Risk assessment of the diabetic foot and wound

Risk assessment of thediabetic foot and woundStephanie Wu, David G Armstrong

Wu S, Armstrong DG. Risk assessment of the diabetic foot and wound. Int Wound J 2005;2:17—24.

ABSTRACTDiabetic foot ulcers are among the most common severe complications of diabetes, affecting up to 68 per 1000persons with diabetes per year in the United States. Over half of these patients develop an infection and 20%require some form of amputation during the course of their malady. The key risk factors of diabetic footulceration include neuropathy, deformity and repetitive stress (trauma). The key factors associated with nonhealing of diabetic foot wounds (and therefore amputation) include wound depth, presence of infection andpresence of ischaemia. This manuscript will discuss these key risk factors and briefly outline steps for simple,evidence-based assessment of risk in this population.

Key words: Diabetic foot . Wound . Risk assessment . Ulcer . Pressure

INTRODUCTIONComplications of the diabetic foot are the mostcommon cause of non traumatic lower extre-mity amputations in the world. Individualswith diabetes have up to 46-fold greater riskof high-level lower extremity amputation thanthose without diabetes (1,2). The single mostcommon factor leading to amputation is theneuropathic diabetic foot ulcer. The diabeticfoot ulcer is amongst the most common ofdiabetic foot complications, affecting some 68per 1000 persons with diabetes per year in theUnited States (US). Over one half of thesepatients develop an infection (3,4). While themajority of these infections may be treated onan outpatient basis, the infected foot ulcer isthe most common reason for hospitalisationamong patients with diabetes, accounting forapproximately one quarter of all diabetes-related admissions in the US and UnitedKingdom (5—7).

Unfortunately, the majority of patientsadmitted to the hospital for diabetic foot com-plications receive a less than adequate lowerextremity evaluation. Edelson and coworkers(8) reported that only 14% of patientsadmitted to the hospital with a diabetic footcomplication received appropriate and ade-quate lower extremity evaluations. It hasbeen estimated that appropriate knowledgeof risk factors and application of evidence-based multidisciplinary treatments couldreduce 85% of diabetic foot and leg amputa-tions (9,10). Prevention is becoming increas-ingly important to overburdened health caresystems in industrialised nations. This isexemplified by the fact that only 2% ofpatients receiving an amputation are admittedfrom an intermediate or long-term care facilityand 25% are discharged to one following theamputation (11).Regular inspection is one of the most effec-

tive mechanisms to prevent diabetic foot com-plications. Even with an increase in diabeticfoot awareness, there still exists a tremendousdeficiency in foot evaluations. Persons withdiabetes often do not have their feetevaluated, even on the most cursory level,during a regular office visit by their primarycare physician, with only 10—19% of patientswith an established diagnosis of diabetes hadtheir feet inspected even after having theirshoes and stocking removed by the nursing

Authors: S Wu, DPM, Dr William M. Scholl College ofPodiatric Medicine at Rosalind Franklin University of Medicineand Science, North Chicago, IL, USA; DG Armstrong, PhD,DPM, MSc, the Center for Lower Extremity AmbulatoryResearch (CLEAR), Dr William M. Scholl College of PodiatricMedicine at Rosalind Franklin University of Medicine andScience, North Chicago, IL, USAAddress for correspondence: S Wu, Dr William M. SchollCollege of Podiatric Medicine at Rosalind Franklin University ofMedicine and Science, 3333 Green Bay Road, North ChicagoIL, 60064, USAE-mail: [email protected]

� Blackwell Publishing Ltd and Medicalhelplines.com Inc 2005 . International Wound Journal . Vol 2 No 1 17

RESEARCH&

Key Points

. complications of the diabeticfoot are the most commoncause of non traumatic lowerextremity amputation

. the diabetic foot ulcer is amongstthe most common of diabeticcomplications

. over half of the patients developinfections

. the majority of the patientsadmitted for diabetic foot com-plications receive a less thanadequate lower extremity eva-luation

. regular inspection is one of themost effective mechanisms toprevent diabetic foot complica-tions

staff (12,13). The majority of the signs andsymptoms associated with ulceration andamputation can be identified by a few focusedquestions, foot inspection and simple exam-ination techniques. This manuscript willreview the risk factors most commonly asso-ciated with lower limb ulceration in thediabetic population and will subsequentlyoutline a treatment-based classification sys-tem for risk stratification and subsequenttreatment.

