Preventing Amputation In Patients With Diabetes

Author(s): 
Lee C. Rogers, DPM

The World Health Organization and the International Diabetes Federation have stated that up to 85 percent of diabetic lower extremity amputations are preventable. There are approximately 82,000 diabetes-related lower extremity amputations (LEA) annually at an estimated cost of over $11 billion.1,2 Eighty-five percent of amputations are preceded by a foot ulcer.3 Diabetic foot ulcers are caused by neuropathy, deformity and repetitive microtrauma.4 The treatment of diabetic foot ulcers may cost the United States healthcare system as much as $19 billion yearly.2 Diabetic foot ulcers lead to amputations and both conditions are largely preventable. Pecoraro reported that 86 percent of amputations in his study were preceded by an identifiable and preventable pivotal event.3
The diagnosis of diabetes is not a condemnation to future amputation. Several “steps” take place prior to the loss of a limb. The six steps are diabetes, neuropathy, ulceration, vascular disease, infection and amputation. Each of these steps is preventable and one can take action to prevent the patient from escalating to the next step.
The first step is the diagnosis of diabetes. Diabetes is associated with the comorbid conditions of macrovascular disease (heart attack, stroke, peripheral arterial disease (PAD)) and microvascular disease (retinopathy, nephropathy, neuropathy). Diabetes is the sixth leading cause of death.1 Type 1 diabetes accounts for approximately 5 percent of all diabetes cases and there are no known methods for prevention.
However, type 2 diabetes (95 percent of cases) is associated with decreased physical activity, obesity, older age and a family history of type 2 diabetes.1 Some of these risk factors are modifiable and one can improve impaired glucose tolerance with exercise and diet modifications.5 If patients make these modifications early in the disease process, they can prevent complications or delay the onset of the disease.

Keys To Screening For Peripheral Neuropathy

Peripheral neuropathy affects up to 65 percent of patients with diabetes.6 The onset is typically eight to 12 years after the diagnosis of diabetes. Diabetic peripheral neuropathy (DPN) affects all three divisions of the peripheral nervous system (sensory, motor, autonomic).
Sensory neuropathy can predispose patients to unperceived repetitive microtrauma and is the main risk factor for foot ulceration.
Motor neuropathy causes muscle atrophy, which leads to hammered digits and equinus. Autonomic neuropathy affects skin sweating and lubrication, which leads to xerosis.
Autonomic neuropathy may also play a role in Charcot foot. Autonomic neuropathy may be mediated through peripheral vasodilation and the “washing out” of the mineral content in the bones.
When it comes to patients with diabetes, one can determine if there is a loss of protective sensation (LOPS) by using a 5.07 Semmes-Weinstein monofilament or a biothesiometer. Diabetic peripheral neuropathy is a length-dependent process and affects the longest nerves first (the nerves to the toes). The 10-point monofilament test was developed for those with leprosy neuropathy, which is not a length-dependent process. Therefore, it is not necessary to test 10 points in those with diabetes.
To uncover LOPS in diabetes, one should test four points in each foot: the plantar hallux and plantar metatarsal heads one, three and five.7 Instruct patients to close their eyes and say “yes” whenever they feel the monofilament. Press the monofilament against the skin until it buckles. Failure to perceive one of the four sites is sufficient for the diagnosis of LOPS. The biothesiometer is a semi-quantitative measure of nerve function. Place the biothesiometer on the distal hallux and slowly turn the dial until the patient feels the vibratory sensation. Greater than 25 volts connotes LOPS and a future risk of ulceration.8
There are currently no FDA-approved or evidence-based treatments that reverse sensory loss due to diabetic neuropathy. Instead, we must prevent progression to the next step of ulceration.

What The Research Reveals About Preventing Ulceration

One must concentrate on measures to reduce pressure or trauma, or use devices that can provide early warning of trauma/inflammation. While physicians commonly prescribe extra-depth shoes, there is disagreement on how effective they are at preventing ulceration.
Uccioli, et al., found a 53 percent reduction in re-ulceration rates with the use of custom extra-depth shoes in high-risk patients who already had a history of ulceration.9 There have been three published randomized, controlled trials showing that home temperature monitoring reduces ulceration rates in high-risk patients.10-12 One could also consider prophylactic surgery to reduce peak plantar pressures and prevent future ulceration.13,14

