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Interventions for Clients with Diabetes Mellitus. Diabetes mellitus. Diabetes mellitus is a common chronic disease requiring lifelong behavioral and lifestyle changes Diabetes is a major public health problem worldwide. The complications of the disease cause many devastating health problems.

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diabetes mellitus
Diabetes mellitus
  • Diabetes mellitus is a common chronic disease requiring lifelong behavioral and lifestyle changes
  • Diabetes is a major public health problem worldwide. The complications of the disease cause many devastating health problems.
  • In the United States, diabetes is the leading cause of new cases of blindness, end-stage renal disease requiring dialysis or transplantation, and lower limb amputations.
  • A large percentage of the U.S. population with diabetes is undiagnosed, and many of those who are diagnosed have unacceptably high blood glucose levels.
classification
Classification
  • For all types of diabetes mellitus, the main feature is chronic hyperglycemia (high blood glucose level) resulting from problems with insulin secretion, insulin action, or both
  • The disease is classified by age of onset, the underlying problem causing a lack of insulin, and the severity of the deficiency
pathophysiology
Pathophysiology
  • The endocrine portion of the pancreas consists of about 1 million small glands, the islets of Langerhans, scattered throughout the gland
  • Four types of islet cells have been identified:
    • alpha – glucagon (is a major "counterregulatory“ hormone that has actions opposite those of insulin and releases glucose from cell storage sites whenever blood glucose levels are low)
    • beta – insulin (plays a key role in allowing body cells to store and use carbohydrate, fat, and protein)
    • D - somatostatin
    • F - pancreatic polypeptide
pathophysiology1
Pathophysiology
  • The liver is the first major organ to be reached by insulin in the blood. In the liver, insulin promotes tissue-building metabolism (anabolism) by causing both the production and storage of glycogen (glycogenesis) at the same time that it inhibits glycogen breakdown into glucose (glycogenolysis)
  • Insulin increases protein and lipid (fat) synthesis and verylow-density lipoprotein (VLDL) formation
pathophysiology2
Pathophysiology
  • Insulin inhibits tissue-degrading metabolism (catabolism) by inhibiting liver glycogenolysis, ketogenesis (conversion of fats to acids), and gluconeogenesis (conversion of proteins to glucose).
  • In muscle, insulin promotes protein and glycogen synthesis. In fat cells, insulin promotes the storage of triglycerides
  • Overall, insulin keeps blood glucose levels from becoming too high and also helps maintain blood lipid levels in the normal range
pathophysiology3
Pathophysiology
  • The pancreas secretes about 40 to 50 units of insulin per day
  • Insulin is secreted directly into liver circulation in a biphasic (two-step) manner. Insulin is secreted at low levels during the fasting state (basal insulin secretion) and at increased levels after eating (prandial)
  • There is an early burst of insulin secretion within 10 minutes of eating, followed by a progressively increasing phase of insulin release that lasts as long as hyperglycemia is present
pathophysiology4
Pathophysiology
  • Without insulin, glucose builds up in the blood, causing hyperglycemia (high blood glucose levels). Hyperglycemia causes fluid and electrolyte imbalances, leading to the classic symptoms of diabetes: polyuria, polydipsia, and polyphagia
  • Polyuria (frequent and excessive urination) results from an osmotic diuresis caused by excess glucose in the urine. As a result of diuresis, sodium, chloride, and potassium are excreted in the urine in large amounts, accompanied by severe water loss.
  • The resulting dehydration stimulates the thirst mechanism, and polydipsia (excessive thirst) occurs.
  • Because the cells are not receiving any food (glucose), the sense of cell starvation results in polyphagia (excessive eating)
pathophysiology5
Pathophysiology
  • With insulin deficiency, fats break down (lipolysis), releasing free fatty acids.
  • Conversion of free fatty acids to ketone bodies (small acids) provides a backup energy source. Because ketone bodies, or "ketones," are incomplete and abnormaldegradation products of free fatty acids, they are not further metabolized and may accumulate in the blood when insulin is not available. This accumulation causes metabolic acidosis
pathophysiology6
Pathophysiology
  • Because of the dehydration associated with diabetes mellitus, hemoconcentration (increased blood concentration) and hypovolemia (decreased blood volume) develop, leading to hyperviscosity (thick, concentrated blood) and hypoperfusion (decreased circulation) of tissues and poor tissue oxygenation (hypoxia).
  • Hypoxic cells are unable to metabolize glucose efficiently, the Kreb\'s cycle is blocked, and lactic acid accumulates, causing more acidosis
pathophysiology7
Pathophysiology
  • Increased concentrations of the hydrogen ion (H+) and carbon dioxide (CO2) in the blood and other extracellular fluids stimulates the respiratory control areas of the brain to increase the rate and depth of respiration in an attempt to excrete more carbon dioxide and acid (Kussmaul respiration)
  • Acetone is exhaled, giving the breath a "fruity" odor
  • When the lungs can no longer offset acidosis, the pH drops. Arterial blood gas studies show a primary metabolic acidosis (decreased pH accompanied by decreased arterial bicarbonate [HCO3] levels) and compensatory respiratory alkalosis (decreased partial pressure of arterial carbon dioxide [Paco2])
pathophysiology8
Pathophysiology
  • Three emergencies related to abnormal blood glucose levels can occur in clients who have diabetes:
    • diabetic ketoacidosis (DKA) caused by lack of insulin and ketosis;
    • hyperglycemic hyperosmolar nonketotic syndrome (HHNS) associated with insulin deficiency, profound dehydration, and the absence of ketosis;
    • hypoglycemia occurring when too much insulin or too little glucose is present.
