1. Diabetic Foot Ulcers Summer 2012 FN 6800 Maryann Walsh

2. Background There are an estimated 150 million people with diabetes worldwide Projected to increase to 366 million by 2030. Current US population is 311 million (just to put the number into perspective.)

3. Background Studies have indicated that diabetic patients have up to a 25% lifetime risk of developing a foot ulcer. Once ulcers develop, there is an increased risk of wound infection which may lead to amputation. At least 40% of amputations in diabetic patients can be prevented with a team approach to wound care.

4. How does it begin? Diabetic foot ulcers typically result from the simultaneous occurrences of: Peripheral neuropathy Ischemia from peripheral vascular disease. More than 60% of Diabetic foot ulcers are the result of underlying neuropathy.

5. Neuropathy In the development of neuropathy: The hyperglycemia state leads to an increase in action of 2 enzymes: Aldose reductase Sorbitol dehydrogenase The result: Conversion of intracellular glucose to sorbitol and fructose

6. Neuropathy The accumulation of sorbitol and fructose result in a decrease in the synthesis of myoinositol. Myoinositol: a nerve cell required for normal neuron conduction. Additionally, the chemical conversion of glucose results in a depletion of nicotinamide adenine dinucleotide phosphate (NADPh) stores. NADPh is necessary for: Detoxification of reactive oxygen Synthesis of nitric oxide (vasodilator)

7. Neuropathy Subsequently, the increase in oxidative stress on the nerve cell and increase in vasoconstriction lead to ischemia. Ischemia promotes nerve cell injury and death. Coupled with the oxidative stress, hyperglycemia contributes to: Abnormal glycation of nerve cell proteins Inappropriate activation of protein kinase C Results in further nerve dysfunction and ischemia.

8. Resultant Damage Damage to the innervations of the intrinsic foot muscles leads to: Imbalance between flexion and extension of the affected foot This creates anatomic foot deformities that create abnormal bony prominences and pressure points. Gradually causes skin breakdown and ulceration

9. Resultant Damage (cont.) Autonomic neuropathy leads to: Diminished sweat and oil gland functionality. As a result the foot loses its natural ability to moisturize the overlying skin. Skin becomes dry and susceptible to tears Tears can lead to subsequent development of infection. Loss of sensation due to the peripheral neuropathy prevents the patient from feeling any trauma that may occur to the wound site. Repetitive pressure and weight bearing on the foot causes the wound to worsen.

10. Peripheral Artery Disease (PAD) Contributing Factor to the development of foot ulcers in up to 50% of cases. Commonly affects tibial and peroneal arteries of the calf. As a result of persistent hypoglycemia: Endothelial cell dysfunction and smooth cell abnormalities develop in peripheral arteries. A result decrease in endothelium-derived vasodilators leading to vasoconstriction.

11. Peripheral Artery Disease Factors that are common in diabetic patients that contribute to PAD: Smoking Hypertension Hyperlipidemia

12. Stages of Ulcers

13. Dietitian’s Role in Pressure Ulcer Treatment Numerous studies have shown that adequate protein and adequate overall nutrition can aid in pressure ulcer healing. Important to work with patient to develop a plan for after they leave the hospital to continue adequate protein intake to promote further healing

14. Nutrition Assessment Assess Pre-albumin (PAB) and Albumin (Alb). PAB: 2-3 day half-life therefore a better indicator of protein depletion in an acute care setting. Ideal range: 16 - 35 mg/dL Alb: Approx. 20 day half-life, less reliable indicator Ideal range: 3.4 – 5.4 g/dL It is very often that a patient suffering from a foot ulcer is protein depleted.

15. Nutrition Intervention Supplement with protein: Calculate protein needs by multiplying body weight in kg x 1.2-1.5 g PRO Example: 200lb man with stage 2 pressure ulcer: 200 / 2.2 = 91kg x 1.3 = 118 g PRO

16. Nutrition Intervention Patient must be placed on a high protein diet: Meats, dairy, beans, etc. Supplements can aid in achieving a patient’s protein goals: Ensure, Boost, standard hospital protein shakes, Beneprotein packets, etc.

17. Sources 1. Patrizio Tatti, Donatella Bloise, Patrizia di Mauro, Leonardo MasselliInt.Extremely accelerated healing of diabetic foot ulcers with Medical NutritionTherapy: report of the first three cases. J Diabetes & Metabolism (2009) 17:115-116 2. Patrizio Tattia, c, Annabel Elisabeth Barber, The Use of a Specialized Nutritional Supplement for Diabetic Foot Ulcers Reduces the Use of Antibiotics. Journal of Endocrinology and Metabolism Volume 2, Number 1, February 2012, pages 26-31 3. Logan, Daniel, etal. Prevention and Treatment of Leg and Foot Ulcers in Diabetes Mellitus. Cleveland Clinic. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/prevention-treatment-diabetic-leg-and- foot-ulcers/ 4. Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA. 2005, 293: 217-228. 5. Clayton, Warren, Elasy, Tom. A Review of the Pathophysiology, Classification, and Treatment of Foot Ulcers in Diabetic Patients Clinical Diabetes 2009 vol. 27 no. 2 52-58 6. National Pressure Ulcer Advisory Panel http://www.npuap.org/http://www.npuap.org/ 7. ADA Evidence Library http://www.adaevidencelibrary.com/topic.cfm?cat=4598&auth=1