Online Learning Center

Diabetes-Related Amputations: Understanding Secondary Conditions and How They Affect Your Practice

• By Ann Fecko, MS, OTR-L, CO

Introduction

Diabetes has attracted significant attention since it and its associated complications were named as the seventh leading cause of death in the United States. Statistics from the Centers for Disease Control and Prevention (CDC) indicate that the number of individuals diagnosed with diabetes has more than tripled from 5.6 million in 1980 to approximately 18.2 million in 2003. The most recent data from the American Diabetes Association (ADA) reveals that as of 2007, 23.6 million adults in the United States (approximately 7.8 percent of the population) has been diagnosed with diabetes, with 1.6 million new cases diagnosed annually.

The underlying disease process and development of secondary conditions make individuals with diabetes eight times more likely than the general population to have an amputation at or proximal to the metatarsal level. The prevalence of lower-limb amputation in the diabetic population is approximately 67 percent, and it is estimated that people with diabetes mellitus account for approximately 60 percent of all non-traumatic lower-limb amputations. As this amputee population continues to grow and seek prosthetic services, it is imperative that prosthetists have a thorough understanding of diabetes and its secondary effects in order to optimize patient care.

Background

Diabetes mellitus is a group of chronic metabolic disorders that affect the way glucose (sugar) is processed by the body. Insulin, a hormone secreted by the pancreas, breaks down sugar in the bloodstream and converts it to an absorbable form of energy to fuel the body's cells. In the absence of insulin, unprocessed glucose accumulates and remains in the bloodstream. This elevation of glucose levels in the bloodstream is the hallmark of diabetes. Insufficiencies in insulin may be related to the body's inability to produce the hormone on its own (type 1 diabetes) or the cells' failure to recognize and effectively use the insulin that the body does produce (type 2 diabetes).

Type 2, often referred to as "adult onset" diabetes, is more common than type 1. Factors that influence the incidence of type 2 diabetes include age, male gender, genetics, ethnic background, poor eating habits, obesity, and limited exercise. Typical age at onset is 30 years, although it is becoming more prevalent in teens and young adults. Increased incidence of type 2 diabetes is noted for individuals over 40 years of age. Approximately 20 percent of individuals between the ages of 65 and 74 have diabetes.

Secondary Conditions

When diabetes mellitus is left untreated or is poorly controlled, it is often accompanied by a number of adverse secondary conditions and complications. Over the long term, diabetes affects the structure and function of both small and large blood vessels of the circulatory system. Compromised blood flow to vital organs and the limbs predisposes these individuals to atherosclerosis, heart disease, heart attack, stroke, hypertension, kidney disease, and amputation. Other common related problems include neurological deficits, visual impairment, and cognitive decline. The latter are important factors for clinicians to consider while treating this population throughout the continuum of prosthetic management.

Diabetic Neuropathy

Diabetic neuropathy is a condition of neurological compromise caused by lack of blood flow to the nerves. It is estimated that 60 to 70 percent of individuals with diabetes experience some degree of neuropathy. Risk factors for the development of neuropathy include poorly controlled blood glucose levels, long duration of diabetic history, hypertension, and obesity. Subtypes of diabetic neuropathy include peripheral, autonomic, proximal, and focal. These neurological deficits significantly heighten the risk for potential lower-limb injury, infection, and amputation.

Peripheral Neuropathy
Peripheral is the most common subtype of diabetic neuropathy. The effects of neuropathy vary among individuals: some experience minimal neurological disruption, while others completely lose sensation. Common symptoms include numbness, tingling, pain, aching, burning, loss of protective sensation, and decreased proprioception in the limbs, including the feet. The lower limbs are typically more involved than upper limbs.

Autonomic Neuropathy
In contrast to peripheral neuropathy, autonomic neuropathy primarily affects the nerves that regulate the "automatic" functions of the body. Examples include actions of the cardiovascular, digestive, respiratory, visual, and endocrine systems. Urinary and sexual functions may also be compromised. Nerves that regulate body temperature, sweat, and oil glands are also affected, leading to dry and brittle skin that is prone to injury and other complications.

Proximal and Focal Neuropathies
These neuropathies are characterized by pain, weakness, and neurological deficits in various areas of the body, but they differ in onset and presentation. Proximal neuropathy disrupts nerve pathways in the lumbar plexus, affecting the thigh, buttocks, hips, and lower limb unilaterally. Focal neuropathy has a more sudden onset and tends to affect nerves in the head, torso, and lower limbs. Both conditions are more prevalent in older adults with type 2 diabetes.

Application for Prosthetists
Goals of prosthetic management for this population include protection of the residual limb and maximization of function. Due to sensation impairment, individuals may not be able to accurately detect volume fluctuations and resultant pressure changes within the socket. Consequently, they are more likely to experience challenges with socket fit and subsequent skin breakdown.

