Nursing care plans for Diabetes Mellitus.

Diabetes mellitus is a disorder in which

the level oI blood glucose is persistently raised above the normal range. Diabetes
mellitus is a syndrome with disordered metabolism and inappropriate hyperglycemia
due to either a deIiciency oI insulin secretion or to a combination oI insulin resistance
and inadequate insulin secretion to compensate. Diabetes mellitus occurs in two
primary Iorms: type 1, characterized by absolute insuIIiciency, and the more prevalent
type 2, characterized by insulin resistance with varying degrees oI insulin secretory
deIects. Diabetes mellitus is a group oI metabolic diseases characterized by elevated
levels oI glucose in the blood (hyperglycemia) resulting Irom deIects in insulin
secretion, insulin action, or both (ADA|, Expert Committee on the Diagnosis and
ClassiIication oI Diabetes Mellitus, 2003.
Causes for Diabetes Mellitus
The cause oI both type 1 and type 2 diabetes remains unknown, although genetic
Iactors may play a role. Diabetes mellitus results Irom insulin deIiciency or resistance.
Insulin transports glucose into the cell Ior use as energy and storage as glycogen. It
also stimulates protein synthesis and Iree Iatty acid storage. Insulin deIiciency or
resistance compromises the body tissues` access to essential nutrients Ior Iuel and
storage. The resulting hyperglycemia can damage many oI 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 Iorm and results Irom insulin resistance with a
deIect in compensatory insulin secretion
Insulin, a hormone produced by the pancreas, controls the level oI glucose in the
blood by regulating the production and storage oI glucose.
Risk Factors For Diabetes Mellitus Include:
O besity.
O !hysiologic or emotional stress, which can cause prolonged elevation oI stress
hormone levels.
O pregnancy, which causes weight gain and increases levels oI estrogen and
placental hormones, which antagonize insulin
O metabolic syndrome, which is considered a precursor to the development oI
type 2 diabetes mellitus
O some medications that can antagonize the eIIects oI insulin, including thiazide
diuretics, adrenal corticosteroids, and hormonal contraceptives
Classification of Diabetes Mellitus
There are several diIIerent types oI diabetes mellitus; they may diIIer in cause,
clinical course, and treatment. The maior classiIications oI diabetes are:
O Type 1 diabetes (insulin dependent diabetes mellitus) is caused by B-cell
destruction, usually leading to absolute insulin deIiciency
a) Immune mediated
b) Idiopathic
O Type 2 diabetes (previously reIerred to as non insulin dependent diabetes
mellitus) ranges Irom those with predominant insulin resistance associated
with relative insulin deIiciency, to those with a predominantly insulin
secretory deIect with insulin resistance
PATHOPHYSIOLOGY OF DIABETES
Insulin is secreted by beta cells, which are one oI Iour types oI cells in the islets oI
Langerhans in the pancreas. Insulin is an anabolic, or storage, hormone. When a
person eats a meal, insulin secretion increases and moves glucose Irom the blood into
muscle, liver, and Iat cells. In those cells, insulin:
Transports and metabolizes glucose Ior energy
Stimulates storage oI glucose in the liver and muscle (in the Iorm oI glycogen)
Signals the liver to stop the release oI glucose
Enhances storage oI dietary Iat in adipose tissue
Accelerates transport oI amino acids (derived Irom dietary protein) into cells
Insulin also inhibits the breakdown oI stored glucose, protein, and Iat. During Iasting
periods (between meals and overnight), the pancreas continuously releases a small
amount oI insulin (basal insulin); another pancreatic hormone called glucagon
(secreted by the alpha cells oI the islets oI 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 oI glucose in the blood by
stimulating the release oI glucose Irom the liver. Initially, the liver produces glucose
through the breakdown oI glycogen (glycogenolysis). AIter 8 to 12 hours without
Iood, the liver Iorms glucose Irom the breakdown oI noncarbohydrate substances,
including amino acids (gluconeogenesis).
