Nursing Management of Patients with Diabetes Mellitus A&P Review, Study Guides, Projects, Research of Nursing

Download Nursing Management of Patients with Diabetes Mellitus A&P Review and more Study Guides, Projects, Research Nursing in PDF only on Docsity! Nursing Management of Patients with Diabetes Mellitus A&P Review: Pancreas • Exocrine & Endocrine functions o Islet of Langerhans: hormone secreting portion of pancreas o Alpha cells: produce and secrete glucagon (counterregulatory hormone) o Beta cells: produce and secrete insulin ▪ Alpha + Beta cells have opposing effects to one another Glucagon & Insulin • Insulin: facilitates glucose transport across cell membranes in most tissues o Continuously released into blood stream in small increments lowers blood glucose and facilitates normal glucose range of 70-120 mg/dL o Transports/carries glucose into cell ▪ Ex. Insulin = Lyft driver (insulin picks glucose up and takes it to cell; the cell receptors open up and allow the insulin to carry glucose in cell) o Insulin is always released/secreted in steady increments from the pancreas ▪ Insulin spikes when we eat because glucose stimulates insulin secretion • Glucagon: released in response to low blood sugar o If glucagon increases, insulin is counteractive by increasing glucose into the cells by removing it from the blood o Opposes effects of insulin o Glucagon increases during times of stress (if you are stressed, you need more energy, and we use glucagon as a source of energy) o Cortisol: stress hormone; opposes effects of insulin ▪ Increases glucose o Epinephrine: counteractive hormone o Growth hormone: counterregulatory hormone ▪ These all increase blood sugar—stimulates glucose production and output from the liver (can lead to liver issues) What is Diabetes? • Diabetes is a chronic disease in which the body either does not make any or enough insulin or cannot utilize the insulin it makes • Chronic disease; persistent in nature; can be treated and controlled but not cured • Type 1: someone does not make ANY insulin (in the initial stages not enough, and then not any) • Type 2: someone cannot utilize insulin (insulin resistance) • About 10% of population in the US has diabetes with more than 80 million considered early/pre-diabetic • What do patients with diabetes die from? o Heart disease (diabetes increases the risk of heart disease and stroke by 2x than the nondiabetic patient) • At risk populations for type 2: o African Americans, Hispanic, Native Americans, Asian Americans, Pacific Islander Americans ▪ African Americans = highest risk for diabetes Causes of Diabetes: Genetics + Environmental Factors • Problem is with glucose metabolism • Absent or insufficient insulin release • And/or • Poor utilization of available insulin • Combination of genetic risks + environmental factors as a primary essential disease Normal Insulin Metabolism • Normally released into bloodstream in small increments o Endogenous/homeostatic insulin secretion: there is always a little there as a buffer and spikes when eating because insulin is secreted from pancreas to transport glucose into the cells • Increased amounts when food is ingested • Type 1: you do not make insulin / are completely dependent on external sources of insulin, so you are always going to need endogenous replacement, and you will have to account for insulin with each meal/food intake (essentially carbohydrates) Type 1 vs. Type 2 • Both have a genetic factor • Type 1: environmental factors o Carries a distribution of younger age o Genetically susceptible person and at some point, the gene is triggered, and you get the autoimmune destruction of beta cells that produce insulin (can occur over many years) o When someone becomes symptomatic with type 1, it is the end result of long-standing beta cell destruction (80-90% have been destroyed) o Destroyed cells that make insulin, so we lose our ability to excrete insulin o If cells cannot get glucose in and are starving, they begin to look at other sources for energy: glucose + oxygen = aerobic metabolism ▪ If cells cannot utilize glucose for aerobic metabolism, then they switch to