Clin Diabetes 2006 Kruse 91 3 Foot

3
P R A C T I C A L P O I N T E R S Evaluation and Treatment of Diabetic Foot Ulcers Ingrid Kruse, DPM, and Steven Edelman, MD D iabetic foot problems, such as ulcerations, infections, and gan- grene, are the most common cause of hospitalization among diabetic patients. Routine ulcer care, treatment of infections, amputations, and hospitaliza- tions cost billions of dollars every year and place a tremendous burden on the health care system. The average cost of healing a single ulcer is $8,000, that of an infected ulcer is $17,000, and that of a major amputa- tion is $45,000. More than 80,000 ampu- tations are performed each year on dia- betic patients in the United States, and ~ 50% of the people with amputations will develop ulcerations and infections in the contralateral limb within 18 months. An alarming 58% will have a contralat- eral amputation 3–5 years after the first amputation. In addition, the 3-year mor- tality after a first amputation has been estimated as high as 20–50%, and these numbers have not changed much in the past 30 years, despite huge advances in the medical and surgical treatment of patients with diabetes. Etiology “The majority of foot ulcers appear to result from minor trauma in the presence of sensory neuropathy.” This famous but simple quote from McNeely et al. 1 best describes the critical triad most com- monly seen in patients with diabetic foot ulcers: peripheral sensory neuropathy, deformity, and trauma. All three of these risk factors are present in 65% of diabet- ic foot ulcers. Calluses, edema, and peripheral vascular disease have also been identified as etiological factors in the development of diabetic foot ulcers. 91 CLINICAL DIABETES Volume 24, Number 2, 2006 Although the pathogenesis of periph- eral sensory neuropathy is still poorly understood, there seem to be multiple mechanisms involved, including the for- mation of advanced glycosylated end products and diacylglycerol, oxidative stress, and activation of protein kinase C. Furthermore, the Diabetes Control and Complications Trial 2 and other prospective studies have confirmed the pivotal role of hyperglycemia in the onset and progression of neuropathy. The data linking glycemic control and neuropathy are not as clear cut as those for retinopathy because of the difficulty in identifying objective measures to assess the many stages of neuropathy over time and because the symptoms, or lack thereof, of neuropathy may be mis- leading if assessed only through patient questionnaires. Finally, the differential diagnosis of peripheral neuropathy is quite large, and patients may have other etiologies, as well. Even so, it is impor- tant for clinicians to know the basics of evaluation and treatment of foot ulcers seen in diabetic patients. Evaluation Foot ulcer evaluation should include assessment of neurological status, vascu- lar status, and evaluation of the wound itself. Neurological status can be checked by using the Semmes-Weinstein monofil- aments to determine whether the patient has “protective sensation,” which means determining whether the patient is sen- sate to the 10-g monofilament (Figure 1). Figure 1. Using the 10-g Semmes-Weinstein monofilament. The monofilament is applied to various areas on the foot (e.g., at the dorsum of the great toe just proxi- mal to the nail bed and the plantar surface of the big toe, metatarsal heads, and heel) with enough pressure to bend the nylon filament. Patients are asked to identi- fy the location of the filament, preferably with their eyes closed. Patients who can- not feel the monofilament on their feet are termed “insensate” and are 10 times more likely to develop a foot ulcer than their “sensate” counterparts.

description

Clin Diabetes 2006

Transcript of Clin Diabetes 2006 Kruse 91 3 Foot

Page 1: Clin Diabetes 2006 Kruse 91 3 Foot

P R A C T I C A L P O I N T E R S

Evaluation and Treatment of Diabetic Foot UlcersIngrid Kruse, DPM, and Steven Edelman, MD

Diabetic foot problems, such asulcerations, infections, and gan-grene, are the most common

cause of hospitalization among diabeticpatients. Routine ulcer care, treatment ofinfections, amputations, and hospitaliza-tions cost billions of dollars every yearand place a tremendous burden on thehealth care system.

