancomycin or teicoplanin are indicatedin cases of infection with methicillin-resistant staphylococcal strains.

• Third generation cephalosporins shouldbe used only in combination withother agents, as they have moderateanti-staphylococcal activity and lacksignificant activity against anaerobes.

• Aminoglycosides are nephrotoxic andthey are inactivated in the acidicenvironment of the soft tissue infectionand have poor penetration into bone.

Keywords: Osteomyelitis; heel ulceration;calcaneus; severe foot infection treatment;below-knee amputation

Chapter IXNEURO-OSTEOARTHROPATHY.THE CHARCOT FOOT

� CLASSIFICATION

� ACUTE NEURO-OSTEOARTHROPATHY

� DIFFERENTIAL DIAGNOSIS BETWEEN ACUTE

NEURO-OSTEOARTHROPATHY AND OSTEOMYELITIS

� PATTERNS OF NEURO-OSTEOARTHROPATHY

� NEURO-OSTEOARTHROPATHY: SANDERS AND

FRYKBERG PATTERNS II AND III; DOUNIS TYPE II:INVOLVEMENT OF THE FIFTH METATARSAL HEAD


FRYKBERG PATTERNS II AND III; DOUNIS TYPE

II: PARTIAL RESORPTION OF LISFRANC’S JOINT

� ACUTE NEURO-OSTEOARTHROPATHY: SANDERS

AND FRYKBERG PATTERN II; DOUNIS TYPE II


FRYKBERG PATTERNS II AND III; DOUNIS TYPE II:FRAGMENTATION OF THE CUBOID BONE


FRYKBERG PATTERNS II AND III; DOUNIS TYPE II:COLLAPSED PLANTAR ARCH


FRYKBERG PATTERNS II AND III; DOUNIS TYPE II:MIDFOOT COLLAPSE





FRYKBERG PATTERNS II AND III; DOUNIS TYPE II:ULCER OVER A BONY PROMINENCE

� ACUTE NEURO-OSTEOARTHROPATHY: SANDERS

AND FRYKBERG PATTERN IV; DOUNIS TYPE IIIa

� NEURO-OSTEOARTHROPATHY: SANDERS

AND FRYKBERG PATTERN IV; DOUNIS

TYPE III (a, b, and c)


FRYKBERG PATTERN IV; DOUNIS TYPE IIIa


FRYKBERG PATTERNS IV AND V; DOUNIS

TYPE III (a, b and c): INVOLVEMENT

OF THE HINDFOOT


FRYKBERG PATTERNS IV AND V; DOUNIS

TYPE III (a, b and c)

� BIBLIOGRAPHY

Neuro-Osteoarthropathy. The Charcot Foot 187

CLASSIFICATIONOF NEURO-

OSTEOARTHROPATHY

Neuro-osteoarthropathy (Charcot arthropa-thy, Charcot osteoarthropathy, neuropathicosteoarthropathy) represents one of themost serious complications of diabetes. Itsprevalence is between 1 and 7.5%; bilateralinvolvement has been reported to occur in6–40% of patients in several series. Thedevelopment of this complication dependson peripheral somatic and autonomic neu-ropathy, together with adequate blood sup-ply to the foot. A minor trauma, oftenunrecognized by the patient, may initiatethe process of joint and bone destruction.Some cases of neuro-osteoarthropathy havebeen reported after infection of the foot,surgery to the ipsilateral or the contralat-eral foot, or restoration of foot circulation.Mean age of presentation is approximately60 years and the majority of the patientshave diabetes of more than 15 years’ dura-tion. Men and women are affected equally.

CLASSIFICATION OFNEURO-OSTEOARTHROPATHY,BASED ON CHARACTERISTIC

ANATOMIC PATTERNS OF BONEAND JOINT DESTRUCTION

Classification Proposed by Sandersand Frykberg (1991)

Pattern I : Forefoot (involvement of inter-phalangeal joints, phalanges, metatarsopha-langeal joints, distal metatarsal bones). Thefrequency of this pattern is 26–67%, and itis often associated with ulceration over themetatarsal heads.

Pattern II : Tarsometatarsal joints. The fre-quency of this pattern is 15–48%; it oftencauses collapse of the midfoot and a rocker-bottom foot deformity.

Pattern III : Naviculocuneiform, talonavic-ular and calcaneocuboid joints. The fre-quency of this pattern is 32%; it oftencauses collapse of the midfoot and a rockerbottom foot deformity, particularly when itis combined with pattern II.

Pattern IV : Ankle and subtalar joints. Al-though this pattern accounts for only3–10% of the cases of neuro-osteoarthrop-athy, it invariably causes severe structuraldeformity and functional instability of theankle.

Pattern V : Calcaneus. Avulsion fractureof the posterior tubercle of the calca-neus. This pattern is not in fact neuro-osteoarthropathy, since no joint involve-ment occurs. This pattern is rare.

Classification Proposed by Dounis(1997)

According to the classification proposed byDounis in 1997, there are three main typesof neuro-osteoarthropathy (Figure 9.1):

Type I : This type is similar to pattern Ias in the above classification proposed bySanders and Frykberg, and involves theforefoot.

Type II : Type II involves the midfoot (tar-sometatarsal, naviculocuneiform, talonavic-ular and calcaneocuboid joints); its mainconsequence is the collapse of the mid-foot and development of rocker-bottom footdeformity.

Type III : Type III involves the rearfoot andis subclassified as:

IIIa (ankle joint): Main consequenceis instability.

IIIb (subtalar joint): Main consequenceis instability and development of varusdeformity of the foot.


Figure 9.1 Dounis classification of neuro-osteoarthropathy. Refer to text

IIIc (resorption of talus and/or calca-neus): This type is associated with theinability to bear weight.

The IIIc subcategory is similar to pat-tern V as proposed by Sanders and Fryk-berg, but it includes some cases withresorption either of the talus or the cal-caneus or both bones. The classificationproposed by Dounis is less complex thanthat suggested by Sanders and Frykberg asit is based on the three anatomic areas ofthe foot.

Other classifications have been alsodescribed (Harris and Brand, 1966; Lennox,1974; Horibe et al., 1988; Barjon, 1993;Brodsky and Rouse, 1993; Johnson, 1995).Detailed descriptions of these classificationsystems can be found in the literature.

CLINICAL PRESENTATIONAND LABORATORY FINDINGS

A typical clinical presentation is a patientwith a swollen, warm and red foot withmild pain or discomfort. Usually there isa difference in skin temperature of morethan 2 ◦C compared to the unaffected foot.Most patients do not report any trauma,although some may recall a minor injury

such as a mild ankle sprain. On examina-tion, pedal pulses are bounding and find-ings of peripheral neuropathy are constantlypresent. The white blood cell count is nor-mal and the erythrocyte sedimentation ratemay be slightly increased (20–40 mm/h).

RADIOLOGICAL FINDINGS

Radiological findings depend on the stageof the disease. Eichenholtz (1966) describedthree clinico-radiologically distinct stages.(a) The development stage, characterizedby soft tissue swelling, hydrarthrosis, sub-luxations, cartilage debris (detritus), erosionof the cartilage and subchondral bone, dif-fuse osteopenia, thinning of the joint spaceand bone fragmentation. (b) The coales-cence stage, characterized by evidence ofrestoration of the tissue damage: inflam-mation subsides, fine debris is absorbed,periosteal bone is formed, bone fragmentsfuse to the adjacent bones and the affectedjoints are stabilized. (c) The reconstruc-tive stage, characterized by subchondralosteosclerosis, periarticular spurring, intra-articular and marginal exuberant osteo-phytes and ossification of ligaments andjoint cartilage. Joint mobility is reduced andfusion and rounding of large bone frag-ments may be seen (Onvlee, 1998).


DIFFERENTIAL DIAGNOSIS

Diagnosis of acute neuro-osteoarthropathyrequires a high level of vigilance for thedisease. The acute development of footswelling in a patient with long-standing dia-betes and peripheral neuropathy is a clueto the presence of acute neuro-osteoarthrop-athy. In the early stages, plain radiographsmay be normal and serial radiographicexamination of the affected foot may bewarranted. Acute infections (osteomyeli-tis, cellulitis) and crystal deposition dis-ease should be excluded. Exclusion ofosteomyelitis in such patients is not alwayseasy. Scintigraphy studies and magneticresonance imaging or computed tomogra-phy may not distinguish neuro-osteoarthrop-athy from osteomyelitis (Shaw and Boul-ton, 1995).