WHAT ARE THE RISK FACTORS OFDIABETIC FOOT ULCERATION?The most common risk factors for ulcerationinclude peripheral neuropathy, history ofulceration and structural deformity (14,15).While myriad other factors exist, such asperipheral arterial disease, poor metaboliccontrol, blindness and poor social supportsystems (16—18), these are generally secondaryfactors that do not in and of themselves leaddirectly to diabetic foot ulceration.

Peripheral neuropathyPeripheral sensory neuropathy is one of themost significant risk factors for both footulceration and amputation in this population(6). People rarely develop foot ulcers whenthey have intact peripheral sensation. Due tothe lack of painful feedback, peripheral neuro-pathy allows an environment where an injurycan occur that is not recognised by the patient.This results in a person being able to wear ahole in the bottom of his or her foot just as onemight wear a hole in a stocking (19). It is theconstant repetitive stress that, in the face ofneuropathy, leads to failure of the tissue andultimately ulceration (20—22).Identification of and diagnosing a patient

with peripheral neuropathy is a critical taskin screening and risk stratification among per-sons with diabetes. Many studies have beenconducted attempting to define methods oftesting for neuropathy and determining thepoint of neuropathy. Several studies haveshown that the 10-g Semmes—Weinsteinmonofilament (SWMF) is one of the mosteffective instruments to screen persons withdiabetes. The instrument is inexpensive andreusable. The test is non invasive, reproduci-ble and easy to perform by a physician or

nurse. Inability to feel of four or more out often sites on the bottom of the foot using theSWMF carried with it a 97% sensitivity and a83% specificity (23). When the SWMF is com-bined with a vibration perception examin-ation, the sensitivity rose to 100% with aspecificity of 77%. Furthermore, a combina-tion of one or more positive questions on afocused neuropathy symptom score coupledwith four out of ten imperceptible sites imper-ceptible to the SWMF yielded a 97% specifi-city and 86% specificity. It should be noted,however, that the SWMF is not a perfect tool.In fact, differences in design and manufacturecan lead to dramatic differences in sensitivityand specificity. Furthermore, the devicebecomes more pliable and therefore oversen-sitive if used repetitively throughout the day.It is therefore recommended that severaldevices be rotated throughout the day toavoid overdiagnosing loss of protective sensa-tion (24,25). As there are no readily availableclinical devices that can simultaneously eval-uate large and small fiber neuropathy, it isprobably prudent for the specialists to con-sider combining modalities (26).

History of ulcerationA history significant for ulceration or amputa-tion heightens the risk of further ulceration,infection and subsequent amputation. This isdue to abnormal distribution of plantar pres-sures that are often the cause of ulceration andthat are often encountered following anamputation (27). It may be assumed thatpatients with a history of ulceration possessall the risk factors necessary to produceanother ulceration. It is therefore not surpris-ing that between 20% and 58% of patientsdevelop another ulcer within a year after heal-ing a wound (28,29).

Structural deformityThere are two main mechanisms by whichfoot deformity and neuropathy bring aboutskin breakdown. The first mechanism refersto prolonged low pressure over a small radiusof curvature. In this scenario, a prominent footdeformity such as a bunion or hammertoedeformity rubs against the shoe. The unrecog-nised pressure and shear forces over thedeformity generally cause wounds over the

Risk assessment of the diabetic foot and wound

� Blackwell Publishing Ltd and Medicalhelplines.com Inc 2005 . International Wound Journal . Vol 2 No 118

Key Points

. only 10—19% of patients withan established diagnosis of dia-betes had their feet inspected evenafter their shoes and stockingswere removed by the nursing staff

. this paper reviews the riskfactors most commonly asso-ciated with lower limb ulcer-ation in the diabetic population

. peripheral sensory neuropathy isone of the most significant riskfactors for both foot ulceration andamputation in this population

