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Diabetes Mellitus - Outline
Generalist Nursing Practice IV: Tertiary Care Across the Lifespan (NURS 4889)
Temple University
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Diabetes Mellitus: - Chronic multisystem disease related to: o abnormal insulin production and/or o impaired insulin utilization - Combination of causative factors o Genetic o Autoimmune o Environmental - Affects 25 million people - 7 th leading cause of death
- Leading cause of o Adult blindness o End-stage kidney disease o Nontraumatic lower limb amputations
- Major contributing factor o Heart disease o Stroke o Hypertension
Type 1 DM: - Formerly known as juvenile-onset or insulin- dependent diabetes - Accounts for 5% of all cases of diabetes - Onset in people younger than 40 years - Incidence increasing - frequently in younger children
- Autoimmune destruction of β-cells
- Total absence of insulin
- Genetic predisposition and viral exposure
- Idiopathic diabetes
- Latent autoimmune diabetes in adults (LADA)
- Onset: o Autoantibodies are present for months to years before symptoms occur o Manifestations develop when pancreas can no longer produce insulin—then rapid onset with ketoacidosis o In type 1 diabetes, the islet cell autoantibodies responsible for β-cell destruction are present for months to years before the onset of symptoms. o Manifestations of type 1 diabetes develop when the person’s pancreas can no longer produce sufficient amounts of insulin to maintain normal glucose levels. o Once this occurs, the onset of symptoms is usually rapid, and patients often present with impending or actual ketoacidosis. o The patient usually has a history of recent and sudden weight loss, as well as the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger). o The individual with type 1 diabetes requires insulin from an outside source (exogenous insulin) to sustain life. Without insulin, the patient will develop diabetic ketoacidosis (DKA), a life- threatening condition resulting in metabolic acidosis. o Patients with newly diagnosed type 1 diabetes may experience a remission, or “honeymoon period,” for 3 to 12 months after treatment is initiated. During this time, the patient requires very little injected insulin because β-cell insulin production remains sufficient for glucose control. Eventually, as more β-cells are destroyed and blood glucose levels increase, the honeymoon period ends, and the patient will require insulin on a permanent basis.
- Clinical Manifestations: o Classic symptoms Polyuria (frequent urination) Polydipsia (excessive thirst) Polyphagia (excessive hunger) o Weight loss o Weakness o Fatigue o Because the onset of type 1 diabetes is rapid, the initial manifestations are usually acute. o The classic symptoms are polyuria, polydipsia, and polyphagia. o The osmotic effect of glucose produces the manifestations of polydipsia and polyuria.
o Polyphagia is a consequence of cellular malnourishment when insulin deficiency prevents utilization of glucose for energy. o Weight loss may occur because the body cannot get glucose and turns to other energy sources, such as fat and protein. o Weakness and fatigue may result because body cells lack needed energy from glucose.
Type 2 DM: - Formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (IDDM) - Most prevalent type (90% to 95%) - Risk factors: overweight, obesity, advancing age, family history - Increasing prevalence in children - Greater prevalence in ethnic groups - Gradual onset
- Hyperglycemia may go many years without being detected
- Many times discovered with routine laboratory testing
- Pancreas continues to produce some endogenous insulin
- Insulin insufficient or poorly utilized
- Obesity is greatest risk factor
- Genetic component increases insulin resistance and obesity
- Metabolic Syndrome o Elevated glucose levels o Abdominal obesity o Elevated blood pressure
o High levels of triglycerides o Decreased levels of HDLs
- Clinical Manifestations: o Nonspecific symptoms Classic symptoms of type 1 may manifest o Fatigue o Recurrent infection
o Recurrent vaginal yeast or candida infection o Prolonged wound healing o Visual changes
Acute Hyperglycemia of Critical Illness: - Intrinsic response to stress, result of increased hepatic insulin resistance and enhanced hepatic glucose production - Extrinsic sources including dextrose-containing fluids, corticosteroids, sympathomimetic drugs, and cardiopulmonary bypass, TPN - Associated with hemodynamic instability & increased risk of infection - Society of Critical Medicine – Moderate Glycemic Control o Initiate insulin infusion for blood glucose level of 150 mg/dL o Titrate an evidence-based insulin infusion protocol to maintain a blood glucose level less than 180 mg/dL with a goal range of 100 to 150 mg/dL Hypoglycemia: - Blood glucose level less than 70 mg/dL o Goal: Moderate glycemic control - Too much insulin in proportion to glucose in the blood - Common manifestations o Shakiness o Palpitations o Nervousness o Diaphoresis
o Anxiety o Hunger o Pallor
- Altered mental functioning o Difficulty speaking o Visual disturbances o Stupor
o Confusion o Coma
- Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death
Hyperosmolar Hyperglycemic Syndrome: (HHS): - Life-threatening syndrome – higher mortality than DKA - Enough circulating insulin to prevent ketoacidosis (pH > 7, HCO3 > 18) - SEVERE Dehydration - osmotic diuresis & extracellular fluid depletion - Fewer symptoms lead to higher BG levels (>600 mg/dL) - Severe neurologic manifestations (lethargy to coma) - ↑ serum osmolality - Ketones absent or minimal in blood and urine - Occurs with type 2 diabetes - Precipitating factors – occurs over several days to weeks o UTIs, pneumonia, sepsis o Acute illness
o Newly diagnosed type 2 diabetes o Impaired thirst sensation and/or inability to replace fluids
- Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion.