Keywords: Classification of neuro-osteoar-thropathy; Charcot foot; Sanders and Fryk-berg classification; Dounis classification;clinical presentation of neuro-osteoarthrop-athy; radiological findings of neuro-osteo-arthropathy; differential diagnosis of neuro-osteoarthropathy; Eichenholtz stage ofneuro-osteoarthropathy

ACUTE NEURO-OSTEOARTHROPATHY:

SANDERS AND FRYKBERGPATTERN I; DOUNIS TYPE I

A 56-year-old female patient with type 2diabetes mellitus diagnosed at the age of43 years and treated with sulfonylureas,was referred to the outpatient diabetic footclinic for a forefoot ulcer and possibleosteomyelitis. Diabetes control was accept-able (HBA1c: 7.6%). She had backgrounddiabetic retinopathy and hypertension. On

examination the forefoot was red, swollen,warm and painful; she had severe periph-eral neuropathy and a clear ulcer under herright fifth metatarsal head of 2 weeks’ dura-tion; peripheral pulses on both feet werenormal. The patient denied any trauma. Ananteroposterior radiograph showed osteo-lytic destruction of her third and fourthmetatarsal heads, widening of the thirdmetatarsophalangeal joints and subluxationof the second metatarsophalangeal joint(Figure 9.2). The white blood cell count(WBC) was within the normal range andthe erythrocyte sedimentation rate (ESR)was 25 mm/h. The patient was diagnosedas a case of acute neuro-osteoarthropathyand, after debridement of the ulcer, atotal-contact cast was fitted and bed restwas advised. She had her cast changedon a weekly basis for 1 month and every2 weeks thereafter for two more months.The ulcer healed completely in 4 weeks andshe had a good recovery. Plain radiographsfollowed 2 weeks later in order to excludeosteomyelitis, but no further bone destruc-tion was seen.

This type of bone destruction is quitesimilar to that seen in osteomyelitis. How-ever, in this patient osteomyelitis was lesspossible due to the short duration of theulcer and lack of infection which must bepresent to cause extensive bone destruc-tion. Bone destruction due to osteomyeli-tis takes at least 2 weeks to become vis-ible on plain radiographs. Involvement ofbones and joints is typical in acute neuro-osteoarthropathy. An increase in the ESR(greater than 70 mm/h) and WBC is acommon feature of acute osteomyelitis.Mild elevation of the ESR (usually lessthan 40 mm/h) is common in acute neuro-osteoarthropathy.

Other roentgenographic findings inpattern I neuro-osteoarthropathy includeconcentric resorption of phalanges and


Figure 9.2 Radiograph of acute neuro-osteoarthropathy showing osteolytic destruction of the thirdand fourth metatarsal heads, widening of the third metatarsophalangeal joint and subluxation of thesecond metatarsophalangeal joint

broadening of the bases of proximal pha-

langes with formation of a cup around

the metatarsal heads. Osteolytic destruction

of the metatarsophalangeal joints with a

pencil-like tapering of the metatarsal shafts,

epiphyseal absorption, thinning of the joint

space and subluxation of the metatarsopha-

langeal and the phalangophalangeal joints,

Figure 9.3 Neuro-osteoarthropathy: concentric resorption of the phalanges of the three lesser toes,osteolytic destruction of the metatarsophalangeal joints and severe epiphyseal absorption are evident


may also be seen (Figure 9.3 exemplifiedby another patient). Pattern I-type neuro-osteoarthropathy is often complicated byplantar ulceration.

Keywords: Acute neuro-osteoarthropathy;plantar ulceration

DIFFERENTIAL DIAGNOSISBETWEEN ACUTE TYPE INEURO-OSTEOARTHROP-

ATHY AND ACUTEOSTEOMYELITIS

A 62-year-old lady with type 2 diabetesdiagnosed at the age of 48 years was

Figure 9.4 Right first ray amputation. Medialdisplacement and an ulcer on the tip of thesecond toe due to repeated trauma of the clawedtoe can be seen

referred to the outpatient diabetic foot clinicfor possible acute osteomyelitis of her rightfoot. The patient had had a first ray ampu-tation on the right side due to osteomyeli-tis 2 years earlier. Eventually second andthird claw toe deformity developed anda chronic ulcer formed at the tip of herright second toe due to repeated trauma(Figure 9.4). During the previous 6 monthsthe patient had been the subject of sev-eral scintigraphic studies which suggestedosteomyelitis of her right second and thirdmetatarsals, she had therefore been treatedwith ciprofloxacin and clindamycin.

On examination, claw toe deformity wasobserved; the dorsum of her right fore-foot was red, swollen, painful and warm;she had severe peripheral neuropathy andbounding feet pulses. A clear non-infected

Figure 9.5 Radiograph of acute neuro-osteoar-thropathy as shown in the patient whose foot isillustrated in Figure 9.4. Osteolytic destructionof the second and third metatarsal heads, widen-ing of the third metatarsophalangeal joint andsubluxation of the second metatarsophalangealjoint are evident


ulcer was seen at the tip of her secondtoe. A plain radiograph (Figure 9.5) showeddisintegration of her right second and thirdmetatarsal heads and an avulsion frac-ture between her second and third proxi-mal phalanges. Her white blood cell count(WBC) was 14,500, the erythrocyte sedi-mentation rate (ESR) was 104 mm/h andthe C-reactive protein level was 45 mg/dl.The patient’s foot was immobilized by theuse of a total-contact cast and she con-tinued with antibiotics as the probabilityof osteomyelitis was high. She continuedusing the cast and the antibiotic treatmentfor 3 months. At that time the WBC wasnormal and the ESR and C-reactive proteinlevels were mildly elevated. One year later,a plain radiograph (Figure 9.6) revealedbroadening of her second metatarsal head,

proliferative changes of her third metatarsalhead and lateral exostosis of the proximalphalanx of her second toe. These findingscorrespond to the reconstructive stage inthe evolution of neuro-osteoarthropathy.

Differential diagnosis in this case incl-uded osteomyelitis and acute neuro-osteo-arthropathy. Scintigraphy and hematologystudies suggested the presence of osteo-myelitis. Radiographic findings are similarin both acute Charcot foot and osteomyeli-tis (see Figure 8.37 which shows scintig-raphy studies of the same patient). Itis also possible that both conditions co-existed for some time, as an acute infectionmay initiate acute neuro-osteoarthropathy.Whatever was the case, the patient had agood outcome and no further foot deformitydeveloped.

Figure 9.6 X-ray showing the pro-gression of neuro-osteoarthropathyin the patient whose foot is illustratedin Figures 9.4 and 9.5. This radio-graph was taken 1 year after thatshown in Figure 9.4. Broadening ofthe second metatarsal head, prolifer-ative changes of the third metatarsalhead and lateral exostosis of theproximal phalanx of the second toeare all evident


Keywords: Acute neuro-osteoarthropathy;type I neuro-osteoarthropathy; acute osteo-myelitis

NEURO-OSTEO-ARTHROPATHY: SANDERS

AND FRYKBERGPATTERNS II AND III;

DOUNIS TYPE II:INVOLVEMENTOF THE FIFTH

METATARSAL HEAD

A 40-year-old male patient with type 1 dia-betes diagnosed at the age of 18 years was

referred to the outpatient orthopedic depart-ment of our hospital for acute osteomyelitisin his left foot. The patient had fair diabetescontrol (HBA1c: 7.2%) and background dia-betic retinopathy.

On examination, redness, edema andwarmth were noted on the dorsolateralaspect of his left foot (Figure 9.7), butno ulceration. A large ecchymosis wasseen below the external malleolus, but thepatient denied any trauma. He had diabeticneuropathy with severe loss of sensation ofpain, light touch and temperature percep-tion, but he could feel vibration. The vibra-tion perception threshold was 10 V in bothfeet. The difference in temperature betweenthe two feet was 3.5 ◦C. Peripheral pulses

Figure 9.7 Redness and edema onthe dorsolateral aspect of this foot isdue to acute neuro-osteoarthropathy. Alarge ecchymosis below the externalmalleolus is due to an avulsion fractureof the base of the fifth metatarsal


were palpable and the ankle brachial indexwas 1.2 bilaterally.

An anteroposterior radiograph showedan avulsion fracture of the tubercle of hisleft fifth metatarsal base together with milderosion of his left cuboid bone (Figure 9.8).Acute neuro-osteoarthropathy was diag-nosed; a total-contact cast was applied andthe patient was advised to limit his activ-ity to a minimal level. He had the castchanged on a weekly basis initially andevery 2 weeks thereafter for 3 months. He

Figure 9.8 Radiograph of acute neuro-osteoar-thropathy in the patient whose foot is shown inFigure 9.7. An avulsion fracture of the tubercleof the left fifth metatarsal base, together withmild erosion of the left cuboid bone can be seen

had a good recovery with minimal footdeformity.

This patient had preserved function ofthe large myelinated fibers as evidenced bynormal sensation of vibration as well as thevibration perception thresholds, and dam-age to the small nerve fibers responsiblefor sensations of pain, light touch and tem-perature. The pattern of nerve fiber dam-age may vary considerably in diabetes. Themost common pattern is impairment of allnerve fibers; however, damage of the largemyelinated fibers with preservation of thesmall unmyelinated fibers and vice versamay also be seen.

Pattern II (or Dounis’ type II) is thecommonest pattern of neuro-osteoarthrop-athy, characterized by involvement of thetarsometatarsal joints (Lisfranc’s joint).Osteolytic destruction at this site mayresult in collapse of cuneiforms and/orcuboid bone and a rocker-bottom footdeformity. Ulcers may develop at the apexof collapsed bones.

The patient’s ecchymosis was probablydue to an avulsion fracture of the base ofhis fifth metatarsal bone.

