Nursing Management of Patients with Diabetes Mellitus PDF

Dr/ Furat Hussein 1  Outlines: 1-What is diabetes. 2- Classification of diabetes. 3-Causes of diabetes. 4- Signs & Symptoms of diabetes. 5-Risk factors of diabetes. 6-- Management of diabetes. 7- Complication of diabetes. 8- Nursing care of diabetes mellit...

Dr/ Furat Hussein 1  Outlines: 1-What is diabetes. 2- Classification of diabetes. 3-Causes of diabetes. 4- Signs & Symptoms of diabetes. 5-Risk factors of diabetes. 6-- Management of diabetes. 7- Complication of diabetes. 8- Nursing care of diabetes mellitus.  What is diabetes? Diabetes mellitus (DM) is a group of diseases characterized by high levels of blood glucose (Hyperglycemia) resulting from defects in insulin production, insulin action, or both. Endocrine Function :  Cells of the Islet of Langerhans synthesize and release hormones into the circulation.  Hormones travel through the bloodstream to target tissues (especially liver and muscle).  At the target cells, hormones bind specific receptors and cause cell changes that control metabolism. Pancreatic endocrine cells regulate carbohydrate, fat, protein metabolism: Alpha cells: secrete the hormone Glucagon. Beta cells: secrete the hormones insulin. Delta cells: secrete the hormones gastrin. F cells: secrete hormone pancreatic polypeptide. Insulin secretion is controlled through several mechanisms: 1- Chemically :high levels of glucose and amino acids in the blood. 2- Hormonally :beta cells are sensitive to several hormones that may inhibit or cause insulin secretion. 2  3- Neurally : stimulation of the parasympathetic nervous system causes insulin to be secreted. Statistics: Diabetes is the leading cause of : -non-traumatic amputations, -blindness among working-age adult, -end-stage renal disease. Diabetes is the 3rd leading cause of death -MI -Stroke -Peripheral vascular disease Hospitalization rates for people with DM are 2.4 times greater for adults and 5.3 times greater for children than for the general population.  Classification of Diabetes:  Type 1 diabetes (previously referred to as insulin-dependent diabetes mellitus) IDDM  Type 2 diabetes (previously referred to as non-insulin dependent diabetes mellitus) NIDDM  Gestational diabetes mellitus  Diabetes mellitus associated with other conditions or syndromes. Type 1 Diabetes ( Insulin-dependent DM)  Caused by a total lack of insulin that, in turn, produces high blood glucose levels. (Approximately 5%- 10% ) (< 30 y)  Genetic factors are thought to be important in most patients. 3  ß-cell destruction, usually leading to absolute insulin deficiency.  Type 1 is most often seen in children.  Beta cells are destroyed by an autoimmune process.Often islet cell antibodies and antibodies to insulin.  Other names: Insulin-dependent diabetes mellitus; IDDM; juvenile onset diabetes. Type 2 Diabetes ( Non-Insulin-dependent DM)  Occurs when the body does not produce enough insulin or cannot properly use insulin.  Most common type in adult above 30 years.  About one-third are undiagnosed and most of them are obese (80%).  As result of decrease sensitivity to insulin (insulin resistance) & impaired Beta cells function lead to insufficient insulin production.  Frequently not diagnosed until complications appear. Gestational Diabetes  Occurs in pregnant women that have high blood glucose levels.  This type of Diabetes can harm both Mother and baby.  any degree of glucose intolerance with onset of first recognition during pregnancy.  Usually in 2nd or 3rd trimester due to hormones secreted by the placenta, which inhibit action of insulin (abnormally large baby) Six weeks or after or more after pregnancy ends disappear. 4  DM associated with other conditions It is accompanied by conditions as  pancreatic disease  Corticosteroids  estrogen-containing preparations Prediabetes  Previous history of hyperglycemia (gestational)  Is classified as Impaired glucose tolerance {IGT} or impaired fasting glucose {IFG}.  IGT refers to a condition in which blood glucose levels fall between normal levels & levels considered diagnostic for diabetes 140 mg/dL – 200mg/dL IFG is defined as a fasting plasma glucose between 110mg/dL – 125 mg/dL Causes and Risk Factors:  Family history of diabetes  More than 20% overweight (BMI ≥27 kg/m2)  Impaired fasting glucose (IGF)or impaired glucose tolerance (IGT)  Had gestational diabetes or had a baby over 9 lbs.  