Medical Surgical Nursing 2 (Theory) (NUR 302) Management of Patients with Diabetes Mellitus

Diabetes Mellitus A metabolic disorder in which the body cannot metabolize glucose. Usually due to the lack of insulin or inadequate insulin production. o o Diabetes mellitus is a group of metabolic diseases characterized by increased levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both (American Diabetes Association [ADA], 2009). Normally, a certain amount of glucose circulates in the blood. The major sources of this glucose are absorption of ingested food in the gastrointestinal tract and formation of glucose by the liver from food substances. Insulin Glucose Major source of energy for the body All cells need it to function As important to the brain as oxygen Allows glucose to pass from the blood stream into cell. Produced in the pancreas Production stimulated by increased blood sugar

Normal blood sugar = 80120mg/dl Hypoglycemia (insulin shock) Low blood sugar (<70mg/dl) Hyperglycemia [diabetic ketoacidosis (DKA)] High blood sugar (>200mg/dl)

Precipitating factors
1. Heredity 2. Obesity 3. Pregnancy 4. Viral infections Classification The major classifications of diabetes are : Type 1 diabetes Type 2 diabetes Gestational Diabetes Diabetes mellitus associated with other conditions or syndromes. Prediabetes is classified as impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) and refers to a condition in which blood glucose concentrations fall between normal levels and those considered diagnostic for diabetes. Pathophysiology During fasting periods (between meals and overnight), 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 stimulates 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). After 8 to 12 hours without food, the liver forms glucose from the breakdown of noncarbohydrate substances, including amino acids (gluconeogenesis). Long term effects on the body 1 Blindness 2. Heart disease 3. Kidney failure 4. Nerve disorders 5. Circulatory disorders Type I (Insulin dependent IDDM) 1. No insulin produced 2. Can significantly shorten life span if not managed 3. Effects on the body are usually more severe than with type II 4. Treated with daily insulin shots Type 1 diabetes affects approximately 5% to 10% of people

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with the disease; it is characterized by an acute onset, usually before 30 years of age (CDC, 2008). Type 1 diabetes is characterized by destruction of the pancreatic beta cells. Combined genetic, immunologic, and possibly environmental (eg, viral) factors are thought to contribute to beta cell destruction. the destruction of the beta cells results in decreased insulin production, unchecked glucose production by the liver, and fasting hyperglycemia. glucose derived from food cannot be stored in the liver but instead remains in the bloodstream and contributes to postprandial (after meals) hyperglycemia. If the concentration of glucose in the blood exceeds the renal threshold for glucose, usually 180 to 200 mg/dL (9.9 to 11.1 mmol/L), the kidneys may not reabsorb all of the filtered glucose; the glucose then appears in the urine (glycosuria). When excess glucose is excreted in the urine, it is accompanied by excessive loss of fluids and electrolytes. This is called osmotic diuresis. Because insulin normally inhibits glycogenolysis (breakdown of stored glucose) and gluconeogenes is (production of new glucose from amino acids and other substrates), these processes occur in an unrestrained fashion in people with insulin deficiency and contribute further to hyperglycemia. In addition, fat breakdown occurs, resulting in an increased production of ketone bodies, which are the byproducts of fat breakdown.