Type 1 Diabetes
This Iorm oI diabetes is immune-mediated in over 90 oI cases and idiopathic in less
than 10. The rate oI 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 beIore 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 Iail to respond to all
insulinogenic stimuli. Exogenous insulin is thereIore 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
Iacilitate screening Ior an autoimmune cause oI diabetes, particularly screening
siblings oI aIIected children, as well as adults with atypical Ieatures oI type 2
Diabetes). Antibody levels decline with increasing duration oI disease. Also, low
levels oI anti-insulin antibodies develop in almost all patients once they are treated
with insulin.
This theory is reIerred to as the hygiene hypothesis. None oI these Iactors has so Iar
been conIirmed as the culprit. !art oI the diIIiculty is that autoimmune iniury
undoubtedly starts many years beIore clinical diabetes mellitus develops.
Idiopathic type 1 diabetes mellitus (type 1B)
Less than 10 oI subiects have no evidence oI pancreatic B cell autoimmunity to
explain their insulinopenia and ketoacidosis. This subgroup has been classiIied as
'idiopathic type 1 diabetes and designated as 'type 1B. Although only a minority oI
patients with type 1 diabetes Iall into this group, most oI these are oI Asian or AIrican
origin.
Type 2 Diabetes Mellitus
Circulating endogenous insulin is suIIicient to prevent ketoacidosis but is inadequate
to prevent hyperglycemia in the Iace oI 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 reIers to a decreased tissue sensitivity to
insulin. Normally, insulin binds to special receptors on cell surIaces and initiates a
series oI reactions involved in glucose metabolism. In type 2 diabetes, these
intracellular reactions are diminished, thus rendering insulin less eIIective 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 Iactors are thought to play a role.
Despite the impaired insulin secretion that is characteristic oI type 2 diabetes, there is
enough insulin present to prevent the breakdown oI Iat and the accompanying
production oI ketone bodies. ThereIore, DKA does not typically occur in type 2
diabetes.
Prediabetes
!rediabetes is an abnormality in glucose values intermediate between normal and
overt diabetes.
Impaired Fasting Glucose
O A new category adopted by the American Diabetes Association in 1997 and
redeIined in 2004.
O ccurs when Iasting blood glucose is greater than or equal to 100 but less than
126 mg/dL.
Impaired Glucose Tolerance
O DeIined 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.
O Asymptomatic; it can progress to type 2 diabetes or remain unchanged.
O May be a risk Iactor Ior the development oI hypertension, coronary heart
disease, and hyperlipidemias.
Gestational Diabetes Mellitus
O Gestational diabetes mellitus (GDM) is deIined as carbohydrate intolerance
occurring during pregnancy.
O ccurs in approximately 4 oI pregnancies and usually disappears aIter
delivery.
O Women with GDM are at higher risk Ior diabetes at a later date.
O GDM is associated with increased risk oI Ietal morbidity.
O Screening Ior GDM Ior all pregnant women other than those at lowest risk
(under age 25, oI normal body weight, have no Iamily history oI diabetes, are
not a member oI an ethnic group with high prevalence oI diabetes) should
occur between the 24th and 28th weeks oI gestation.
Diabetes Associated with Other Conditions
O Certain drugs can decrease insulin activity resulting in hyperglycemia
corticosteroids, thiazide diuretics, estrogen, phenytoin.
O Disease states aIIecting the pancreas or insulin receptors pancreatitis, cancer
oI the pancreas, Cushing`s disease or syndrome, acromegaly,
pheochromocytoma, muscular dystrophy, Huntington`s chorea.
CLINICAL MANIFESTATIONS
Clinical maniIestations oI all types oI diabetes include the 'three !s: polyuria,
polydipsia, and polyphagia. !olyuria (increased urination) and polydipsia (increased
thirst) occur as a result oI the
excess loss oI Iluid associated with osmotic diuresis. The patient also experiences
polyphagia (increased appetite) resulting Irom the catabolic state induced by insulin
deIiciency and the breakdown oI proteins and Iats. ther symptoms include Iatigue
and weakness, sudden vision changes, tingling or numbness in hands or Ieet, dry skin,
skin lesions or wounds that are slow to heal, and recurrent inIections. The onset oI
type 1 Diabetes may also be associated with sudden weight loss or nausea, vomiting,
or abdominal pains, iI DKA has developed.