anaerobic metabolism – they utilize alternate food sources such as fat and protein ▪ If type 1 diabetics have polyphagia and weight loss resulting from cellular starvation due to not giving the cells insulin from not producing it anymore, the cells start looking at other sources and ketones are the byproduct of fat metabolism, and ketones lead to metabolic acidosis ▪ Pts that still have insulin production do not get DKA (type 2 diabetics with good insulin secretion do not get DKA—Insulin or no insulin is the biggest difference in the complication DKA) • Acute complication of type 1: DKA (if you do not produce insulin, you are at higher risk for DKA) • Malaise and fatigue: low energy • Recurrent or frequent infections o Immune system is impaired, pro-inflammation, susceptibility o Bugs like sugar—someone who has hyperglycemia chronically will be more susceptible to infection o UTI, yeast infections (candidiasis), etc. • Visual changes o Retinopathy (target organ damage of the eyes from hyperglycemia) • Parasthesias / Neuropathy o Nerve damage from diabetes (also a target organ problem) • “Target organs”: organs that diseases target: hyperglycemia being the initial problem— it causes damage to the vessels in the eyes, heart, brain, lower extremities, damage to nerves, nervous system, damage/sclerosis of kidneys/nephrons ▪ Problems related to diabetes damage these target organs—if you see target organ damage, you see longer term complications ▪ Ex. If someone diagnosed with diabetes has retinopathy, that tells us that the diabetes has affected vision Type 2 Diabetes Mellitus • Onset—Gradual (most prevalent: 90% of people with diabetes) o Does not have the same presentation as type 1 (type 1 can present as DKA) • May go undetected for many years • Usually people >35 years • 80-90% overweight at time of dx • Now being seen in children—ethnicity + weight contribute to increased risk in children • Run in families—genetic based • Prevalence increases with age • Ethnicity risk Incidence • 25.8 million Americans have diabetes • 79 million Americans have what I used to call “pre-diabetes” • 215,000 cases in people <20 years of age • 7.1% of non-Hispanic whites • 8.4% of Asian Americans • 12.6% of non-Hispanic blacks • 11.8% of Hispanics • Major cause of cardiovascular disease • 7th leading cause of death in the US Type 2 Diabetes • Sedentary lifestyle (genetics + lifestyle) • Familial tendency • Average age 50 years • Hx of increased BP (HTN) • Fatigue (decreased energy) • Obese • Recurrent infections • Polyuria • Polydipsia • FBS: >126 mg/dL • Hgb A1C: >/6.5% Metabolic Syndrome • Hypertension: o BP >130/85 • Triglycerides: o >/ 150 mg/dL • Impaired fasting glucose: o >/ 110 mg/dL • HDL-cholesterol: o <40 mg/dL (males) o <50 mg/dL (females) • Abdominal obesity: o Waist >/40” (males) o Waist >/ 35” (females) Metabolic Abnormalities • Role of developing type 2 diabetes: o Insulin resistance o Decreased ability of pancreas to produce insulin (after it has been overworked) o Inappropriate glucose production by the liver o Pro-inflammatory nature of adiposity Diagnostic Testing • HgBA1C o Normal is <6.5% o “Early diabetes”: 5.7-6.4% o “Corn flakes versus frosted flakes” o Best way to measure improvement over time—when they come back in 3 months and has an increased A1C, or their A1C has not changed, then the interventions have not been effective- we need to reevaluate the effectiveness of our interventions (meds, lifestyle changes, etc.) • Plasma glucose tolerance test o 2-hour plasma glucose >200 o Used most frequently in pregnancy • Symptoms of DM plus a random plasma glucose >200 o Pt admitted to hospital with fatigue and other S&S, and the glucose is elevated during a BMP- this is technically enough to say pt has diabetes, and should definitely be followed up on o When pts are sick, what is their blood sugar more likely to be? High, why? Sickness/illness is a stressful state- will see higher levels of cortisol and glucagon which opposes affects of insulin • 2 fasting glucose levels >126 o Normal fasting level is 70-126 Diabetes Mellitus: Collaborative Care • Goals of diabetes management: decrease symptoms, promote wellbeing, control BS, reduce target organ damage • We need to know what the acute and chronic complications are, so we know what to monitor/assess for and prevent • Triangle of diabetes management: o MED: ▪ Medication, exercise, diet • The oral meds mostly increase insulin receptor sensitivity o Not compatible with anything—will not mix anything with Lantus (given separately) • ONE insulin can be given IV infusion or IVP: Regular o The ONLY insulin you can give IV: regular ▪ Will give for someone in an acute hyperglycemic state Mixing Insulins 1. Wash hands 2. Gently rotate NPH insulin bottle 3. Wipe off tops of insulin vials with alcohol sponge 4. Draw back amount of air into the syringe that equals that dose 5. Inject air equal to NPH dose into NPH vial. Remove syringe from vial 6. Inject air equal to regular dose into regular vial a. Cloudy – clear – clear – cloudy • If long acting insulin gets mixed into the regular vial, it can cause profound hyperglycemia o Ex. You pull up 8 U of regular insulin that was contaminated with NPH and give it IV, your pt can go into hypoglycemia Insulin Syringes • Can only be used to give insulin • Measured in units NOT mL’s: pull back units to the top of the plunger • Insulin is considered High Hazard medication: o Needs to be double checked by 2 RNs (not at Mo Bap) • Administered subcutaneously at 45*, 60*, or 90* angle into sub-q tissue: do not aspirate o The angle is based on how much SQ pt has Insulin Administration • Fastest absorption is in the abdomen, then arm thigh, then buttock o Teach patients: pick an area, divide it into incremints for a week and then switch (rotate among same site for a week)—if you use same site over and over, a pad forms (lipodystrophy) under skin and decreases absorption • Caution: when injecting insulin into area such as thigh and then exercising: why? • Lipodystrophy: bumps / dents in skin from repeated injections • Where should insulin be stored? Where it is available, room temp or refrigerated • Each click is a unit Insulin Pump • Connected with plastic tube inserted into subcutaneous tissue in abdominal wall o Waterproof - can shower with it o Can alert you when glucose levels are abnormal • Delivers Regular insulin 24-hours “basal rate” • Provides tight glucose control: can increase amounts during meals, exercise • Patient must check blood sugars more often 4-6 times a day • Insertion site must be checked frequently • Biggest risks with insulin pump: o When it malfunctions, it increases risk for DKA (acidosis) o They can also cause infection at the site o Pump is more expensive than insulin syringes • A: Insulin pump • B: Insulin infusion set • G: Glucose sensor • D: Transmitter Complications of Insulin • Somogyi Effect: hyperglycemic in the AM o Insulin overdose o Overnight, between midnight and 4 AM, the pts BS will drop and they will become hypoglycemic overnight—glucagon, cortisol, epi kicks in, etc. and when the nurse checks the BS in the morning, it is hyperglycemic o The nurse may think the pt is not on enough insulin, but actually they are getting too much o If you see this pattern in a pt with diabetes, what do you do? Check BS between 2-4 AM • Dawn Phenomenon: hyperglycemic in the AM o Related to insulin/diabetes, but does not mean someone is getting too much insulin o Most commonly occurs during adolescence when they have a lot of growth hormone on board, and it raises BS in the morning o Key: check BS in the middle of the night ▪ Pt may need a snack before bed or insulin adjustments, etc. ▪ Want to assess for pre-dawn hyperglycemia by checking BS between 2-4 Medication: Oral Agents • Used for Type 2 only • Used in combination with each other o Can start Metformin and add a drug to it, etc. • Many times, used with daily Lantus or other long-acting insulin • Elevated sugars covered by rapid or short acting • Goal is to control sugar throughout day with oral agent and possibly some insulin regimen Oral Drug Therapy • Biguanides (1st line for most people with type 2 DM) o Reduces rate of glucose production by the liver: improves/increases glucose transport into the