Type II (Non-insulin dependent NIDDM) Usually appears later in life 2. Patient produces inadequate insulin or insulin doesnt function correctly 3. Treated with diet/exercise and/or oral medications 4. Can progress to type I diabetes Type 2 diabetes affects approximately 90% to 95% of people with the disease (CDC, 2008). It occurs more commonly among people who are older than 30 years of age and obese. The two main problems related to insulin in type 2 diabetes are : 1- insulin resistance. 2- impaired insulin secretion. Insulin resistance refers to a decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism. In type 2 diabetes, these intracellular reactions are diminished, making insulin less effective at stimulating glucose uptake by the tissues and at regulating glucose release by the liver. To overcome insulin resistance and to prevent the buildup of glucose in the blood, increased amounts of insulin must be secreted to maintain the glucose level at a normal or slightly elevated level. This is called metabolic syndrome, which includes hypertension, hypercholesterolemia, and abdominal obesity. However, if the beta cells cannot keep up with the increased demand for insulin, the glucose level rises and type 2 diabetes develops. Despite the impaired insulin secretion that is characteristic of type 2 diabetes, there is enough insulin present to prevent the breakdown of fat and the accompanying production of ketone bodies. Therefore, DKA does not typically occur in type 2 diabetes. uncontrolled type 2 diabetes may lead to another acute problem hyperglycemic hyperosmolar nonketotic syndrome (see later discussion). Because type 2 diabetes is associated with a slow, progressive glucose intolerance, its onset may go undetected for many years. If the patient experiences symptoms, they are frequently mild and may include fatigue, irritability, polyuria, polydipsia, poorly healing skin wounds, vaginal infections, or blurred vision (if glucose levels are very high). For most patients (approximately 75%), type 2 diabetes is detected incidentally (eg, when routine laboratory tests or ophthalmoscopic examinations are performed). One consequence of undetected diabetes is that long-term diabetes complications (eg, eye disease, peripheral neuropathy, peripheral vascular disease).

Gestational Diabetes
Gestational diabetes mellitus (GDM) is any degree of glucose intolerance with its onset during pregnancy. Hyperglycemia develops during pregnancy because of the secretion of placental hormones, which causes insulin resistance. Gestational diabetes occurs in as many as 14% of pregnant women and increases their risk for hypertensive disorders during pregnancy.

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Women who are considered to be at high risk for GDM and who should be screened by blood glucose testing at their first prenatal visit are those with marked obesity, a personal history of GDM, glycosuria, or a strong family history of diabetes. Goals for blood glucose levels during pregnancy are 105 mg/dL (5.8 mmol/L) or less before meals and 130 mg/dL (7.2 mmol/L) or less 2 hours after meals (ADA, 2009a).

Clinical manifestations of DM
depend on the patients level of hyperglycemia. Classic clinical manifestations of all types of diabetes include the three Ps: polyuria, polydipsia, and polyphagia . Polyuria (increased urination) and polydipsia (increased thirst) occur as a result of the excess loss of fluid associated with osmotic diuresis. Patients also experience polyphagia (increased appetite) that results from the catabolic state induced by insulin deficiency and the breakdown of proteins and fats. Other symptoms include fatigue and weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent infections. The onset of type 1 diabetes may also be associated with sudden weight loss or nausea, vomiting, or abdominal pains, if DKA has developed.

Assessment and Diagnostic Findings

An abnormally high blood glucose level is the basic criterion for the diagnosis of diabetes. Fasting plasma glucose (FPG), random plasma glucose, and glucose level 2 hours after receiving glucose (2-hour postload) may be used.

Medical Management
The main goal of diabetes treatment is to : normalize insulin activity and blood glucose levels to reduce the development of vascular and neuropathic complications. intensive glucose control dramatically reduced the development and progression of complications such as retinopathy, nephropathy, and neuropathy. Intensive treatment is defined as three or four insulin injections per day or continuous subcutaneous insulin infusion, insulin pump therapy plus frequent blood glucose monitoring and weekly contacts with diabetes educators. Diabetes management has five components: 1- nutritional therapy 2- exercise 3- Monitoring 4- pharmacologic therapy 5- education

One of the main goals of diet therapy in diabetes is to avoid sharp, rapid increases in blood glucose levels after food is eaten. The term glycemic index is used to describe how much a given food increases the blood glucose level compared with an equivalent amount of glucose. Dietary recommendations: Combining starchy foods with protein-containing and fat-containing foods tends to slow their absorption and lower the glycemic response. In general, eating foods that are raw and whole results in a lower glycemic response than eating chopped, pured, or cooked foods. Eating whole fruit instead of drinking juice decreases the glycemic response, because fiber in the fruit slows absorption. Adding foods with sugars to the diet may result in a lower glycemic response if these foods are eaten with foods that are m ore slowly absorbed.