DIABETES MANAGEMENT
The main goal oI diabetes treatment is to normalize insulin activity and blood glucose
levels to reduce the development oI vascular and neuropathic complications.
Drugs for Treating Hyperglycemia
The drugs Ior treating type 2 diabetes Iall into several categories:
1) Drugs that primarily stimulate insulin secretion by binding to the sulIonylurea
receptor. SulIonylureas remain the most widely prescribed drugs Ior treating
hyperglycemia. The meglitinide analog repaglinide and the D-phenylalanine
derivative nateglinide also bind the sulIonylurea receptor and stimulate insulin
secretion.
2) Drugs that alter insulin action: MetIormin works in the liver. The
thiazolidinediones appear to have their main eIIect on skeletal muscle and adipose
tissue.
3) Drugs that principally aIIect absorption oI glucose: The glucosidase inhibitors
acarbose and miglitol are such currently available drugs.
4) Drugs that mimic incretin eIIect or prolong incretin action: Exenatide and D!!
1V inhibitors Iall into this category.
5) ther: !ramlintide lowers glucose by suppressing glucagon and slowing gastric
emptying.
Insulin
Insulin is indicated Ior type 1 diabetes as well as Ior type 2 diabetic patients with
insulinopenia whose hyperglycemia does not respond to diet therapy either alone or
combined with other hypoglycemic drugs.
ThereIore, the therapeutic goal Ior diabetes management is to achieve normal blood
glucose levels (euglycemia) without hypoglycemia and without seriously disrupting
the patient`s usual liIestyle and activity.
There are Iive components oI diabetes management
Nutritional management
Exercise
Monitoring
!harmacologic therapy
Education
Nursing Process Nursing Care Plans For Diabetes Mellitus
Nursing Assessment Nursing Care Plans For Diabetes Mellitus
O btain a history oI current problems, Iamily history, and general health
history.
4 Has the patient experienced polyuria, polydipsia, polyphagia, and any
other symptoms?
4 Number oI years since diagnosis oI diabetes
4 Family members diagnosed with diabetes, their subsequent treatment,
and complications
O !erIorm a review oI systems and physical examination to assess Ior signs and
symptoms oI diabetes, general health oI patient, and presence oI
complications.
4 General: recent weight loss or gain, increased Iatigue, tiredness,
anxiety
4 Skin: skin lesions, inIections, dehydration, evidence oI poor wound
healing
4 Eyes: changes in visionIloaters, halos, blurred vision, dry or burning
eyes, cataracts, glaucoma
4 Mouth: gingivitis, periodontal disease
4 Cardiovascular: orthostatic hypotension, cold extremities, weak pedal
pulses, leg claudication
4 GI: diarrhea, constipation, early satiety, bloating, increased Ilatulence,
hunger or thirst
4 Genitourinary (GU): increased urination, nocturia, impotence, vaginal
discharge
4 Neurologic: numbness and tingling oI the extremities, decreased pain
and temperature perception, changes in gait and balance
Nursing Diagnosis Nursing care plans for Diabetes Mellitus
Common nursing diagnosis Iound in Nursing care plans Ior Diabetes Mellitus
O Imbalanced Nutrition: More than Body Requirements related to intake in
excess oI activity expenditures
O Fear related to insulin iniection
O Risk Ior Iniury (hypoglycemia) related to eIIects oI insulin, inability to eat
O Activity Intolerance related to poor glucose control
O DeIicient Knowledge related to use oI oral hypoglycemic agents
O Risk Ior Impaired Skin Integrity related to decreased sensation and circulation
to lower extremities
O IneIIective Coping related to chronic disease and complex selI-care regimen
Nursing Intervention and Evaluation Nursing care plans for Diabetes Mellitus
No Nursing
Diagnose
utcome Intervention Evaluation
1 Imbalanced
Nutrition: More
than Body
Requirements
Nutrition
balance
between
needs and
O Assess current timing and
content oI meals.