Keywords: Pattern II neuro-osteoarthropa-thy; fracture; cuboid bone; fifth metatarsal



DOUNIS TYPE II: PARTIALRESORPTION

OF LISFRANC’S JOINT

A 38-year-old lady with type 1 diabetesdiagnosed at the age of 19 years attendedthe outpatient diabetic foot clinic becauseof mild discomfort in her right midfoot.


Symptoms persisted for 1 week and thepatient denied any trauma.

On examination, the right midfoot wasred and swollen. She had claw toe defor-mity, and a small superficial neuropathiculcer on the dorsum of the second righttoe (Figure 9.9). Peripheral pulses werenormal. Severe peripheral neuropathy wasfound with loss of sensation of light touch,pain, temperature and vibration. She couldnot feel 5.07 monofilaments. The vibra-tion perception threshold was 40 V at thetip of the halluxes. A plain radiograph(Figure 9.10) revealed a partial disruptionof the Lisfranc’s joint with mild sub-luxation of the second metatarsal boneand mild lateral displacement of the lastthree metatarsals. Diagnosis of acute neuro-osteoarthropathy was made; a total-contactcast was fitted and 3 months later a prefab-ricated walker was fitted and used for a fur-ther 6 months (Figure 9.11). The outcome

was good and no significant foot deformitydeveloped.

Minimal second metatarsal dislocationmay be easily overlooked in patients withmild symptoms. This type of neuro-osteoar-thropathy should be diagnosed and man-aged early as it invariably results in collapseof the midfoot. A minimal (of a few mil-limeters) lateral deviation or a fracture ofthe base of the second metatarsal may be anearly sign of acute neuro-osteoarthropathy.If the foot is not immobilized, dislocationof all metatarsals develops. Lateral dis-placement of the metatarsal bases on thecuneiform and cuboid bones occurs andeventually the midfoot collapses.

Prefabricated walkers are suitable alter-natives to a total-contact cast, although theydo not provide total contact. Application ofinflatable pads improves contact. They areindicated in patients with impaired vascu-lar circulation or in patients who require

Figure 9.9 Claw toe deformity and a small superficial neuropathic ulcer on the dorsum of thesecond right toe. No other apparent foot deformity is visible in this patient with early acuteneuro-osteoarthropathy


Figure 9.10 Radiograph of acuteneuro-osteoarthropathy in the patientwhose foot is shown in Figure 9.9.Partial disruption of the Lisfranc’sjoint with mild subluxation of thesecond metatarsal bone and mild lat-eral displacement of the last threemetatarsals can be seen

Figure 9.11 Prefabricated walker forthe patient whose foot is illustratedin Figures 9.9 and 9.10. Prefabricatedwalkers are suitable alternatives to thetotal-contact cast. As they do not pro-vide total contact, inflatable pads areused to improve contact. They are indi-cated in patients with impaired vascularcirculation or in patients who requirefrequent removal of the cast for thetreatment of concurrent ulcers


frequent removal of the cast for treatmentof concurrent ulcers.

Keywords: Second metatarsal subluxation;pattern II neuro-osteoarthropathy


SANDERS AND FRYKBERGPATTERN II; DOUNIS

TYPE II

A 54-year-old male patient with long-standing type 1 diabetes was referred tothe orthopedic department because of mildpain, foot swelling and deformity, whichdeveloped 2 weeks after a foot sprain. Hehad a history of an intermediate ampu-tation of the fifth metatarsal bone dueto osteomyelitis resulting from a perfo-rated ulcer on his fifth metatarsal head andmetaphysis, which had occurred 2 yearsearlier.

On examination he had bounding feetpulses and severe diabetic neuropathy; the

vibration perception threshold was above50 V bilaterally. His left foot was painful,swollen and warm. A prominence on thedorsal aspect of his first metatarsopha-langeal joint was visible and crepitus couldbe heard on passive foot flexion andextension. A radiograph revealed signsof acute neuro-osteoarthropathy involvingthe midfoot: osteolysis and fragmentationof the cuneiforms, tarsometatarsal jointinvolvement and dislocation of the firstmetatarsal joint (Figure 9.12). The patientwas hospitalized and arthrodesis of the dis-located metatarsal bone was carried out bymeans of Steinmann pins (Figure 9.13). Anon-weight-bearing total-contact cast wasapplied for 3 months, followed by 6 monthsin a weight-bearing total-contact cast. Twomonths later no major deformity was vis-ible (Figure 9.14, immediately after castremoval).

As a rule, reconstructive surgery ofneuro-osteoarthropathy is contraindicatedin the acute dissolution phase (Eichenholtzstage I). The main reconstructive proce-dures carried out in patients with neuro-osteoarthropathy are osteotomy of a bony

Figure 9.12 Radiograph of acute neuro-osteoarthropathy involving the midfoot: osteolysis andfragmentation of the cuneiforms, tarsometatarsal joint involvement and dislocation of the firstmetatarsal joint are evident


Figure 9.13 Postoperative radiographs of the condition shown in Figure 9.12; fusion of thetarsometatarsophalangeal joints (arthrodesis) with the placement of Steinmann pins can be seen

Figure 9.14 Postoperative photo-graph of the patient whose condi-tion is illustrated in Figures 9.12 and9.13, 9 months after arthrodesis anduse of a total-contact cast. No majorfoot deformity is seen


prominence and arthrodesis. When indi-cated, surgery is undertaken during thereconstructive stage (Eichenholtz stage III).During the acute phase surgery resultsin high rates of fixation failure, recurrentfoot deformity and infection. Other con-traindications to arthrodesis in such patientsinclude soft tissue and bone infection,insufficient bone stock to achieve rigid fix-ation and non-compliance with postoper-ative regimens. However, in this patientarthrodesis in the acute phase was neces-sary, as major foot deformity and func-tional dysfunction was anticipated if themetatarsal head was left untreated. In addi-tion, a prerequisite for successful arthrode-sis is the presence of a sufficient bone stockfor rigid fixation. If the operation had beenpostponed, this procedure might have beenimpossible as the cuneiforms and navicu-lar bones were fragmented and collapsed.After the operation, patients with neuro-osteoarthropathy need long-term immobi-lization, irrespective of stage. In gen-eral, the immobilization period followingan arthrodesis is double that required bypatients without neuropathy.

Keywords: Acute pattern II neuro-osteoar-thropathy; arthrodesis; reconstructive sur-gery; Steinmann pins



DOUNIS TYPE II:FRAGMENTATION

OF THE CUBOID BONE

A 64-year-old female patient with long-standing type 2 diabetes attended the out-patient diabetic foot clinic because of red-ness, edema, swelling and mild pain on thedorsum of the right midfoot, which hadbeen present for the previous 2 months.She did not report any trauma. The feetpulses were normal but she had severediabetic neuropathy. A plain radiographshowed fragmentation of the cuboid bone,a pseudoarthrosis of an old fracture atthe base of the fifth metatarsal and bone

Figure 9.15 Plain radiograph showing neuro-osteoarthropathy. Fragmentation of the cuboid, apseudoarthrosis of an old fracture at the base of the fifth metatarsal and bone fragments at thetalonavicular joint dorsally can be seen


fragments in the talonavicular joint dor-sally (Figure 9.15). Neuro-osteoarthropathywas diagnosed, and the foot was put intoa total-contact cast for 8 weeks. A fibrousunion was present despite the absence ofradiographic signs of healing of the frac-tured fifth metatarsal. The patient worehigh-arched custom-made shoes. No fur-ther bone destruction was found during thenext 6 months.

Keywords: Neuro-osteoarthropathy; pat-terns II and III; type II; cuboid fragmentation



DOUNIS TYPE II: COL-LAPSED PLANTAR ARCH

A 56-year-old insulin-treated female patientwith type 2 diabetes since the age of45 years attended the outpatient diabeticfoot clinic. She had background retinopa-thy — treated with laser — hypertension,

diabetic nephropathy and dyslipidemia, aswell as a left foot deformity which she hadhad since the age of 52 years. She was aheavy smoker. She had an ulcer on the outeraspect of her left foot which had developedwhen she was 53 years old and had startedas a bulla following a trauma caused byher shoe.

On examination, a collapsed left mid-foot and claw toe deformity were present.She had a painful irregular ulcer on thelateral aspect of her left foot with localedema, erythema and purulent discharge(Figure 9.16). A hemorrhagic callus wasnoted on the dorsum of her fifth left toe.Peripheral pulses were weak. The vibrationperception threshold was over 50 V and shehad reduced sensation of pain, light touchand temperature. Achilles tendon reflexeswere absent.

Triplex ultrasonography of her leg arter-ies showed severe obstruction of her com-mon femoral arteries on both sides. Amethicillin-resistant Staphylococcus aureuswas isolated from the base of the ulcerand the patient was treated with intramus-cular teicoplanin and ciprofloxacin. The

Figure 9.16 Chronic neuro-osteoarthropathy with collapsed plantar arch and claw toe deformity.An irregular neuro-ischemic ulcer is present over the lateral aspect of the fifth metatarsal head withlocal edema, erythema and a sloughy bed superimposing osteomyelitis. A hemorrhagic callus isseen on the dorsum of the fifth left toe


patient was referred to the Vascular SurgeryDepartment for bypass surgery. Appropri-ate footwear was prescribed and the ulcerhealed in 3 months.