Glycemic Index

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Patients can create their own glycemic index by monitoring their blood glucose level after ingestion of a particular food. This can help improve blood glucose control through individualized manipulation of the diet. Many patients who use frequent monitoring of blood glucose levels can use this information to adjust their insulin doses in accordance with variations in food intake.

Testing for Glycated Hemoglobin

Glycated hemoglobin (also referred to as glycosylated hemoglobin, HgbA1C, or A1C) is a blood test that reflects average blood glucose levels over a period of approximately 2 to 3 months (ADA, 2009b). When blood glucose levels are elevated, glucose molecules attach to hemoglobin in red blood cells. The longer the amount of glucose in the blood remains above normal, the more glucose binds to hemoglobin and the higher the glycated hemoglobin level becomes. This complex (hemoglobin attached to the glucose) is permanent and lasts for the life of an individual red blood cell, approximately 120 days. Glycated hemoglobin (also referred to as glycosylated hemoglobin, HgbA1C, or A1C) is a blood test that reflects average blood glucose levels over a period of approximately 2 to 3 months (ADA, 2009b). When blood glucose levels are elevated, glucose molecules attach to hemoglobin in red blood cells. The longer the amount of glucose in the blood remains above normal, the more glucose binds to hemoglobin and the higher the glycated hemoglobin level becomes. This complex (hemoglobin attached to the glucose) is permanent and lasts for the life of an individual red blood cell, approximately 120 days. If near-normal blood glucose levels are maintained, with only occasional increases, the overall value will not be greatly elevated. However, if the blood glucose values are consistently high, then the test result is also elevated. If the patient reports mostly normal SMBG results but the glycated hemoglobin is high, there may be errors in the methods used for glucose monitoring, errors in recording results, or frequent elevations in glucose levels at times during the day when the patient is not usually monitoring blood sugar levels. Normal values typically range from 4% to 6% and indicate consistently near-normal blood glucose concentrations. The target range for people with diabetes is less than 7% (ADA, 2009b). Pharmacologic Therapy Insulin Therapy In type 1 diabetes, exogenous insulin must be administered for life because the body loses the ability to produce insulin. In type 2 diabetes, insulin may be necessary on a long-term basis to control glucose levels if meal planning and oral agents are ineffective.

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Oral Antidiabetic Agents Oral antidiabetic agents may be effective for patients who have type 2 diabetes that cannot be treated effectively with MNT and exercise alone. Oral antidiabetic agents include first-generation and second generation sulfonylureas, biguanides, alpha-glucosidase inhibitors, non-sulfonylurea insulin secretogogues (meglitinides and phenylalanine derivatives) thiazolidinediones (glitazones), and dipeptide-peptidase-4 (DPP-4) inhibitors Sulfonylureas and meglitinides are considered insulin secretagogues because their action increases the secretion of insulin by the pancreatic beta cells. ACUTE COMPLICATIONS OF DIABETES There are three major acute complications of diabetes related to short-term imbalances in blood glucose levels: 1- hypoglycemia. 2- DKA. 3- hyperglycemic hyperosmolar nonketotic syndrome.

Hypoglycemia (Insulin Reactions) Hypoglycemia occurs when the blood glucose falls to less than 50 to 60 mg/dL (2.7 to 3.3 mmol/L), because of too much insulin or oral hypoglycemic agents, too little food, or excessive physical activity. Hypoglycemia may occur at any time of the day or night. It often occurs before meals, especially if meals are delayed or snacks are omitted. Clinical Manifestations Sweating, tremor, tachycardia, palpitation, nervousness, and hunger. In moderate hypoglycemia, the drop in blood glucose level deprives the brain cells of needed fuel for functioning. Signs of impaired function of the CNS may include 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. In severe hypoglycemia, Symptoms may include disoriented behavior, seizures, difficulty arousing from sleep, or loss of consciousness.