. a history significant for ulcer-ation or amputation heightensthe risk of further ulceration,infection and subsequent ampu-tation

medial, lateral and dorsal prominences of theforefoot. The second and most commonmechanism involves prolonged repetitivemoderate stress. This normally occurs on theball of the foot and is thought to be associatedwith prominent metatarsal heads with a dis-placed or atrophied fat pad. Foot deformitiesare believed to be more common in the per-sons with diabetes due to atrophy of theintrinsic musculature associated with motorneuropathy. The intrinsic musculature of thefoot functions to stabilise the toes duringgait. In the presence of neuropathy, thelesser digits tend to contract and formhammertoes. The metatarsophalangeal jointstend to sublux and dislocate, which increasethe prominence of the metatarsal heads andanteriorly displace the fat pad that normallydissipates stresses directly under the ball ofthe foot (30,31). Rigid deformities and/orlimited range of motion at the subtalar ormetatarsophalangeal joints have also beenassociated with the development of diabeticfoot ulcers (32,33). Decrease in joint mobilityhas been observed in the hand, foot andankle of persons with diabetes and asso-ciated with soft tissue glycosylation (34,35).Decreased motion in weight-bearing jointsincreases the load on adjacent joints andinterrupts the normal transfer of pressuresthat occur on the foot during normal ambul-ation (36).Additional, more complex deformities may

also be present on a screening examination.The most widely recognised of these is theso-called ‘rocker bottom’ foot caused by Char-cot arthropathy. This deformity, which isthought to be caused by a combination oflarge and small fibre peripheral neuropathy,relatively good vascular outflow and repeti-tive stress or a single (often unrecognised)traumatic event in the at-risk patient, canlead to profound swelling and bony defor-mity. Its incidence appears to be similar tothat of lower extremity amputations in theUS (3). This deformity often occurs in thearch area due to a combination of plantarflex-ory pull from the Achilles tendon andelevated plantar pressure, causing dislocationin the midfoot (33,37). Charcot arthropathy ofthe foot should be included in the differentialdiagnosis of a patient presenting with a red,hot, swollen foot, particularly in the absenceof any open wound (38).

Poor metabolic controlPoor systemic control of blood glucose is asso-ciated with a host of systemic complications.These include neuropathy (39), impairedwhite blood cell function (40,41), soft tissuecross-linking through production of advancedglycosylation products (42) and ulceration(43). In a direct sense, this cross-linking canmake the skin more friable and more prone torepetitive stress injury (44). Aggressive meta-bolic control with appropriate lower extremitycare may reduce overall risk for ulcerationand amputation (14).

ARE RISK FACTORS OF ULCERA-TION CUMULATIVE?It has been reported that neuropathy, defor-mity, high plantar pressure, poor glucose con-trol and male gender are significant risk factorsof ulceration in diabetic patients. Additionally,it has also been noted that these risks arecumulative. Patients with neuropathy aloneare at approximately 1�7 times greater risk ofpresenting with ulceration than patients with-out neuropathy. This risk increases to 12�1times when patients present with neuropathyand deformity. Patients with neuropathy,deformity and a history of ulcer or amputationare at approximately 36 times greater risk ofdeveloping another ulcer (14). These evidence-based categories and corresponding treatmentstrategies are essentially incorporated into theInternational Working Group Classification fordiabetic foot risk (Table 1) (45,46).While classifying basic risk of ulceration is

important, one must also be adept in describ-ing and classifying a pre-existing wound.There have been numerous wound classifica-tion systems proposed and utilised (47—51).Unfortunately, few have concisely and consist-ently included the three key factors associatedwith risk of amputation. These three keyfactors can be summed up as depth, infectionand ischaemia (47). Presently, the most vali-dated system used that includes these factorsconsistently is the system proposed by theUniversity of Texas (Table 2) (52). While thereare other systems either in place or in devel-opment that address these issues, it seems alogical starting point to use this system forpurposes of discussion. Again, there arethree key questions to ask when assessing awound.