  • All three conditions require emergency treatment and can result in death if inappropriately treated or not treated at all
chronic complications of diabetes
Chronic complications of diabetes
  • Diabetes mellitus is a major risk factor for morbidity andmortality because of changes in the larger or generalized bodyblood vessels (macrovascular), as well aschanges in smallblood vessels (microvascular)
chronic complications of diabetes1
Chronic complications of diabetes
  • Macrovascular complications:
    • cardiovascular disease (coronary artery disease – acute myocardial infarction)
    • cerebrovascular disease (infarction and stroke)
  • Microvascular complications:
    • eye and vision complications (Nonproliferative diabetic retinopathy (NPDR); Microaneurysms; Venous beading; Proliferative diabetic retinopathy (PDR))
    • diabetic neuropathy:
      • diffuse (distal symmetric polyneuropathy; autonomic neuropathy)
      • focal (focal ischemia; entrapment neuropathies)
chronic complications of diabetes2
Chronic complications of diabetes
  • diabetic nephropathy (microalbuminuria (presence of very small amounts of albumin in the urine)
  • male erectile dysfunction (ED)
assessment
Assessment
  • History
    • risk factors
    • age
    • women are asked how large theirchildrenwere at birth (9 pounds or more – maybe they have glucose intolerance during the pregnancy)
  • assessing weight and weight change (obesity or weight loss)
  • fatigue,polyuria, and polydipsia
  • majoror minor infections
  • all clients are asked if theyhave noticed whether small skin injuries become infectedmore easily or seem to take a longer time to heal
  • family history
assessment1
Assessment
  • Laboratory assessment
    • blood tests
      • fasting blood glucose test
      • oral glucose tolerance test
      • glycosylated hemoglobin assays
      • glycosylated serum proteins and albumin
    • urine tests
      • urine testing for ketone bodies
      • tests for renal function
      • urine testing for glucose
insulin administration3
Insulin administration
  • Rapid-, short-, intermediate-, and long-acting forms of insulin can be injected separately or mixed in the same syringe.
  • Insulin is available in concentrations of 100 units/mL (U-100) and 500 units/mL (U-500). U-500 is used only in rare cases of insulin resistance
  • Most of the insulin regimens use NPH insulin for basal insulin coverage
  • Humulin U Ultralente insulin provides a lower basal rate and may be used instead of NPH insulin when frequent hypoglycemic episodes occur
  • Insulinglargine (Lantus), a long-acting insulin analog, is available for once-daily subcutaneous injection at bedtime to provide basal insulin coverage
  • The client determines the effect of long-acting insulin by monitoring fasting blood glucose values
insulin administration4
Insulin administration
  • Single Daily Injection Protocol. Many clients inject insulin only once daily.
    • This protocol may include only intermediate acting insulin or a combination of short- and intermediate acting insulin.
    • A single dose of intermediate-acting insulin may not match the blood insulin level with food intake.
    • When fasting glucose levels become elevated, a multiple-injection protocol should be considered
insulin administration5
Insulin administration
  • Two-Dose Protocol. Combinations of short- and intermediate-acting insulin are injected twice daily.
    • Two thirds of the daily dose is given before breakfast, and one third is given before the evening meal.
    • Initially, intermediate-acting and regular insulin are usually given in a 2:1 ratio, and the evening (or bedtime) dose is given in a 1:1 ratio.
    • Changes in these ratios are then based on results of blood glucose monitoring.
    • Disadvantages of this schedule are that nighttime hypoglycemia is common and the blood glucose value in the morning is higher than desired
insulin administration6
Insulin administration
  • Three-Dose Protocol. A combination of short- and intermediate-acting insulin is given before breakfast, short-acting insulin is given before the evening meal, and intermediateacting insulin is given at bedtime.
  • Giving intermediate-acting insulin at bedtime results in lower fasting and after-breakfast blood glucose levels.
  • This schedule avoids nighttime hypoglycemia but may not provide enough coverage for the noon meal
insulin administration7
Insulin administration
  • Four-Dose Protocol. Giving short-acting insulin 30 minutes before meals allows the greatest amount of insulin to be present during the greatest insulin need.
  • Basal insulin is provided by twice-daily injection of intermediate-acting insulin or a bedtime injection of long-acting insulin.
  • Injection of premeal short-acting insulin based on anticipated carbohydrate intake allows some highly motivated clients with type 1 diabetes to have more flexibility in meal timing and size.
  • Insulin lispro should be given within 15 minutes of eating a meal; peak action usually occurs within 30 to 90 minutes.
  • Because this insulin duration of action is short, the client taking insulin lispro also requires longer-acting insulin for basal insulin requirements
insulin administration8
Insulin administration
  • Injections are usually made into the subcutaneous tissue.
  • Most individuals are able to lightly grasp a fold of skin and inject at a 90-degree angle. Aspiration for blood is not necessary.
  • Thin individuals may need to pinch the skin and inject at a 45-degree angle to avoid intramuscular (IM) injection
  • Injecting regular insulin 30 minutes before meals provides a greater amount of plasma free-insulin at mealtime. Eating within a few minutes after (or before) injecting short-acting insulin reduces insulin\'s ability to prevent rapid rises in postmeal blood glucose and may increase the risk of delayed hypoglycemia.
  • Insulin lispro should be given 15 minutes before a meal
hypoglycemia
Hypoglycemia
  • Many diabetic clients have symptoms of hypoglycemia at levels above 50 mg/dL.
  • A blood glucose level below 70 mg/dL alerts the nurse to assess for signs and symptoms of hypoglycemia
diabetic ketoacidosis dka
Diabetic ketoacidosis (DKA)