Management
Treating with Carbohydrates - Immediate treatment must be given when hypoglycemia occurs. Initiating Emergency Measures In emergency situations, for adults who are unconscious and cannot swallow, an injection of glucagon 1 mg can be administered either subcutaneously or intramuscularly. In hospitals and emergency departments, for patients who are unconscious or cannot swallow, 25 to 50 mL of 50% dextrose in water (D50W) may be administered IV. Providing Patient Education

Diabetic Ketoacidosis
DKA is caused by an absence or markedly inadequate amount of insulin. This deficit in available insulin results in disorders in the metabolism of carbohydrate, protein, and fat. The three main clinical features of DKA are : Hyperglycemia Dehydration and electrolyte loss Acidosis

Clinical Manifestations
The hyperglycemia of DKA leads to polyuria and polydipsia (increased thirst). blurred vision, weakness, and headache. Orthostatic hypotension (drop in systolic blood pressure of 20 mm Hg or more on changing from a reclining to a standing position). Volume depletion may also lead to frank hypotension with a weak, rapid pulse. The ketosis and acidosis of DKA lead to gastrointestinal symptoms such as anorexia, nausea, vomiting, and abdominal pain.

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The abdominal pain and physical findings on examination can be so severe that they resemble an acute abdominal disorder that requires surgery. The patient may have acetone breath (a fruity odor), which occurs with elevated ketone levels. hyperventilation (with very deep, but not labored, respirations) may occur. Kussmaul respirations represent the bodys attempt to decrease the acidosis, counteracting the effect of the ketone buildup. mental status in DKA varies widely. The patient may be alert, lethargic, or comatose.

Assessment and Diagnostic Findings

Blood glucose levels may vary between 300 and 800 mg/dL (16.6 to 44.4 mmol/L). Some patients have lower glucose values, and others have values of 1000 mg/dL (55.5 mmol/L) or higher (usually depending on the degree of dehydration). The severity of DKA is not necessarily related to the blood glucose level. 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 partial pressure of carbon dioxide (PCO2; 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 concentrations may be low, normal, or high, depending on the amount of water loss (dehydration). Despite the plasma concentration, there has been a marked total body depletion of these (and other) electrolytes and they will need to be replaced. Increased levels of creatinine, blood urea nitrogen (BUN), and hematocrit may also be seen with dehydration. After rehydration, continued elevation in the serum creatinine and BUN levels suggests underlying renal insufficiency.

Prevention
Drinking fluids every hour is important to prevent dehydration. Blood glucose and urine ketones must be assessed every 3 to 4 hours. If the patient cannot take fluids without vomiting, or if elevated glucose or ketone levels persist, the physician must be contacted. Patients are taught to have foods available for use on sick days. In addition, a supply of urine test strips (for ketone testing) and blood glucose test strips should be available. The patient must know how to contact his or her physician 24 hours a day. After the acute phase of DKA has resolved, the nurse should assess for underlying causes of DKA. If there are psychological reasons for the patients deliberately missing insulin doses, the patient and family may be referr ed for evaluation and counseling or therapy.

Management Rehydration In dehydrated patients, rehydration is important for maintaining tissue perfusion. In addition, fluid replacement enhances the excretion of excessive glucose by the kidneys. The patient may need as much as 6 to 10 L of IV fluid to replace fluid losses caused by polyuria, hyperventilation, diarrhea, and vomiting. Restoring Electrolytes The major electrolyte of concern during treatment of DKA is potassium. Reversing Acidosis Ketone bodies (acids) accumulate as a result of fat breakdown. The acidosis that occurs in DKA is reversed with insulin, which inhibits fat breakdown, thereby stopping acid buildup. Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) is a serious condition in which hyperosmolarity and hyperglycemia predominate, with alterations of the sensorium (sense of awareness). At the same time, ketosis is usually minimal or absent. The basic biochemical defect is lack of effective insulin (ie, insulin resistance). Persistent hyperglycemia causes osmotic diuresis, which results in losses of water and electrolytes. To maintain osmotic equilibrium, water shifts from the intracellular fluid space to the extracellular fluid space. With glycosuria and dehydration, hypernatremia and increased osmolarity occur.