• Prosthetic Design
  The use of gel liners as a means of suspension and interface has become common with this population, as it affords greater protection to the insensate residuum when compared to alternative methods. If the neuropathy also affects the upper limbs, liners and sockets may need to be adapted to facilitate independent donning/doffing of the prosthesis.
• Skin Care/Hygiene
  Patient education regarding appropriate skin care and hygiene will also prevent potential problems. Although gel liners afford significant protection of the limb, they also create an environment where bacteria and other microorganisms thrive. Patients must be instructed to clean gel liners after each use and to wash the residuum and inspect it for areas of breakdown, rash, or irritation. After washing, patients should dry the residual limbs completely and apply a thin layer of petroleum jelly or unscented cream. Excessive application of moisturizers and soaking the limb for long periods of time should be avoided.

Vision Loss

In addition to diabetic neuropathy, individuals with diabetes are vulnerable to various eye complications that may lead to visual impairment and blindness. These include, but are not limited to, diabetic retinopathy, glaucoma, and cataracts.

Diabetic Retinopathy
Diabetic retinopathy (Figure 1) refers to any disorder of the retina that is caused by diabetes. The retina is the blanket of nerve cells that lines the interior posterior wall of the eye. It is responsible for converting images and light into electrical signals that the brain can interpret. The ADA estimates that blindness caused by diabetic retinopathy grows by 12,000 to 24,000 new cases each year and reports that diabetic retinopathy is the leading cause of blindness in adults between the ages of 20 and 74. Diabetic retinopathy is most commonly found in individuals who have had diabetes five years or more, with nearly 50 percent of individuals with diabetes experiencing some degree of vision loss after ten years and 80 percent after 15 years. Factors that influence the development of diabetic retinopathy include control of blood sugar and blood pressure, duration since onset of diabetes, and genetics.

Damage to the retina occurs because of interruptions to its vascular supply. In nonproliferative retinopathy, the small blood vessels in the eyes weaken and form small pockets. Despite damage to the internal structures, vision loss in mild cases is rare.

If left untreated, nonproliferative retinopathy may progress to proliferative retinopathy, a condition characterized by the growth of new blood vessels to replace those that have been damaged or blocked. These new vessels are inherently weak and are prone to hemorrhages that restrict vision. Revascularization attempts contribute to the development of scar tissue along the surface of the retina, which may lead to retinal detachment, vision distortion, blurred vision, patchy spots, decreased contrast sensitivity, or total blindness.

Depending on the stage of the disease, laser treatments designed to seal the blood vessels and stop them from leaking can prevent further damage and restore some vision. In more severe cases, scar tissue may be removed from the eye along with cloudy fluids. When retinal detachment is involved, attempts to reattach it are only moderately successful (50 percent).

Glaucoma
Glaucoma (Figure 2) is related to an increase in pressures within the eye due to insufficient drainage of ocular fluid (aqueous humor). This pressure exerts a force on the small vessels of the eye, occluding blood flow to the retina and optic nerve. Prolonged exposure to this environment causes permanent damage to these important structures and results in vision loss. Vision-related changes associated with glaucoma include blurred vision, patchy vision, and the development of "tunnel" vision. The incidence of glaucoma is 40 percent higher in individuals with diabetes and the risk for development increases with age. Treatments for glaucoma include drugs, eye drops, and surgery.

Cataracts
Individuals with diabetes are also at increased risk for developing cataracts (Figure 3)—approximately 60 percent more likely than the general population. This condition affects the lens of the eye, the structure that focuses light on the back of the retina and adjusts to accommodate focal distance. Cataracts occur when the proteins inside the lens form small clusters that prevent light from passing through it. Treatment for this condition generally involves surgery to repair or replace the damaged lens. Another factor that affects how the lens functions is directly related to sugar concentrations in the blood. Because the lens allows water to pass through it by means of osmosis, changes in sugar concentration will cause the lens to retain or lose water. As a result, the lens' ability to focus is compromised and vision becomes blurred.

Application for Prosthetists
Depending on the severity of the condition, these visual disruptions may present unique challenges to the patient and practitioner throughout the course of treatment. Consideration of visual deficits during the evaluation process may influence patient interaction, goals, prosthetic design, and approach to patient education. Use of effective communication practices and incorporation of simple visual accommodation strategies will foster positive patient experiences and prosthetic outcomes.

Communication: Inquiries about a patient's visual abilities should be routine.

Visual accommodations: General strategies to maximize visual function include provision of an appropriately lit environment, application of tactile markers and techniques, and heightened contrast. Contrast refers to a person's ability to discriminate between similar shades of light and dark.