cells o Side effects: ▪ Renal: nausea & diarrhea • Potentially nephrotoxic: it is metabolized and excreted in the kidneys: check creatinine before beginning Metformin ▪ Nursing implications: monitor creatinine (10-20) ▪ HOLD when patient is having test with contrast media: day of procedure and 48 hours after • Can reinitiate sooner if creatinine is normal: check creatinine, and if it is normal you may resume it before the 48 hours is up o Example: ▪ Glucophage (Metformin): only form available in the US • Sulfonylureas (-ides) o Stimulates the release of insulin by the beta cells of the pancreas and causes tissues to take up and store glucose more readily, and helps decrease insulin resistance ▪ Because they stimulate insulin release, a complication is hypoglycemia o Decreased change of prolonged hypoglycemia o Major side effect is hypoglycemia—why? Due to stimulation of insulin release o Examples: • Pts with type 1 or type 2 diabetes can eat whatever they want, but the key is moderation and well-balanced meals with all the food groups Food Composition • Carbohydrates: primary source of energy: min of 130 g/day o Whole grains, fruits, vegetables, and low-fat milk • Fats: whole grains, fruits, vegetables and low-fat milk (<7%) • Carbs should provide 45-65% of the total energy intake for the day • Protein: should be 15-20% o High protein NOT recommended with DM patients Nutritional Related Strategies • Calorie restriction • Moderate weight loss • Consistent carbohydrate intake • Decrease fat, especially saturated fat intake • Increase physical activity • Self-monitoring of pre and post blood sugars Exercise & Diabetes • Best done after meals when glucose level is rising • Monitor levels before, during and after exercise—adjust oral intake accordingly • Delayed exercise induced hypoglycemia: o May occur several hours after completion of exercise o When you exercise, what are you utilizing for energy? Carbohydrates – glucose ▪ When you exercise, you will have increase glucose utilization (risk = hypoglycemia) o If someone is going for a 10-15-minute run, short/little planning is necessary (make sure you have carbohydrates before) ▪ Will not have long lasting affect- when you stop running, you stop utilizing glucose o Exercise that has longer lasting effects will continue to affect glucose ▪ Ex. weight-lifting – glucose will still be utilized awhile after and can cause delayed exercise induced hypoglycemia ▪ Make sure pt has carbs on board, brings some with them depending on how long they are exercising, and monitor blood sugar more frequently • Glucose lowering effects of exercise can last up to 48 hours after activity • Exercise 1-hour after meal or have 10-15-gram carb snack and check blood glucose level before exercising (every 60 minutes) • Have fast acting source of carbohydrates glucose tablets hard candies Stressful Situations and Diabetics • Diabetes in stressful situations: o Blood glucose goes up (cortisol, glucagon, epi) in response to stress ▪ They still need to maintain a steady intake of PO if they can ▪ It is important that you increase the amount of noncaloric fluid intake (water or calorie free other drinks); it is common for pts to get dehydrated due to the diuresis when hyperglycemia occurs, so we push fluids ▪ Should a pt that is in this situation continue to take their oral meds and insulin? Yes • Glucose levels tend to be higher in stressful events, and if you stop taking your insulin, an acute hyperglycemic crisis can occur • If you are sick, you should continue to check blood sugar and take blood sugar more frequently when sick • Risk factor for acute hyperglycemic crisis: o Stress (hospitalization) o Sick • Acute: o Illness—infection o Surgery o Injury o Hospitalizations o Physiological stress • Attempt to continue same calorie intake—not always possible • Check blood sugar every 4 hours and PRN • If glucose greater than 240 mg/dL test urine for ketones every 3-4 hours o The presence of ketones in urine or blood is always abnormal—of we are checking and seeing the presence in a pt with diabetes, what does this indicate? Could indicate the development of