OBJECTIVES

GENERAL OBJECTIVE:

At the end of the class the students will be able to acquire knowledge
about Diabetes mellitus, and develop positive attitude towards Diabetes mellitus
and practice these skills in the clinical area.

SPECIFIC OBJECTIVES: At the end of the class the group will be able to

 identify the risk factors

 identify the causative agents
 describe the clinical signs and symptoms
 discuss medical and nursing management
 discuss possible investigations
 discuss medications that may be used
 discuss infection control measures

DIABETES MELLITUS
DEFINITION:
 Diabetes mellitus is characterized by hyper glycaemia due to absolute or
relative insulin deficiency
  Diabetes mellitus, or simply diabetes, is a group of metabolic diseases in
which a person has high blood sugar, either because the pancreas does not
produce enough insulin, or because cells do not respond to the insulin that is
produced This high blood sugar produces the classical symptoms
.

of polyuria (frequenturination), polydipsia (increasedthirst)and

polyphagia (increased hunger).
TYPES
There are three main types of diabetes mellitus (DM).

 Type 1 DM results from the body's failure to produce insulin, and currently
requires the person to inject insulin or wear an insulin pump. This form was
previously referred to as "insulin-dependent diabetes mellitus" (IDDM) or
"juvenile diabetes".
severe insulin deficiency due to autoimmune destruction of the pancreatic islets

 Type 2 DM results from insulin resistance, a condition in which cells fail to use
insulin properly, sometimes combined with an absolute insulin deficiency. This
form was previously referred to as non insulin-dependent diabetes mellitus
(NIDDM) or "adult-onset diabetes".
 The third main form, gestational diabetes occurs when pregnant women without
a previous diagnosis of diabetes develop a high blood glucose level. It may
precede development of type 2 DM.
Other forms of diabetes mellitus include congenital diabetes, which is due
to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid
diabetes induced by high doses of glucocorticoids, and several forms of monogenic
diabetes.