Key Points

. foot deformities, shear andstress are generally the maincauses of wounds in the diabeticfoot

. the most widely recognised isthe Charcot foot

. poor systemic control of bloodglucose is associated with a hostof systemic complications

. neuropathy deformity, highplantar pressure, poor glucosecontrol and male gender aresignificant risk factors of ulcer-ation in diabetic patients

. there are three key questions toask when assessing a wound

1. How deep is it?Depth of the wound and involvement ofunderlying structures are the most commonlyutilised descriptors in wound classification.Wounds are graded by depth. Grade 0 repre-sents a preulcerative or postulcerative site.Grade 1 wounds are superficial woundsthrough the epidermis or epidermis and der-mis but do not penetrate to tendon, capsule orbone (Figure 1). Grade 2 wounds penetrate totendon or capsule. Grade 3 wounds penetrateto bone or into a joint. We have known forsome time that wounds that penetrate tobone are highly prone to osteomyelitis (53).Additionally, we have observed that morbidoutcomes are intimately associated with pro-gressive wound depth. When this question isanswered and graded as 0, 1, 2 or 3, we maythen move on to the wound’s stage, which isdivided into four groups (clean, infected,ischaemic and both infected and ischaemic).

2. Is infection present?The definition of infection is not an easy one.Cultures, laboratory values and subjectivesymptoms are all helpful. However, the diag-

nosis of an infection’s genesis and resolutionhas to be, and continues to be, a clinical one(4). The presence of purulent exudate and/orlocal signs of inflammation, sinus tractformation, fluctuance or crepitation may behighly indicative of infection (54,55). How-ever, it is important to note that, due to often-profound loss of protective sensation, painis not always noted with infected diabeticfoot ulcers (56). Furthermore, while systemicsigns and symptoms of sepsis should provideimportant cues to the treating clinician, theyare frequently absent in persons with evensignificant diabetic foot infections (57—59).While criteria for infection may be somethingless than clear-cut, there is little question thatpresence of infection is a prime cause of lowerextremity morbidity and frequently developsinto gangrene and subsequent amputation.Nonetheless, if a wound is clean, it falls intostage A. If it is infected, it falls into stage B.

3. Is it ischaemic?The condition of ischaemia in tissue oftenresults in amputation (6). Few other qualita-tive factors can necessitate amputation alone.

Table 1 International Working Group Classification of diabetic foot risk (44)

Grade 0 No neuropathy present

Grade 1 Neuropathy without deformity or history of ulceration

Grade 2 Neuropathy with deformity or peripheral vascular disease

Grade 3 History of ulcer, amputation

Table 2 The University of Texas Diabetic Wound Classification System (46,51)

Grade

Stage 0 1 2 3

A Preulcerative or postulcera-

tivelesion completely epithe-

lialised

Superficial wound not invol-

vingtendon, capsule or bone

Wound penetrating to ten-

donor capsule

Wound penetrating to

bone or joint

B Preulcerative or postulcera-


lialisedwith infection


vingtendon, capsule or

bonewith infection


donor capsule with infection


bone or jointwith infec-

tion

C Preulcerative or postulcera-


lialisedwith ischaemia


vingtendon, capsule or

bonewith ischaemia


donor capsule with ischae-

mia


bone or jointwith

ischaemia

D Preulcerative or postulcera-


lialisedwith infection and

ischaemia


vingtendon, capsule or bone

withinfection and ischaemia


donor capsule with infection

andischaemia


bone or jointwith infec-

tion and ischaemia



Key Points

. how deep is it?; is infectionpresent?; is it ischaemia?

. wound depth is assessed andquantified by a grading system

. the diagnosis of infection shouldbe based on the clinical signs forthe presence of infection

