Dietetics Professional Portfolio



Type 2 Diabetes Mellitus:A Case StudyAmy LofleyIntroductionED was an elderly female admitted to the University Hospital. She was diagnosed with type 2 diabetes mellitus (DM) and had a 2 -3 cm ulcer on her lateral left foot. The following case study will discuss the etiology and treatment of type 2 DM and pressure ulcers as it relates to this patient.Patient Profile and Social HistoryED was a 71-year-old African American widow who lived in low-income housing with her sister who had type 2 DM. She was a homemaker. She completed schooling through the tenth grade (11 years). She was of the Protestant faith. She denied use of alcohol and tobacco. She had no known medical allergies. Medical HistoryED presented to the University Hospital with complaints of a two month old cut on her left lateral foot, blurry vision, frequent bladder infections, and peripheral neuropath of the feet. She had a history of hypertension, which was controlled with the antihypertensive agent, Capoten.Type 2 DM Literature Review In the United States, there are more than 13 million people living with DM (1). Of which, 90-95% of cases are type 2 DM (2). Type 2 DM is a progressive disease that is often manifested in adulthood. The etiology of type 2 DM is multifactorial and not completely known. It is characterized by impaired insulin secretion and cellular resistance causing increased gluconeogenesis and hyperglycemia. . This phenomenon takes many years to develop, but overtime, reliance on oral antidiabetic agents and exogenous insulin to maintain euglycmia may be necessary. Genetics plays a role in the development of type 2 DM, but the extent of it remains unclear (3). Regardless, certain ethnic groups and populations are at increased risk for type 2 DM. Groups at increased risk include African Americans, Native Americans, and Mexican Americans (2). Obesity is a strong risk factor for the development of type 2 DM (3). Weight gain is often related to lifestyle factors, such as poor dietary choices and physical inactivity. Moreover, adiposity may increase risk independently. Adiposity appears to impair insulin-stimulated glucose transport as well as function as an endocrine organ that release factors that affect glucose metabolism (3). In conjunction with the rise in childhood obesity, incidence of type 2 DM has increased among children who are overweight and obese Forty-50% of childhood cases of DM are type 2 (3). Complications of DM usually affect both micro- and macro vascular systems. Vessel damage occurs due to chronic hyperglycemia causing glycosylation of serum and tissue proteins (3). Vessel damage occurs due to chronic hyperglycemia causing hypertension, dyslipidemia, impaired immune function, and hyperinsulinemia to name a few. Macro vascular disease affects the large vessels resulting in atherosclerosis and endothelial damage, which increases risk for coronary heart disease, metabolic syndrome and bacterial and fungal infections (3). Micro vascular disease results in the classic complications of DM including: retinopathy, nephropathy, and neuropathy (3). Retinopathy is the leading cause of blindness in adults in the United States (3). Initially, this is manifested by small capillary aneurisms and over time, it can lead to blindness. Better control of glucose Euglycemia, early detection and treatment can help prevent vision loss. Nephropathy is the thickening of the glomerular basement membrane, mesangial expansion and glomerular sclerosis (3). Diabetic nephropathy is one of the leading causes of chronic kidney disease and end stage renal failure in the United States, which is evidenced by aluminuria. Neuropathy is defined as impaired nerve function from hyperglycemia (3). Neuropathy often affects the extremities causing a tingling and numbing sensation, which over time, leads to loss of sensation. As a result, abrasions to the feet often remain undetected until an ulcer has developed. Diabetic foot wounds are the leading cause of amputation in the