ketoacidosis ▪ May not yet indicate ketoacidosis, but could be the development ▪ Ketones tell us that the pt is utilizing other things for energy-- byproduct of fat metabolism is ketones (we know they are using fat for energy because of the + ketones) • Blood sugar is high which means they are not breaking down sugar for energy which means they are breaking down fat for energy—as evidenced by presence of ketones o Pt has BS >240, they need to check ketones, and if positive, call physician and go to ER Diabetic Ketoacidosis (DKA) • Pts can have undiagnosed type 1 that presents as DKA • 4 major characteristics of DKA that really feed the problem: o 1. Hyperglycemia: profound deficiency of insulin that causes blood sugar to continue increasing o 2. Ketosis: cannot utilize glucose because you have profound insulin deficiency (ex. type 1) ▪ Outsourcing for energy to other things we usually do not break down (fat) ▪ Leads to acidosis o 3. Acidosis: ▪ How does ketosis lead to acidosis? • By-product of fat metabolism: ketones • Ketones alter pH – ketones are acidic and cause the acidosis • Acidosis: life-threatening nature of DKA that leads to increased mortality rates – this can kill you o 4. Dehydration: Increased plasma osmolality ▪ Losing fluids because blood glucose is high and is acting as a diuretic • Hyperglycemia—osmotic diuresis ▪ Electrolyte imbalances: pt will be vascularly dry—will see potassium imbalances result • Monitor for electrolyte imbalances—particularly potassium o When we get into the management of DKA, it is about managing these characteristics/problems • Causes: o Increase calories/caloric intake o Too little insulin o Stress from physical illness—infection (and physiological stress) o Undiagnosed DM ▪ Type 1 can appear as DKA when it is first symptomatic • Process: o Glucose cannot be used > cellular o Starvation > (ketogenesis) breakdown of protein and fats > free fatty acids > ketones > ketoacidosis – neurological manifestations of DKA • Results: o Metabolic acidosis o Increase plasma osmolality o BMP comes back and lab calls and says, “we have a critical lab we need to report! Your pts BS is 1200, k+ is 5.5, and anion gap is elevated = 18.” ▪ Prioritize interventions: pt coming in with DKA ▪ Anion gap: indirect measurement of acidosis (normal range 3-10) • When the anion gap is elevated, there is unmeasured anions present in the blood (indirectly reflects acidosis) • When this gap is open, acidosis is still occurring—noninvasive way, not as good as ABG, becomes important when you consider continuing treatment for DKA (especially if hyperglycemia is resolved) ▪ Assess: VS, BS (accucheck), Labs—BMP (will be repeated every hour while being treated for DKA until anion gap normalizes), Hx info, ECG/Cardiac monitor (can cause dysrhythmias from K+ imbalances), head-to-toe / neuro / respiratory, UO (important when evaluating the effectiveness of interventions), ABGs if pt has fruity breath and ketones, and UA to check for ketones and glucose + specific gravity • Continue treatment until you fix the acidosis (anion gap will close) • Monitor trends in anion gap as well (trends in the anion gap tell us whether our patient is responding to treatment) ▪ Treatment: Interventions- • IV—IVFs (NS or LR -- isotonic fluids-) o Antiemetic • Insulin: Regular (IV)—at least 20 G if not an 18 o Always have 2 IVs placed in case one goes bad because DKA is a life-threatening ER o IV insulin 12 units per hour o Will also be giving boluses of NS ▪ BMP will be even more important now—we will be replacing fluids which dilutes concentrated blood to even it out and will see shifts in K+ • Insulin drives potassium inside cells which is when you will see K+ decrease • Many times, potassium will need to be supplemented after DKA is treated o Sometimes IV bolus of insulin will also be ordered • The interventions begin working—anion gap is beginning to decrease (it is now 13), BP 120/80, HR is 90, RR is improving, and his BS is now 200. Do we stop insulin? o NO because the anion gap still indicates acidosis—we will switch to D5½NS to buffer the insulin ▪ We cannot keep giving him insulin without