The average cost of healing a singleulcer is $8,000, that of an infected ulceris $17,000, and that of a major amputa-tion is $45,000. More than 80,000 ampu-tations are performed each year on dia-betic patients in the United States, and ~ 50% of the people with amputationswill develop ulcerations and infections inthe contralateral limb within 18 months.An alarming 58% will have a contralat-eral amputation 3–5 years after the firstamputation. In addition, the 3-year mor-tality after a first amputation has beenestimated as high as 20–50%, and thesenumbers have not changed much in thepast 30 years, despite huge advances inthe medical and surgical treatment ofpatients with diabetes.

Etiology“The majority of foot ulcers appear toresult from minor trauma in the presenceof sensory neuropathy.” This famous butsimple quote from McNeely et al.1 bestdescribes the critical triad most com-monly seen in patients with diabetic footulcers: peripheral sensory neuropathy,deformity, and trauma. All three of theserisk factors are present in 65% of diabet-ic foot ulcers. Calluses, edema, andperipheral vascular disease have alsobeen identified as etiological factors inthe development of diabetic foot ulcers.

91CLINICAL DIABETES • Volume 24, Number 2, 2006

Although the pathogenesis of periph-eral sensory neuropathy is still poorlyunderstood, there seem to be multiplemechanisms involved, including the for-mation of advanced glycosylated endproducts and diacylglycerol, oxidativestress, and activation of protein kinaseC�. Furthermore, the Diabetes Controland Complications Trial2 and otherprospective studies have confirmed thepivotal role of hyperglycemia in theonset and progression of neuropathy.The data linking glycemic control andneuropathy are not as clear cut as thosefor retinopathy because of the difficultyin identifying objective measures toassess the many stages of neuropathyover time and because the symptoms, orlack thereof, of neuropathy may be mis-

leading if assessed only through patientquestionnaires. Finally, the differentialdiagnosis of peripheral neuropathy isquite large, and patients may have otheretiologies, as well. Even so, it is impor-tant for clinicians to know the basics ofevaluation and treatment of foot ulcersseen in diabetic patients.

EvaluationFoot ulcer evaluation should includeassessment of neurological status, vascu-lar status, and evaluation of the wounditself. Neurological status can be checkedby using the Semmes-Weinstein monofil-aments to determine whether the patienthas “protective sensation,” which meansdetermining whether the patient is sen-sate to the 10-g monofilament (Figure 1).

Figure 1. Using the 10-g Semmes-Weinstein monofilament. The monofilament isapplied to various areas on the foot (e.g., at the dorsum of the great toe just proxi-mal to the nail bed and the plantar surface of the big toe, metatarsal heads, andheel) with enough pressure to bend the nylon filament. Patients are asked to identi-fy the location of the filament, preferably with their eyes closed. Patients who can-not feel the monofilament on their feet are termed “insensate” and are 10 timesmore likely to develop a foot ulcer than their “sensate” counterparts.

Page 2: Clin Diabetes 2006 Kruse 91 3 Foot

prolonged. If pedal pulses are nonpalpa-ble, the patient should be sent to a nonin-vasive vascular laboratory for furtherassessment, which may include checkinglower extremity arterial pressures byDoppler and recording pulse volumewaveforms. The ankle brachial index isoften not helpful because of high pres-sures resulting from noncompressiblearteries. However, toe pressures are veryuseful in determining the healing poten-tial of an ulcer. In addition, transcuta-neous oxygen measurements are oftenuseful in determining whether a footwound can heal.

Ulcer evaluation should include doc-umentation of the wound’s location, size,shape, depth, base, and border. A sterilestainless steel probe is useful in assess-ing the presence of sinus tracts anddetermining whether a wound probes toa tendon, joint, or bone. X-rays shouldbe ordered on all deep or infectedwounds, but magnetic resonance imag-ing often is more useful because it ismore sensitive in detecting osteomyelitisand deep abscesses. Signs of infection,such as the presence of cellulites, odor,or purulent drainage, should be docu-mented, and aerobic and anaerobic cul-tures should be obtained of any purulentexudates. Culturing a dry or clean

P R A C T I C A L P O I N T E R S

Another useful instrument is the 128C tuning fork, which can be used todetermine whether a patient’s vibratorysensation is intact by checking at theankle and first metatarsal-phalangealjoints. The notion is that metabolic neu-ropathies have a gradient in intensity andare most severe distally. Thus, a patientwho cannot sense vibration at the big toebut can detect vibration at the anklewhen the tuning fork is immediatelytransferred from toe to ankle demon-strates a gradient in sensation suggestiveof a metabolic neuropathy. In general,you should not be able to sense vibrationof the tuning fork in your fingers formore than 10 seconds after the timewhen the patient can no longer sensevibration at the great toe. Many patientswith normal sensation only demonstratea difference between sensation at theirtoe and sensation in the practitioner’shand of ≤ 3 seconds.