A plain radiograph revealed cuneiformfragmentation and disruption of the tar-sometatarsal joint (Lisfranc’s joint). Osteo-myelitis of the head of the fifth metatarsalwas also present (Figure 9.17). Calcifica-tion of the digital arteries was also noted, acommon finding in patients with diabetes.

Adequate blood supply is a prerequisitefor neuro-osteoarthropathy. In this patient,

Figure 9.17 Plain radiograph showing chronicneuro-osteoarthropathy in the patient whosefoot is illustrated in Figure 9.16. Fragmen-tation of the cuneiforms and disruption atthe tarsometatarsal joint (Lisfranc’s joint) withosteomyelitis of the head of the fifth metatarsaland calcification of the digital arteries, a com-mon finding in patients with diabetes, are allevident

peripheral vascular disease occurred afterneuro-osteoarthropathy.

Keywords: Neuro-ischemic ulcer; neuro-osteoarthropathy

NEURO-OSTEOARTHROPATHY:

SANDERS AND FRYKBERGPATTERNS II AND III;

DOUNIS TYPE II: MIDFOOTCOLLAPSE

A lateral radiograph shows midfoot col-lapse (collapse of naviculocuneiform, talon-avicular and calcaneocuboid joints) dueto chronic neuro-osteoarthropathy of com-bined patterns II and III (Figure 9.18). Inaddition, localized bone resorption at thenaviculocuneiform joints can be seen.

Osteotomy of protruding bone is rec-ommended if recurrent ulceration occursdespite the use of custom-made shoesand insoles.

Keywords: Midfoot collapse; neuro-osteo-arthropathy


SANDERS AND FRYKBERGPATTERNS II AND III;

DOUNIS TYPE II: ULCEROVER A BONYPROMINENCE

A 64-year-old insulin treated male patientwith type 2 diabetes diagnosed at the ageof 46 years and acceptable diabetes con-trol (HBA1c: 7.4%), was referred to theoutpatient diabetic foot clinic for a chronicplantar ulcer on his left midfoot. The


Figure 9.18 Plain radiograph of a midfoot collapse (collapse of naviculocuneiform, talonavicularand calcaneocuboid joints) due to chronic neuro-osteoarthropathy. Localized bone resorption at thenaviculocuneiform joints is also seen

Figure 9.19 Chronic neuro-osteo-arthropathy with collapsed midfoot,hallux valgus deformity and amputa-tion of the second toe. Gross callusformation is seen at the borders ofthe neuropathic ulcer. Healthy gran-ulating tissue can be seen on its bed


patient had background retinopathy, hyper-tension and diabetic nephropathy (protein-uria of 1.5 g/24 h).

One year earlier he had been hospitalizedfor almost 3 months because the ulcer wascomplicated by a severe deep tissue infec-tion. During hospitalization he had exten-sive surgical debridement and was treatedwith intravenous antibiotics. A below-kneeamputation was suggested, but the patientdid not consent and he sustained a secondtoe amputation instead, due to osteomyeli-tis. The patient wore his usual shoes andrefused the total-contact cast which hadbeen suggested.

On examination, he had severe periph-eral neuropathy (the vibration perceptionthreshold was above 50 V bilaterally) andbounding peripheral pulses. He had chronicneuro-osteoarthropathy of his left foot. Hal-lux valgus deformity and a collapsed mid-foot were observed. Bony prominencescould be palpated at the base of the neuro-pathic ulcer (Figure 9.19).

An anteroposterior radiograph showedcollapsed cuboid and navicular bones(Figure 9.19), extensive destruction and

resorption of the cuneiforms with osteoscle-rotic changes and complete destruction ofthe tarsometatarsal, naviculocuneiform andtalonavicular joints (Figures 9.20–9.22).Extensive resorption of the metatarsal dia-physes with a pencil-like appearance of thefifth metatarsal could be seen (Figure 9.21).

Debridement of the ulcer was carriedout and the patient was advised to rest athome. Custom-made shoes were prescribedin order to offload the pressure from theulcerated area and to accommodate thedeformity. The ulcer healed in 12 weeks(Figure 9.23). Within the next 2 years thepatient suffered two relapses of the footulcer at the same site.

In this case, chronic neuro-osteoarthrop-athy involves the Chopart’s joint (talonav-icular and/or calcaneocuboid) or naviculo-cuneiform joints, as well as Lisfranc’s jointand, if left untreated, results in collapseof the midfoot and a rocker-bottom footdeformity. Recurrent foot ulceration at theapex of the collapsed bones is a commoncomplication.

Keywords: Chronic neuro-osteoarthrop-athy; neuropathic ulcer

Figure 9.20 Plain radiograph of chronic neuro-osteoarthropathy in the patient whose foot is shownin Figure 9.19. Collapsed cuboid and navicular bones, extensive destruction and resorption of thecuneiforms and destruction of the talonavicular joint are evident


Figure 9.21 Plain radiograph of chronic neuro-osteoarthropathy in the patient whose foot isillustrated in Figures 9.19 and 9.20. Osteosclerotic changes and complete destruction of thetarsometatarsal and naviculocuneiform joints can be seen in addition to the pencil-like appearanceof the fifth metatarsal

Figure 9.22 Plain radiograph of chronic neuro-osteoarthropathy in the patient whose foot is shownin Figures 9.19–9.21. Osteosclerotic changes and complete destruction of the tarsometatarsal jointstogether with bone resorption of the metatarsal shafts and osteophyte formation can be seen


SANDERS AND FRYKBERGPATTERN IV; DOUNIS

TYPE IIIa

A 41-year-old male patient with type 1diabetes diagnosed at the age of 19 years

was referred to the orthopedic departmentof the hospital because of erythema andswelling of his right ankle, the onset ofwhich had occurred rapidly some daysearlier. No history of trauma was reported.

On examination, he had severe periph-eral neuropathy and normal feet pulses. Hisright ankle was red, warm and swollen(Figure 9.24). A radiograph showed erosion


Figure 9.23 Healed ulcer in the patient whose foot is shown in Figures 9.19–9.22. Recurrentulceration of the midsole in a patient with midfoot collapse is an indication of osteotomy in theprotruding bones

Figure 9.24 Clinical presentation ofacute neuro-osteoarthropathy of theright ankle which is red, warm andswollen


of the articular surfaces of the right tibiaand talus. Bone fragments protruded medi-ally (Figure 9.25). A diagnosis of acuteneuro-osteoarthropathy was made and thepatient was advised to rest, with his rightfoot in a total-contact cast. The cast waschanged fortnightly for the first monthand monthly for the next year. After thistime osteoarthritic changes remained onlyin the affected joint and no major deformitywas sustained.

Neuro-osteoarthropathy in the ankle isthe third most common pattern of this

Figure 9.25 Plain radiograph of chronicneuro-osteoarthropathy of the right ankle andfoot as illustrated in Figure 9.24. There iserosion of the articular surfaces of the righttibia and talus and bone fragments protrudingmedially

condition (frequency of 13%) and mayresult in severe structural deformity andinstability. An extensive period of immo-bilization is required in order to preventdeformities.

Keywords: Acute neuro-osteoarthropathy


SANDERS AND FRYKBERGPATTERN IV; DOUNISTYPE III (a, b, and c)

A 67-year-old patient with type 2 diabetesdiagnosed at the age of 41 years attendedthe outpatient orthopedic clinic because ofworsening painful ankle swelling after astrain in his right ankle 2 weeks previously.He had severe peripheral neuropathy andnormal feet pulses.

A plain film showed resorption of thedistal parts of the tibial and peronealbones and involvement of the ankle joint(Figure 9.26). Pattern IV neuro-osteoarth-ropathy was diagnosed and the foot wasplaced in a total-contact cast and bed restwas advised. The patient did not complywith the advice and continued to be activewhile wearing the cast. One month laterextensive resorption and fragmentation ofthe talus and resorption of the distal areas ofthe tibia and fibula was observed on a sec-ond radiograph. A bone fragment protrudedposteriorly (Figure 9.27). Six months latera plain film showed extensive resorp-tion of the talus, subchondral osteosclero-sis of the tibia and calcaneus and exten-sive ligament ossification (the reconstruc-tive stage of neuro-osteoarthropathy). Bonefragments protruded laterally (Figure 9.28).The patient admitted that during this timehe had been active. He had significant


Figure 9.26 Plain radiograph showing acute neuro-osteoarthropathy. Resorption of the distal areasof the tibia and fibula and involvement of the ankle joint are evident

Figure 9.27 Plain radiograph showing pro-gress of neuro-osteoarthropathy 1 month afterthe X-ray shown in Figure 9.25 was taken.There is extensive resorption and fragmentationof the talus and resorption of distal areas of thetibia and fibula and a bone fragment protrudesposteriorly

instability and varus foot deformity. Even-tually the patient sustained a below-kneeamputation.