Hypertension (≥140/90 mm Hg)  HDL cholesterol level ≤ 35 mg/dL and or triglyceride level ≥ 250 mg/dL Risk Factors for type 2 DM:  Family history of DM(parents or sibling with DM)  Lack of physical activities.  Previously identified IFG or IGT.  Hypertension (more than140/90 mmHg in adult).  HDL cholesterol less than 35 mg/dl and/or triglyceride level 250 mg/dl.  History of vascular disease. 5  Obesity (significant risk factor) More than 20% overweight (BMI ≥27 kg/m2).  Age ≥ 45 years Physiology: Insulin moves glucose from blood into muscle, liver and fat cells. Insulin action:  Transport & metabolize glucose for energy  Stimulates storage of glucose in the liver & muscle (gluconeogenesis).  Signals the liver to stop the release of glucose glycogenolysis  Enhances storage of dietary fat in adipose tissue  Accelerates transport of amino acids (derived from dietary protein) into cells  Inhibits the breakdown of stored glucose, protein , and fats. Pathophysiology:  During fasting periods the pancreas continuously releases a small amount of insulin (basal insulin); another pancreatic hormone called glucagon (secreted by the alpha cells of the islets of Langerhans) is released when blood glucose levels decrease and stimulate the liver to release stored glucose.  The insulin and the glucagon together maintain a constant level of glucose in the blood by stimulating the release of glucose from the liver. Initially, the liver produces glucose through the breakdown of glycogen (glycogenolysis). Type 1 diabetes: Total lack of insulin due to the destruction of the pancreatic beta cells. Signs & Symptoms: Symptoms of Type I &Type II Diabetes  Polyuria  Polydipsia  Polyphagia 6   Fatigue  Muscle Weakness Type I Diabetes  Nausea  Severe Vomiting  Abdominal Pains Type II Diabetes  Muscle wasting  Vision Changes  Numbness & tingling in hands or feet  Dry skin  Skin lesion that are slow to heal Assessment & diagnosis:  Symptoms of DM  Fasting plasma glucose (normal: 70 – 110 mg/dL) (>126mg/dL ,  2-hour post-load glucose (>200mg/dL)  Random blood glucose ( = or > 200 + presence of diabetic Ss). Management 1-Nutritional Management: Nutritional management of diabetes is control of total caloric intake to attain or maintain a reasonable body weight and control of blood 7  glucose levels. Provide optimal nutrition including all essential food constituents to;  Meet energy needs  Achieve and maintain a reasonable weight.  Prevent wide fluctuations of blood glucose levels  Decrease serum lipids, if elevated Caloric requirement in Diabetic Patients the American Dietetic Association & American Heart Association recommend that for all levels of caloric intake,  50% to 60% of calories should be derived from carbohydrates,  20% to 30% from fat,  and the remaining 10% to 20% from protein. Role of the Nurse: Be knowledgeable about dietary Management. Communicate important information to the dietician or other management specialists. Reinforce patient understanding. Support dietary and lifestyle changes. Glycemic index (how much a given food raises blood glucose level compare to equivalent amount of glucose) One of the main goals of diet therapy in diabetes is to avoid sharp, rapid increases in blood glucose levels after food is eaten.  Combine starchy food with protein-fat to slow absorption & lower glycemic response.  Eating raw foods & whole to lower glycemic response than pureed, or cooked food.  Eating whole fruit instead of drinking juice because fiber slow absorption.  Other Dietary Concerns: Alcohol  if a diabetic patient takes alcohol on an empty stomach, there is an increased likelihood that hypoglycemia will develop. In addition, excessive alcohol intake may impair the patient’s ability to recognize and treat hypoglycemia. 8  Sweeteners Nutritive (fructose) and sorbitol , (contain calories cause less elevation in blood sugar levels than sucrose. Non-nutritive (saccharin) (produce minimal or no elevation in blood glucose levels. 