CLASSIFICATION

Comparison of type 1 and 2 diabetes

Feature Type 1 diabetes Type 2 diabetes

Onset Sudden Gradual

Age at onset Mostly in children Mostly in adults

Body built Thin or normal Often obese

Ketoacidosis Common Rare

Auto antibodies Usually present Absent

Normal,decrease
Endogenous insulin Low or absent d
or increased

Concordance
50% 90%
in identical twins

Prevalence 10% 90%

Diabetes mellitus is classified into four broad categories: type 1, type 2, gestational
diabetes and "other specific types".
The "other specific types" are a collection of a few dozen individual causes. The
term "diabetes", without qualification, usually refers to diabetes mellitus.
The rare disease diabetes insipidus has similar symptoms as diabetes mellitus, but
without disturbances in the sugar metabolism (insipidus means "without taste" in
Latin).
The term "type 1 diabetes" has replaced several former terms, including childhood-
onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM).
Likewise, the term "type 2 diabetes" has replaced several former terms, including
adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes
mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard
nomenclature.
Type 1 diabetes
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta
cells of the islets of Langerhans in the pancreas, leading to insulin deficiency. This
type can be further classified as immune-mediated or idiopathic.
The majority of type 1 diabetes is of the immune-mediated nature, in which beta
cell loss is a T-cell-mediated autoimmune attack. There is no known preventive
measure against type 1 diabetes, which causes approximately 10% of diabetes
mellitus cases in North America and Europe.
Most affected people are otherwise healthy and of a healthy weight when onset
occurs. Sensitivity and responsiveness to insulin are usually normal, especially in
the early stages. Type 1 diabetes can affect children or adults, but was traditionally
termed "juvenile diabetes" because a majority of these diabetes cases were in
children.
"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that
was traditionally used to describe to dramatic and recurrent swings
in glucose levels, often occurring for no apparent reason in insulin-dependent
diabetes.
This term, however, has no biologic basis and should not be used. There are many
reasons for type 1 diabetes to be accompanied by irregular and
unpredictable hyperglycemias, frequently with ketosis, and sometimes
serious hypoglycemias, including an impaired counter regulatory response to
hypoglycemia, occult infection, gastroparesis (which leads to erratic absorption of
dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These
phenomena are believed to occur no more frequently than in 1% to 2% of persons
with type 1 diabetes.
Type 2 diabetes
Type 2 diabetes mellitus is characterized by insulin resistance, which may be
combined with relatively reduced insulin secretion.
The defective responsiveness of body tissues to insulin is believed to involve
the insulin receptor. However, the specific defects are not known. Diabetes
mellitus cases due to a known defect are classified separately. Type 2 diabetes is
the most common type.
In the early stage of type 2, the predominant abnormality is reduced insulin
sensitivity. At this stage, hyperglycemia can be reversed by a variety of measures
and medications that improve insulin sensitivity or reduce glucose production by
the liver.
Gestational diabetes
Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects,
involving a combination of relatively inadequate insulin secretion and
responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or
disappear after delivery.
Gestational diabetes is fully treatable, but requires careful medical supervision
throughout the pregnancy. About 20%–50% of affected women develop type 2
diabetes later in life.
Though it may be transient, untreated gestational diabetes can damage the health of
the fetus or mother.
Risks to the baby include macrosomia (high birth weight), congenital
cardiac and central nervous system anomalies, and skeletal muscle malformations.
Increased fetal insulin may inhibit fetal surfactant production and cause respiratory
distress syndrome.
Hyper bilirubinemia may result from red blood cell destruction. In severe
cases, perinatal death may occur, most commonly as a result of poor placental
perfusion due to vascular impairment. Labor induction may be indicated with
decreased placental function.
A Caesarean section may be performed if there is marked fetal distress or an
increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Pre diabetes indicates a condition that occurs when a person's blood glucose
levels are higher than normal but not high enough for a diagnosis of type 2 DM.
Many people destined to develop type 2 DM spend many years in a state of pre
diabetes which has been termed "America's largest healthcare epidemic."
Latent autoimmune diabetes of adults (LADA) is a condition in which type 1
DM develops in adults. Adults with LADA are frequently initially misdiagnosed as
having type 2 DM, based on age rather than etiology.
Some cases of diabetes are caused by the body's tissue receptors not responding to
insulin (even when insulin levels are normal, which is what separates it from type 2
diabetes); this form is very uncommon.
Genetic mutations (autosomal or mitochondrial) can lead to defects
in beta cell function. Abnormal insulin action may also have been genetically
determined in some cases. Any disease that causes extensive damage to
the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic
fibrosis).
 Diseases associated with excessive secretion of insulin-
antagonistic hormones can cause diabetes (which is typically resolved once the
hormone excess is removed). Many drugs impair insulin secretion and some toxins
damage pancreatic beta cells.
Causes
The cause of diabetes depends on the type.
Type 1 diabetes is partly inherited, and then triggered by certain infections, with
some evidence pointing at Coxsackie B4 virus.
A genetic element in individual susceptibility to some of these triggers has been
traced to particular HLA genotypes (i.e., the genetic "self" identifiers relied upon
by the immune system). However, even in those who have inherited the
susceptibility, type 1 DM seems to require an environmental trigger. The onset of
type 1 diabetes is unrelated to lifestyle.
Type 2 diabetes is due primarily to lifestyle factors and genetics.
The following is a comprehensive list of other causes of diabetes:
 Genetic defects of β-cell function
 Maturity onset diabetes of the young
 Mitochondrial DNA mutations
Genetic defects in insulin processing or insulin action
 Defects in proinsulin conversion
 Insulin gene mutations
 Insulin receptor mutations
Exocrine pancreatic defects
 Chronic pancreatitis
 Pancreatectomy
 Pancreatic neoplasia
 Cystic fibrosis
 Hemochromatosis
 Fibrocalculous pancreatopathy