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Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) What distinguishes HHNS from DKA is that ketosis and acidosis generally do not occur in HHNS, partly because of differences in insulin levels. In DKA, no insulin is present, and this promotes the breakdown of stored glucose, protein, and fat, which leads to the production of ketone bodies and ketoacidosis. Clinical Manifestations The clinical picture of HHNS is one of hypotension, profound dehydration (dry mucous membranes, poor skin turgor), tachycardia, and variable neurologic signs (eg, alteration of sensorium, seizures, hemiparesis). Assessment and Diagnostic Findings Diagnostic assessment includes a range of laboratory tests, including blood glucose, electrolytes, BUN, complete blood count, serum osmolality, and arterial blood gas analysis. The blood glucose level is usually 600 to 1200 mg/dL, and the osmolality exceeds 350 mOsm/kg. Electrolyte and BUN levels are consistent with the clinical picture of severe dehydration. Mental status changes, focal neurologic deficits, and hallucinations are common secondary to the cerebral dehydration that results from extreme hyperosmolality. Postural hypotension accompanies the dehydration. Management fluid replacement, correction of electrolyte imbalances, and insulin administration. Because patients with HHNS are typically older, close monitoring of volume and electrolyte status is important for prevention of fluid overload, heart failure, and cardiac dysrhythmias. Fluid treatment is started with 0.9% or 0.45% NS, depending on the patients sodium level and the severity of volume depletio n. Central venous or hemodynamic pressure monitoring guides fluid replacement. Potassium is added to IV fluids when urinary output is adequate and is guided by continuous ECG monitoring and frequent laboratory determinations of potassium. Extremely elevated blood glucose concentrations decrease as the patient is rehydrated. Insulin plays a less important role in the treatment of HHNS because it is not needed for reversal of acidosis, as in DKA. Nevertheless, insulin is usually administered at a continuous low rate to treat hyperglycemia, and replacement IV fluids with dextrose are administered (as in DKA) after the glucose level has decreased to the range of 250 to 300 mg/dL ( 13.8 to 16.6 mmol/L) . Other therapeutic modalities are determined by the underlying illness and the results of continuing clinical and laboratory evaluation. It may take 3 to 5 days for neurologic symptoms to clear, and treatment of HHNS usually continues well after metabolic abnormalities have resolved. After recovery from HHNS, many patients can control their diabetes with MNT alone or with MNT and oral antidiabetic medications. Insulin may not be needed once the acute hyperglycemic complication is resolved. Frequent SBGM is important in prevention of recurrence of HHNS.

THE PATIENT WITH DIABETIC KETOACIDOSIS OR HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME

Assessment
nurse monitors the ECG for dysrhythmias indicating abnormal potassium levels. Vital signs (especially blood pressure and pulse), arterial blood gases, breath sounds, and mental status are assessed every hour and recorded on a flow sheet. Neurologic status checks are included as part of the hourly assessment as cerebral edema can be a severe and sometimes fatal outcome. For the patient with HHNS, the nurse assesses vital signs, fluid status, and laboratory values. Fluid status and urine output are closely monitored because of the high risk of renal failure secondary to severe dehydration. Because HHNS tends to occur in older patients, the physiologic changes that occur with aging should be considered. Careful assessment of cardiovascular, pulmonary, and renal function throughout the acute and recovery phases of HHNS is important.

Nursing Diagnoses
Based on the assessment data, major nursing diagnoses may include the following: Risk for fluid volume deficit related to polyuria and dehydration Fluid and electrolyte imbalance related to fluid loss or shifts Deficient knowledge about diabetes self-care skills or information Anxiety related to loss of control, fear of inability to manage diabetes, misinformation related to diabetes, fear of diabetes complications.

Planning and Goals

The major goals for the patient may include maintenance of fluid and electrolyte balance, optimal control of blood glucose levels, ability to perform diabetes survival skills and self-care activities, and absence of complications.