O Advise patient on the
importance oI an
Maintains
ideal body
weight with
body mass
related to intake
in excess oI
activity
expenditures
intake individualized meal plan in
meeting weight-loss goals.
Reducing intake oI
carbohydrates may beneIit
some patients; however, Iad
diets or diet plans that stress
one Iood group and eliminate
another are generally not
recommended.
O Discuss the goals oI dietary
therapy Ior the patient. Setting
a goal oI a 10 (oI patient`s
actual body weight) weight
loss over several months is
usually achievable and
eIIective in reducing blood
sugar and other metabolic
parameters.
O Assist patient to identiIy
problems that may have an
impact on dietary adherence
and possible solutions to these
problems. Emphasize that
liIestyle changes should be
maintainable Ior liIe.
O Explain the importance oI
exercise in
maintaining/reducing body
weight.
4 Caloric expenditure
Ior energy in exercise
4 Carryover oI enhanced
metabolic rate and
eIIicient Iood
utilization
O Assist patient to establish
goals Ior weekly weight loss
and incentives to assist in
achieving them.
O Strategize with patient to
address the potential social
pitIalls oI weight reduction.
index less than
25
2 Fear related to
insulin iniection
Fear less or
discrease
O Assist patient to reduce Iear
oI iniection by encouraging
verbalization oI Iears
regarding insulin iniection,
conveying a sense oI
empathy, and identiIying
supportive coping techniques.
Demonstrates
selI-iniection
oI insulin with
minimal Iear
O Demonstrate and explain
thoroughly the procedure Ior
insulin selI-iniection
O Help patient to master
technique by taking a step-by-
step approach.
4 Allow patient time to
handle insulin and
syringe to become
Iamiliar with the
equipment.
4 Teach selI-iniection
Iirst to alleviate Iear oI
pain Irom iniection.
4 Instruct patient in
Iilling syringe when
he or she expresses
conIidence in selI-
iniection procedure.
O Review dosage and time oI
iniections in relation to meals,
activity, and bedtime based on
patient`s individualized
insulin regimen.
3 Risk Ior Iniury
(hypoglycemia)
related to
eIIects oI
insulin,
inability to eat
Iniury is
not appears
O Closely monitor blood
glucose levels to detect
hypoglycemia.
O Instruct patient in the
importance oI accuracy in
insulin preparation and meal
timing to avoid
hypoglycemia.
O Assess patient Ior the signs
and symptoms oI
hypoglycemia.
4 Adrenergic (early
symptoms) sweating,
tremor, pallor,
tachycardia,
palpitations,
nervousness Irom the
release oI adrenalin
when blood glucose
Ialls rapidly
4 Neurologic (later
symptoms) light-
headedness, headache,
conIusion, irritability,
slurred speech, lack oI
Hypoglycemia
identiIied and
treated
appropriately
coordination,
staggering gait Irom
depression oI central
nervous system as
glucose level
progressively Ialls
O Treat hypoglycemia promptly
with 15 to 20 g oI Iast-acting
carbohydrates.
O Encourage patient to carry a
portable treatment Ior
hypoglycemia at all times.
O Assess patient Ior cognitive or
physical impairments that
may interIere with ability to
accurately administer insulin.
O Between-meal snacks as well
as extra Iood taken beIore
exercise should be
encouraged to prevent
hypoglycemia.
O Encourage patients to wear an
identiIication bracelet or card
that may assist in prompt
treatment in a hypoglycemic
emergency.
O Encourage patient to carry a
portable treatment Ior
hypoglycemia at all times.
O Assess patient Ior cognitive or
physical impairments that
may interIere with ability to
accurately administer insulin.
O Between-meal snacks as well
as extra Iood taken beIore
exercise should be
encouraged to prevent
hypoglycemia.
O Encourage patients to wear an
identiIication bracelet or card
that may assist in prompt
treatment in a hypoglycemic
emergency.