 Endocrinopathies
 Growth hormone excess (acromegaly)
 Cushing syndrome
 Hyperthyroidism
 Pheochromocytoma
 Glucagonoma
Infections
 Cytomegalovirus infection
 Coxsackievirus B
 Drugs
 Glucocorticoids
 Thyroid hormone
 β-adrenergic agonists
 Statins

Pathophysiology
Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells
(primarily muscle and fat cells, but not central nervous system cells). Therefore, deficiency of
insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.
Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the
pancreas, in response to rising levels of blood glucose, typically after eating.
Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use
as fuel, for conversion to other needed molecules, or for storage.
Insulin is also the principal control signal for conversion of glucose to glycogen for internal
storage in liver and muscle cells.
Lowered glucose levels result both in the reduced release of insulin from the β-cells and in the
reverse conversion of glycogen to glucose when glucose levels fall.
This is mainly controlled by the hormone glucagon, which acts in the opposite manner to
insulin. Glucose thus forcibly produced from internal liver cell stores (as glycogen) re-enters the
bloodstream; muscle cells lack the necessary export mechanism.
Normally, liver cells do this when the level of insulin is low (which normally correlates with low
levels of blood glucose).
Higher insulin levels increase some anabolic ("building up") processes, such as cell growth and
duplication, protein synthesis, and fat storage.
Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of
metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin
level is the trigger for entering or leaving ketosis (the fat-burning metabolic phase).
If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin
(insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not have
its usual effect, so it will not be absorbed properly by those body cells that require it, nor will it
be stored appropriately in the liver and muscles.
Insulin resistance, which is the inability of cells to respond adequately to normal levels of
insulin, occurs primarily within the muscles, liver, and fat tissue.
In the liver, insulin normally suppresses glucose release. However, in the setting of insulin
resistance, the liver inappropriately releases glucose into the blood.
The net effect is persistent high levels of blood glucose, poor protein synthesis, and other
metabolic derangements, such as acidosis.
When the glucose concentration in the blood is raised to about 9-10 mmol/L (except certain
conditions, such as pregnancy), beyond its renal threshold(i.e. when glucose level surpasses
the transport maximum of glucose reabsorption), reabsorption of glucose in the proximal renal
tubuli is incomplete, and part of the glucose remains in the urine (glycosuria). This increases
the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in
increased urine production (polyuria) and increased fluid loss.
Lost blood volume will be replaced osmotically from water held in body cells and other body
compartments, causing dehydration and increased thirst.

SIGNS AND SYMPTOMS

Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually
develop much more slowly and may be subtle or absent in type 2 diabetes.
Diabetes may present with the classical triad of symptoms:
 polyuria (frequent urination), : due to osmotic diuresis caused by glycosuria
 polydipsia (increased thirst): due to the resulting loss of fl uid and electrolytes
 weight loss : due to fluid depletion and breakdown of fat and muscle secondary to insulin
deficiency.
 polyphagia (increased hunger).
Other common symptoms include tiredness, blurred vision (due to glucose-induced changes in
lens refraction) and itching of the genitalia (pruritus vulvae in women or balanitis in men) due to
Candida yeast infection (thrush).
Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to
changes in its shape, resulting in vision changes. Blurred vision is a common complaint leading
to a diabetes diagnosis. A number of skin rashes that can occur in diabetes are collectively
known as diabetic dermadromes.
Diabetic emergencies
People (usually with type 1 diabetes) may also present with diabetic ketoacidosis, a state of
metabolic dysregulation characterized by the smell of acetone, a rapid, deep breathing known
as Kussmaul breathing, nausea, vomiting and abdominal pain, and altered states of
consciousness.
A rare but equally severe possibility is hyperosmolar nonketotic state, which is more common in
type 2 diabetes and is mainly the result of dehydration.
Diagnostic Tests
Health history
Physical examination
Lab tests
On examination there may be evidence of weight loss and dehydration, and in diabetic
ketoacidosis the breath may have the sweet smell of ketones.
Skin infections with boils and abscesses are common.
Acanthosis nigricans (soft, velvety, brown skin) is a sign of hyperinsulinism and is seen
frequently in the axillae and groins of patients with insulin-resistant type 2 diabetes.
Necrobiosis lipoidica, due to collagen degeneration, may occur on the shins of some patients
with type 1 diabetes and often causes chronic ulceration.
The causes of diabetic foot ulceration are sites for evidence of lipohypertrophy (which may
cause unpredictable insulin release), lipoatrophy (now rare) or signs of infection (very rare).
Insulin-dependent patients are particularly susceptible to acute metabolic decompensation due
to hypoglycaemia or ketoacidosis, both of which require prompt clinical and biochemical
recognition.