United States. Pressure ulcers occur due to tissue necrosis in the layers of the skin where individuals apply constant pressure or load. There are four factors that impact the development of ulcers: pressure, shear force, friction, and moisture. As an area of the body sustains pressure, blood flow is impaired and tissue necrosis occurs. Shear force is refers to the motion of the bone and tissue against the pressure. Friction is one surface moving against another, and a moist environment increases susceptibility of an ulcer (4). It has been shown that the amount of pressure does not impact ulcer development as much as the time the pressure is applied (5). Shorter pressure times and loads create superficial ulcers and longer, heavier loads develop deep tissue ulcers that affect the muscle and bone (5). Thus, due to lack of positioning, ulcers are frequently observed in people who are bedridden, wheelchair bound, or wear prosthetics (5). Moreover, advanced age, uncontrolled diabetes, spinal cord damage, malnutrition, and trauma can increase risk (6). As stated, malnutrition increases risk for pressure ulcers. Malnutrition also impairs wound healing (7). In the British population, 5% of those with type 2 DM develop a foot ulcer at some point in time (8). As aforementioned, patients with diabetes are prone to ulcer development due to neuropathy (3). This is due in part to the fact that neuropathy causes loss of sensation in the extremities, which diminishes the natural shift of limb movement increasing affects stress and pressure to the affected area.Pressure ulcers are prevalent in both young and old and greatly affect quality of life. Pressure ulcers occur in about 1.3 to 3 million patients in the United States with the highest number observed among the institutionalized elderly (3). The prevalence of pressure ulcers in long-term geriatric wards is 3-30 %( 9).As previously mentioned, pressure ulcers can either form superficially on the skin or deep within the tissue (4). The superficial ulcers are a detachment of the skin from stress exerted on the skin. Deep tissue ulcers occur over bony prominences deep within the tissue that occur with sustained pressure. Such ulcers develop much faster and are more difficult to treat (4). Prevention of pressure ulcers is key to the management of diabetes (10). Education on food care and glycemic control is a key component to the prevention and/or recurrence of ulcers (10). Other ways to prevent pressure ulcers include: pressure reduction, pressure-relieving devices, and repositioning (11). Pressure can occur by using foam, fiber-filled, or gel-filled mattresses or overlays. Pressure-relieving devises include powered devices that operate using an air system to alternate pressure sites on patients. Repositioning is one of the most important steps because it is changes how the body is putting its weight. Repositioning should occur every two to three hours (11). Another preventative measure is checking limbs and other areas where there is limited sensation for abrasions Nutrition plays a vital role in healing and preventing ulcers. “Some investigators have found that patients who receive extra nutritional support dent to develop fewer pressure ulcers and to heal existing pressure ulcers faster compared to patients who do not receive nutritional support. Furthermore, a number of studies have investigated the potential value of specific, single nutrients such as vitamin C and zinc in regulating wound healing and have found promising results” (6). In addition, recent it has been shown that supplementation of arginine, zinc and antioxidants in cases of advanced pressure ulcers for three weeks, improves healing, but does not prevent occurrence (6). Bedridden patients with ulcers also have an increased protein needs due to the healing mechanism. Twelve recommendations have been proposed to treat and prevent ulcers (10). One of the recommendations is maximizing nutritional status. Nutritional assessment of the patient involves energy