Examples of visual accommodations include:

Lighting

• Provide task-specific lighting (e.g., incandescent light focused over the workspace).



Figure 4: Socket views. Photograph
courtesy of Ortho Rehab Designs,
www.ordesignslv.com/images/
ischialsocket.jpg

• Reduce glare.
• Close curtains.
• Don prosthesis away from a window.
• Wear a baseball cap while donning prosthesis.

Prosthetic Design

• Keep it simple.
• Pin-lock systems work well for some patients due to the auditory feedback. However, it might be difficult for some patients to line up the pin appropriately.
• High contrast between the inner and outer surface of the socket (Figure 4).
• High contrast between the socket and interfaces/liners.

Donning/Doffing

• Mark the socket/interface with a tactile marker (e.g., puff paint, bump-ons, adhesive-backed felt, small notch) (Figure 5).
• Apply tactile markers (e.g., button, washable puff paint, stitching) to differentiate between different ply socks or multiple liners.
• Label socks and liners with high-contrast or large-print markings.
• Tactile markers can be a helpful strategy with these patients. However, exercise caution with regard to location of placement and the security with which they are attached. If a marker falls into a socket, it may irritate the patient's insensate limb and cause skin breakdown.

Skin Inspection

• When upper-limb neuropathy is not involved, teach the patient to use the fingers to feel for differences in skin texture, temperature, etc.
• When upper-limb neuropathy is an issue, encourage the patient to use a lighted magnifier to inspect the limb.
• Teach the patient to use all senses to determine the condition of the limb (e.g., feel socks to see if they are damp or "crusty," take note of changes in odor).

Education Materials

• Written materials provided to the patient should be in clear fonts (e.g., Arial or Times New Roman), be 14-point or larger, and should be high contrast (e.g., black on white).

Cognition

In addition to diabetes' adverse effects on vision and the peripheral nervous system, research suggests that the disease also has a negative influence that is not as easily perceived—an impact on cognition. Recent findings indicate that proteins that serve as insulin receptors in the brain also play a role in the regulation of blood glucose levels. Interruptions to these pathways and fluctuations in sugar concentrations in the blood prevent the brain from receiving the energy that it needs to function properly. The hippocampus, a brain structure that plays an important role in learning and memory function, is affected most by this disease process. Elevated insulin levels also appear to stimulate proteins that fuel the formation of degenerative plaques on the brain's surface. As a result, individuals with diabetes are said to be at greater risk of dementia and Alzheimer's disease. On specific tests of cognitive function, individuals with diabetes demonstrated significant declines in performance over various periods in comparison to their counterparts without diabetes.

Application for Prosthetists
Practitioners must be sensitive to the cognitive challenges that individuals with diabetes may experience. This patient population may require additional time and instruction when receiving a prosthesis for the first time. A number of strategies may be employed to support the patient throughout the continuum of care. Examples include:

• Asking the patient about his or her preferred learning style (e.g., learn by watching, learn by doing) can guide the practitioner in determining how to most effectively interact with and teach the patient throughout the course of treatment.
• Speak in clear and simple language with step-by-step directions that the patient understands.
• Simplify prosthetic design when possible.
• Provide instructions in a format that the patient understands (e.g., language, pictures).
• If present, instruct caregiver(s) in all aspects of prosthetic care (e.g., donning/doffing, skin inspection, volume management).
• When appropriate, consult other members of the patient's rehabilitation team (e.g., occupational/physical therapist, speech therapist, physiatrist, and ophthalmologist) for further evaluation and services to maximize the patient's function and independence with prosthetic management.

Conclusion

Diabetes is a complex disease that has the potential to significantly affect various body structures and functions. As a result, providing comprehensive treatment across the entire continuum of prosthetic care can be particularly challenging for this population. Developing a positive rapport and providing thorough and effective patient education are two important components to successful prosthetic outcomes. Adopting a holistic approach to working with these patients and tailoring treatment to accommodate their unique needs will facilitate the achievement of goals outlined by both the patient and practitioner.

Acknowledgments

Sue Berger, PhD, OTR/L, BCG, FAOTA, clinical associate professor, Boston University, College of Health & Rehabilitation Sciences: Sargent College, Massachusetts.

Jennifer Kaldenberg, MSA, OTR/L, SCLV, CLVT, FAOTA, director of the occupational therapy service at New England Eye, Boston, Massachusetts, and assistant professor of vision rehabilitation at The New England College of Optometry, Boston.

Anne Fecko, MS, OTR/L, CO, is affiliated with Hanger Prosthetics & Orthotics, Woburn, Massachusetts.

