Nursing care plans for Diabetes Mellitus, Diabetes mellitus is a disorder in which

the level of blood glucose is persistently raised above the normal range. Diabetes
mellitus is a syndrome with disordered metabolism and inappropriate hyperglycemia
due to either a deficiency of insulin secretion or to a combination of insulin resistance
and inadequate insulin secretion to compensate. Diabetes mellitus occurs in two
primary forms: type 1, characterized by absolute insufficiency, and the more prevalent
type 2, characterized by insulin resistance with varying degrees of insulin secretory
defects. Diabetes mellitus is a group of metabolic diseases characterized by elevated
levels of glucose in the blood (hyperglycemia) resulting from defects in insulin
secretion, insulin action, or both (ADA], Expert Committee on the Diagnosis and
Classification of Diabetes Mellitus, 2003.

Causes for Diabetes Mellitus

The cause of both type 1 and type 2 diabetes remains unknown, although genetic
factors may play a role. Diabetes mellitus results from insulin deficiency or resistance.
Insulin transports glucose into the cell for use as energy and storage as glycogen. It
also stimulates protein synthesis and free fatty acid storage. Insulin deficiency or
resistance compromises the body tissues’ access to essential nutrients for fuel and
storage. The resulting hyperglycemia can damage many of the body’s organs and
tissues.

Type 1 diabetes is due to pancreatic islet B cell destruction predominantly by an

autoimmune process, and these patients are prone to ketoacidosis.

Type 2 diabetes is the more prevalent form and results from insulin resistance with a
defect in compensatory insulin secretion

Insulin, a hormone produced by the pancreas, controls the level of glucose in the
blood by regulating the production and storage of glucose.

Risk Factors For Diabetes Mellitus Include:

 Obesity.
 Physiologic or emotional stress, which can cause prolonged elevation of stress
hormone levels.
 pregnancy, which causes weight gain and increases levels of estrogen and
placental hormones, which antagonize insulin
 metabolic syndrome, which is considered a precursor to the development of
type 2 diabetes mellitus
 some medications that can antagonize the effects of insulin, including thiazide
diuretics, adrenal corticosteroids, and hormonal contraceptives

Classification of Diabetes Mellitus

There are several different types of diabetes mellitus; they may differ in cause,
clinical course, and treatment. The major classifications of diabetes are:

 Type 1 diabetes (insulin dependent diabetes mellitus) is caused by B-cell

destruction, usually leading to absolute insulin deficiency
a)    Immune mediated

b)   Idiopathic

 Type 2 diabetes (previously referred to as non insulin dependent diabetes

mellitus) ranges from those with predominant insulin resistance associated
with relative insulin deficiency, to those with a predominantly insulin
secretory defect with insulin resistance

PATHOPHYSIOLOGY OF DIABETES

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. 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 stimulate 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).

Type 1 Diabetes

This form of diabetes is immune-mediated in over 90% of cases and idiopathic in less
than 10%. The rate of pancreatic B cell destruction is quite variable, being rapid in
some individuals and slow in others. Type 1 diabetes is usually associated with
ketosis in its untreated state. It occurs at any age but most commonly arises in
children and young adults with a peak incidence before school age and again at
around puberty. It is a catabolic disorder in which circulating insulin is virtually
absent, plasma glucagon is elevated, and the pancreatic B cells fail to respond to all
insulinogenic stimuli. Exogenous insulin is therefore required to reverse the catabolic
state, prevent ketosis, reduce the hyperglucagonemia, and reduce blood glucose.

Immune-mediated type 1 diabetes mellitus (type 1A)

Most patients with type 1 diabetes mellitus have circulating antibodies to islet cells
(ICA), insulin (IAA), glutamic acid decarboxylase (GAD65), and tyrosine
phosphatases (IA-2 and IA2-) at the time the diagnosis is made. These antibodies
facilitate screening for an autoimmune cause of diabetes, particularly screening
siblings of affected children, as well as adults with atypical features of type 2
Diabetes). Antibody levels decline with increasing duration of disease. Also, low
levels of anti-insulin antibodies develop in almost all patients once they are treated
with insulin.

This theory is referred to as the hygiene hypothesis. None of these factors has so far
been confirmed as the culprit. Part of the difficulty is that autoimmune injury
undoubtedly starts many years before clinical diabetes mellitus develops.