requirements, protein requirements, and micronutrient requirements. Energy requirements are based on the basal metabolic rate (BMR) in addition to account for physical activity and stress. Protein requirements are determined by the stress and nutrition status, and stage of the ulcer of the patient. Micronutrient requirements are usually increased during times of stress, as is often the case with ulcers (10). Vitamins A, C, and E, zinc, and some amino acids have been shown to assist in wound healing and the rate in which the healing occurs (10). Treatment and ProgressThe patient was admitted to University Hospital on June 8, 2010 and discharged on June 13, 2010. It was found that she had a 2-3 cm ulcer on her lateral left foot due to undiagnosed type 2 Dm. Upon admit, surgical debridement of the wound took place. She was prescribed sliding scale insulin, 1,200-kcal ADA exchange diet, and an anti-lipidemic agent. She was taught DM self-management. Anthropometrics Patient’s anthropometrics upon admit were 155 pounds (70.45 kg), 5’0” (152.4 cm). Calculations done were ideal body weight 100 pounds (45.45 kg), percent ideal body weight 155, body mass index 31, and adjusted body weight 114 pounds (52 kg). The patient was overweight for her height. She was classified as class I obese as determined by her body mass index (BMI). Laboratory InformationDateDateTestAdmitDay 5NormalGluc*32512170-110 mg/dLAlb4.04.13.5-5 g/dLHct30.427.737-47 %Hgb9.910.112-15 g/dLBUN26258-18 mg/dLCrea1.21.2.6-1.2 mg/dLChol300250120-199 mg/dLNa140145136-145 mEq/LK4.24.53.5-5.5 mEq/LHbA1C8.53.9-5.2 %TG40030035-135 mg/dLUpon admit, ED had an elevated blood glucose and hemoglobin A1C (HbA1c) consistent with her new diagnosis of type 2 DM. Her blood urea nitrogen (BUN) was slightly high due to stress. Her cholesterol and triglycerides were high reflective of dyslipidemia. Medications ED was prescribed Capoten 50 mg bid for hypertension prior to admission, and continued with this prescription during her hospitalization. Upon admit, she was prescribed Lipitor 10 mg qd to correct her dyslipidemia. In addition, she was prescribed sliding scale insulin throughout her hospital stay to correct her elevated blood glucose. ClinicalED did not appear malnourished upon admit. There were no signs or symptoms of a nutrient deficiency. She was obese and wore glasses. She had a 2-3 cm ulcer on her lateral foot that was not healing. Diet EvaluationUsing the Harris Benedict equation to estimate ED’s needs her calories came out to be 1507, carbohydrates 207 g, protein 94 g, and fats 33.5 g. Using Kcal/Kg her energy needs were 1090-1181, protein 55 g, and fluid needs 1090-1181 mL. Upon admit, the patient was prescribed a 1,200 kcal ADA exchange diet, which she tolerated well. She was consuming 75-100% of her meals, which was adequate to meet her needs. DM was given high protein supplements to assist in wound healing. A diet history was obtained from ED. ED reported that she had tried to avoid starchy foods and concentrated sweets since her sister was diagnosed with type 2 DM 10 years prior to admission. Her diet analysis revealed a diet high in saturated fat, total fat, and sodium. Her carbohydrate choices were low in fiber and high in refined sugar. ED was provided with a carbohydrate exchange meal plan based on her diet history. She was prescribed 165 g per day, which amounted to 11 carbohydrate exchanges per day. Her meal plan was as follows: Breakfast – ? cup black coffee; ? cup oatmeal; 1 cup 1% milk, 1 small appleLunch – Whole wheat turkey sandwhich (2 pieces whole wheat bread, 1 oz turkey, 1 oz American Cheese, mustard, lettuce); 8 oz unsweetened ice teaDinner – 1 cup turnip greens steamed with salt and pepper; 2 small new potatoes, boiled; 2 inch square piece of cornbread; ? cup great northern beans seasoned with ham. 1 cup coffeeSnacks – ? banana; 5 whole wheat crackers; In addition the patient was educated on protein and wound healing. The patient verbalized understanding and was likely to comply with