AC, eds.
The Diabetic Foot.
Amsterdam: Excerpta Medica; 1991:137, 149. 24.
McInnes AD.
The role of the chiropodist.
In: Boulton AJM, Connor H, Cavanagh PR, eds.
The Foot in Diabetes. 2nd edn.
Chichester: Wiley; 1994:77, 91. 25.
Hampson JP, Roberts RI, Morgan DA.
Shared care: a review of the literature.
Fam Pract 1996;13:264, 279. 26.
Hickman M, Drummond N, Grimshaw J.
A taxonomy of shared care for chronic disease.
J Public Health 1994;16:447, 454. 27.
Abbott C, Carrington AL, Ashe H, et al The North-West Diabetes Foot Care Study: incidence of, and risk factors for, new diabetic foot ulceration in a community-based cohort.
Diabet Med 2002;19:377, 384. 28.
Middleton A, Young RJ, Webb F, Brown C, Chadwick P.
An integrated, district wide team approach to diabetic foot care (letter).
Diabet Foot 2000;3:124. 29.
NICE Clinical Guideline 10.
Type 2 diabetes , prevention and management of foot problems.
Available at: www.nice.org.uk/CGO10NICEguideline2004. 30.
Rayman G, Baker NR, Barnett S.
Diabetes specialist podiatrists: time for recognition.
Diabet Foot 2000;3:38, 40.
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40 Algorithms for Assessing Risks for Ulcerations and Amputations David G. Armstrong, Stephanie C. Wu and Ryan C. Crews
Foot ulceration is one of the commonest precursors to lower extremity amputations among persons with diabetes.1,2 Ulceration allows an avenue for infection3 and can cause pro- gressive tissue necrosis and poor wound healing, particularly in the presence of critical is- chaemia.
Foot ulcers therefore play a pivotal role in the causal pathway to lower extremity amputation.4 Diabetic foot ulceration is commonly associated with the presence of peripheral neuropathy and repetitive trauma from normal walking activities to areas of the foot exposed to moderate or high pressure and increased shear forces.5 Foot deformities, limited joint mobility, partial foot amputations and other structural deformities often predispose diabetics with peripheral neuropathy to abnormal weight bearing, areas of concentrated pressure and abnormal shear forces that may significantly increase their risk of ulceration.6−8 Brand9 theorised that when these types of forces were applied to a discrete area over an extended period, they would cause a local inflammatory response, focal tissue ischaemia, tissue destruction and ulceration.
Since most ulcerations are entirely avoidable, the concept of prevention takes on an entirely new urgency.
Clearly, identification of persons at risk for ulceration is of central importance in any plan for amputation prevention and diabetes care.
In this chapter, we will discuss the key, evidence-based risk factors for diabetic foot ulcer- ation as well as those for assessing amputation risk.
ASSESSING THE RISK FOR ULCERATION
Preventing foot complications begins with identifying those at risk. When screening to identify patients at risk for diabetic foot ulcers, there are three key words that can help identify ulcer risk10 , history, numbness and deformity.
The Foot in Diabetes, 4th Edition. Edited by Andrew J.M. Boulton, Peter R. Cavanagh and Gerry Rayman. C 2006 John Wiley & Sons, Ltd. ISBN: 0-470-01504-7
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432 ALGORITHMS FOR ASSESSING RISKS FOR ULCERATIONS AND AMPUTATIONS
History Does the patient have a previous history of foot amputation, ulceration or Charcot arthropathy?
Clinicians should inquire about factors known to be associated with foot ulcers, such as previous foot ulceration, prior lower extremity amputation or the presence of neuropathic fractures,10−12 as these risk factors heighten the risk for further ulceration, infection and sub- sequent amputation.4,10,13 Following ulceration, the skin at that site is often less resilient and less well fortified to accept repetitive stress and therefore more prone to subsequent breakdown.
Partial foot amputation changes the architecture of the foot and may therefore affect its intrin- sic stability.
Thus, persons with a partial foot amputation often develop local foot deformities secondary to biomechanical imbalances that may cause further foci of increased pressure.14−16 Patients with a high-level amputation such as below or above the knee tend to be much more reliant on their remaining limb for transfer or ambulation and may therefore increase the risk for tissue breakdown.
In general, people with a history of ulceration or amputation have all the risk factors to re-ulcerate.
This is evidenced by the fact that up to six in ten persons with a history of ulceration will develop another one within 1 year of wound healing.17,18
Numbness Is there loss of protective sensation?