Hyperglycemia management

  • The nurse checks the client\'s blood pressure, pulse, and respirations every 15 minutes until stable.
  • The nurse records urine output, temperature, and mental status every hour. When a central venous catheter has been placed, the nurse assesses central venous pressure as ordered, usually every 30 minutes.
  • Assessing the client\'s airway patency, level of consciousness, hydration status, status of fluid and electrolyte replacement, and levels of blood glucose are primary nursing measures. After treatment is underway and these variables are stable, monitoring vital signs and recording values every 4 hours is acceptable.
  • Blood glucose values can be measured either by laboratory or bedside glucose monitoring.
  • Results indicate the adequacy of insulin replacement and establish when to switch from saline to dextrose-containing solutions
diabetic ketoacidosis dka1
Diabetic ketoacidosis (DKA)

Fluid and electrolyte management

  • Close assessment of the fluid status of the diabetic client is essential
  • Treatment is initiated to correct a fluid volume deficit. The initial goal of fluid therapy is to restore circulating volume and protect against cerebral, coronary, or renal hypoperfusion.
  • The nurse administers 1 L of isotonic saline over a period of 30 to 60 minutes, followed by a second liter in the next hour, or as ordered.
  • The second objective of fluid therapy, which is to replace total body and intracellular losses, is achieved more slowly, usually using 0.45% saline. When blood glucose levels reach 250 mg/dL (13.8 mmol/L), 5% dextrose in 0.45% saline is administered.
diabetic ketoacidosis dka2
Diabetic ketoacidosis (DKA)
  • This measure prevents hypoglycemia and the development of cerebral edema, which can occur when serum osmolality is reduced too rapidly.
  • During the first 24 hours of treatment, the client needs enough fluids to replace both the volume deficit and ongoing losses. This volume can be as much as 6 to 10 L.
  • The nurse monitors for signs of congestive heart failure and pulmonary edema with infusions of this magnitude. Central venous pressure monitoring may be needed for older clients and those with myocardial disease
diabetic ketoacidosis dka3
Diabetic ketoacidosis (DKA)

