Download (120 days). Assessment and Management of Patients With Diabetes

Assessment and
Management of Patients
With Diabetes Mellitus
Chapter 41
1
On completion of this chapter, the learner will be
able to:
1- Differentiate between type 1 and type 2 diabetes.
2- Describe etiologic factors associated with diabetes.
3- Relate the clinical manifestations of diabetes to the associated
pathophysiologic alterations.
4- Identify the diagnostic and clinical significance of blood glucose test results.
5- Explain the dietary modifications used for management of people with
diabetes.
6- Describe the relationships among diet, exercise, and medication (ie, insulin or
oral antidiabetic agents) for people with diabetes.
7- Develop a plan for teaching insulin self-management.
8- Identify the role of oral antidiabetic agents in diabetic therapy.
9- Differentiate between hyperglycemia with diabetic ketoacidosis and
hyperosmolar nonketotic syndrome.
10- Describe the major macrovascular, microvascular, and neuropathic
complications of diabetes and the self-care behaviors that are important in their
prevention.
2
Diabetes mellitus
• 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.
3
4
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.
5
Pathophysiology
• Insulin is secreted by beta cells, which are one of four
types of cells in the islets of Langerhans in the pancreas.
• Insulin is an anabolic, or storage, hormone. When a person
eats a meal, insulin secretion increases and moves glucose
from the blood into muscle, liver, and fat cells. In those
cells, insulin:
• Transports and metabolizes glucose for energy
• Stimulates storage of glucose in the liver and muscle (in the
form of glycogen)
• Signals the liver to stop the release of glucose
• Enhances storage of dietary fat in adipose tissue
• Accelerates transport of amino acids (derived from dietary
protein) into cells. Insulin also inhibits the breakdown of
stored glucose, protein, and fat.
6
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).
7
Type 1 Diabetes
• Type 1 diabetes affects approximately 5% to 10% of people
• 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.
8
Type 1 Diabetes
• 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.
9
10
Type 2 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 .
11
Type 2 Diabetes
• 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).
12
Type 2 Diabetes
• 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).
13
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.
• 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).
14
Clinical manifestations
• depend on the patient’s 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.
15
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.
• See Next chart please .
16
17
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.
18
Medical Management
• Diabetes management has five components:
1- nutritional therapy
2- exercise
3- Monitoring
4- pharmacologic therapy
5- education
19
Glycemic Index
• 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, puréed, 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 more slowly absorbed.
- 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.
20
21
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.
22
Testing for Glycated Hemoglobin
• 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).
23
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.
24
25
26
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
• See (Table 41-6).
• Sulfonylureas and meglitinides are considered insulin
secretagogues because their action increases the secretion
of insulin by the pancreatic beta cells.
27
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.
28
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.
29
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.
30
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
31
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
32
•
•
•
•
•
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.
33
•
•
•
•
•
Clinical Manifestations
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 body’s
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.
34
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.
35
Assessment and Diagnostic Findings
• 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.
36
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 patient’s deliberately missing
insulin doses, the patient and family may be referred for evaluation and
counseling or therapy.
37
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.
38
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.
• Table 41-8 compares DKA and HHNS.
39
40
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.
41
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).
42
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.
43
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 patient’s sodium level and the
severity of volume depletion.
44
Management
• 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) .
45
Management
• 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.
46
THE PATIENT WITH DIABETIC
KETOACIDOSIS OR
HYPERGLYCEMIC
HYPEROSMOLAR NONKETOTIC
SYNDROME
47
NURSING PROCESS
THE PATIENT WITH DIABETIC
KETOACIDOSIS OR HYPERGLYCEMIC
HYPEROSMOLAR NONKETOTIC
SYNDROME
48
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.
49
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.
50
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.
51
Nursing Interventions
• Maintaining Fluid and Electrolyte Balance
• Increasing Knowledge About Diabetes
Management
• Monitoring and Managing Potential
Complications
• Teaching Patients Self-Care
52
Evaluation
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
1. Achieves fluid and electrolyte balance
a. Demonstrates intake and output balance
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
53