Interventions for Clients with Diabetes Mellitus

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Interventions for Clientswith Diabetes Mellitus
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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.

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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

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Classification
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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

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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

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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

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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

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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)

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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

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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

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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)

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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

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Chronic complications of diabetes

• Diabetes mellitus is a major risk factor for
  morbidity and mortality because of changes in the
  larger or generalized body blood vessels
  (macrovascular), as well as changes in small
  blood vessels (microvascular)

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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)

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Chronic complications of diabetes

• diabetic nephropathy (microalbuminuria (presence
  of very small amounts of albumin in the urine)
• male erectile dysfunction (ED)

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Diabetes type 1 2
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Assessment

• History
• risk factors
• age
• women are asked how large their children were 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
• major or minor infections
• all clients are asked if they have noticed
  whether small skin injuries become infected more
  easily or seem to take a longer time to heal
• family history

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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

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Blood tests
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Insulin administration
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Insulin administration
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Insulin administration
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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

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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

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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 21 ratio, and the
  evening (or bedtime) dose is given in a 11
  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

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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

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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

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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

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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

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Hypoglycemia
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Hypoglycemia. Interventions
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Hypoglycemia. Client education
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Diabetic ketoacidosis (DKA)Hyperglycemic-hyperosm
olar nonketotic syndrome (HHNS)
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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

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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.

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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

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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.

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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

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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).

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Diabetic ketoacidosis (DKA)Client education
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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

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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

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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.

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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

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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