A major problem in this pattern ofneuro-osteoarthropathy is functional insta-bility and foot deformity. Reconstructive

Figure 9.28 Plain radiograph showing pro-gress of neuro-osteoarthropathy 6 months afterthe X-ray shown in Figure 9.27 was taken.There is extensive resorption of the talus, sub-chondral osteosclerosis of the tibia and calca-neus and extensive ligament ossification. Bonefragments can be seen to protrude laterally


procedures (such as arthrodesis) were notpossible due to extensive bone absorption.With this type of articular destruction reha-bilitation will be more successful if thepatient uses a below-knee prosthesis ratherthan a patellar-tibial-bearing orthosis.

Keywords: Ankle neuro-osteoarthropathy;talus resorption; reconstructive stage


SANDERS AND FRYKBERGPATTERN IV; DOUNIS

TYPE IIIa

A type 2 diabetic female patient with bilat-eral chronic neuro-osteoarthropathy (in the

reconstructive stage) resulting in markedbilateral varus foot deformity (Figures 9.29and 9.30), attended the outpatient orthope-dic clinic. She was unable to walk with-out crutches due to significant instability.On a plain radiograph complete destruc-tion of the ankle joint and subchondralosteosclerosis at the distal ends of the tibiaand fibula were seen, together with lat-eral resorption of the talus. Bone frag-ments were observed laterally in the anklejoint as were medial exuberant osteo-phytes (Figure 9.31). The patient under-went a realignment arthrodesis of the anklejoint by lateral ankle incisions and theankle joint was fixed with a Huckstepnail (Figure 9.32). The postoperative resultswere excellent (Figure 9.33).

Significant deformity and instability isthe main indication for arthrodesis in

Figure 9.29 Bilateral varus deformity of the feet due to chronic neuro-osteoarthropathy. Signifi-cant instability resulted in the patient’s inability to walk without crutches


Figure 9.30 Lateral view of Figure 9.29

Figure 9.31 Plain radiograph ofneuro-osteoarthropathy of the rightfoot of the patient whose feet areshown in Figures 9.29 and 9.30. Thereis complete destruction of the anklejoint, subchondral osteosclerosis inthe distal areas of the tibia and fibula,together with lateral resorption oftalus. Bone fragments are seen later-ally in the ankle joint and exuberantosteophytes medially


Figure 9.32 Plain postoperative radiograph ofthe right foot of the patient whose feet areillustrated in Figures 9.29–9.31. Arthrodesis ofthe ankle joint with the use of a Huckstep nailhas been carried out

patients with neuro-osteoarthropathy. Inexperienced hands it is possible in almost80% of cases to achieve the goal of a sta-ble and shoeable foot after an arthrodesis inpatients with neuro-osteoarthropathy. Theuse of modern techniques of internal fix-ation has significantly improved prognosisin these patients. The period of immobi-lization after an arthrodesis in patients withneuro-osteoarthropathy is prolonged, usu-ally more than 4 months.

Keywords: Neuro-osteoarthropathy; arthro-desis; Huckstep nail

Figure 9.33 Postoperative photograph of theright foot of the patient whose feet are shown inFigures 9.29–9.32 after successful arthrodesisof the ankle joint


AND FRYKBERG PATTERNSIV AND V; DOUNIS TYPE III

(a, b and c): INVOLVE-MENT OF THE HINDFOOT

Chronic neuro-osteoarthropathy often leadsto extensive resorption of the hindfoot(talus and calcaneus), navicular and cuboidbones (Figure 9.34). The patient whose


Figure 9.34 Plain radiograph showing chronic neuro-osteoarthropathy. Extensive resorption ofthe hindfoot (talus and calcaneus), navicular and cuboid bones is evident

X-ray is shown in Figure 9.34 is a 45-year-old female with long-standing type 1diabetes who developed this complicationafter a severe ankle sprain. She sufferedcomplete loss of sensation in her feetand symptomatic autonomic neuropathy

(gastroparesis, diabetic diarrhea and ortho-static hypotension). Gait instability devel-oped within 8 months, to the point wherethe patient was unable to walk with-out crutches. Although she used a total-contact cast, bone resorption was rapid and

Figure 9.35 Plain radiograph showing extensive resorption of most of the talus and calcaneus andof the distal end of the tibia–fibula in a patient with chronic neuro-osteoarthropathy. Osteolysis inthe lower part of the calcaneus is due to osteomyelitis following a perforated ulcer


relentless, so that eventually the patient suc-cumbed to a below-knee amputation.

Keywords: Chronic neuro-osteoarthrop-athy


SANDERS AND FRYKBERGPATTERNS IV AND V;

DOUNIS TYPE III (a, b and c)

Figure 9.35 shows extensive resorption ofmost of the talus and calcaneus, in additionto the distal end of the tibia–fibula ina patient with neuro-osteoarthropathy. Theosteolysis in the lower part of the calca-neus is due to osteomyelitis. A chronic

Figure 9.36 Chronic neuro-osteoarthropathy.The osteomyelitis in the heel has been super-imposed with a deep neuropathic ulcer inthe patient whose X-rays are illustrated inFigure 9.35

neuropathic heel ulcer is present, causedby a foreign body (Figure 9.36). Eventuallythe patient, who had long-standing diabetesand severe diabetic neuropathy, sustained abelow-knee amputation.

Keywords: neuro-osteoarthropathy; heelulcer; osteomyelitis

BIBLIOGRAPHY

1. Sanders LJ, Frykberg RG. Diabetic neuro-pathic osteoarthropathy: the Charcot foot.In Frykberg RG (Ed.), The High Risk Footin Diabetes Mellitus. New York: ChurchillLivingstone, 1991.

2. Dounis E. Charcot neuropathic osteoarthrop-athy of the foot. Acta Orthopaed Hellenica1997; 48: 281–295.

3. Harris JR, Brand PW. Patterns of disinte-gration of the tarsus in the anaesthetic foot.J Bone Joint Surg 1966; 5: 95–97.

4. Lennox WM. Surgical treatment of chronicdeformities of the anaesthetic foot. InMcDowell F, Enna CD (Eds), SurgicalRehabilitation in Leprosy, and in OtherPeripheral Nerve Disorders. Baltimore:Williams and Wilkins, 1974; 350–372.

5. Horibe S, Tada K, Nagano J. Neuroarthrop-athy of the foot in leprosy. J Bone Joint Surg(Br) 1988; 70-B: 481–485.

6. Brodsky JW, Rouse AM. Exostectomy forsymptomatic bony prominences in diabeticCharcot foot. Clin Orthop 1993; 296: 21–26.

7. Barjon MC. Les osteoarthropathies destruc-trices du pied diabetique. In Herisson C,Simon L (Eds), Le Pied Diabetique. Paris:Masson, 1993; 77–91.

8. Johnson JE. Neuropathic (Charcot) arthrop-athy of the foot and ankle. AAOS 1995Instructional course #349. Handoutcover.

9. Eichenholtz SN. Charcot Joints. Spring-field, IL: Charles C Thomas, 1966.

10. Onvlee GJ. The Charcot foot. A criticalreview and an observational study of 60patients. Thesis, Universiteit van Amster-dam, 1998.

11. Shaw JE, Boulton AJM. The Charcot foot.Foot 1995; 5: 65–70.

Appendix 1ANATOMY OF THE FOOT



Anatomy of the Foot 215

Figure A1 Dorsal aspect of the bones inthe foot

Figure A3 Plain radiograph of the foot shownin lateral view

Figure A2 Plantar aspects of the bones inthe foot

Appendix 2MANUFACTURERS OF PREVENTIVEAND THERAPEUTIC FOOTWEAR



Manufacturers of Preventive and Therapeutic Footwear 219

The therapeutic and preventive footwear and insoles described in this book are productsof various companies including:

Acor Orthopedic, USAAircast, Inc., USAAliMed, Inc., USABuratto Advanced Technology, ItalyDarco International, Inc., USAF. W. Kraemer KG, GermanyOrthopaedic Systems, UK