Idiopathic type 1 diabetes mellitus (type 1B)

Less than 10% of subjects have no evidence of pancreatic B cell autoimmunity to

explain their insulinopenia and ketoacidosis. This subgroup has been classified as
“idiopathic type 1 diabetes” and designated as “type 1B.” Although only a minority of
patients with type 1 diabetes fall into this group, most of these are of Asian or African
origin.

Type 2 Diabetes Mellitus

Circulating endogenous insulin is sufficient to prevent ketoacidosis but is inadequate

to prevent hyperglycemia in the face of increased needs owing to tissue insensitivity
(insulin resistance).

The two main problems related to insulin in type 2 diabetes are insulin resistance and
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, thus rendering insulin less effective at
stimulating glucose uptake by the tissues and at regulating glucose release by the
liver.

The exact mechanisms that lead to insulin resistance and impaired insulin secretion in
type 2 diabetes are unknown, although genetic factors are thought to play a role.
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.

Prediabetes

Prediabetes is an abnormality in glucose values intermediate between normal and

overt diabetes.

Impaired Fasting Glucose

  A new category adopted by the American Diabetes Association in 1997 and
redefined in 2004.
 Occurs when fasting blood glucose is greater than or equal to 100 but less than
126 mg/dL.

Impaired Glucose Tolerance

 Defined as blood glucose measurement on a glucose tolerance test greater than

or equal to 140 mg/dl but less than 200 in the 2-hour sample.
 Asymptomatic; it can progress to type 2 diabetes or remain unchanged.
 May be a risk factor for the development of hypertension, coronary heart
disease, and hyperlipidemias.

Gestational Diabetes Mellitus

 Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance

occurring during pregnancy.
 Occurs in approximately 4% of pregnancies and usually disappears after
delivery.
 Women with GDM are at higher risk for diabetes at a later date.
 GDM is associated with increased risk of fetal morbidity.
 Screening for GDM for all pregnant women other than those at lowest risk
(under age 25, of normal body weight, have no family history of diabetes, are
not a member of an ethnic group with high prevalence of diabetes) should
occur between the 24th and 28th weeks of gestation.

Diabetes Associated with Other Conditions

 Certain drugs can decrease insulin activity resulting in hyperglycemia

corticosteroids, thiazide diuretics, estrogen, phenytoin.
 Disease states affecting the pancreas or insulin receptors pancreatitis, cancer
of the pancreas, Cushing’s disease or syndrome, acromegaly,
pheochromocytoma, muscular dystrophy, Huntington’s chorea.

CLINICAL MANIFESTATIONS

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. The patient also experiences
polyphagia (increased appetite) resulting 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.

DIABETES 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.

Drugs for Treating Hyperglycemia

The drugs for treating type 2 diabetes fall into several categories:

1)      Drugs that primarily stimulate insulin secretion by binding to the sulfonylurea
receptor. Sulfonylureas remain the most widely prescribed drugs for treating
hyperglycemia. The meglitinide analog repaglinide and the D-phenylalanine
derivative nateglinide also bind the sulfonylurea receptor and stimulate insulin
secretion.

2)      Drugs that alter insulin action: Metformin works in the liver. The
thiazolidinediones appear to have their main effect on skeletal muscle and adipose
tissue.

3)      Drugs that principally affect absorption of glucose: The glucosidase inhibitors
acarbose and miglitol are such currently available drugs.

4)      Drugs that mimic incretin effect or prolong incretin action: Exenatide and DPP
1V inhibitors fall into this category.

5)       Other: Pramlintide lowers glucose by suppressing glucagon and slowing gastric
emptying.

Insulin

Insulin is indicated for type 1 diabetes as well as for type 2 diabetic patients with
insulinopenia whose hyperglycemia does not respond to diet therapy either alone or
combined with other hypoglycemic drugs.

Therefore, the therapeutic goal for diabetes management is to achieve normal blood
glucose levels (euglycemia) without hypoglycemia and without seriously disrupting
the patient’s usual lifestyle and activity.