some sugar or he will become hypoglycemic ▪ Once BS gets to 250 or below but anion gap is still elevated, you will switch the fluids on the pump to D5½NS (at a slower rate: 125 mL/hr.) – the sugar should still be enough to buffer the BS levels so they do not become hypoglycemic • After you switch the pump to D5, you come back and hour later, and now the anion gap is 9. What do we do? o Stop the insulin and D5½NS o Maintenance fluids of NS for hydration will still be given Hyperosmolar Hyperglycemic Syndrome • Occurs in patients that are able to produce some insulin but not enough to prevent hyperglycemia o Hyperglycemia + dehydration just like DKA but with the absence of ketoacidosis (they are still producing some insulin) • Rare, occurs less often than DKA • Usually in patient’s older than 60 and with Type 2 Diabetes o Typically occurs in type 2 diabetics that are older • Produces fewer symptoms in early stages: blood sugar can raise quite high before symptoms are seen • The absence of ketoacidosis because they are still producing some insulin (there is not a profound deficiency of insulin), so they do not have to break down fats and proteins which is what causes ketones • Same interventions except not managing the acidosis o Massive fluids o IV: regular insulin o Same assessments • Type 1: most prominent population in DKA o Can still see DKA in type 2, but it is all about the insulin and how much is being produced or not Acute Complications Continued [Hypoglycemia Related] • Hypoglycemia: TIRED o T: tachycardia o I: irritability o R: restless o E: excessive hunger o D: diaphoresis, depression • <70 is technically considered abnormally low o However, most patients are symptomatic at <50 • Ex. Pt lives at 350, but now they are 180 – they have perceived hypoglycemia o Normal, but not for pt o Pt will need glucose – trend it and do some investigation • Detect it, teach pt about it, take time to investigate why it occurred o If it occurred once, it could absolutely occur again (and this kills people) • Other S&S of hypoglycemia: o Cool, clammy skin/diaphoresis o Tachycardia: counterregulatory hormone kicks in when BS drops (epinephrine- stress response- can also cause diaphoresis) o Restlessness o Hunger (low BS) Hypoglycemia • Too much insulin for available glucose • Less than 50 mg/dL • Sudden shift and fall of glucose • Symptoms: result of epinephrine o Nervousness, irritability, increased HR, diaphoresis, impaired mental status • Treatment: o For glucose replacement, assess their ability to take PO o Simple carbohydrate foods if pt is alert, commercial gels o Glucagon IV or D50 IV push in acute situation • Clinical manifestations: o Cool, clammy skin o Rapid heartbeat o Hunger o Nervousness, tremor o Faintness, dizziness o Unsteady gait, slurred and/or incoherent speech o Vision changes o Seizures, coma o Severe hypoglycemia can result in death • Hypoglycemia: “great mimicker” o Mimics stroke and alcohol intoxication o CHECK BS if you think your pt is having a stroke (part of stroke protocol) ▪ Especially if they have a history of diabetes o Seizure, coma, death= when hypoglycemia is critically low-- end of neurological cascade ▪ Without glucose, you almost get hypoxic brain injury as a result Hypoglycemia Treatment • Elderly patients and patients that use beta-blockers are at risk for hypoglycemic unawareness due to blocking of the beta-adrenergic receptors o Disease of small blood vessels ▪ Eyes, heart, skin, nerves o Specific to diabetes o Endothelial dysfunction o Thickening of the basement membrane in the capillaries and arterioles ▪ Eyes, kidneys, nerves, heart, and skin o Seen prior to or onset of disease o Symptoms do not occur for 15-20 years Retinopathy • Microvascular damage to the retina due to: o Chronic hyperglycemia o Hypertension • Microaneurysms (non-proliferative; most common form)—causes hemorrhages • And capillary walls weak • Retinal edema • If retinopathy is a problem, what do I recommend for my pt with diabetes? What is the intervention to detect/prevent retinopathy? o Prevent by: control BP and BS ▪ If you want to optimize eye function, and you’re a