Neuropathy and wound depth are not stand-alone factors for the need for amputation of anaffected limb; to generate an infection, onemust frequently have an open wound. There-fore, the identification of ischaemia is of theutmost importance when evaluating a wound.If pulses are not palpable, or if a wound issluggish to heal even in the face of appropri-ate off-loading and local wound care, appro-priate non invasive vascular studies arewarranted followed by a prompt vascular sur-gery consultation and possible intervention toimprove perfusion and thereby effect healing.Recent guidelines have suggested that regularscreening for vascular disease through the useof ankle-brachial systolic pressure index (ABI)may be of benefit for not only identifying

peripheral ischaemia, but also potentially foridentifying risk of cardiovascular morbidityand mortality if it is either low (<0�9) or high(>1�4) (60—62). While the ABI may not be sen-sitive enough to detect subtle signs of ischae-mia, it might be useful as an initial measureprior to embarking on further investigations ifthere is a clinical index of suspicion. Regard-less of what type of assessment is used toinitially assess for ischaemia, it is clearly arisk factor for poor healing. If a wound isischaemic, it falls into stage C (Figure 2). Ifthe wound is both infected and ischaemic, itis categorised into stage D.Once these three questions are accom-

plished, a wound may be classified based onthe above listed criteria. For instance, an

Figure 1. Superficial diabetic foot wound.

Figure 2. Mummifying second digit secondary to ischaemia.



Key Points

. it should be considered thatpain as an indicator may beabsent due to neuropathy

. there is little question that thepresence of infection is a primecause of lower extremity mor-bidity

. the condition of ischaemia intissue often results in amputa-tion

. the identification of ischaemia isof the utmost importance whenevaluating a wound

infected wound that probes to tendon with nobone involvement and adequate blood flowwould be termed a UT grade 2B wound.When the infection is resolved by appropriatemedical care, the wound classification wouldbe revised to 2A.Subsequent to the appropriate diagnosis of

and classification of a diabetic neuropathiculceration, treatment may then commence. Aplethora of treatment modalities exist and fewphysicians would attempt to state that there isone treatment that may be used successfullyon all wounds. What is paramount is thatproper wound care tenets be observed. Theseinclude appropriate debridement of necroticand undermining tissue and reduction ofpressure through offloading of the diabeticfoot wound (63).In conclusion, it is observed that many of

the most common component causes forneuropathic ulceration, infection and subse-quent amputation may be identified usingsimple, inexpensive equipment in a primarycare setting (Table 3). However, to initiatetreatment based on the information gathered,a thorough knowledge of the risk factors’interactions and cumulative effect are of para-mount important. Also of critical import is theappropriate communication of these risk fac-tors to other members of the diabetic limb sal-vage team. Only when these goals have beenmet will we be able to make a meaningful long-term, widespread impact on the unnecessarilyhigh prevalence of diabetes-related lowerextremity amputations both in our nation andthroughout the industrialised world.

REFERENCES1 Lavery LA, Ashry HR, van Houtum W, Pugh JA,

Harkless LB, Basu S. Variation in the incidenceand proportion of diabetes-related amputationsin minorities. Diabetes Care 1996;19(1):48—52.

2 Armstrong DG, Lavery LA, Quebedeaux TL, WalkerSC. Surgical morbidity and the risk of amputationfollowing infected puncture wounds of the foot in

diabetic and non-diabetic adults. South Med J1997;90(4):384—9.

3 Lavery LA, Armstrong DG, Wunderlich RP, BoultonAJM, Tredwell JL. Diabetic foot syndrome: evalu-ating the prevalence and incidence of foot pathol-ogy in mexican americans and non-hispanicwhites from a diabetes disease managementcohort. Diabetes Care 2003;26:1435—8.

4 Armstrong DG, Lipsky BA. Advances in the treat-ment of diabetic foot infections. Diabetes TechnolTher 2004;6:167—77.

5 Gibbons G, Eliopoulos GM. Infection of the diabeticfoot. In: Kozak GP, Hoar CS, Rowbotham, JL,editors. Management of Diabetic Foot Problems.Philadelphia: W.B. Saunders 1984:97—102.

6 Pecoraro RE, Reiber GE, Burgess EM. Pathways todiabetic limb amputation: basis for prevention.Diabetes Care 1990;13:513—21.

7 Levin M. Pathophysiology of diabetic foot lesions.In: Davidson JK, editors. Clinical DiabetesMellitus: A Problem-Oriented Approach. NewYork: Theime Medical, 1991:504—10.

8 Edelson GW, Armstrong DG, Lavery LA, Caicco G.The acutely infected diabetic foot is not ade-quately evaluated in an inpatient setting. ArchIntern Med 1996;156:2373—6.