Diabetes diagnostic criteria

Condition 2 hour glucose Fasting glucose HbA1c

mmol/l(mg/dl) mmol/l(mg/dl) %

Normal <7.8 (<140) <6.1 (<110) <6.0

≥ 6.1(≥110) &
Impaired fasting glycaemia <7.8 (<140) 6.0–6.4
<7.0(<126)

Impaired glucose tolerance ≥7.8 (≥140) <7.0 (<126) 6.0–6.4

Diabetes mellitus ≥11.1 (≥200) ≥7.0 (≥126) ≥6.5

Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by

demonstrating any one of the following:

 Fasting plasma glucose level ≥ 7.0 mmol/l (126 mg/dl)

 Plasma glucose ≥ 11.1 mmol/l (200 mg/dL) two hours after a 75 g oral glucose load as in
a glucose tolerance test
 Symptoms of hyperglycemia and casual plasma glucose ≥ 11.1 mmol/l (200 mg/dl)
 Glycated hemoglobin (Hb A1C) ≥ 6.5%.
It is preferable to measure a fasting glucose level because of the ease of measurement and the
considerable time commitment of formal glucose tolerance testing, which takes two hours to
complete and offers no prognostic advantage over the fasting test.
According to the current definition, two fasting glucose measurements above 126 mg/dl
(7.0 mmol/l) is considered diagnostic for diabetes mellitus.
People with fasting glucose levels from 110 to 125 mg/dl (6.1 to 6.9 mmol/l) are considered to
have impaired fasting glucose.
Patients with plasma glucose at or above 140 mg/dL (7.8 mmol/L), but not over 200 mg/dL
(11.1 mmol/L), two hours after a 75 g oral glucose load are considered to have impaired glucose
tolerance.
Of these two prediabetic states, the latter in particular is a major risk factor for progression to
full-blown diabetes mellitus, as well as cardiovascular disease.
Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular
disease and death from any cause.
Management
Diabetes mellitus is a chronic disease which cannot be cured except in very specific situations.
Management concentrates on keeping blood sugar levels as close to normal ("euglycemia") as
possible, without causing hypoglycemia.
This can usually be accomplished with diet, exercise, and use of appropriate medications
(insulin in the case of type 1 diabetes, oral medications, as well as possibly insulin, in type 2
diabetes).
Patient education, understanding, and participation is vital, since the complications of diabetes
are far less common and less severe in people who have well-managed blood sugar levels.
Attention is also paid to other health problems that may accelerate the deleterious effects of
diabetes.
These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of
regular exercise.
Specialised footwear is widely used to reduce the risk of ulceration, or re-ulceration, in at-risk
diabetic feet.
Lifestyle
A proper diet and exercise are the foundations of diabetic care, with a greater amount of exercise
yielding better results. Aerobic exercise leads to a decrease in HbA1c and improved insulin
sensitivity.
Resistance training is also useful and the combination of both types of exercise may be most
effective.
A diabetic diet that promotes weight loss is important. While the best diet type to achieve this is
controversial a low glycemic index diet has been found to improve blood sugar control.
Culturally appropriate education may help people with type 2 diabetes control their blood sugar
levels, for up to six months at least.
If changes in lifestyle in those with mild diabetes has not resulted in improved blood sugars
within six weeks, medications should then be considered.
Medications
Oral medications
Metformin 500mg is generally recommended as a first line treatment for type 2 diabetes, as
there is good evidence that it decreases mortality. Routine use of aspirin, however, has not been
found to improve outcomes in uncomplicated diabetes.
Other classes of medications include: sulfonylureas, nonsulfonylurea secretagogues, alpha
glucosidase inhibitors, thiazolidinediones, glucagon-like peptide-1 analog, and dipeptidyl
peptidase-4 inhibitors.
Metformin should not be used in those with severe kidney or liver problems. Injections
of insulin may either be added to oral medication or used alone.
Most people do not initially need insulin. When it is used, a long-acting formulation is typically
added at night, with oral medications being continued.