Essential Pointers On Managing Diabetic Foot Ulceration

Once a diabetic foot ulceration has occurred, it is important to determine the etiology. One should initially consider the “VIPs” (vascular, infection and pressure). Increased plantar pressure is a common reason for non-healing of ulcerations.15 Podiatrists must examine the ankle and the first metatarsophalangeal joint for limited joint mobility.16 Plantar forefoot ulcers occur (or fail to heal in a timely fashion) in the presence of equinus. A percutaneous tendo-Achilles lengthening can reduce plantar forefoot pressures and speed the healing of ulcers.17 Likewise, plantar hallux ulcers are usually a result of loss of protective sensation combined with hallux limitus. A Keller arthroplasty can be a curative procedure for these wounds.18
Debridement is key in the management of diabetic foot wounds as it removes fibrotic/necrotic tissue and reduces the bioburden. Serial debridements are often necessary to maintain this positive effect.
In an oral abstract at the most recent American Podiatric Medical Association (APMA) annual meeting, Armstrong showed that diabetic foot wounds that were debrided every study visit over 12 weeks had a 5.3 times greater chance of healing than those debrided less often.19 Clinicians can accomplish debridement by a number of mechanisms including scalpel, hydrosurgery (Versajet, Smith and Nephew) or maggot debridement therapy (Monarch Labs, Irvine, Ca.). See “A Guide To Modalities For Facilitating Debridement And Granulation Tissue” below. Most wounds will heal expeditiously if one manages the VIPs. If an ulcer fails to heal by 50 percent (length multiplied by width) in four weeks, it has a 91 percent chance of not healing in 12 weeks.20 In these cases, one should prescribe more advanced treatments.
A good granular wound base is required before one can close the wound. Negative pressure wound therapy (NPWT) can help accelerate granulation tissue formation and wound bed preparation.21 Marrow-derived stem cells from a bone marrow aspirate have also shown promise in speeding the preparation of the wound bed for an allogenic or autogenic graft.22 Dermagraft (Advanced Biohealing) offers cryopreserved neonatal fibroblasts on a bioabsorbable mesh and researchers have shown that this modality speeds ulcer healing.23 Other skin substitutes and bioengineered tissues can be of benefit. The key is knowing when to use each modality.
After a wound has become granular and level with the surrounding tissue, attaining wound closure as soon as possible will limit the risk of infection.

Emphasizing The Importance Of Screening For Vascular Disease

When it comes to peripheral arterial disease (PAD) or macrovascular disease, one can diagnose these diseases via the ankle-brachial index (ABI), segmental arterial pressures or pulse volume recordings. Clinical signs and symptoms might include gangrene or pallor on elevation, and rubor on dependency. Those with type 2 diabetes should have a screening for PAD every five years after diagnosis.24 Peripheral arterial disease is a marker for coronary artery disease and cerebrovascular disease. Those who are diagnosed with one disease usually have the other two. If the diagnosis is PAD, it would greatly benefit the patient to obtain a referral for cardiovascular risk reduction.
If an ulcer is present and vascular disease is significant, critical limb ischemia (CLI) is the diagnosis. Peripheral arterial disease is a serious risk factor for limb amputation in the presence of a foot wound.3 Patients with PAD or CLI require a consultation by a vascular surgeon to determine if an endovascular procedure or open bypass can restore flow.
One can investigate microvascular function via transcutaneous oxygen measurement, the OxyVu (HyperMed) or skin perfusion pressure. These measures can predict wound healing and the level of amputation.

How To Detect And Treat Infected Ulcers In The Diabetic Foot
Infection is often the coup de grace that precipitates an amputation. Infection is a clinical diagnosis that is based on the presence of two or more of the following: purulence, erythema, tenderness/pain or warmth.25 Laboratory assessment is of little value in diagnosing a diabetic foot infection. If you suspect an infection, you can be fairly confident that gram-positive organisms are the main pathogens. If the infection is mild, in which the erythema extends less than 2 cm, one can utilize empiric antibiotics to cover gram-positive organisms and obtain a tissue specimen for culture and sensitivity. Physicians can also adjust or narrow antimicrobial therapy based on the culture results.
As the incidence of methicillin-resistant Staphylococcus aureus (MRSA) is increasing, one should consider risk factors for MRSA such as previous MRSA infection, a history of multiple antibiotic usage and/or a history of hospitalization or institutionalization.26,27 If there are one or more risk factors present and the infection is moderate or severe, one should begin “de-escalation therapy” with vancomycin, linezolid (Zyvox, Pfizer) or tigecycline (Tygacil, Wyeth). After getting the culture and sensitivity reports, physicians can narrow the antibiotic spectrum.
If the infection is moderate or severe, hospitalization and surgery may be necessary to limit the spread of the infection. Intravenous antibiotics are often necessary in these cases and can be broad-spectrum. However, gram-positive bacteria are still generally the major causative organisms.