References

1. Arvanitakis Z, Wilson RS, Li Y, Aggarwal NT, Bennett DA. Diabetes and function in different cognitive systems in older individuals without dementia. Diabetes Care. 2006;29(3):560-5.
2. Centers for Disease Control. National Diabetes Fact Sheet, 2007. Centers for Disease Control, www.cdc.gov/diabetes/pubs/estimates07.htm#1. Accessed December 28, 2009.
3. Diabetes Statistics. American Diabetes Association, www.diabetes.org/diabetes-basics/diabetes-statistics. Accessed December 27, 2009.
4. Diabetic neuropathies: The Nerve Damage of Diabetes. February 2009. National Diabetes Information Clearinghouse (NDIC), diabetes.niddk.nih.gov/DM/pubs/neuropathies. Accessed January 4, 2010.
5. Diabetic retinopathy. 2009. Retrieved January 12, 2010 from the National Eye Institute website: www.nei.nih.gov/health/diabetic/retinopathy.asp.
6. Duffy MA. Making life more livable: Simple adaptations for living at home after vision loss. (Rev. ed.). American Foundation for the Blind. 2002; New York, NY.
7. Eye complications (n.d.). American Diabetes Association, www.diabetes.org/living-withdiabetes/complications/eye-complications.html. Accessed December 27, 2009.
8. Eye conditions (n.d.). Canadian National Institute for the Blind, www.cnib.ca/en/your-eyes/eye-conditions/preventionstrategies1107/Default.aspx9. Accessed January 12, 2010.
9. Fontbonne A, Beer C, Duchimetiere P, et al. Changes in cognitive abilities over a 4-year period are unfavorably affected in elderly diabetic subjects. Diabetes Care. 2001;24(2):366-70.
10. Gregg EW, Yaffe K, Cauley JA, Rolka DB, Blackwell TL, Narayan V, Cummings S. Is diabetes associated with cognitive impairment and cognitive decline among older women? Archives of Internal Medicine. 2000;160:174-80.
11. Interacting with visually impaired individuals. Olmstead Center for Sight, www.ollmsteadcenter.org/Home/About/News-Information/Interacting. Accessed December 27, 2009.
12. Johannesson A, Larsson G, Ramstrand N, Turkiewicz A, Wirehn A, Atroshi I. Incidence of lower-limb amputation in the diabetic and nondiabetic general population: A 10-year population-based cohort study of initial Diabetes-Related Amputations unilateral and contralateral amputations and reamputations. Diabetes Care. 2009;32(2):27580.
13. Lee J, Bailey M. (2009). Cataracts. www.allaboutvision.com/conditions/cataracts.htm. Accessed December 29, 2009.
14. Mathur R. (2008). Diabetes Mellitus. MedicineNet, www.medicinenet.com/script/main/art.asp?articlekey=343&pf=3&page=1. Accessed December 28, 2009.
15. Mogk LG. Eye conditions that cause low vision in adults. In MW (e.d.), Low vision: Occupational therapy evaluation and intervention with older adults. (Rev. ed., 2008; pp. 1-24). Bethesda, MD: American Occupational Therapy Association.
16. National Limb Loss Information Center. Preventing Further Limb Loss Among People with Diabetes. 2008. Retrieved from the Amputee Coalition, www.amputeecoalition.org/fact_sheets/preventingamp.html. Accessed December 28, 2009.
17. Neuropathy (Nerve Damage). (n.d.). American Diabetes Association, www.diabetes.org/living-with-diabetes/complications/neuropathy. Accessed December 27, 2009.
18. Society for Neuroscience. Brain briefings: Diabetes, the brain, and cognition. February 2008. www.sfn.org/index.aspx?pagename=brainBriefings_diabetes. Accessed December 27, 2009.
19. Sokol-McKay DA. (2007) Adaptive Diabetes Self-Management Tools and Techniques. In Scheiman M, Scheiman M, Whittaker S, Eds. Low Vision Rehabilitation: A Practical Guide for Occupational Therapists. 2007; 265-86: Thorofare, NJ: SLACK Incorporated.
20. Steinbrook R. Facing the diabetes epidemic: Mandatory reporting of glycosylates hemoglobin in New York City. New England Journal of Medicine. 2006;354(6):545-8.
21. Stewart R, Liolitsa D. Type 2 diabetes mellitus, cognitive impairment and dementia. Diabetic Medicine. 1999;16(2): 93-112.
22. "Type 2." (n.d.). American Diabetes Association, www.diabetes.org/diabetes-basics/type-2. Accessed December 28 2009.
23. Warren M. An overview of low vision rehabilitation and the role of occupational therapy. In M.W. (e.d.), Low Vision: Occupational Therapy Evaluation and Intervention with Older Adults. (Rev. ed). 2008: 1-24. Bethesda, MD: American Occupational Therapy Association.

Earn PCE Credits from this article

Take the quiz at the Academy's Online Learning Center.