Neuropathy is the major component of nearly all diabetic ulcerations.19 Diabetic persons who have lost the gift of pain will wear a hole in their foot similar to the way we may wear a hole in our sock.
Without loss of protective sensation, patients generally will not ulcerate.
This is defined as a level of sensory loss that allows patients to injure themselves without recognising the injury.
The consequent vulnerability to physical and thermal trauma increases the risk of foot ulceration sevenfold.20 The absence of protective sensation may be determined by a number of means described elsewhere in this book.
These methods include, but are not limited to, a Semmes, Weinstein log 5.07 (10, g) nylon monofilament, a calibrated vibration perception threshold (VPT) meter (biothesiometer) or a comprehensive physical examination.12
Deformity Is there deformity or limited joint mobility?
The second causative factor in foot ulceration is excessive plantar pressure from foot de- formities.
Neuropathy and foot deformity, in combination with repetitive or constant stress, will ultimately lead to failure of the protective integument and ulceration.
Characteristically, ulceration occurs at the site of highest plantar pressure.5,6,21−23 Foot deformity may be defined as any contracture or prominence that cannot be manually reduced.
Diabetic peripheral neu- ropathy may also affect motor nerves, often causing atrophy of intrinsic musculature of the hand and foot.
When this occurs, the extrinsic musculature functions unopposed, thus caus- ing hammering of the toes, anterior displacement of the fat pad and retrograde buckling of the metatarsal heads.
This results in bony prominences of the metatarsal heads on the plantar aspect of the foot, and of the dorsal surface of the proximal interphalangeal joints of the toes, predisposing these areas to neuropathic ulceration.24−26 In addition, foot deformity is often accompanied by limited joint mobility secondary to the non-enzymatic glycosylation of periarticular soft tissues.
Limitation of motion reduces the foot’s ability to accommodate for ambulatory ground reactive force and, therefore, increases
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ASSESSMENT FOR AMPUTATION RISK 433
plantar pressures.8,27−30 We have previously defined limited joint mobility as simply less than 50◦ of non-weight-bearing passive dorsiflexion of the hallux.10,31 Glycosylation may also dele- teriously affect the resiliency of the Achilles tendon, thereby functionally pulling the foot into plantar flexion. This leads to increased forefoot pressure (increasing risk for plantar ulceration) and, in some patients, may be a component of midfoot collapse and Charcot arthropathy. Clinicians should therefore also examine the feet for structural abnormalities including hammer or claw toes, flat feet, bunions and calluses and reduced joint mobility, to help identify pressure points that are susceptible to future ulceration.
CUMULATIVE RISK When the above three questions have been answered, one may then begin to assess degree of risk for ulceration.
Lavery et al. reported that a patient with neuropathy but no deformity or history of ulcer or amputation has a 1.7 times greater risk for ulceration, compared with a patient without neuropathy.10 Neuropathy with concomitant deformity or limited joint mobility yields a 12.1 times greater risk.
Lastly, a patient with a history of previous ulceration or amputation has a 36.4 times greater risk for presenting with another ulcer.
The assessment of these three risk questions correlates well with those promoted by the International Working Group on the Diabetic Foot32 as well as by other authors.33
CONTRIBUTORY FACTORS
Clinicians should also examine the patient for other contributing risk factors.
Footwear should be inspected to ensure proper fit.
Among 699 persons with a foot ulcer, 21% of the foot ulcers were attributed to rubbing from footwear.34 Cutaneous manifestations associated with diabetes such as dry or fissured skin, calluses, tinea or onychomycosis should also be noted.
Persons with diabetes have a higher rate of onychomycosis and digital interspace tinea infections that can lead to skin disruption.35,36 When present, the callused tissue (as with all callused tissues) should generally be debrided and inspected for the possible presence of underlying neuropathic ulceration or abscess.
Failure to do this could lead to exacerbation of the condition by both covering up a potential fluid collection and further increasing plantar pressure.19,37−42
ASSESSMENT FOR AMPUTATION RISK The three key risk factors for lower extremity amputation are ischaemia, infection and wound depth.43 However, of these key factors, ischaemia is the only one that can, in and of itself, precipitate a primary amputation. The other two factors listed rely on a host of concomitant or preceding factors to develop. For instance, most ulcers are preceded by neuropathy, deformity and repetitive stress. In turn, most diabetic foot infections are preceded by an ulcer.
Is the Wound Ischaemic? In general, vascular disease is not the commonest cause of foot ulceration, being a component factor in only about a quarter of all cases.44,45 It is, however, a powerful risk factor for the non-healing of an ulcer once present, and therefore a risk factor for amputation.