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Interventions for Clients with Diabetes Mellitus

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Title: Interventions for Clients with Diabetes Mellitus


1
Interventions for Clientswith Diabetes Mellitus
2
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.

3
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

4
Classification
5
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

6
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

7
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

8
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

9
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)

10
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

11
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

12
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)

13
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

14
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)

15
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)

16
Chronic complications of diabetes
  • diabetic nephropathy (microalbuminuria (presence
    of very small amounts of albumin in the urine)
  • male erectile dysfunction (ED)

17
Diabetes type 1 2
18
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

19
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

20
Blood tests
21
Insulin administration
22
Insulin administration
23
Insulin administration
24
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

25
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

26
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

27
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

28
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

29
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

30
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

31
Hypoglycemia
32
Hypoglycemia. Interventions
33
Hypoglycemia. Client education
34
Diabetic ketoacidosis (DKA)Hyperglycemic-hyperosm
olar nonketotic syndrome (HHNS)
35
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

36
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.

37
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

38
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.

39
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

40
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).

41
Diabetic ketoacidosis (DKA)Client education
42
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

43
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

44
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.

45
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

46
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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