- HHS is less common than DKA. It often occurs in patients older than 60 years with type 2 diabetes.
- Common causes of HHS are urinary tract infections, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes.
- HHS is often related to impaired thirst sensation and/or a functional inability to replace fluids.
- There is usually a history of inadequate fluid intake, increasing mental depression, and polyuria.
DKA and HHS: Treatment: - Establish IV access - BMP, serum/urine ketones, ABG or venous pH, osmolality, CBC o Is the pt acidotic? Diagnosis of infection (High WBC), potassium - Begin fluid resuscitation (FIRST THING TO DO) o 0% NaCl - 1 to 1 L in the first hour o 0% or 0% at 250 – 500 ml/hr (subsequent hours) o Change to 5% Dextrose with 0% NaCl at 150 – 250 ml/hr when: DKA – BG 200 – 250 mg/dL, HHS – BG 300 mg/dL Prevents hypoglycemia & cerebral edema While on insulin drip, until gap closes and normalizes Q4H BMP - Bicarbonate for pH < 6 until pH 7 (DKA) - DKA is a serious condition that proceeds rapidly and must be treated promptly. - Ensure an patent airway and administer oxygen via nasal cannula or non-rebreather mask. - Because fluid imbalance is potentially life-threatening, the initial goal of therapy is to establish IV access and begin fluid and electrolyte replacement. o Typically, the initial fluid therapy regimen consists of an infusion of 0% or 0% NaCl at a rate to restore urine output to 30 to 60 mL/hr and to raise blood pressure. o When blood glucose levels approach 250 mg/dL (13 mmol/L), 5% to 10% dextrose is added to the fluid regimen to prevent hypoglycemia, as well as a sudden drop in glucose that can be associated with cerebral edema. o Overzealous rehydration, especially with hypotonic IV solutions, can result in cerebral edema. o Monitor patients with renal or cardiac compromise for fluid overload. - Measure serum potassium level before starting insulin. If the patient is hypokalemic, insulin administration will further decrease the potassium levels, making early potassium replacement is essential. Although initial serum potassium value may be normal or high, levels can decrease rapidly once therapy starts, as insulin drives potassium into the cells, leading to life-threatening hypokalemia.
- IV insulin administration is therapy directed toward correcting hyperglycemia and hyperketonemia. o Insulin is immediately started at 0 U/kg/hr by a continuous infusion. o It is important to prevent rapid drops in serum glucose to avoid cerebral edema. A blood glucose reduction of 36 to 54 mg/dL (2 to 3 mmol/L) per hour will avoid complications. o Insulin allows water and potassium to enter the cell along with glucose and can lead to a depletion of vascular volume and hypokalemia; therefore, monitor the patient’s fluid balance and potassium levels.
- REGULAR INSULIN only for IV!!! Bolus or Drip
- Potassium (K+) replacement as needed o K+ < 3 mEq/L – hold insulin and give KCL IVPB 20 - 30 mEq/L/hr until > 3. o K+ 20 – 30 mEq in each liter of IV fluid to keep K+ 4 – 5 mEq/L
- Serum K+ levels may decrease rapidly as K+ moves into the cells once insulin becomes available o High K+, PVCs, more frequent -> possible vtach
- Hourly bedside BG
- BMP, venous pH every 2 – 4 hours until stable
Nursing Management: - Assess o Level of consciousness – Cerebral Edema o Renal status o Cardiopulmonary status – Pulmonary Edema
- Signs/Symptoms of Hypoglycemia
- Cardiac monitoring – K+
- Patient education – Discharge planning o Diet o Home BG monitoring o Medications
- Closely monitor blood glucose and urine for output and ketones, as well laboratory data to determine appropriate patient care.
- Monitor the administration of (1) IV fluids to correct dehydration, (2) insulin therapy to reduce blood glucose and serum acetone levels, and (3) electrolytes given to correct electrolyte imbalance.