IndexNote: page numbers in italics refer to figures and tables

abscessdrainage 146plantar 133

Achilles tendon reflexes 5Acinetobacter baumannii 181amputation

arteriography prior to 20below-knee 129, 140, 147

chronic neuro-osteoarthropathy 212deep-tissue infection 163, 166osteomyelitis of heel 181

biomechanics of foot 69Charcot foot 95Chopart disarticulation 68–9foot deformities 31hallux 109, 110, 169heel ulcers 98limited distal 127prevalence 3ray 140, 178

fifth 178first 61–3, 176fourth 70

risk 3toe 140, 146

fifth 121, 122fourth 134second 203

wet gangrene 143, 146–7angiography 29

digital subtraction 132, 134, 136, 137–8stenosis location 135, 140, 141

angioplastysuboptimal 135see also percutaneous transluminal

angioplastyanhidrosis 3

anklearthrodesis 208, 210bone fragments 208, 209disarticulation 181edema 53, 110, 112

deep-tissue infection 162, 163neuro-osteoarthropathy 204, 205, 206, 207osteophytes 208, 209pressure 8, 20swelling 204, 205, 206

ankle brachial indexcalculation 20cardiovascular risk 18foot ulcer classification 26ischemic ulcers 28monitoring 18, 20neuropathic ulcer 28peripheral vascular disease detection 16

antibiotics 154bone bioavailability 182broad-spectrum 154intravenous 154osteomyelitis of heel 182–3resistance 154

antifungal drugs 160aorta, abdominal, stenosis 138aorto — femoral bypass graft 127aorto — popliteal bypass graft 150Apligraf see Graftskinarterial calcification 9, 10arterial insufficiency, antibiotic therapy 154arterial stenosis 11

criteria in spectral analysis 13ultrasonography 12see also named arteries

arteriography 20arthrodesis, realignment 208, 210



222 Index

aspirin 16autolytic debridement 119

becaplermin see platelet-derived growth factorβ (PDGF-β)

bedridden patients 97–8biosurgery 119, 121biothesiometer 6blisters

rupture 146, 167soft tissue infection 156, 157

blood pressure control 16bone demineralization 92bone scintigraphy imaging 175, 178–9, 181

phases 179, 181bony prominence

osteotomy 197, 199ulcer 201, 202, 203, 204–5

bunion 48–9chronic neuropathic ulcer 177ulcers 49

bunionette formation 43–4, 46ulceration 46varus deformity 48

burnsforefoot 98, 99, 100, 101, 102squamous cell carcinoma in scars 81toes 98, 99, 100, 101, 102

bursitis 48–9bypass grafting 127, 201

neuro-ischemic ulcers 113wet gangrene 147

calcaneocuboid jointChopart dislocation 69collapse 201, 202neuro-osteoarthropathy 203

calcaneusbone resorption 183exposure 180osteolysis 211, 212resorption 210, 211, 212subchondral osteosclerosis 206, 207

calcium pyrophosphate dihydrate (CPPD)deposition disease 77–8

calf support device 129, 131callus formation 3

under bone prominence 63–4claw toe 155hemorrhagic 65–6, 67, 68, 88, 200metatarsal heads 45, 50–1

neuropathic ulcers 89, 94prominent 64–5second toe removal 59, 60, 61, 62

plantar pressure 88pressure loading 87–8prevention 67removal 65ulcer under 66–7

Candida albicans 71fungal infection with multimicrobial

colonization 160wound colonization 121

cardiovascular risk factors 16cast, total-contact 34, 195–7, 198, 200,

206, 211contraindications 34

cellulitisdeep-tissue infection 166infected foot ulcer 153infected plantar ulcer with osteomyelitis

172neuro-ischemic ulcers 114, 115non-ulcerated skin 154treatment 154wet gangrene 146wound infections 153

Charcot foot 27amputation 95with neuropathic ulcer and deep-tissue

infection 163–4, 165, 166, 167radiography 192ulcers 95–6

Chopart dislocation, bilateral 68–9Chopart’s joint 203claw toe 30, 31, 46–8

bunionette formation 46callus formation 155

under bone prominence 64hemorrhagic 65–6

convex triangular foot 51fungal infection 159hallux valgus with overriding toes 52–4,

56with heloma durum 48–9infection

under callus at tip 155soft-tissue 156

muscle atrophy 103neuro-ischemic ulcers 120, 121neuro-osteoarthropathy 191, 195neuropathic ulcers of metatarsal heads

93–4onychodystrophy 155pes cavus 45phlegmon 169plantar arch collapse 200prominent metatarsal heads 58–9

Index 223

second 99ulcers 58, 59, 93–4, 120, 121

under callus area 66–7wet gangrene 150

cocked-up toes see claw toecoeliac aortic bifurcation stenosis 134, 137collagen bundles, hyalinized 80, 81collagenase 119collateral circulation 8, 15, 19, 122

development 138, 150popliteal artery 132, 135

collateral vessel development 142compliance with medical instructions 3computed tomography (CT)

osteomyelitis diagnosis 175phlegmon imaging 171spiral 14

convex triangular foot 51–2corns 49–50

see also heloma durumcritical leg ischemia 127cuboid bone

collapsed 203fragmentation 199–200resorption 210, 211

cuneiform bonefragmentation 201osteolysis 197resorption 203

curly toe deformity 48hemorrhagic callus formation 65–6

debridement 119, 121depth — ischemia classification 26Dermagraf 38dermatofibrosarcoma protruberans 82–3dermis, bioengineered 38dextranomers 119diabetes 3diabetic bullae 157diabetic neuropathy 3–6

definition 4painful — painless foot 90peripheral vascular disease co-existence 7

digital arteriescalcification 201thrombosis 158

digital subtraction angiography seeangiography, digital subtraction

dorsalis pedis palpation 18dressings 36, 37–8

ecchymosis 193, 194eczema, hyperkeratotic 78, 79

edemaankle 53, 110, 112

deep-tissue infection 162, 163foot 158forefoot deep-tissue infection 162, 163neuro-osteoarthropathy 193wet gangrene 140

Enterobacter 103, 104fungal infection with multimicrobial

colonization 160Enterobacter cloacae 168Enterococci 156, 178, 181enzymatic debridement 119Epidermophyton floccosum 158, 160Escherichia coli 62, 98

deep-tissue after interphalangeal mycosis161

infected ulcers 154osteomyelitis 104, 171web space infection 158wet gangrene 146

femoral arterybruits 18obstruction 122, 123stenosis 7, 132, 134, 138

femoral artery, commonatheromatous disease 114, 146obstruction 200peak systolic velocity 148, 150stenosis 17, 148, 150

femoral artery, superficial 19atheromatous disease 139, 144, 146atherosclerosis 117spectral waveform 13, 16stenosis 7, 10, 15, 17, 140, 141

collateral vessel development 142dry gangrene 127neuro-ischemic ulcers 114stents 135wet gangrene 150

stents 135, 141femoro — popliteal bypass graft 117, 127,

140neuro-osteoarthropathy 95

femoro — tibial bypass graft 123fibroblasts 39fibula

resorption 206, 207, 211, 212subchondral osteosclerosis 208, 209

flat foot see pes planusFontaine clinical staging 7–8

neuro-ischemic ulcers 116

224 Index

footanatomy 215see also forefoot; heel; hindfoot; midfoot;

sole of foot; toe(s)foot care, patient education 31–2foot deformities 3

definition 31see also pes cavus; pes planovalgus; pes

planus; varus deformityfoot ischemia, hyperbaric oxygen 38foot pulses

palpation 7peripheral 28

footwear, preventive 29, 31, 111, 219commercially-available 120prescription 117pressure relief shoes 35–6refusal to wear 116see also shoes

forefootburns 98, 99, 100, 101, 102edema with deep-tissue infection 162, 163neuro-ischemic ulcers with osteomyelitis

114, 116–17foreign objects

neuropathic heel ulcer 212in shoes 156, 157

fracturesavulsion of metatarsal base 193see also stress fractures

fungal infection 158claw toe 159interphalangeal deep-tissue infection 161,

162with multimicrobial colonization 160palmoplantar keratoderma 76–7web space 158see also onychomycosis

gait instability 211gallium-67 citrate 179, 181gangrene 7–8

bedridden patients 97–8critical limb ischemia 18diabetic 133dry

heel 129–30with ischemic necrosis of skin 129patient education 143toes 127, 128, 130, 131, 133–4, 136 –8

infection 127ischemic ulcers 29necrosis 127, 128, 139transcutaneous oxygen pressure 10

wet 127amputation 143, 146–7blistering 146cellulitis 146Escherichia coli 146extensive of foot 143–4, 146–7foot 140, 144hallux 147, 148, 149–50leading to mid-tarsal disarticulation

142–3, 145necrotic tissue debridement 146sepsis 130, 132–3, 134, 135, 136Staphylococcus aureus 132, 146toes 139–40, 144

wound infections 153Graftskin 38–9granulocyte colony stimulating factor (G-CSF)

39

halluxamputation 109, 110, 169disarticulation 63, 95, 99, 102, 109, 110hemorrhagic callus 55infection 103ingrown nails 146neuro-ischemic ulcers 107, 108

osteomyelitis 107–9, 110, 117–21osteomyelitis 168–9, 176, 178

neuro-ischemic ulcers 107–9, 110,117–21

removal 63subungual hematoma 110ulcer under 67, 68wet gangrene 147, 148, 149–50

hallux valgus 31, 45after second toe removal 59, 60, 61, 62bunionette formation 46callus over prominent metatarsal heads 65collapsed midfoot 202, 203hammer toes 57onychomycosis 54–6, 57with overriding toe 50–1, 52–4, 56, 57phlegmon 169with quintus varus 51–2

hammer toe 31, 47, 58hallux valgus 57onychomycosis 54–6, 57

hands, hyperkeratosis of palms 76heel

cracks 65, 67–8dry gangrene 129–30osteomyelitis 179–83ulcers

debridement 132–3

Index 225

neuro-ischemic 114, 115neuropathic 96–8, 212

heel protector ring 129, 130heloma durum 48–9, 50heloma molle 49–50

hemorrhagic callus formation 66kissing 50

hindfootpreservation 69resorption 210, 211

Huckstep nail 208, 210Hyaff 39hydrocolloids 119hydrogels 119hydrotherapy 119hyperhidrosis 158hyperkeratosis

eczema 78, 79fifth toe 155metatarsal heads 95

hypoesthesianeuropathic ulcers 27zone 5

iliac arteryatheromatous disease 114, 139, 144common, stenosis 127proximal, stenosis 134, 137stenosis 7, 132, 134, 135, 140

infectionunder callus

over fifth toe 155–6at tip of claw toe 155

deep-tissue 161–3after interphalangeal mycosis 161, 162Charcot foot with neuropathic ulcer