Doses are then increased to effect (blood sugar levels being well controlled).
When nightly insulin is insufficient twice daily insulin may achieve better control.
The long acting insulins, glargine and detemir, do not appear much better than neutral
protamine Hagedorn (NPH) insulin but have a significantly greater cost making them, as of
2010, not cost effective.
In those who are pregnant insulin is generally the treatment of choice.[7]
Insulin
Type 1 diabetes is typically treated with a combinations of regular and NPH insulin, or
synthetic insulin analogs.
When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially,
while continuing oral medications. Doses of insulin are then increased to effect.
Surgery
Weight loss surgery in those who are obese is an effective measure to treat diabetes. Many are
able to maintain normal blood sugar levels with little or no medications following surgery and
long term mortality is decreased. There however is some short term mortality risk of less than
1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet
clear. It however is recommended that this option be considered in those who are unable to get
both their weight and blood sugar under control.
Complications
Untreated, diabetes can cause many complications.
Acute complications include diabetic ketoacidosis and nonketotic hyperosmolar coma.
Serious long-term complications include cardiovascular disease, chronic renal failure,
and diabetic retinopathy (retinal damage).
Adequate treatment of diabetes is thus important, as well as blood pressure control and lifestyle
factors such as stopping smoking and maintaining a healthy body weight.
All forms of diabetes have been treatable since insulin became available in 1921, and type 2
diabetes may be controlled with medications. Insulin and some oral medications can
cause hypoglycemia (low blood sugars), which can be dangerous if severe. Both types 1 and 2
are chronic conditions that cannot be cured.
Pancreas transplants have been tried with limited success in type 1 DM; gastric bypass
surgery has been successful in many with morbid obesity and type 2 DM. Gestational diabetes
usually resolves after delivery.
All forms of diabetes increase the risk of long-term complications. These typically develop after
many years (10–20), but may be the first symptom in those who have otherwise not received a
diagnosis before that time.
The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk
of cardiovascular disease. The main "macrovascular" diseases (related to atherosclerosis of
larger arteries) are ischemic heart disease (angina and myocardial
infarction), stroke and peripheral vascular disease.
Diabetes also damages the capillaries (causes micro angiopathy). Diabetic retinopathy, which
affects blood vessel formation in the retina of the eye, can lead to visual symptoms, reduced
vision, and potentially blindness.
Diabetic nephropathy, the impact of diabetes on the kidneys, can lead to scarring changes in
the kidney tissue, loss of small or progressively larger amounts of protein in the urine, and
eventually chronic kidney disease requiring dialysis.
Diabetic neuropathy is the impact of diabetes on the nervous system, most commonly causing
numbness, tingling and pain in the feet and also increasing the risk of skin damage due to altered
sensation. Together with vascular disease in the legs, neuropathy contributes to the risk
of diabetes-related foot problems (such as diabetic foot ulcers) that can be difficult to treat and
occasionally require amputation.
Complications of diabetes mellitus
Microvascular/neuropathic
● Retinopathy, cataract,Impaired vision
● Nephropathy, Protein loss, renal failure
● Peripheral neuropathy, Sensory loss, motor weakness
● Autonomic neuropathy, Postural hypotension, vomiting, diarrhoea
● Foot disease, Ulceration, arthropathy
Macrovascular
● Coronary circulation, Myocardial ischaemia/ infarction
● Cerebral circulation, Transient ischaemic attack(TIA), stroke
● Peripheral circulation, Claudication, gangrene, Amputation, multifactorial, including diabetic
neuropathy, arterial insufficiency and increased susceptibility to infection.