- Assess renal status and the cardiopulmonary status related to hydration and electrolyte levels.
- Monitor the level of consciousness.
- Assess for signs of potassium imbalance resulting from hypoinsulinemia and osmotic diuresis.
- When treatment with insulin begins, serum potassium levels may decrease rapidly as potassium moves into the cells once insulin becomes available. This movement of potassium into and out of extracellular fluid influences cardiac functioning.
- Cardiac monitoring is a useful aid in detecting hyperkalemia and hypokalemia because characteristic changes indicating potassium excess or deficit are observable on electrocardiographic tracings.
- Assess vital signs often to determine the presence of fever, hypovolemic shock, tachycardia, and Kussmaul respirations.
Insulin Regimens: - Basal-bolus regimen o Most closely mimics endogenous insulin production o Rapid- or short-acting (bolus) insulin before meals o Intermediate- or long-acting (basal) background insulin once or twice a day - Less intense regimens can also be used - The insulin regimen that most closely mimics endogenous insulin production is the basal-bolus regimen: o Rapid- or short-acting (bolus) insulin before meals and intermediate- or long-acting (basal) background insulin once or twice a day o Intensive insulin therapy, consisting of multiple daily insulin injections together with frequent self-monitoring of blood glucose o Goal: to achieve a near-normal glucose level of 70 to 130 mg/dL before meals - Other, less intense regimens can also achieve good glucose control for some people. Ideally, the patient and the health care provider should mutually select regimens.
(Basal) Background Insulin: - Used to control glucose levels between meals & overnight - Long-acting (basal) o Insulin glargine (Lantus) and detemir (Levemir) o Released steadily and continuously with no peak action o Administered once or twice a day o Do not mix with any other insulin or solution - Intermediate-acting insulin o NPH o Duration 12 to 18 hours - Peak 4 to 12 hours o Cloudy; must agitate to mix o Can mix with short- and rapid-acting insulins o ”Clear to Cloudy” - In addition to mealtime insulin, people with type 1 diabetes must also use a long-acting basal or intermediate-acting (background) insulin to control blood glucose levels in between meals and overnight. o Without 24-hour background insulin, people with type 1 diabetes are more prone to developing diabetic ketoacidosis. o Many people with type 2 diabetes who use mealtime insulin injections or oral medications also require basal insulin to adequately control blood glucose levels. - Insulin glargine (Lantus) and detemir (Levemir) are long-acting insulins that are released steadily and continuously and, for most people, do not have a peak of action. - Although they are typically used for once-daily subcutaneous administration, detemir can be given twice daily. Because they lack peak action time, the risk for hypoglycemia from this type of insulin is greatly reduced. - Do not mix or dilute glargine or detemir with any other insulin or solution in the same syringe.
Subcutaneous Injection Sites: - Absorption is fastest from abdomen, followed by arm, thigh, and buttock - Abdomen is preferred site - Do not inject in site to be exercised - Rotate injections within one particular site
Insulin Pump: - Continuous subcutaneous infusion - Battery-operated device - Connected to a catheter inserted into subcutaneous tissue in abdominal wall - Program basal and bolus doses that can vary throughout the day - Potential for tight glucose control - Continuous subcutaneous insulin infusion can be administered with an insulin pump, a small battery- operated device that resembles a standard paging device in size and appearance. - Most insulin pumps are worn on the belt or under clothing and loaded with rapid-acting insulin, which is connected via plastic tubing to a catheter inserted into the subcutaneous tissue in the abdominal wall. - All insulin pumps are programmed to deliver a continuous infusion of rapid-acting insulin 24 hours a day, known as the “basal rate.” Basal insulin can be temporarily increased or decreased on the basis of
carbohydrate intake, activity changes, or illness. Some individuals require different basal rates at different times of the day.
- At mealtime, the user programs the pump to deliver a bolus infusion of insulin appropriate to the amount of carbohydrate ingested and an additional amount, if needed to bring down high premeal blood glucose levels.
- Insulin pump users must check their blood glucose level at least four times per day. Testing eight times or more per day is common.
- A major advantage of the insulin pump is the potential for tight glucose control. This is possible because insulin delivery becomes very similar to the normal physiologic pattern.
Diabetes Mellitus - Outline
Course: Generalist Nursing Practice IV: Tertiary Care Across the Lifespan (NURS 4889)
University: Temple University
- Discover more from:Generalist Nursing Practice IV: Tertiary Care Across the LifespanNURS 4889Temple University30 Documents
- More from:Generalist Nursing Practice IV: Tertiary Care Across the LifespanNURS 4889Temple University30 Documents