2-Exercise: Blood glucose should not exceed 250 mg/dL before exercise. Exercise with elevated blood glucose level increase secretion of glucagon, growth hormone. The liver then release more glucose. Exercise in same time & same amount each day. Patients who require insulin should be taught to eat a 15-g carbohydrate snack (a fruit exchange) or a snack of complex carbohydrates with a protein before engaging in moderate exercise. To avoid post exercise hypoglycemia after strenuous or prolonged exercise, the patient may need to eat a snack at the end of the exercise session - and at bedtime and monitor the blood glucose level more frequently. 3-Frequency of Self-Monitoring of Blood Glucose Who take insulin before each meal at least 3times daily before meals to determine each dose. Who take insulin at bedtime or who use an insulin infusion pump should also test once. Not receiving insulin may be instructed to assess their blood glucose levels at least 2 or 3 times per week, including a 2-hour postprandial test. For all patients, testing is recommended whenever hypoglycemia, hyperglycemia , changes in medications, activity, diet, with stress or illness. Every 6-12 months compare with lab. (Q 3 months) Glycosylated Hemoglobin HgbA1c. Continuous Glucose Monitoring System Urine test Ketones test 9  Glycosylated Hemoglobin; When blood glucose levels are elevated, glucosemolecules attach to hemoglobin in the red blood cell.The longer the amount of glucose in the blood remains above normal, The more glucose binds to the red blood cell and the higher the glycosylated hemoglobin level. This complex (the hemoglobin attached to the glucose) is permanent and lasts for the life of the red blood cell, approximately 120 days. 4-Pharmacological therapy (Insulin): Types Human insulin Manufacture (NPH) Complications of insulin Allergy (urticaria) Insulin lipo-dys-trophy (lipoatrophy, lipohypertrophy) Lipoatrophy is loss of subcutaneous fat and appears as slight dimpling or more serious pitting of subcutaneous fat. The use of human insulin has almost eliminated this disfiguring. Lipohypertrophy, the development of fibrofatty masses at the injection site. Insulin resistance (daily requirement of >200 units) Morning hyperglycemia Methods of insulin delivery: Insulin Pens. Jet Injectors. Insulin Pumps. Future Insulin Delivery 10  Transplantation of Pancreatic Cells Injection sites: -Abdominal areas is the most preferred because of rapid absorption. -Do not aspirate insulin injections. list of new treatment options that are currently being researched  Insulin Pump Implants - a permanently implanted pump that will measure blood sugar levels and deliver the exact amount of insulin needed.  Insulin Capsule Implant - an insulin capsule that can be implanted to continuously release insulin into the bloodstream.  Insulin Inhaler - a rapid-acting insulin that is inhaled into the mouth.  Insulin Pill – Currently, the pill form has only been tested in animals.  Continuous Monitoring Device - The GlucoWatch Biographer, a wristwatch-like device, has been approved by the FDA. It is intended as a companion for the fingertip blood test to monitor glucose, in order to ensure accurate results.  Islet Cell Transplant – For people with Type 1 Diabetes, helps patients become insulin free for up to 14 months after treatment.  Gene Therapy  A Diabetes Vaccine – To prevent or slow the progress of Type 1 Diabetes. general principles for rotation of Insulin Injections  First, patients should try not to use the same site more than once in 2 to 3 weeks.  In addition, if the patient is planning to exercise, insulin should not be injected into the limb that will be exercised, because it will be absorbed faster, result in hypoglycemia. 11   patients should be encouraged to use all available injection sites within one area (0.5 to 1 inch away from the previous) injection rather than randomly rotating sites from area to area.  The speed of absorption is greatest in the abdomen and decreases progressively in the arm, thigh, and hip.  When rapid acting or short acting insulin is mixed with longer acting insulin, draw the short acting insulin into the syringe first.  Prevents contamination of the shorter acting insulin with the longer acting insulin.  Draw up clear, then cloudy.  Insuling glargine (Lantus) should not be mixed with any other insulin. Mixing  insulin  Self Injection Of Insulin Oral Anti-Diabetic Agents  If glycaemic control is not achieved (HbA1c > 6.5% with lifestyle modification within 1 –3 months, ORAL ANTI-DIABETIC AGENT should be initiated.  