Drug therapy

  • The goal of insulin therapy is to lower the serum glucose by approximately 75 to 150 mg/dL/hr.
  • "Low-dose" insulin therapy is associated with less hypokalemia and hypoglycemia than is seen with "high-dose" regimens.
  • Although both IM and IV administration have been used, most protocols for treating DKA recommend continuous IV administration of regular insulin because absorption from intramuscular or subcutaneous sites may be erratic.
diabetic ketoacidosis dka4
Diabetic ketoacidosis (DKA)
  • A steady-state level of insulin can be reached in 25 to 30 minutes. Effective blood insulin concentrations are reached almost immediately when an IV bolus dose is given at the start of the infusion.
  • Usually, regular insulin is administered in an initial IV bolus dose of 0.1 units/kg, followed by an IV drip of 0.1 units/kg/hr. Continuous infusion of insulin is required because of the 4-minute half-life of IV insulin.
  • Subcutaneous insulin is started when the client can take oral nourishment and ketosis has stopped. The effects of insulin therapy are assessed by hourly blood glucose measurements
diabetic ketoacidosis dka5
Diabetic ketoacidosis (DKA)

Acidosis management

  • Bicarbonate therapy is indicated only for severe acidosis.
  • Inappropriate use of bicarbonate may reverse acidosis too rapidly and result in severe hypokalemia, which can cause fatal cardiac dysrhythmias. Rapid correction of acidosis can worsen the client\'s mental status. Metabolic acidosis is corrected with fluid replacement and insulin therapy.
  • Sodium bicarbonate, administered by slow IV infusion over several hours, is indicated when the arterial pH is 7.0 or less or the serum bicarbonate level is less than 5 mEq/L (5 mmol/L).
hyperglycemic hyperosmolar nonketotic syndrome hhns
Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
  • Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS) is a hyperosmolar (increased blood osmolarity) state caused by hyperglycemia of any origin
  • Although both HHNS and diabetic ketoacidosis (DKA) are associated with hyperglycemia, HHNS is different from DKA because of the absence of ketosis and the much higher than average blood glucose levels and osmolality.
  • Often blood glucose levels are greater than 800 mg/dL (44.5 mmol/L) and blood osmolarity is greater than 350 mOsL when HHNS is present.
  • Other biochemical problems with HHNS tend to be more severe than those with DKA
hyperglycemic hyperosmolar nonketotic syndrome hhns1
Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)

Fluid therapy

  • The goal of therapy is to complete rehydration and obtain normal blood glucose levels within 36 to 72 hours.
  • The choice of fluid replacement and the rate of administration are critical in the management of HHNS.
  • The severity of the CNS problems is related to the level of blood hyperosmolarity and cellular dehydration. Re-establishing fluid balance in brain cells is a difficult and slow process, and many clients do not recover baseline CNS function until several hours after blood glucose levels have returned to normal
hyperglycemic hyperosmolar nonketotic syndrome hhns2
Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
  • As with DKA, the initial objective for fluid replacement in HHNS is to increase circulating blood volume.
  • If shock or severe hypotension is present, normal saline is given initially.
  • Otherwise, half-normal saline is preferable because it more rapidly corrects the free-water deficit.
  • The fluids are infused at a rate of 1 L/hr until central venous pressure or pulmonary capillary wedge pressure begins to rise or until the blood pressure and urine output are adequate. The rate is then reduced to 100 to 200 mL/hr.
  • Half of the estimated water deficit is replaced in the first 12 hours, and the remainder is given during the next 36 hours.
  • Body weight, urine output, kidney function, and the presence or absence of pulmonary congestion and jugular venous distention determine the rate of fluid administration.
hyperglycemic hyperosmolar nonketotic syndrome hhns3
Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
  • In clients with known congestive heart failure, renal insufficiency, or acute kidney failure, central venous pressure monitoring is indicated.
  • The nurse assesses the client hourly for signs of cerebral edema.
  • Changes in the level of consciousness; changes in pupil size, shape or reaction; or seizures are reported immediately to the physician.
  • Lack of any improvement in level of consciousness may indicate inadequate rates of fluid replacement or reduction in plasma osmolarity.
  • Regression after initial improvement may indicate too rapid reduction in plasma osmolarity
hyperglycemic hyperosmolar nonketotic syndrome hhns4
Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
  • A slow but steady improvement in CNS function is the best evidence that fluid management is satisfactory

Continuing therapy

  • IV insulin given at a rate of 10 units/hr is usually required to reduce blood glucose levels. Although fluid replacement reduces hyperglycemia, it cannot by itself return blood glucose levels to normal. A reduction of 10% per hour in the blood glucose level is a reasonable goal
  • Potassium loss occurs in HHNS, although not to the degree that it does in DKA.
  • Because of the initial low urine output (oliguria) or absent urine output (anuria), potassium replacement may not be needed at the onset of therapy.
  • Client education and interventions to minimize dehydration are similar to those for ketoacidosis
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