9 National Diabetes Advisory Board. The NationalLong-Range Plan to Combat Diabetes. Bethesda:National. Institutions of Health, 1987:88—1587.

10 Edmonds ME. Experience in a multidisciplinarydiabetic foot clinic. In: Connor H, Boulton AJM,Ward JD, editors. The Foot in Diabetes. Chiche-ster: John Wiley and Sons, 1987:121—31.

11 Lavery LA, van Houtum WH, Armstrong DG.Institutionalization following diabetes-relatedlower extremity amputation. Am J Med 1997;103(5):383—8.

12 Wylie-Rosset J, Walker EA, Shamoon H, Engel S,Basch C, Zybert P. Assessment of documentedfoot examinations for patients with diabetes ininner-city primary care clinics. Arch Fam Med1990;4:46—50.

13 Cohen SJ. Potential barriers to diabetes care.Diabetes Care 1983;6:499—500.

14 Lavery LA, Armstrong DG, Vela SA, Quebedeaux TL,Fleischli JG. Practical criteria for screening patientsat high risk for diabetic foot ulceration. Arch InternMed 1998;158:158—62.

15 Reiber GE, Vileikyte L, Boyko EJ, del Aguila M,Smith DG, Lavery LA, Boulton AJ. Causalpathways for incident lower-extremity ulcers inpatients with diabetes from two settings. DiabetesCare 1999;22(1):157—62.

Table 3 Three key, take-home messages for appropriate assessment of the diabetic foot

1. Persons with diabetes should have their shoes and socks removed on every visit to the family physician to facilitate a brief,

focused assessment.

2. The key risk factors for most diabetic foot wounds include neuropathy, deformity and repetitive stress. Ischaemia is a critical

factor but is generally considered a risk factor for not healing a wound and subsequent amputation.

3. The key risk factors associated with a poor prognosis when an ulcer is present are depth, infection and ischaemia. These

should be evaluated whenever assessing a wound.



Key Points

. recent guidelines have sug-gested that regular screeningfor vascular disease throughthe use of ABI

. while the ABI may not besensitive enough to detectsubtle signs of ischaemia itmight be useful as an initialmeasure prior to further investi-gation

. once these three questions areaccomplished a wound may beclassified based on the abovelisted criteria

. subsequent to the appropriatediagnosis and classification of adiabetic neuropathic ulceration,treatment may then commence

16 Boyko EJ, Ahroni JH, Stensel V, Forsberg RC,Davignon DR, Smith DG. A prospective study ofrisk factors for diabetic foot ulcer. The SeattleDiabetic Foot Study. Diabetes Care 1999;22(7):1036—42.

17 Boyko EJ, Ahroni JH, Stensel V, Forsberg RC,Heagerty PJ. Prediction of diabetic foot ulcerusing readily available clinical information: theSeattle Diabetic Foot Study. Diabetes 2002;51(2Suppl):A18.

18 Reiber GE. Epidemiology of foot ulcers and ampu-tations in the diabetic foot. In: Bowker JH, PfeiferMA, editors. The Diabetic Foot. St Louis: Mosby,2001:13—32.

19 Birke JA, Sims DS. Plantar sensory threshold in theulcerated foot. Lepr Rev 1986;57:261—7.

20 Armstrong DG, Abu Rumman PL, Nixon BP, Boul-ton AJM. Continuous activity monitoring in per-sons at high risk for diabetes-related lowerextremity amputation. J Am Podiatr Med Assoc2001;91:451—5.

21 Armstrong DG, Boulton AJM. Activity monitors:Should we begin dosing activity as we dose adrug? J Am Podiatr Med Assoc 2001;91:152—3.

22 Armstrong DG, Lavery LA, Kimbriel HR, Nixon BP,Boulton AJ. Activity patterns of patients withdiabetic foot ulceration: patients with activeulceration may not adhere to a standard pressureoff-loading regimen. Diabetes Care 2003;26(9):2595—7.