Look for xanthomata in all newly presenting diabetic patients; their presence indicates
significant hyperlipidaemia ( Fig. 5.8D ). Examine insulin injection sites for evidence of
lipohypertrophy (which may cause unpredictable insulin release), lipoatrophy (now rare) or
signs of infection (very rare). Insulin-dependent patients are particularly susceptible to acute
metabolic decompensation due to hypoglycaemia or ketoacidosis, both of which require prompt
clinical and biochemical recognition.

Prevention
Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular
exercise.
Intensive lifestyle measures may reduce the risk by over half.
The benefit of exercise occurs regardless of the person's initial weight or subsequent weight
loss.
Evidence for the benefit of dietary changes alone, however, is limited, with some evidence for a
diet high in green leafy vegetables and some for limiting the intake of sugary drinks.
In those with impaired glucose tolerance, diet and exercise either alone or in combination
with metformin or acarbose may decrease the risk of developing diabetes.

Nursing Diagnosis for Diabetes Mellitus

1) Fluid Volume Deficit related to osmotic diuresis from hyperglycemia, polyuria, decreased
fluid intake as evidenced by increased urine output
2) Imbalanced Nutrition Less Than Body Requirements related to reduction of carbohydrate
metabolism due to insulin deficiency, inadequate intake due to nausea and vomiting as
evidenced by weight loss

3) Impaired Skin Integrity related to decreased sensory sensation, impaired circulation,

decreased activity / mobilization, lack of knowledge of skin care as evidenced by dry
skin ,itching, acne

4) Activity Intolerance related to weakness due to decreased energy production as evidenced

by unable to do ADL.

5) High risk of injury associated with decreased sensation sensory (visual), weakness, and
hypoglycemia.

6) Anxiety related to a lack of knowledge (diabetes management), the ability to remember the
less, diagnosis or treatment of a new way, cognitive limitations as evidenced by asking
questions.

7) Risk for ineffective management of therapeutic rules at home due to a lack of knowledge
about the condition of the therapeutic management, inadequate support systems.
Nursing Diagnosis : Fluid Volume Deficit related to osmotic diuresis.

Goal:
Demonstrate adequate hydration evidenced by stable vital signs, palpable peripheral pulse, skin
turgor and capillary refill well, individually appropriate urinary output, and electrolyte levels
within normal limits.

Nursing Intervention:
1.) Monitor vital signs.
Rational: hypovolemia can be manifested by hypotension and tachycardia.
2.) Assess peripheral pulses, capillary refill, skin turgor, and mucous membranes.
Rational: This is an indicator of the level of dehydration, or an adequate circulating volume.
3.) Monitor input and output, record the specific gravity of urine.
Rational: To provide estimates of the need for fluid replacement, renal function, and
effectiveness of the therapy given.

4.) Measure weight every day.

Rational: To provide the best assessment of fluid status of ongoing and further to provide a
replacement fluid.

5.) Provide fluid therapy as indicated.