Recognizing The Realities Of Amputation

Amputation is often the unfortunate preventable end effect of the aforementioned pathway. The higher the level of amputation, the more energy is required for ambulation with the prosthesis.28 The five-year mortality rate after diabetes-related lower extremity amputation is nearly 50 percent. This mortality rate is higher than many types of cancers.29 About half of amputees suffer a serious lesion on the contralateral limb within two years.30 Lower extremity amputation often results in disability and a loss of independence. Amputation is often more costly than limb salvage.31,32
Given these data, podiatrists should limit amputations to cases of life-threatening infection, non-reconstructible ischemia or an uncorrectable deformity. Podiatric physicians can salvage most limbs with a combination of surgery and offloading.

In Conclusion
There is an opportunity for prevention at each step in the aforementioned pathway to an amputation. If we achieve the proper intervention, we can prevent the patient from escalating along the stairway and avoid a complicated diabetic foot or amputation. Research has shown that multidisciplinary teamwork, the addition of a podiatry service, prescription footwear and home temperature monitoring can prevent diabetic foot ulcers and amputation.9,10,12,33,34
Prevention of foot complications in diabetes is key in improving the patient’s quality of life, reducing mortality and lowering healthcare costs. These sentiments are getting national press with recent articles in the New York Times and U.S. News and World Report.35,36 Additionally, presidential candidates have been using references to podiatry and amputation prevention in their stump speeches about health policy.37 Podiatrists are arriving at a time when the tools to treat and prevent this devastating condition are improving, and shortly the health system may have the means by which to pay for them.

Dr. Rogers is the Director of the Amputation Prevention Center at Broadlawns Medical Center in Des Moines, Iowa.

 

 

 

 

 

 

References:

1. Centers for Disease Control and Prevention. National diabetes fact sheet: general information and national estimates on diabetes in the United States, 2005. In: US Department of Health and Human Services. Atlanta, GA; 2005.
2. Rogers LC, Lavery LA, Armstrong DG. The right to bear legs - An amendment to healthcare; how preventing amputations can save billions to the US healthcare system. J Am Podiatr Med Assoc. 2008;98(2):Early Release - in press.
3. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation: basis for prevention. Diabetes Care. 1990;13:513-521.
4. Reiber GE, Vileikyte L, Boyko EJ, et al. Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Diabetes Care. 1999;22(1):157-162.
5. Chiasson JL. Prevention of Type 2 diabetes: fact or fiction? Expert Opin Pharmacother. Dec 2007;8(18):3147-3158.
6. Dyck PJ, Kratz KM, Karnes JL, et al. The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: the Rochester Diabetic Neuropathy Study. Neurology. Apr 1993;43(4):817-824.
7. Smieja M, Hunt DL, Edelman D, Etchells E, Cornuz J, Simel DL. Clinical examination for the detection of protective sensation in the feet of diabetic patients. International Cooperative Group for Clinical Examination Research. J Gen Intern Med. Jul 1999;14(7):418-424.
8. Miranda-Palma B, Sosenko JM, Bowker JH, Mizel MS, Boulton AJ. A comparison of the monofilament with other testing modalities for foot ulcer susceptibility. Diabetes Res Clin Pract. Oct 2005;70(1):8-12.
9. Uccioli L, Faglia E, Monticone G, et al. Manufactured shoes in the prevention of diabetic foot ulcers. Diabetes Care. 1995;18(10):1376-1378.
10. Lavery LA, Higgins KR, Armstrong DG, Holguin D, Athanasiou KA. Randomized clinical trial to evaluate a novel home temperature monitoring device to reduce the incidence of diabetic foot complications. Diabetologia. 2002;Suppl1:A1058.
11. Lavery LA, Higgins KR, Lanctot DR, et al. Home monitoring of foot skin temperatures to prevent ulceration. Diabetes Care. Nov 2004;27(11):2642-2647.
12. Armstrong DG, Holtz-Neiderer K, Wendel C, Mohler MJ, Kimbriel HR, Lavery LA. Skin temperature monitoring reduces the risk for diabetic foot ulceration in high-risk patients. Am J Med. Dec 2007;120(12):1042-1046.
13. Armstrong DG, Lavery LA, Stern S, Harkless LB. Is Prophylactic Diabetic Foot Surgery Dangerous? J Foot Ankle Surg. 1996;35(6):585-589.
14. Frykberg R, Giurini J, Habershaw G, Rosenblum B, Chrzan J. Prophylactic Surgery in the Diabetic Foot. In: Kominsky SJ, ed. Medical and Surgical Management of the Diabetic Foot. Saint Louis: Mosby; 1993.
15. Lavery LA, Vela SA, Lavery DC, Quebedeaux TL. Reducing dynamic foot pressures in high-risk diabetic subjects with foot ulcerations. A comparison of treatments. Diabetes Care. 1996;19(8):818-821.
16. Fernando DJ, Masson EA, Veves A, Boulton AJ. Relationship of limited joint mobility to abnormal foot pressures and diabetic foot ulceration. Diabetes Care. 1991;14(1):8-11.
17. Mueller MJ, Sinacore DR, Hastings MK, Strube MJ, Johnson JE. Effect of achilles tendon lengthening on neuropathic plantar ulcers. A randomized clinical trial. J Bone Joint Surg. 2003;85A(8):1436-1445.
18. Berner A, Sage R, Niemela J. Keller procedure for the treatment of resistant plantar ulceration of the hallux. J Foot Ankle Surg. Mar-Apr 2005;44(2):133-136.
19. Armstrong DG. Serial surgical debridement increases healing rates in chronic lower extremity wounds. Paper presented at: American Podiatric Medical Association Oral Abstracts, 2007; Philadelphia, PA.
20. Sheehan P, Jones P, Caselli A, Giurini JM, Veves A. Percent Change in Wound Area of 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(6):1879-1882.
21. Armstrong DG, Lavery LA. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomised controlled trial. Lancet. Nov 12 2005;366(9498):1704-1710.
22. Rogers LC, Bevilacqua NJ, Armstrong DG. The use of marrow-derived stem cells to accelerate healing in chronic wounds. Int Wound J. 2008:In press.
23. Marston WA, Hanft J, Norwood P, Pollak R. The efficacy and safety of Dermagraft in improving the healing of chronic diabetic foot ulcers: results of a prospective randomized trial. Diabetes Care. Jun 2003;26(6):1701-1705.
24. Peripheral arterial disease in people with diabetes. Diabetes Care. Dec 2003;26(12):3333-3341.
25. Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis. Oct 1 2004;39(7):885-910.
26. Dang CN, Prasad YD, Boulton AJ, Jude EB. Methicillin-resistant Staphylococcus aureus in the diabetic foot clinic: a worsening problem. Diabet Med. Feb 2003;20(2):159-161.
27. Rogers LC, Bevilacqua NJ, Armstrong DG. MRSA in the Diabetic Foot. In: Weigelt JA, ed. MRSA. London: Informa Healthcare; 2007:71-87.
28. Waters RL, Perry J, Antonelle D, Hislop H. Energy cost of walking of amputees: the influence of level of amputation. J Bone Joint Surg. 1976;58A:42-46.
29. Armstrong DG, Wrobel J, Robbins JM. Guest Editorial: are diabetes-related wounds and amputations worse than cancer? Int Wound J. Dec 2007;4(4):286-287.
30. Goldner MG. The fate of the second leg in the diabetic amputee. Diabetes. 1960;9:100-103.
31. MacKenzie EJ, Jones AS, Bosse MJ, et al. Health-care costs associated with amputation or reconstruction of a limb-threatening injury. J Bone Joint Surg Am. Aug 2007;89(8):1685-1692.
32. Williams MO. Long-term cost comparison of major limb salvage using the Ilizarov method versus amputation. Clin Orthop Relat Res. Apr 1994(301):156-158.
33. Dargis V, Pantelejeva O, Jonushaite A, Vileikyte L, Boulton AJ. Benefits of a multidisciplinary approach in the management of recurrent diabetic foot ulceration in Lithuania: a prospective study. Diabetes Care. 1999;22(9):1428-1431.
34. Van Gils CC, Wheeler LA, Mellstrom M, Brinton EA, Mason S, Wheeler CG. Amputation prevention by vascular surgery and podiatry collaboration in high-risk diabetic and nondiabetic patients. The Operation Desert Foot experience. Diabetes Care. May 1999;22(5):678-683.
35. Feder BJ. New priority: Saving the feet of diabetics. New York Times. Aug 30, 2005. http://www.nytimes.com/2005/08/30/health/30foot.html (accessed Feb 3, 2008)
36. Lyon L. Preventing foot ulcers caused by diabetes. U.S. News & World Report; Jan 28, 2008. http://health.usnews.com/articles/health/diabetes/2008/01/28/preventing-... (accessed Feb 3, 2008)
37. Alter J. Big ideas from boring old stump speeches; Today's throwaway campaign lines often wind up as tomorrow's best programs. Newsweek; Dec 31, 2007. http://www.newsweek.com/id/81596 (accessed Feb 3, 2008)
38. Lavery LA, et al. Validation of the Infectious Diseases Society of America's Diabetic Foot Infection Classification System. CID 2007;44:562-5.

 

Add new comment