Diabetic foot care: Tips and tools to streamline your approach

,; ,

Applied Evidence

Diabetic foot care: Tips and tools to streamline your approach

J Fam Pract. 2009 December;58(12):646-653

PDF Download

References

1. LeMaster JW, Reiber GE. Epidemiology and economic impact of foot ulcers. In: Boulton AJM, Cavanaugh PR, Rayman G, eds. The Foot in Diabetes. 4th ed. London, England: John Wiley & Sons Ltd; 2006:1–16.

2. Department of Health and Human Services Centers for Disease Control and Health Prevention. National Diabetes Fact Sheet 2007. Available at: http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2007.pdf. Accessed May 15, 2009.

3. Pinzur M. Amputations in the diabetic foot. In: Boulton AJM, Cavanaugh PR, Rayman G, eds. The Foot in Diabetes. 4th ed. London, England: John Wiley & Sons Ltd; 2006:308–322.

4. Margolis DJ, Allen-Taylor L, Hoffstad O, et al. Diabetic neuropathic foot ulcers and amputation. Wound Repair Regen. 2005;13:230-236.

5. Moss SE, Klein R, Kelin BE. The prevalence and incidence of lower extremity amputation in a diabetic population. Arch Intern Med. 1992;152:610-616.

6. Leese GP, Reid F, Green V, et al. Stratification of foot ulcer risk in patients with diabetes: a population based study. Int J Clin Pract. 2006;60:541-545.

7. Litzelman DR, Slemenda CW, Langefeld CD. Reduction of lower extremity clinical abnormalities in patient with non-insulin-dependent diabetes mellitus: a randomized controlled trial. Ann Intern Med. 1993;119:36-41.

8. Palumbo PJ, Melton LJ, III. Peripheral vascular disease and diabetes. In: National Diabetes Data Group, National Institute of Diabetes and Digestive and Kidney Disease, eds. Diabetes in America. 2nd ed. Bethesda, Md: National Institutes of Health, NIDDKD; 1995:401–408.

9. Boulton AJM, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the foot care interest group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care. 2008;31:1679-1685.

10. Jude EB. Charcot foot: what’s new in pathogensis and medical management? In: Boulton AJM, Cavanaugh PR, Rayman G, eds. The Foot in Diabetes. 4th ed. London, England: John Wiley & Sons Ltd; 2006: 265–273.

11. Pitocco D, Ruotolo V, Caputo S, et al. Six month treatment with alendronate in acute Charcot neuroarthropathy: a randomized controlled trial. Diabetes Care. 2005;28:1214-1215.

12. LeMaster JW, Reiber GE, Smith DG, et al. Daily weight-bearing activity does not increase the risk of diabetic foot ulcers. Med Sci Sports Exerc. 2003;35:1093-1099.

13. Lott DJ, Malug KS, Sinacore DR, et al. Relationship between changes in activity and plantar ulcer recurrence in a patient with diabetes mellitus. Phys Ther. 2005;85:579-588.

14. LeMaster JW, Mueller MJ, Reiber GE, et al. Effect of weight-bearing activity on foot ulcer incidence in people with diabetic peripheral neuropathy: Feet First randomized controlled trial. Phys Ther. 2008;88:1-13.

15. Margolis DJ, Kantor J, Santanna J, et al. Risk factors for delayed healing of neuropathic foot ulcers: a pooled analysis. Arch Dermatol. 2000;136:1531-1535.

16. Wagner FW, Jr. The diabetic foot. Orthopedics. 1987;10:163-172.

17. Rith-Najarian S, Branchaid C, Beaulieu O, et al. Reducing lower-extremity amputations due to diabetes: application of the staged diabetes management approach in a primary care setting. J Fam Pract. 1998;47:127-132.

18. Canavan RJ, Unwin NC, Connolly VM, et al. Diabetes and non-diabetes related lower extremity amputation incidence before and after the introduction of better organized diabetic foot care. Diabetes Care. 2008;31.-

19. Krishnan St, Nash F, Baker NR, et al. Reduction in diabetes amputations over 11 years in a defined UK population. Diabetes Care. 2008;31:99-101.