There are five components of diabetes management

• Nutritional management

• Exercise

• Monitoring

• Pharmacologic therapy

• Education

Nursing Process Nursing Care Plans For Diabetes Mellitus

Nursing Assessment Nursing Care Plans For Diabetes Mellitus

 Obtain a history of current problems, family history, and general health

history.
o Has the patient experienced polyuria, polydipsia, polyphagia, and any
other symptoms?
o Number of years since diagnosis of diabetes
o Family members diagnosed with diabetes, their subsequent treatment,
and complications
 Perform a review of systems and physical examination to assess for signs and
symptoms of diabetes, general health of patient, and presence of
complications.
o General: recent weight loss or gain, increased fatigue, tiredness,
anxiety
o Skin: skin lesions, infections, dehydration, evidence of poor wound
healing
o Eyes: changes in vision”floaters, halos, blurred vision, dry or burning
eyes, cataracts, glaucoma
o Mouth: gingivitis, periodontal disease
o Cardiovascular: orthostatic hypotension, cold extremities, weak pedal
pulses, leg claudication
o GI: diarrhea, constipation, early satiety, bloating, increased flatulence,
hunger or thirst
o Genitourinary (GU): increased urination, nocturia, impotence, vaginal
discharge
o Neurologic: numbness and tingling of the extremities, decreased pain
and temperature perception, changes in gait and balance

Nursing Diagnosis Nursing care plans for Diabetes Mellitus

Common nursing diagnosis found in Nursing care plans for Diabetes Mellitus

 Imbalanced Nutrition: More than Body Requirements related to intake in

excess of activity expenditures
 Fear related to insulin injection
 Risk for Injury (hypoglycemia) related to effects of insulin, inability to eat
 Activity Intolerance related to poor glucose control
 Deficient Knowledge related to use of oral hypoglycemic agents
 Risk for Impaired Skin Integrity related to decreased sensation and circulation
to lower extremities
 Ineffective Coping related to chronic disease and complex self-care regimen

Nursing Intervention and Evaluation Nursing care plans for Diabetes Mellitus

No Nursing Outcome Intervention Evaluation

Diagnose
1 Imbalanced Nutrition  Assess current timing and Maintains
Nutrition: More balance content of meals. ideal body
 than Body between  Advise patient on the weight with
Requirements needs and importance of an body mass
related to intake intake individualized meal plan in index less than
in excess of meeting weight-loss goals. 25
activity Reducing intake of
expenditures carbohydrates may benefit
some patients; however, fad
diets or diet plans that stress
one food group and eliminate
another are generally not
recommended.
 Discuss the goals of dietary
therapy for the patient.
Setting a goal of a 10% (of
patient’s actual body weight)
weight loss over several
months is usually achievable
and effective in reducing
blood sugar and other
metabolic parameters.
 Assist patient to identify
problems that may have an
impact on dietary adherence
and possible solutions to
these problems. Emphasize
that lifestyle changes should
be maintainable for life.
 Explain the importance of
exercise in
maintaining/reducing body
weight.
o Caloric expenditure
for energy in exercise
o Carryover of enhanced
metabolic rate and
efficient food
utilization
 Assist patient to establish
goals for weekly weight loss
and incentives to assist in
achieving them.
 Strategize with patient to
address the potential social
pitfalls of weight reduction.

2 Fear related to Fear less or  Assist patient to reduce fear Demonstrates

insulin discrease of injection by encouraging self-injection
injection verbalization of fears of insulin with
regarding insulin injection, minimal fear
 conveying a sense of
empathy, and identifying
supportive coping techniques.
 Demonstrate and explain
thoroughly the procedure for
insulin self-injection
 Help patient to master
technique by taking a step-by-
step approach.
o Allow patient time to
handle insulin and
syringe to become
familiar with the
equipment.
o Teach self-injection
first to alleviate fear of
pain from injection.
o Instruct patient in
filling syringe when
he or she expresses
confidence in self-
injection procedure.
 Review dosage and time of
injections in relation to meals,
activity, and bedtime based
on patient’s individualized
insulin regimen.

3 Risk for Injury Injury is  Closely monitor blood Hypoglycemia

(hypoglycemia) not appears glucose levels to detect identified and
related to hypoglycemia. treated
effects of  Instruct patient in the appropriately
insulin, importance of accuracy in
inability to eat insulin preparation and meal
timing to avoid
hypoglycemia.
 Assess patient for the signs
and symptoms of
hypoglycemia.
o Adrenergic (early
symptoms) sweating,
tremor, pallor,
tachycardia,
palpitations,
nervousness from the
release of adrenalin
when blood glucose
falls rapidly
o Neurologic (later
 symptoms) light-
headedness, headache,
confusion, irritability,
slurred speech, lack of
coordination,
staggering gait from
depression of central
nervous system as
glucose level
progressively falls
 Treat hypoglycemia promptly
with 15 to 20 g of fast-acting
carbohydrates.