Both of these tests can be performedquickly in any office setting. Achillesand patellar reflexes can also be checkedeasily but are unreliable in the assess-ment of diabetic peripheral neuropathy.More in-depth analysis can be performedusing a vibrometer (a device designed tomore objectively measure vibratorysense), assessing temperature sense, per-forming nerve conduction studies, andchecking position sense and balance.These tests are usually performed in aneurological laboratory. A much moredetailed review of peripheral neuropathyhas been published in the journal Dia-betes Care and is available online in fulltext at no charge.3

Vascular assessment is important foreventual ulcer healing and is essential inthe evaluation of diabetic ulcers. Vascu-lar assessment includes checking pedalpulses, the dorsalis pedis on the dorsumof the foot, and the posterior tibial pulsebehind the medial malleolus, as well ascapillary filling time to the digits. Thecapillary filling time is assessed bypressing on a toe enough to cause theskin to blanch and then counting the sec-onds for skin color to return. A capillaryfilling time > 5 seconds is considered

Volume 24, Number 2, 2006 • CLINICAL DIABETES92

wound base has proven to be uselessbecause most wounds are colonized, andthis practice leads to overprescribing ofantibiotics.

After all physical findings have beennoted, a differential diagnosis should beestablished. One cannot assume that anulcer is a diabetic foot ulcer without con-sidering other possibilities, such asmalignancies or vasculitic disorders(Figure 2).

TreatmentSuccessful treatment of diabetic footulcers consists of addressing these threebasic issues: debridement, offloading,and infection control.

DebridementDebridement consists of removal of allnecrotic tissue, peri-wound callus, andforeign bodies down to viable tissue.Proper debridement is necessary todecrease the risk of infection and reduceperi-wound pressure, which can impedenormal wound contraction and healing.After debridement, the wound should beirrigated with saline or cleanser, and adressing should be applied.

Dressings should prevent tissuedessication, absorb excess fluid, andprotect the wound from contamination.

Figure 2. A foot lesion confirmed as malignant melanoma. The patient was origi-nally referred for suspected gangrene on the heel.

Page 3: Clin Diabetes 2006 Kruse 91 3 Foot

~ 30% of the time they are walking (usually to and from the doctor’s office).5

Postoperative shoes or wedge shoesare also used and must be large enoughto accommodate bulky dressings. Properoffloading remains the biggest challengefor clinicians dealing with diabetic footulcers.

Infection controlLimb-threatening diabetic foot infec-tions are usually polymicrobial.Commonly encountered pathogensinclude methicillin-resistant staphylo-coccus aureus, �-hemolytic streptococ-ci, enterobacteriaceae, pseudomonasaeruginosa, and enterococci. Anaerobes,such as bacteroides, peptococcus, andpeptostreptococcus, are rarely the solepathogens but are seen in mixed infec-tions with aerobes. Antibiotics selectedto treat severe or limb-threatening infec-tions should include coverage of gram-positive and gram-negative organismsand provide both aerobic and anaerobiccoverage. Patients with such woundsshould be hospitalized and treated withintravenous antibiotics.

Mild to moderate infections withlocalized cellulitis can be treated on anoutpatient basis with oral antibioticssuch as cephalexin, amoxicillin withclavulanate potassium, moxifloxacin, orclindamycin. The antibiotics should bestarted after initial cultures are taken andchanged as necessary.

SummaryThe etiology of diabetic foot ulcers ismultifactorial, but minor trauma in thepresence of peripheral sensory neuropa-thy remains the primary culprit.Prevention of foot ulcers in high-riskindividuals, such as those with neuropa-thy, peripheral vascular disease, or struc-tural foot abnormalities, is of primaryimportance through appropriate patienteducation, the use of emollients, and theuse of appropriately fitting shoes. Thepatient information page that accompa-nies this article (p. 94) offers a completelist of self-care behaviors that should beprovided to patients with high-risk feet.