In the presence of marked hyperglycaemia in newly diagnosed symptomatic type 2 diabetes (HbA1c > 8%, oral anti-diabetic agents can be considered at the outset together with lifestyle modification. 12   Combining insulin and the following oral anti-diabetic agents has been shown to be effective in people with type 2 diabetes:  Biguanide (metformin).  Insulin secretagogues (sulphonylureas).  α-glucosidase inhibitor (acarbose).  Insulin dose can be increased until target Fasting blood glucose (FPG) is achieved. 5-Education:  Foot care  Eye care  General hygiene (eg, skin care, oral hygiene)  Risk factor management (eg, control of blood pressure and,  Blood lipid levels, and normalizing blood glucose levels). Acute Complications of Diabetes:  Hypoglycemia  DKA  HHNS, which is also called hyperglycemic hyperosmolar nonketotic syndrome. Hypoglycemia: (abnormally low blood glucose level) occurs when the blood glucose falls to less than 50 to 60 mg/dL. Caused by; - too much insulin or oral hypoglycemic agents, - too little food, or excessive physical activity. Signs & Symptoms : impaired function of the CNS may include; 13  sweating, pallor, coldness,  inability to concentrate,  headache, lightheadedness,  confusion, memory lapses,  numbness of the lips and tongue,  slurred speech,  impaired coordination,  emotional changes, irrational or combative behavior,  double vision, and drowsiness. feeling dizzy/shaking profuse sweating headache pins and needles around mouth excessive hunger DPMI Workforce Development – The Alfred Workforce Development Team June 2005 Treatment :  -Provide glucose (I.V. if unconscious).  -Observe for relapse.  -Never give food to an unconscious person. DIABETIC KETOACIDOSIS: Caused by an absence or markedly inadequate amount of insulin. Occurs when Diabetes Type 1 is undiagnosed Three main clinical features of DKA  Hyperglycemia  Dehydration and electrolyte loss  Acidosis 14 Clinical Manifestations Polyuria and Polydipsia Blurred vision, weakness, and headache Orthostatic hypotension Anorexia, nausea, vomiting and abdominal pain Acetone breath (a fruity odor), with elevated ketone levels ,very deep, but not labored respirations) may occur. Assessment and Diagnostic Findings:  Blood glucose levels may vary from 300 to 800 mg/dL (16.6 to 44.4 mmol/L).  Evidence of ketoacidosis is reflected in low serum bicarbonate (0 to 15 mEq/L) and low pH (6.8 to 7.3) values.  A low PCO2 level (10 to 30 mm Hg) reflects respiratory compensation (Kussmaul respirations) for the metabolic acidosis.  Accumulation of ketone bodies (which precipitates the acidosis) is reflected in blood and urine ketone measurements.  Sodium and potassium levels may be low, normal, or high, depending on the amount of water loss (dehydration).  Medical Management:1- REHYDRATION Fluid replacement enhances the excretion of excessive glucose by the kidneys. IV fluid to replace fluid losses caused by polyuria, hyperventilation, diarrhea, and vomiting. Monitoring fluid volume status. Vital signs 15 2-RESTORING ELECTROLYTES Plasma concentration of potassium may be low, normal, or even high. Insulin administration, which enhances the movement of potassium from the extracellular fluid into the cells. potassium replacement is vital to avoid dysrhythmias that may occur with hypokalemia 3-REVERSING ACIDOSIS Ketone bodies (acids) accumulate as a result of fat breakdown Insulin inhibits fat breakdown, thereby stopping acid buildup Insulin is usually infused intravenously at a slow, continuous rate (eg, 5 units per hour) Hourly blood glucose values and IV fluid solutions with higher concentrations of glucose to avoid too rapid a drop in the blood glucose level. Nursing Management  Monitoring fluid and electrolyte status as well as blood glucose levels.  Urine output is monitored to ensure adequate renal function before potassium is administered to prevent hyperkalemia.  