 Encourage patient to carry a

portable treatment for
hypoglycemia at all times.
 Assess patient for cognitive
or physical impairments that
may interfere with ability to
accurately administer insulin.
 Between-meal snacks as well
as extra food taken before
exercise should be
encouraged to prevent
hypoglycemia.
 Encourage patients to wear an
identification bracelet or card
that may assist in prompt
treatment in a hypoglycemic
emergency.

 Encourage patient to carry a

portable treatment for
hypoglycemia at all times.
 Assess patient for cognitive
or physical impairments that
may interfere with ability to
accurately administer insulin.
 Between-meal snacks as well
as extra food taken before
exercise should be
encouraged to prevent
hypoglycemia.
 Encourage patients to wear an
identification bracelet or card
that may assist in prompt
treatment in a hypoglycemic
 emergency.

4 Activity Normal  Advise patient to assess blood Exercises

Intolerance Activity is glucose level before and after daily
related to poor appears strenuous exercise.
glucose control  Instruct patient to plan
exercises on a regular basis
each day.
 Encourage patient to eat a
carbohydrate snack before
exercising to avoid
hypoglycemia.
 Advise patient that prolonged
strenuous exercise may
require increased food at
bedtime to avoid nocturnal
hypoglycemia.
 Instruct patient to avoid
exercise whenever blood
glucose levels exceed 250
mg/day and urine ketones are
present. Patient should
contact health care provider if
levels remain elevated.
 Counsel patient to inject
insulin into the abdominal site
on days when arms or legs are
exercised.

5 Deficient Knowledge  Assess level of knowledge of Verbalizes

Knowledge is sufficient disease and ability to care for appropriate
related to use of self use and action
oral  Assess adherence to diet of oral
hypoglycemic therapy, monitoring hypoglycemic
agents procedures, medication agents
treatment, and exercise
regimen
 Assess for signs of
hyperglycemia: polyuria,
polydipsia, polyphagia,
weight loss, fatigue, blurred
vision
 Assess for signs of
hypoglycemia: sweating,
tremor, nervousness,
tachycardia, light-headedness,
confusion
 Perform thorough skin and
extremity assessment for
 peripheral neuropathy or
peripheral vascular disease
and any injury to the feet or
lower extremities
 Assess for trends in blood
glucose and other laboratory
results
 Make sure that appropriate
insulin dosage is given at the
right time and in relation to
meals and exercise
 Make sure patient has
adequate knowledge of diet,
exercise, and medication
treatment
 Immediately report to health
care provider any signs of
skin or soft tissue infection
(redness, swelling, warmth,
tenderness, drainage)
 Get help immediately for
signs of hypoglycemia that do
not respond to usual glucose
replacement
 Get help immediately for
patient presenting with signs
of either ketoacidosis (nausea
and vomiting, Kussmaul
respirations, fruity breath
odor, hypotension, and altered
level of consciousness) or
hyperosmolar hyperglycemic
nonketotic syndrome (nausea
and vomiting, hypothermia,
muscle weakness, seizures,
stupor, coma).

6 Risk for Impaired  Assess feet and legs for skin No skin
Impaired Skin Skin temperature, sensation, soft breakdown
Integrity related Integrity is tissue injuries, corns, calluses,
to decreased not appears dryness, hammer toe or
sensation and bunion deformation, hair
circulation to distribution, pulses, deep
lower tendon reflexes.
extremities
 Maintain skin integrity by
protecting feet from
breakdown.
o Use heel protectors,
 special mattresses,
foot cradles for
patients on bed rest.
o Avoid applying drying
agents to skin (eg,
alcohol).
o Apply skin
moisturizers to
maintain suppleness
and prevent cracking
and fissures.
 Instruct patient in foot care
guidelines

 Advise the patient who

smokes to stop smoking or
reduce if possible, to reduce
vasoconstriction and enhance
peripheral blood flow. Help
patient to establish behavior
modification techniques to
eliminate smoking in the
hospital and to continue them
at home for smoking-
cessation program.

7 Ineffective Effective  Discuss with the patient the Verbalizes

Coping related coping perceived effect of diabetes initial
to chronic on lifestyle, finances, family strategies for
disease and life, occupation. coping with
complex self-  Explore previous coping diabetes
care regimen strategies and skills that have
had positive effects.

 Encourage patient and family

participation in diabetes self-
care regimen to foster
confidence.
 Identify available support
groups to assist in lifestyle
adaptation.
 Assist family in providing
emotional support.