20. Clayton W, Elasy TA. A review of the pathophysiology, classification, and treatment of foot ulcers in diabetic patients. Clin Diabetes. 2009;27:52-58.

21. Majno G, Joris I. Cells, Tissues, and Disease: Principles of General Pathology, 2nd ed. Oxford, England: Oxford University Press; 2004.

22. Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2004;39:885-910.

23. Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders: a clinical practice guideline (2006 revision). J Foot Ankle Surg. 2006;45(5 suppl):S2-S66.

24. Edmonds M, Foster A. The use of antibiotics in the diabetic foot. Am J Surg. 2004;187:S25-S28.

25. Eddy JJ, Gideonsen MD. Topical honey therapy for diabetic foot ulcers. J Fam Pract. 2005;54:533-535.

26. Remmen R, Coenen S, Seuntjens R, et al. Honey for refractory diabetic foot ulcers. J Fam Pract. 2005;54:863.-

27. Sheehan P, Jones P, Caselli A, et al. Percent change in wound area in diabetic foot ulcers over a 4-week period is a robust predictor of complete healing in a 12-week prospective trial. Diabetes Care. 2003;26:1879-1882.

28. Lavery LA, Murdoch DP. Conventional offloading and activity monitoring. In: The Foot in Diabetes. 4th ed. Boulton AJM, Cavanaugh PR, Rayman G, eds. London, England: John Wiley & Sons Ltd; 2006: PG NUM.

29. Armstrong DG, Lavery LA, Kimbrel HR, et al. Activity patterns of patients with diabetic foot ulceration: patients with active ulceration may not adhere to a standard pressure off-loading regimen. Diabetes Care. 2003;26:2595-2597.

30. Ubbink DT, Westerbos SJ, Evans D, et al. H. Topical negative pressure for treating chronic wounds. Cochrane Database Syst Rev. 2008(3);CD001898.-

31. Kranke P, Bennett M, Roeckl-Wiedmann I, et al. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev. 2004(2);CD004123.-

32. Edwards J. Debridement of diabetic foot ulcers. Cochrane Database Syst Rev. 2002(4);CD003556.-

33. Sherman RA. Maggot therapy for treating diabetic foot ulcers unresponsive to conventional therapy. Diabetes Care. 2003;26:446-451.

34. Spencer SA. Pressure relieving interventions for preventing and treating diabetic foot ulcers. Cochrane Database Syst Rev. 2000(3);CD002302.-

35. Valk GD, Kriegsman DM, Assendelft WJ. Patient education for preventing diabetic foot ulceration. Cochrane Database Syst Rev. 2001(4);CD001488.-(AU: 2005 update..?)

36. The Diabetes Control and Complications Trial Research Group. The effect of intensive diabetes therapy on the development and progression of neuropathy. Ann Intern Med. 1995;122:561-568.

37. Boulton AJM, Viniv AL, Arezzo JC, et al. Diabetic neuropathies: a statement by the American Diabetes Association. Diabetes Care. 2005;28:956-962.

38. Wong MC, Chung JW, Wong TK. Effects of treatments for symptoms of painful diabetic neuropathy: systematic review. BMJ. 2007;335:87.-

FAST TRACK

Weight-bearing activity that is increased gradually does not appear to increase the likelihood that patients with neuropathy will develop a foot ulcer.

Non-weight-bearing activity can be safely recommended to patients with diabetic neuropathy. So can daily weight-bearing activity, which actually decreases the risk of foot ulcer by maintaining leg muscle tone and plantar tissue tolerance to stress.^12,13 Recent studies suggest that increasing weight-bearing activity slowly–walking daily and adding a total of 100 additional steps every 2 weeks, for example—in a carefully monitored program is not associated with increased risk of foot ulceration.¹⁴ You report these findings to Mr. F.