23 Armstrong DG, Lavery LA, Vela SA, Quebedeaux TL,Fleischli JG. Choosing a practical screening instru-ment to identify patients at risk for diabetic footulceration. Arch Intern Med 1998;158:289—92.

24 Booth J, Young MJ. Differences in the performanceof commercially available 10-g monofilaments.Diabetes Care 2000;23(7):984—8.

25 Armstrong DG. The 10-g monofilament: the diag-nostic divining rod for the diabetic foot? [editor-ial] [In process citation]. Diabetes Care 2000;23(7):887.

26 Singh N, Armstrong DG, Lipsky BA. Preventingfoot ulcers in patients with diabetes. Jama2005;293(2):217—8.

27 Armstrong DG, Lavery LA. Plantar pressures arehigher in diabetic patients following partial footamputation. Ostomy Wound Manage 1998;44(3):30—2, 34, 36 passim.

28 Helm PA, Walker SC, Pulliam GF. Recurrence ofneuropathic ulcerations following healing in a totalcontact cast. Arch Phys Med Rehabil 1991;72(12):967—70.

29 Uccioli L, Faglia E, Monticone G, Favales F, Durola L,Aldeghi A, Quarantiello A, Calia P, Menzinger G.Manufactured shoes in the prevention of diabeticfoot ulcers. Diabetes Care 1995;18(10): 1376—8.

30 Quebedeaux TL, Lavery LA, Lavery DC. The devel-opment of foot deformity and ulcers after greattoe amputation in diabetes. Diabetes Care1996;19(2):165—7.

31 Brand PW. The insensitive foot (including leprosy).In: Jahss M, editors. Disorders of the Foot andAnkle, 2nd edition. Philadelphia: Saunders, 1991:2170—5.

32 Fernando DJ, Masson EA, Veves A, Boulton AJ.Relationship of limited joint mobility to abnormalfoot pressures and diabetic foot ulceration. Dia-betes Care 1991;14(1):8—11.

33 Grant WP, Sullivan R, Soenshine DE, Adam M,Slusser JH, Carson KA, Vinik AI. Electronmicroscopic investigation of the effects of diabetesmellitus on the achilles tendon. J Foot Ankle Surg1997;36(4):272—8.

34 RosenbloomAL, Silverstein JH, Lezotte DC, RileyWJ,Maclaren NK. Limited joint mobility in diabetesmellitus of childhood: natural history and relation-ship to growth impairment. J Pediatr 1982;101(5):874—8.

35 Rosenbloom AL. Skeletal and joint manifestations ofchildhood diabetes. Pediatr Clin North Am 1984;31:569—89.

36 Armstrong DG, Lavery LA, Bushman TR. Peak footpressures influence healing time of diabetic ulcerstreated with total contact casting. J Rehabil ResDev 1998;35:1—5.

37 Armstrong DG, Lavery LA. Elevated peak plantarpressures in patients who have Charcot arthropa-thy. J Bone Joint Surg Am 1998;80(3):365—9.

38 Armstrong DG, Todd WF, Lavery LA, Harkless LB.The natural history of acute Charcot’s arthropathyin a diabetic foot specialty clinic. Diabet Med1997;14:357—63.

39 Dahl-Jorgensen K, Brinchmann-Hansen O, HanssenKF, Ganes T, Kierulf P, Smeland E, Sandvik L,Aagenaes O. Effect of near normoglycemia fortwo years on progression of early diabeticretinopathy, nephropathy, and neuropathy: theoslo study. Br Med J 1986;293:1195—9.

40 Reeves WG, Wilson RM. Infection, immunity, anddiabetes. In: Alberti MM, DeFronzo RA, Kleen H,Zimmet P, editors. International Textbook of Dia-betes Mellitus, 1st edition. West Sussex: JohnWiley and Sons, 1992.

41 Larkin LG, Frier BM, Ireland JT. Diabetes mellitusand infection. Postgrad Med J 1985;61:233—7.

42 Brownlee M. Glycation products and the pathogen-esis of diabetic complications. Diabetes Care1992;15:1835—43.

43 Moss SE, Klein R, Klein BEK. The prevalence andincidence of lower extremity amputation in a dia-betic population. Arch Intern Med 1992;152:610—6.