Nursing Interventions
Maintaining Fluid and Electrolyte Balance Increasing Knowledge About Diabetes Management Monitoring and Managing Potential Complications Teaching Patients Self-Care

Evaluation
1. Achieves fluid and electrolyte balance a. Demonstrates intake and output balance

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b. Exhibits electrolyte values within normal limits c. Exhibits vital signs that remain stable, with resolution of orthostatic hypotension and tachycardia 2. Demonstrates knowledge about DKA and HHNS a. Identifies factors leading to DKA and HHNS b. Describes signs and symptoms of DKA and HHNS c. Describes short-term and long-term consequences of DKA and HHNS d. Identifies strategies to prevent the development of DKA and HHNS e. States when contact with health care provider In needed to treat early signs of DKS and HHNS 3. Absence of complications a. Exhibits normal cardiac rate and rhythm and normal breath sounds b. Exhibits no jugular venous distention c. Exhibits blood glucose and urine ketone levels within target range d. Exhibits no manifestations of hypoglycemia or hyperglycemia e. Shows improved mental status without signs of cerebral edema

Diabetic Medical Emergencies

DKA (Diabetic ketoacidosis) 1. Decreased insulin which results in increased blood sugar 2. Slow in onset 3. Mimics dehydration

Pathophysiology of Hyperglycemia (DKA)

Decreased insulin and/or increased blood sugar

Increased sugar in the urine

Starving cells

Water is pulled into urine

Fat and protein breakdown

Increased urine output

Production of ketones and other acids/byproducts Irritability

Dehydration

Diabetic coma

Death
Common causes a. Infection raises metabolism

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b. c. d. e.

Stress raises metabolism Exercise/diet changes Pregnancy Some drugs (prescription or street)

Pertinent questions (may have to ask family members)

a. Do you take insulin or control your diabetes with diet/oral meds? b. Have you taken your insulin/oral meds today? c. Have your meds been changed lately? d. When did you last eat, and how much? e. Have you been unusually stressed? (heat, cold, sickness, physical or emotional stress) f. When did you last take your blood sugar reading and what was it? Signs/symptoms a. Altered LOC b. Skin warm/dry c. Tachycardia d. Kussmaul respirations Rapid/deep respirations in an attempt to blow e. Blood pressure normal or low (dehydration) f. Smell of acetone on the breath (fruity odor) acids g. ABD pain h. Polydipsia Thirsty i. Polyphagia Hungry j. Polyuria Increased urine output

off acids (CO2)

Treatment
a. ABCs, High flow O2 b. Position as per blood pressure c. Rapid transport d. ALS support e. If unsure treat as hypoglycemia

Hypoglycemia (Insulin shock)

Increased insulin which leads to low blood sugar Rapid onset Mimics shock True medical emergency Can be seen in non-diabetic patients

Pathophysiology of Hypoglycemia

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Increased insulin

Decreased blood sugar

Starved brain (brain damage)

Sugar stores used up

Irritability

Seizures/Coma/Death
Common causes
a. b. c. d. e. f. g. h. i. Too much insulin Normal insulin/not enough food Starvation Alcohol Hypothermia Exercise Tumors of the pancreas Liver problems ASA overdose Pertinent questions (same as for DKA) Do you take insulin or control your diabetes with diet/oral meds? Have you taken your insulin/oral meds today? Have your meds been changed lately? When did you last eat, and how much? Have you been unusually stressed? (heat, cold, sickness, physical or emotional stress) When did you last take your blood sugar reading and what was it? Signs/symptoms Altered LOC (combatitive) Skin pale/cool/diaphoretic Tachycardia Rapid/shallow respirations Blood pressure usually normal Seizures Stroke like symptoms Rapid onset

a. b. c. d. e. f.

a. b. c. d. e. f. g. h.

Treatment
a. b. c. d. e. f. ABCs, High flow O2 Oral glucose between cheek and gum DO NOT place anything into mouth of patient if they cant protect their own airway Position of comfort Rapid transport ALS support

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Major Differences in presentation

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