Vital signs, arterial blood gases, and other clinical findings are recorded on a flow sheet. HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME: Potential complication of Diabetes Type 2 Life threatening medical emergency, high mortality rate, as high as 50% Enough insulin is secreted to prevent ketosis, but not enough to prevent hyperglycemia High blood sugar causes an extreme diuresis with severe electrolyte and fluid loss 16  Characterized by: -Plasma osmolarity 340 mOsm/l or greater- normal 280-300 mOsm/l -Blood glucose severely elevated, 600-1200 mg/dL -Altered level of consciousness Precipitating factors:  Infection (most common) pneumonia  Therapeutic agent or surgery  Acute or chronic illness MI, Stroke Pancreatitis, pregnancy Slow onset 1 – 14 days Clinical Manifestations:  Hypotension, profound dehydration (dry mucous membranes, poor skin turgor). - tachycardia and variable neurological signs (e.g alteration of sensorium ,seizures , hemi paresis). Assessment and Diagnostic Findings  Blood glucose, electrolytes, BUN, complete blood count, serum osmolarity, and arterial blood gas analysis  Blood glucose level is usually 600 to 1,200 mg/dl  Serum osmolarity exceeds 350 mOsm/l Medical Management:  Fluid replacement  Correction of electrolyte imbalances  Insulin administration Nursing Management  Monitoring of vital signs  Fluid status and laboratory values 17  Maintain safety and prevent injury related to changes in the patient’s sensorium secondary to HHNS DIABETES MELLITUS (DM) Complications - Long Term Vascular -Accelerated Atherosclerosis with Associated: -Coronary Heart Disease - MI’s -Cerebrovascular Disease-Strokes (CVA’s) -Peripheral Vascular Disease. - Extremity Gangrene. -Hypertension. -Diabetic Retinopathy. -Blindness. -Diabetic Nephropathy. -Renal Failure. -Diabetic Neuropathy -Loss of Nerve Function. Long Term Complications of Diabetes:– Macrovascular complications  coronary artery disease  Cerebrovascular disease  Peripheral vascular disease Microvascular complications  Retinopathy  Nephropathy  Neuropathies  Foot & leg problems Management of the Diabetic Foot:  Control of blood sugar  Control of infection 18  Local treatment of the ulcer  Vascular assessment  Surgery  Care of the patient as a whole  Patient / public education Quit smoking Smoking can worsen heart and vascular problems and reduce circulation to feet. Avoid activities that can injure the feet; walking barefoot using, heating pads or hot water bottles on the feet , and stepping into a bath before testing the temperature. FOOT CARE:  Use care when trimming nails. Trim nails to the shape of toes and file the nails to remove any sharp edges.  Never cut cuticles , open blisters.  Wash feet daily  Use warm water and mild soap to clean feet. Gently pat feet, dry and apply a moisturizing cream or lotion. FOOT CARE:  Check feet daily  Check the entire surface of both feet for skin breaks, blisters, swelling, or redness.  Don't forget to look between and underneath toes where damage can be hidden.  Use a mirror if it is difficult to see all parts of feet or ask a caregiver to help you.  Don’t walk bare feet  Protect feet from hot and cold  Choose socks and shoes carefully  Select cotton socks that fit loosely and change socks every day.  Select shoes that are snug but not tight,  Make good foot care a habit.  Ask for foot exams 19 NURSING DIAGNOSES:  Risk for fluid volume deficit related to polyuria and dehydration.  Imbalanced nutrition related to imbalance of insulin, food, and physical activity.  Deficient knowledge about diabetes self-care skills/information.  Potential self-care deficit related to physical impairments or social factors.  Anxiety related to loss of control, fear of inability to manage diabetes, misinformation related to diabetes, fear of diabetes complications. NURSING PROCESS:  Risk for impaired skin integrity: Proper foot care Daily inspection of feet Checking temperature of any water before washing feet. Need for lubricating cream after drying but not between toes. Patients should be followed by a podiatrist Early reporting of any wounds or blisters Risk for infection Frequent hand washing Early recognition of signs of infection and seeking treatment Meticulous skin care. Regular dental examinations and consistent oral hygiene care. Risk for injury: -Prevention of accidents, falls and burns -Sexual dysfunction 20  Ineffective coping Assisting clients with problem-solving strategies for specific concerns. Providing information about diabetic resources, community education programs, and support groups. Utilizing any client contact as opportunity to review coping status and reinforce proper diabetes management and complication prevention. Evaluation Achieves fluid and electrolyte balance Achieves metabolic balance Demonstrates/verbalizes diabetes survival skills 21