44 Maluf KS, Mueller MJ. Novel Award 2002. Compari-son of physical activity and cumulative plantar tis-sue stress among subjects with andwithout diabetesmellitus and a history of recurrent plantar ulcers.Clin Biomech (Bristol, Avon) 2003;18(7):567—75.

45 Peters EJ, Lavery LA. Effectiveness of the diabeticfoot risk classification system of the internationalworking group on the diabetic foot. Diabetes Care2001;24(8):1442—7.

46 Armstrong DG. The University of Texas DiabeticFoot Classification System. Ostomy Wound Man-age 1996;42(8):60—1.

47 Armstrong DG, Peters EJ. Classification of woundsdiabetic foot. Curr Diab Rep 2001;1:233—8.

48 Jeffcoate WJ, Macfarlane RM, Fletcher EM. Thedescription and classification of diabetic footlesions. Diabet Med 1993;10:676—9.



49 Arlt B, Protze J. Diabetic foot. Langenbecks ArchChir Suppl Kongressbd 1997;114:528—32.

50 Wagner FW. The dysvascular foot: a system fordiagnosis and treatment. Foot Ankle 1981;2: 64—122.

51 Meggitt B. Surgical management of the diabetic foot.Br J Hosp Med 1976;16:227—332.

52 Armstrong DG, Lavery LA, Harkless LB. Validationof a diabetic wound classification system. Thecontribution of depth, infection, and ischemia torisk of amputation [see comments]. Diabetes Care1998;21(5):855—9.

53 Grayson ML, Balaugh K, Levin E, Karchmer AW.Probing to bone in infected pedal ulcers. A clinicalsign of underlying osteomyelitis in diabeticpatients. JAMA 1995;273(9):721—3.

54 International Working Group on the Diabetic Foot.International Consensus on the diabetic foot.Maastricht: International Working Group on theDiabetic Foot, 1999.

55 Lipsky BA, Berendt AR, Deery HG, Embil JM,Joseph NS, Karchmer AW, Le Frock JL, Lew DP,Mader JT, Norden C, Tan JS. Diagnosis and treat-ment of diabetic foot infections. Clin Infect Dis2004;39:885—910.

56 Edelman D, Hough DM, Glazebrook KN, Oddone EZ.Prognostic value of the clinical examination ofthe diabetic foot ulcer. J Gen Intern Med 1997;12(9):537—43.

57 Lavery LA, Armstrong DG, Quebedeaux TL, WalkerSC. Puncture wounds: the frequency of normal

laboratory values in the face of severe foot infec-tions of the foot in diabetic and non-diabeticadults. Am J Med 1996;101:521—5.

58 Armstrong DG, Lavery LA, Sariaya M, Ashry H.Leukocytosis is a poor indicator of acute osteo-myelitis of the foot in diabetes mellitus. J FootAnkle Surg 1996;35(4):280—3.

59 Armstrong DG, Perales TA, Murff RT, Edelson GW,Welchon JG. Value of white blood cell count withdifferential in the acute diabetic foot infection. JAm Podiatr Med Assoc 1996;86(5):224—7.

60 American Diabetes Association. Peripheral arterialdisease in people with diabetes. Diabetes Care2003;26(12):3333—41.

61 Resnick HE, Lindsay RS, McDermott MM,Devereux RB, Jones KL, Fabsitz RR, Howard BV.Relationship of high and low ankle brachialindex to all-cause and cardiovascular diseasemortality: the Strong Heart Study. Circulation2004;109(6):733—9.

62 Hirsch AT, Gloviczki P, Drooz A, Lovell M,Creager MA. Special communication: mandatefor creation of a national peripheral arterial dis-ease public awareness program: an opportunityto improve cardiovascular health. Angiology2004;55(3):233—42.

63 ArmstrongDG,NguyenHC,LaveryLA,vanSchieCH,Boulton AJM, Harkless LB. Offloading the diabeticfoot wound: a randomized clinical trial. DiabetesCare 2001;24:1019—22.



Risk assessment of the diabetic foot and wound

Documents

Transcript of Risk assessment of the diabetic foot and wound