P R A C T I C A L P O I N T E R S

There are hundreds of dressings on themarket, including hydrogels, foams,calcium alginates, absorbent polymers,growth factors, and skin replacements.Becaplermin contains the �-chainplatelet–derived growth factor and hasbeen shown in double-blind placebo-controlled trials to significantlyincrease the incidence of completewound healing. Its use should be con-sidered for ulcers that are not healingwith standard dressings.

In case of an abscess, incision anddrainage are essential, with debridementof all abscessed tissue. Many limbs havebeen saved by timely incision anddrainage procedures; conversely, manylimbs have been lost by failure to per-form these procedures. Treating a deepabscess with antibiotics alone leads todelayed appropriate therapy and furthermorbidity and mortality.

OffloadingHaving patients use a wheelchair orcrutches to completely halt weight bear-ing on the affected foot is the mosteffective method of offloading to heal afoot ulceration. Total contact casts(TCCs) are difficult and time consumingto apply but significantly reduce pres-sure on wounds and have been shown toheal between 73 and 100% of allwounds treated with them. Armstrong etal.4 have achieved similar healing rateswith an “instant TCC,” made by wrap-ping a removable cast walker with alayer of cohesive bandage or plaster ofParis. Inappropriate application of TCCsmay result in new ulcers, and TCCs arecontraindicated in deep or drainingwounds or for use with noncompliant,blind, morbidly obese, or severely vas-cularly compromised patients.

Clinicians often prefer removablecast walkers because they do not havesome of the disadvantages of TCCs.Removability is an advantage in that itallows for daily wound inspection, dress-ing changes, and early detection ofinfection. But removability is also thegreatest disadvantage in that studies haveshown that patients wear them only

93CLINICAL DIABETES • Volume 24, Number 2, 2006

Evaluation of foot ulcers includeschecking vascular and neurological sta-tus and accurately assessing wounds.The depth of infection is arguably themost critical assessment and one that isnot commonly performed in many cli-nicians’ offices because it requires atleast partial debridement and a probe tobone.

Treatment should address all threemajor concerns: debridement,offloading, and infection control. Notall physicians need to be capable oftreating diabetic foot ulcers them-selves, but it is extremely importantto be knowledgeable enough to per-form an initial evaluation, referpatients promptly, and help with fol-low-up of patients with healingwounds.

REFERENCES

1McNeely MJ, Boyko EJ, Ahroni JH, StenselVL, Reiber GE, Smith DG, Pecoraro RF: Theindependent contributions of diabetic neuropathyand vasculopathy in foot ulceration: how greatare the risks? Diabetes Care 18:216–219, 1995

2The DCCT Research Group: The effect ofintensive treatment of diabetes on the develop-ment and progression of long-term complicationsin insulin-dependent diabetes mellitus. N Engl JMed 329:977–986, 1993

3Boulton AJ, Malik RA, Arezzo JC, SosenkoJM: Diabetic somatic neuropathies. DiabetesCare 27:1458–1486, 2004. Also available in freefull text online from http://care.diabetes journals.org/cgi/content/full/27/6/1458

4Armstrong DG, Lavery LA, Kimbriel HR,Nixon BP, Boulton AJ: Activity patterns ofpatients with diabetic foot ulceration. DiabetesCare 26:2595–2597, 2003

5Armstrong DG, Lavery LA, Wu S, BoultonAJ: Evalution of removable and irremovable castwalkers in the healing of diabetic foot wounds.Diabetes Care 28:551–554, 2005

Ingrid Kruse, DPM, is a staff podiatristat the VA San Diego Healthcare Systemand a clinical instructor in the Depart-ment of Family Medicine at the Universi-ty of California, San Diego (UCSD)Medical School. Steven Edelman, MD, isa professor of medicine at the UCSDSchool of Medicine and founder anddirector of Taking Control of Your Dia-betes, a nonprofit organization to edu-cate and motivate people with diabetes.