4 Activity
Intolerance
related to poor
glucose control
Normal
Activity is
appears
O Advise patient to assess blood
glucose level beIore and aIter
strenuous exercise.
O Instruct patient to plan
Exercises daily
exercises on a regular basis
each day.
O Encourage patient to eat a
carbohydrate snack beIore
exercising to avoid
hypoglycemia.
O Advise patient that prolonged
strenuous exercise may
require increased Iood at
bedtime to avoid nocturnal
hypoglycemia.
O Instruct patient to avoid
exercise whenever blood
glucose levels exceed 250
mg/day and urine ketones are
present. !atient should contact
health care provider iI levels
remain elevated.
O Counsel patient to iniect
insulin into the abdominal site
on days when arms or legs are
exercised.
5 DeIicient
Knowledge
related to use oI
oral
hypoglycemic
agents
Knowledge
is suIIicient
O Assess level oI knowledge oI
disease and ability to care Ior
selI
O Assess adherence to diet
therapy, monitoring
procedures, medication
treatment, and exercise
regimen
O Assess Ior signs oI
hyperglycemia: polyuria,
polydipsia, polyphagia,
weight loss, Iatigue, blurred
vision
O Assess Ior signs oI
hypoglycemia: sweating,
tremor, nervousness,
tachycardia, light-headedness,
conIusion
O !erIorm thorough skin and
extremity assessment Ior
peripheral neuropathy or
peripheral vascular disease
and any iniury to the Ieet or
lower extremities
O Assess Ior trends in blood
glucose and other laboratory
results
Verbalizes
appropriate
use and action
oI oral
hypoglycemic
agents
O Make sure that appropriate
insulin dosage is given at the
right time and in relation to
meals and exercise
O Make sure patient has
adequate knowledge oI diet,
exercise, and medication
treatment
O Immediately report to health
care provider any signs oI
skin or soIt tissue inIection
(redness, swelling, warmth,
tenderness, drainage)
O Get help immediately Ior
signs oI hypoglycemia that do
not respond to usual glucose
replacement
O Get help immediately Ior
patient presenting with signs
oI either ketoacidosis (nausea
and vomiting, Kussmaul
respirations, Iruity breath
odor, hypotension, and altered
level oI consciousness) or
hyperosmolar hyperglycemic
nonketotic syndrome (nausea
and vomiting, hypothermia,
muscle weakness, seizures,
stupor, coma).
6 Risk Ior
Impaired Skin
Integrity related
to decreased
sensation and
circulation to
lower
extremities
Impaired
Skin
Integrity is
not appears
O Assess Ieet and legs Ior skin
temperature, sensation, soIt
tissue iniuries, corns, calluses,
dryness, hammer toe or
bunion deIormation, hair
distribution, pulses, deep
tendon reIlexes.
O Maintain skin integrity by
protecting Ieet Irom
breakdown.
4 Use heel protectors,
special mattresses,
Ioot cradles Ior
patients on bed rest.
4 Avoid applying drying
agents to skin (eg,
alcohol).
4 Apply skin
moisturizers to
No skin
breakdown
maintain suppleness
and prevent cracking
and Iissures.
O Instruct patient in Ioot care
guidelines
O Advise the patient who
smokes to stop smoking or
reduce iI possible, to reduce
vasoconstriction and enhance
peripheral blood Ilow. Help
patient to establish behavior
modiIication techniques to
eliminate smoking in the
hospital and to continue them
at home Ior smoking-
cessation program.
7 IneIIective
Coping related
to chronic
disease and
complex selI-
care regimen
EIIective
coping
O Discuss with the patient the
perceived eIIect oI diabetes
on liIestyle, Iinances, Iamily
liIe, occupation.
O Explore previous coping
strategies and skills that have
had positive eIIects.
O Encourage patient and Iamily
participation in diabetes selI-
care regimen to Ioster
conIidence.
O IdentiIy available support
groups to assist in liIestyle
adaptation.
O Assist Iamily in providing
emotional support.
Verbalizes
initial
strategies Ior
coping with
diabetes