163–4, 165, 166, 167gangrene 127ulceration 153–4web space 157–9see also abscess; cellulitis; fungal infection;

sepsis; soft-tissue infectioninsoles, flat 174insoles, shock-absorbing 31, 32

convex triangular foot 52custom-molded 32, 33pes cavus 46

intermittent claudication 7, 16digital subtraction angiography 138ischemic ulcers 28

internal fixation 210interphalangeal joint, distal

calcium pyrophosphate dihydrate depositiondisease 77, 78

plantar flexion 47, 56interphalangeal joint, proximal

osteomyelitis 109plantar flexion 47

intrinsic muscles of foot, atrophy 47

joint mobility, limited 3plantar pressure 33

keratinocytes 38keratoderma, palmoplantar 75–7Klebsiella, deep-tissue 162Klebsiella pneumoniae 168

larval therapy 119, 121latissimus dorsi musculocutaneous flap 81,

82, 83leuconychia mycotica 160lichenification 78ligament ossification 206, 207limb ischemia, critical 18lipid level reduction 16Lisfranc joint see tarsometatarsal jointlymphangitis 153

maggot debridement 119, 121magnetic resonance angiography (MRA) 14,

16magnetic resonance imaging (MRI)

osteomyelitis diagnosis 175, 177phlegmon imaging 171

male patients, foot ulcers 3malleolus, ulcer 43mallet toe 56, 58Marjolin’s ulcer 81mechanical debridement 119medial arterial calcification 8Meggitt — Wagner classification of ulcers 25

modification 26metastases, dermatofibrosarcoma protruberans

83metatarsal bone

avulsion fracture 193diaphysis resorption 203, 204fifth

pencil-like appearance 203, 204pseudoarthrosis 199

lateral displacement 195, 196osteomyelitis 191phlegmon under base 170, 171subluxation of second 195, 196

metatarsal epiphysis, osteolytic lesions 178metatarsal heads

broadening 192

226 Index

metatarsal heads (continued )callus formation 45, 50–1, 53

hallux disarticulation 99second toe removal 59, 60, 61, 62

cup formation 190erosion in osteomyelitis 103fat pad

displacement 47, 65, 90, 91, 103reduced thickness 91–2

fifthcallosity 132exostosis 46neuro-ischemic ulcer with osteomyelitis

121–3neuro-osteoarthropathy 193–4neuropathic ulcer 99osteomyelitis 121–3, 201pseudoarthrosis in stress fractures 178ulcer 51

firstneuro-ischemic ulcer with osteomyelitis

113–14neuropathic ulcer 87–8osteomyelitis 62, 113–14, 176,

177, 178fourth

erosion 175, 177neuropathic ulcer 69–71, 90–2,

174hyperkeratosis 43, 95necrosis 61osteolysis 172, 191proliferative changes 192prominent 3, 5, 31, 58–9

callus 64–5neuropathic ulcer 87–90, 93–5phlegmon 169plantar pressure 66soft tissue infection 156ulcer under callus area 66–7

stress fractures 92third and hemorrhagic callus 65–6ulcer formation 67

metatarsal joint, dislocation of first 197metatarsophalangeal joint

arthrodesis 61, 62bone resorption 178dorsiflexion 47fourth toe disarticulation 70–1hallux disarticulation 63, 95osteoarthritis 134, 139osteolytic destruction 190subluxation 190

methicillin-resistant Staphylococcus aureus(MRSA) 121, 156

infected plantar ulcer with osteomyelitis171

painful ulcer 200mid-tarsal disarticulation 127, 129, 130

wet gangrene 142–3, 145midfoot

chronic ulcer 201, 202, 203collapsed 90, 200–1, 202

midsole, neuro-ischemic ulcers 114, 115Moh’s micrographic surgery 83monofilaments 5–6muscles, small 5musculocutaneous flap, latissimus dorsi 81,

82, 83mycosis, interphalangeal 161, 162

nailsdeformities 75, 76ingrown 71, 146repetitive trauma 75

navicular bonecollapsed 203resorption 210, 211

naviculocuneiform jointbone resorption 201, 202collapse 201, 202destruction 203, 204neuro-osteoarthropathy 203

necrobiosis lipoidica 78–80, 81necrotizing fasciitis 153nephropathy, diabetic 53neuro-osteoarthropathy 3, 164, 165, 166

acute 189–91, 193, 197, 206acute osteomyelitis differential diagnosis

191–3acute dissolution phase 197ankle 204, 205, 206, 207arthrodesis 199blood supply 201bone destruction 189bone/joint destruction anatomic patterns

187–8calcaneocuboid joint 203classification 187–9claw toe 191clinical presentation 188cuboid bone fragmentation 199–200differential diagnosis 189Dounis classification 187–8

type I 189–91type II 193–203, 204–5type III (a, b and c) 206–8, 210–12

Index 227

neuro-osteoarthropathy (continued )type IIIa 208, 209, 210type IIIα 204, 205, 206

edema 193Eichenholtz stage I 197Eichenholtz stage III 199femoral — popliteal bypass graft 95foot deformities 31, 207functional instability 207immobilization 199, 206, 210internal fixation 210metatarsal heads 193–4midfoot ulcers 36naviculocuneiform joint 203osteophyte formation 204radiological findings 188reconstructive stage 206, 208Sanders and Frykberg classification 187

pattern I 189–91pattern II and III 193–203, 204–5pattern IV 204, 205, 206–8, 209,

210pattern IV and V 210–12

stages 188talonavicular joint 203tarsometatarsal joint 193, 197, 203

neurothesiometer 6

onychocryptosis 71wet gangrene 150

onychodystrophy 134, 136claw toe 155ischemic ulcers 28peripheral vascular disease 132phlegmon 169wet gangrene 146

onychogryposis 75, 76onychomycosis 54–6, 57, 159–60

callus under bone prominence 64distal subungual 159–60neuropathic ulcers of metatarsal heads 94proximal subungual 160

orthosis, patellar-tibial-bearing 208osteoarthritis, metatarsophalangeal joint 134,

139osteomyelitis 95, 96, 167–8

bone destruction 189bone scintigraphy imaging 179, 181burns 102calcaneus osteolysis 211, 212chronic neuro-osteoarthropathy 211chronic ulcer 203diagnosis 175

Escherichia coli 104hallux 168–9, 176, 178

with neuro-ischemic ulcers 117, 118,119, 120, 121

heel 179–83infected ulcer 153

plantar 171–3Klebsiella pneumoniae 168metatarsal head

fifth 201first 62, 176, 177, 178

metatarsals 191neuro-ischemic ulcer

fifth metatarsal head 121–3first metatarsal 113–14forefoot 114, 116–17hallux 117, 118, 119, 120, 121

neuropathic ulcer complication 102–4,173–5, 176, 177chronic 176, 178, 180

pathogens 103, 104proximal phalanx 63Pseudomonas aeruginosa 119radiographic evaluation 154radiography 192Staphylococcus aureus 103, 104, 108,

113–14, 116, 168–9treatment regimens 104

acute infection 172osteophytes 204

ankle 208, 209oxygen

hyperbaric 36, 38transcutaneous pressure (TcPO2) 9–10

painneuropathic 4plantar heel spur 43see also rest pain, ischemic

painful — painless foot 90Palmaz stent 137papain 119papules, violaceous 79paronychia 71

progression to gangrene 7–8patellar-tibial-bearing orthosis 208peak systolic velocity (PSV) ratio 12, 14, 15,