When he returns to your office in 2 months, Mr. F. has lost 7 pounds and his HbA1c has fallen to 6.5. Despite these positive developments, an examination of his feet reveals a full thickness ulcer on the left metatarsal head, which the patient had not noticed.

You recognize the clinical urgency of effectively treating Mr. F.’s diabetic foot ulcer, as size, duration, and grade are the greatest predictors of healing. Ulcers that are larger than 2 cm, have been present for more than 6 months,¹⁵ or have a higher grade on a scale such as the Wagner Foot Classification System¹⁶ (TABLE 2) are far less likely to heal than smaller, low-grade ulcers of shorter duration.

AIM DOC mnemonic guides ulcer care

Comprehensive, coordinated care improves outcomes for diabetic ulcers and has repeatedly been shown to reduce amputation rates.^17-19 Large clinical trials have not evaluated each aspect of diabetic ulcer care, however, so the recommendations that follow are based on expert opinion and available evidence. These include assessing the limb’s arterial supply and ensuring that the patient undergoes revascularization, as needed; promptly treating infection; and providing optimal wound care, including debridement of callused and necrotic tissue, off-loading pressure, and applying moist wound dressings.²⁰

AIM DOC, developed by 1 of the authors (JE), is a handy treatment tool. The mnemonic represents both the elements of treatment and the order in which they should be carried out. The letters stand for:

Arterial disease
Infection
Measure
Debride
Off-load
Cover
Here’s how to use AIM DOC, step by step:

Step 1: Assess for arterial disease

Start by assessing the vascular supply to the affected limb, which can be presumed to be adequate if pulses are palpable. If pulses cannot be palpated, the patient should undergo an ankle-brachial index (ABI) test and, if necessary, referred to a specialist to be evaluated for angioplasty or vascular bypass surgery. An ABI <0.9 is abnormal; 0.5 is considered the threshold for healing without such intervention.³ Keep in mind, however, that the ABI is falsely elevated in approximately 15% of patients with diabetes. If classic signs and symptoms of arterial disease are present, further evaluation is needed even if the ABI is normal.

FAST TRACK

Ulcers on the outside of the foot or between the toes are generally associated with vascular disease; the classic mal perforans ulcer on the metatarsal head is neuropathic.

Classic signs and symptoms of arterial disease include cool, hairless feet with shiny skin, and claudication. Location may provide another clue to etiology: Ulcers located on the heel, the outside of the foot, or between the toes tend to be associated with vascular disease, while ulcers with surrounding callus, such as the classic mal perforans ulcer on the metatarsal head, are neuropathic.

Step 2: Treat—or rule out—infection

While patients with diabetes have a 5-fold increase in risk of infection²¹ compared with individuals without the disease, there is no value in treating an uninfected ulcer with antibiotics. Diagnosing infection can be challenging because patients with diabetes may be less likely to demonstrate evidence of infection.²¹

An elevated white blood cell count, purulent drainage, foul odor, and/or erythema >2 cm around the wound clearly indicates a need for systemic antibiotics.^22,23 Tissue necrosis, often assumed to represent ischemia, may result from neutrophilic vasculitis from soft tissue infection.²⁴ Superficial cultures reflect colonization and should not be used to diagnose infection. In inspecting the wound for signs of infection, probe the ulcer and evaluate for osteomyelitis if it reaches bone.

Gram-positive cocci, especially Staphylococcus aureus, are the predominant pathogens in diabetic foot infections, and antibiotics effective against them may be sufficient for mild-to-moderate infections in patients who have not recently received antibiotic therapy. Gram-negative rods may be found in chronic wounds, however, and anaerobic pathogens may be present in patients with foot ischemia or gangrene; in both cases, broader-spectrum antimicrobials are required.²² Highly bioavailable oral antibiotics are indicated for infection, including some cases of osteomyelitis. Silver dressings may be helpful as a topical antimicrobial; there have been reports of successful treatment with honey, as well.^25,26