recommendations. Nutrition NoteSubjective-Sister has DM and received DM handout 10 yrs pta. Avoids “starch” foods as a result. C/o unhealed cut on foot and blurry vision.Objective-71 yof dx with type 2 DM resides in low income housing. Wt. 155# BMI: 31, No recent wt. change. Alb: 4.0, Pre alb: 23, Gluc: 325, HgbA1c: 3.5, 2-3 cm ulcer on foot. Diet order: diabetic, PO: 75-100%. Obtained diet hxAssessment-Moderate nutrition risk 2o to new dx of DM and wound. Nutrition Dx.Impaired nutrient utilization R/t new dx of DM AEB HgbA1c of 8.5.Increased nutrient needs (protein, vitamin c, vitamin A, zinc) R/t healing AEB 2-3 cm foot wound.Plan-Nutrition InterventionPurpose of nutrition education – DM care, CHO counting, and increased protein for wound mercial beverage – DM Boost tidCoordination of nutrition care – refer to SSW for financial assistanceWill reassess in 3-5 days and monitor and assist as needed. Assessment-Moderate nutrition risk dt new type 2 DM dx and unhealed 2-3 cm foot wound. Admit BG of 325 and HbgA1c. Lives in low-income housing and cares for her sister with DM. Avoids “starch” foods as a result. Diet hx revealed high fat diet and low fiber foods. Given BMI of 31 and diet prefs will create CHO controlled meal plan lower in fat and higher in protein to promote wt. loss and wound healing. Could also benefit from meal assistance.Diagnosis- Nutrition Dx.Impaired nutrient utilization R/t new dx of DM AEB HgbA1c of 8.5.Increased nutrient needs (protein, vitamin c, vitamin A, zinc) R/t healing AEB 2-3 cm foot wound.Intervention- Nutrition InterventionPurpose of nutrition education – DM care, CHO counting, and increased protein for wound mercial beverage – DM Boost tidCoordination of nutrition care – refer to SSW for financial assistanceWill reassess in 3-5 days and monitor and assist as needed. Monitor-Will monitor BG and PO/Diet choicesEvaluate-Will evaluate knowledge of DM edu BG 80-150. Reassess in 3-5 daysSummary and ConclusionED’s condition has improved while hospitalized. She was achieving glycemic control and had received debridement of the wound. By adhering to the recommendations given, she was less likely to develop complications associated with DM. ReferencesCharney P. Diabetes Mellitus. In: Lysen LK. Quick Reference to Clinical Dietetics. Sudbury, Massachusetts: Jones and Bartlett Publishers; 2006: 50-35.Franz MJ. Medical Nutrition Therapy for Diabetes Mellitus and Hypoglycemia of Nondiabetic Origin. In: Mahan LK, Escott-Stump S. Krause’s Food & Nutrition Therapy. St. Louis, MO: Saunders Elsevier; 2008: 764-807.Beers MH, Porter RS, Jones TV, et al, ed. The Merck Manual of Diagnosis and Therapy. West Point, PA: Merck & Co; 2006.Grey JE, Enoch S, Harding KG. ABC of wound healing: Pressure Ulcers. BMJ. 2006; 332 (7539): 472-475. Bouten CV, Oomens CW, Baaijens FP, Bader DL. The etiology of pressure ulcers: skin deep or muscle bound? Arch Phys Med Reahabil 2003; 84: 616-619.Desneves KJ, Rodorovic BE, Cassar A, Crowe TC. Treatment with supplementary arginine, vitamin c and zinc in patients with pressure ulcers: a randomized controlled trial. Clin Nutr. 2005; 24: 979-987.Wellman NS, Kamp BJ. Nutrition in Aging. In: Mahan LK, Escott-Stump S. Krause’s Food & Nutrition Therapy. St. Louis, MO: Saunders Elsevier; 2008: 764-807. Mason J, O’Keeffet C, Hutchinson A, McIntosh A, Young R, Booth A. A systematic review of foot ulcer in patients with type 2 diabetes mellitus. II: treatment. Diab Med. 1999; 16: 889-909. Cereda E, Gini A, Pedrolli C, Vanotti A. Disease-Specific, versus standard, nutritional support for the treatment of pressure ulcers in institutionalized older adults: A randomized controlled trial. J Am Geriatr Soc. 2009; 57: 1395-1402. Dolynchuck K, Keast D, Campbell K, et al. Best Practices for the Prevention and treatment of pressure ulcers. Ostomy/Wound Manag. 2000; 46 (11): 38-52. Dini V, Bertone M, Romanelli M. Prevention and management of pressure ulcers. Derm There. 2006; 19: 356-364. ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download