16, 17wet gangrene 148, 150

pedal arteriescalcification 112pressure index 10reconstitution 140

228 Index

percutaneous transluminal angioplasty 135gangrene 127neuro-ischemic ulcers 113popliteal artery 168wet gangrene 147

peripheral neuropathy 3claw toes 47painless ulcer 30prevalence 4symptoms 5tests 5–6

peripheral vascular disease 3, 6–14, 15, 16,17, 18, 19, 20

detection and follow-up 16, 18, 20gender differences 140neuropathy co-existence 7prevalence 6–7

peroneal artery stenosis 140pes cavus 44–6

callus over prominent metatarsal heads 65pes planovalgus 51pes planus 43, 112

bunionette 43–4phalanges, concentric resorption 189–90phalangophalangeal joint

hemorrhagic callus 67, 68subluxation 190

phalanx, proximal, osteomyelitis 63phlegmon 169–71photoplethysmography 11plantar abscesses 133plantar arch

collapse 200–1high 45

plantar arteries, reconstitution 140plantar branch artery, medial 181, 183plantar cracks 30plantar heel spur pain 43plantar ligament preservation 90plantar pressure

callus formation 88convex triangular foot 52fat pad thickness reduction 91–2high 3in-shoe measurement 52, 54, 91, 92limited joint mobility 33offloading 33–6prominent metatarsal heads 66redistribution 32reduction 31, 32ulcer under callus area 67

platelet-derived growth factor β (PDGF-β)38, 172

plethysmography, segmental 11

ischemic ulcers 29popliteal artery

atheromatous disease 146collateral supply 132, 135obstruction 122, 123percutaneous transluminal angioplasty 168stenosis 114, 127

popliteal — peripheral bypass 117, 150pre-ulcer formation 88pressure loading 87–8pressure offloading 103, 107, 114

heel 131neuropathic ulcer 174

pressure perception 5–6pressure ulcers 129

gangrenous 132, 133probe-to-bone tests 175prosthesis, below-knee 208Proteus infection 153Proteus mirabilis 181Proteus vulgaris 178pseudo-gout see calcium pyrophosphate

dihydrate (CPPD) deposition diseasePseudomonas 153

infected ulcers 154Pseudomonas aeruginosa 104

fungal infection with multimicrobialcolonization 160

osteomyelitis 119wet gangrene 132wound colonization 121

Pseudomonas maltophila 168pulsed Doppler imaging 12

quality of life 3quintus varus 51–2

radiographyCharcot foot 192magnification 175neuro-osteoarthropathy 188osteomyelitis 154, 175, 192

Regranex see platelet-derived growth factorβ (PDGF-β)

rest pain, ischemic 7persistent recurring 127toe pressure 9transcutaneous oxygen pressure 10

revascularization procedures 114heel gangrene 130

rocker bottom deformity 90

scars, squamous cell carcinoma formation 81scintigraphy see bone scintigraphy imagingScotch-cast boot 35

Index 229

segmental pressure measurement 10–11ischemic ulcers 29

Semmes — Weinstein monofilaments 5–6sensation loss 4, 5

footwear 31sensory deficit 5

neuropathic ulcers 27sepsis, wet gangrene 130, 132–3, 134, 135,

136sesamoid bones 63shear stress

reduction 32ulcers 54

shoesathletic 31foreign objects 156, 157half 35, 36, 66heel-free 36, 97manufacturers 219pressure relief 35–6rocker-style 33, 35, 88roller-style 33selection 29–30therapeutic for neuropathic ulcers 87, 88trauma 3ulcer on dorsum of foot 110–11see also footwear, preventive; insoles

silicone ring 111, 112skin

atrophy 112changes

critical limb ischemia 18ischemic ulcers 28

ischemic necrosis with dry gangrene 129lesions

shoe friction 111toe pressure 9

pathogens 154scaling 134see also ulcers/ulceration; wound(s); wound

healingskin, dry 3

callusunder bone prominence 64over prominent metatarsal heads 65

heel 79cracks 67–8

phlegmon 169smoking cessation 16socks, padded 31soft-tissue infection 102, 156–7

under callus at tip of claw toe 155soft-tissue sarcoma 82–3sole of foot

hyperkeratosis 76midsole neuro-ischemic ulcers 114, 115

squamous cell carcinoma 81–2S(AD)SAD classification for foot ulcers 26staphylococcal toxins 133Staphylococcus aureus 62, 97, 98

antibiotics 182, 183callus over fifth toe 155deep-tissue 162

after interphalangeal mycosis 161fungal infection with multimicrobial

colonization 160infected ulcers 154non-limb-threatening infections 156osteomyelitis 103, 104, 108, 113–14, 116,

168–9chronic neuropathic ulcer 178

web space infection 158wet gangrene 132, 146see also methicillin-resistant Staphylococcus

aureus (MRSA)Staphylococcus epidermidis 104Steinmann pins 197stents 135, 137, 140, 141

aortic 134, 138aorto-iliac intravascular 132, 136

Strenotropomonas maltophilia 122streptococci

non-limb-threatening infections 156toxins 133

stress fracturesmetatarsal heads 92, 178pseudoarthrosis in fifth metatarsal 178toes 134, 139

surgical debridement 119sweating inhibition 3Syme ankle disarticulation 181

tailor’s bunion see bunionette formationtalonavicular joint

Chopart dislocation 69collapse 201, 202destruction 203, 204fragments 199, 200neuro-osteoarthropathy 203

talus resorption 206, 207, 208, 209, 210, 211,212

tardus pardus waveform 19, 149, 150tarsometatarsal joint

destruction 203, 204disruption 164, 165, 201Lisfranc joint line 43neuro-osteoarthropathy 193, 197, 203partial resorption 194–5, 196, 197phlegmon 170

230 Index

tarsometatarsal joint line, front transverseconvexity 43

tarsometatarsophalangeal joint fusion 198technetium-99m 179, 181thermal injury see burnstibia

resorption 206, 207, 211, 212subchondral osteosclerosis 206, 207, 208,

209tibial artery

atheromatous disease 138, 146occlusion 140stenosis 117, 140

tibial artery, anteriorobstruction 150spectral waveform 149stenosis 16, 18

tibial artery, posterior 14, 16calcification 112calcinosis 181, 183palpation 18stenosis 18, 148

tibioperoneal artery 140tinea pedis 76

interdigital 158toe(s)

amputation 121, 122, 134, 146, 202, 203ray 140

burns 98, 99, 100, 101, 102deformities 30, 31

incidence 56varus deformity 46, 48

dry gangrene 127, 128, 130, 131, 133–4,136 –8

fifthamputation 121, 122hemorrhagic callus 200infection under callus 155–6stress fracture 134, 139

fourthamputation 134disarticulation 70–1ulceration by pressure from little toe 111

overriding 50–1causes 55hallux valgus 52–4, 56, 57

pressures 8–9sausage-like appearance 167, 168second

amputation 202, 203disarticulation 116, 132lateral exostosis 192medial displacement 99removal 59, 60, 61, 62

silicone ring 111, 112ulcer formation 67wet gangrene 139–40, 144see also claw toe; curly toe deformity;

hammer toe; mallet toe; nailstoe, great see halluxtranscutaneous oximetry 9–10transcutaneous oxygen pressure (TcPO2)

9–10transparent films 119trauma 3

progression to gangrene 7–8Trichophyton 158, 160triplex scan, wet gangrene of foot 148, 149,

150trypsin 119

ulcers/ulceration 29under callus area 66–7cellulitis 114, 115Charcot foot 95–6classification 25–6critical limb ischemia 18curettage 153depth — ischemia classification 26under hallux 67, 68infection 25–6, 27, 153–4

clinical assessment 153cultures 153diagnosis 153plantar with osteomyelitis 171–3wet gangrene 142–3, 145

ischemia 25–6clinical presentation 26, 28–9

load reduction 34midfoot 201, 202, 203necrobiosis lipoidica 80neuro-ischemic 26, 30

claw toes 120, 121clinical presentation 29dorsum of foot 109–11fifth metatarsal with osteomyelitis 121–3first metatarsal with osteomyelitis

113–14forefoot with osteomyelitis 114, 116–17under hallux 107, 108hallux with osteomyelitis 117, 118, 119,

120, 121under hallux with osteomyelitis 107–9,

110heel 114, 115, 180, 182interdigital 111, 112medial side of foot 112–13midsole 114, 115

Index 231

neuropathic 4, 26, 69–71bunion 177callus formation 169Charcot foot and deep-tissue infection

163–4, 165, 166, 167chronic and osteomyelitis complication

176, 178, 180clinical presentation 26–8collapsed midfoot 90under fifth metatarsal head 99first metatarsal head 87–8foreign body 212under fourth metatarsal head 90–2under heel 96–8neuro-osteoarthropathy 195osteomyelitis complication 102–4,

173–5, 176, 177prominent metatarsal heads 87–90under prominent metatarsal heads 93–5

new treatments 36, 38–9pathways to 4prevalence 3, 67prevention 29–33progression to gangrene 7–8recurrence 116–17risk categories 30, 31–3risk factors 3–4

reduction 117total-contact cast 34see also pressure ulcers

ultrasonographyarterial 11–14, 16, 17, 18, 19color frequency mapping 12duplex scanning 12ischemic ulcers 28–9

phlegmon imaging 171pulsed Doppler 12sensitivity 14waveform analysis 12–14wet gangrene of foot 148, 149, 150

University of Texas classification system fordiabetic foot wounds 25–6

varus deformity 208ulcer under callus area 66–7

vascular status assessment 6–14, 15, 16, 17,18, 19, 20

invasive 20noninvasive 8–14, 15, 16, 17, 18, 19, 20

vascular surgery 113, 121femoro — tibial bypass graft 123

vibration perception 5thresholds 6

walkersprefabricated 195, 196, 197removable cast 34–5

walking, Chopart disarticulation 69web space infection 157–9wet-to-dry dressings 119windlass mechanism maintenance 63wound(s)

bacterial contamination 121classification 25–6infection 153irrigation 119

wound healingaccelerating factors 38–9failure 10

Date post:	17-Aug-2015
Category:	Health & Medicine
Upload:	scu-hospital
View:	287 times
Download:	1 times

Atlas of diabetic foot

Health & Medicine