diabetic, you want good glucose control and BP o To detect it: get annual eye exam (at least) ▪ If pt is telling you that they are changing glasses/prescriptions frequently, they need to do a dilated retinopathy exam • This is the only way you can see retinopathy o Good eye health: sunglasses outside, etc. Nephropathy (Kidney Damage) • Glomerular sclerosis leads to nephropathy / kidney disease o Will see in 20-40% of people with diabetes • How can we prevent? o #1 thing we can do to prevent this: control BP o Tight glucose control o Smoking cessation o Use of ace or arb (Valsartin or Lisinopril)—helps prevent kidney damage from diabetes ▪ Helps if they have macro or micro albuminemia ▪ Can be used even if pt does not have HTN ▪ Helps decrease progression of nephropathy • How do you know if pt has nephropathy? o Protein in urine—get UA o Proteinuria tells us that kidney issues are occurring • Microvascular complication associated with damage that supply glomeruli of kidney • Risk Factors: o Hypertension o Genetic predisposition o Smoking o Chronic hyperglycemia Neuropathy • Nerve damage due to metabolic disturbances associated with diabetes • Sensory Neuropathy: o Loss of protective sensation in lower extremities • Exam feet: avoid injury, proper footwear, proper nail care • Autonomic Neuropathy: o Can affect nearly all body systems: hypoglycemic unawareness, postural hypotension, painless MI • Common in diabetics—at least 60-70% of diabetics have some degree of neuropathy o Spectrum of severity o Nerve damage • More than 60% of nontraumatic amputations result from diabetes • Autonomic: o Hypoglycemic unawareness • How do I prevent neuropathy? BS control (this is pretty much it) o HTN does not impact this • Erectile dysfunction, orthostatic hypotension, delayed gastric emptying • How do we know if pt has neuropathy? o It can manifest in different ways: ▪ Pins & needles, tingling, numbness, decreased sensation (these are some S&S) • Monofilament testing: o Tests for sensation o Should be done annually—detects changing in sensation ▪ One way they can differentiate between sharp and dull—before you lose sensation, you will begin losing the ability to differentiate these • Avoiding injury: o Proper footwear: thick-soled shoes that are not too tight- must have breathing room so it does not cause skin breakdown and infection Foot Care • Of all things chronic complication related—foot issues/wounds/complications are the most common in hospitalizations for diabetics o Not many times life-threatening, but causes hospitalization • Examine feet daily • Wash feet with warm water and mild soap • Pat dry—don’t rub • Keep feet from drying and cracking o Can lightly moisturize, but do not leave then wet • Extra care with toenail care • Diabetic foot ulcer: o Primary risk for ulcer in foot or lower extremity ▪ Loss of protection of sensation • This is why monofilament testing is so important (annually) ▪ Decreased sensation + poor perfusion o Screen for PAD also ▪ Increased O2 demands, decreased perfusion to lower extremities ▪ Intermittent claudication—early sign of PAD • Pain with ambulation: increased O2 demands and decreased perfusion—ischemia ▪ Pallor, shiny, cool, dry, hairless areas ▪ Decreased cap refill (<2+) • Necrotic toe before and after amputation- Priority Problems: Risk for Infection • Diabetic more susceptible to infection • May have recurrent infections • Persistent glycosuria: predisposes to bladder infections and yeast/candidiasis infections o Increased urinary glucose leads to UTI, etc. • Decreased circulation: delay in immune response o Decreased circulation decreases immune response ▪ Ex. if you have an injury to lower extremity, they may not be able to get adequate blood to heal it • r/t decreased tactile sensation o Caution about potential sources of injury to feet o Teach pt to inspect inside of shoes for foreign objects • r/t hypoglycemia o Monitor for s/s of hypoglycemia o Teach pt to have simple carbs available • Type 2: increases with age Care of the Older Patient with Diabetes • Care of diabetic older patients o More than 25% of all clients with diabetes are over age 65