Rational: The type and amount of liquid depends on the degree of lack of fluids and the
response of individual patients.
Nursing Diagnosis : Imbalanced Nutrition Less than Body Requirements related to
insufficiency of insulin, reduction of oral input, anorexia, nausea, increased metabolism of
protein, fat.
Goal:
Digest the amount of calories / nutrients right
Shows the energy level is usually Stable or increasing weight.
Nursing Interventions:
1.) Determine the patient's diet and eating patterns and compared with food that can be spent
by the patient.
Rationale: Identify deficiencies and deviations from the therapeutic needs.
2.) Weigh weight per day or as indicated.
Rational: Assessing an adequate food intake (including absorption and utilization).
3.) Identification of preferred food / desired include the needs of ethnic / cultural.
Rational: If the patient's food preferences can be included in meal planning, this cooperation
can be pursued after discharge.
4.) Involve patients in planning the family meal as indicated.
Rationale: Increase the sense of involvement; provide information on the family to understand
the patient's nutrition.
5.) Give regular insulin treatment as indicated.
Rational: regular insulin has a rapid onset and quickly and therefore can help move glucose
into cells.
1. Auscultation bowel sounds, record the existence of abdominal pain / abdominal bloating,
nausea, vomit that has not had time to digest food, maintain a state of fasting according to
the indication.
2. Give the liquid diet containing foods (nutrients) and the electrolyte immediately if the
patient has to tolerate it orally.
3. Observation of the signs of hypoglycemia, such as changes in level of consciousness, skin
moist / cold, rapid pulse, hunger, sensitive to stimuli, anxiety, headaches.
 4. Collaboration examination of blood sugar
Nursing Diagnosis : Risk for Infection related to hyperglycemia.
Goal:
Identify interventions to prevent / reduce the risk of infection.
Demonstrate techniques, lifestyle changes to prevent infection.
Nursing Interventions:
1). Observed signs of infection and inflammation.
Rationale: Patients may be entered with an infection that usually has sparked a state of
ketoacidosis or may have nosocomial infections.
2). Improve efforts to prevention by good hand washing for all people in contact with patients
including the patients themselves.
Rationale: Prevents cross infection.

3). Maintain aseptic technique in invasive procedures.

Rational: high glucose levels in blood would be the best medium for the growth of germs.

4). Give regular skin care.

Rational: the peripheral circulation may be disturbed that puts patients at increased risk of
damage to the skin / skin irritation and infection.

5). Make changes to the position, effective coughing and encourage deep breathing.
Rational: Assist in all areas and mobilize pulmonary secretions.
Diagnostic Studies - Diabetes Mellitus Nursing Care Plan (NCP)

 Serum glucose: Increased 200–1000 mg/dL or more.

 Serum acetone (ketones): Strongly positive.
 Fatty acids: Lipids, triglycerides, and cholesterol level elevated.
 Serum osmolality: Elevated but usually less than 330 mOsm/L.
 Glucagon: Elevated level is associated with conditions that produce (1) actual hypoglycemia,
(2) relative lack of glucose (e.g., trauma, infection), or (3) lack of insulin. Therefore, glucagon
may be elevated with severe DKA despite hyperglycemia.
 Glycosylated hemoglobin (HbA1C): Evaluates glucose control during past 8–12 wk with the
previous 2 wk most heavily weighted. Useful in differentiating inadequate control versus
incident-related DKA (e.g., current upper respiratory infection [URI]). A result greater than
8% represents an average blood glucose of 200 mg/dL and signals a need for changes in
treatment.
 Serum insulin: May be decreased/absent (type 1) or normal to high (type 2), indicating insulin
insufficiency/improper utilization (endogenous/exogenous). Insulin resistance may develop
secondary to formation of antibodies.
 Electrolytes:
 Sodium: May be normal, elevated, or decreased.
 Potassium: Normal or falsely elevated (cellular shifts), then markedly decreased.
 Phosphorus: Frequently decreased.
 Arterial blood gases (ABGs): Usually reflects low pH and decreased HCO3 (metabolic
acidosis) with compensatory respiratory alkalosis.
 CBC: Hct may be elevated (dehydration); leukocytosis suggest hemoconcentration, response
to stress or infection.
 BUN: May be normal or elevated (dehydration/decreased renal perfusion).
 Serum amylase: May be elevated, indicating acute pancreatitis as cause of DKA.
 Thyroid function tests: Increased thyroid activity can increase blood glucose and insulin
needs.
 Urine: Positive for glucose and ketones; specific gravity and osmolality may be elevated.
 Cultures and sensitivities: Possible UTI, respiratory or wound infections

Nursing Interventions Rationale

Observe for signs of infection and Patient may be admitted with infection, which
inflammation, e.g., fever, flushed could have precipitated the ketoacidotic state, or
appearance, wound drainage, may develop a nosocomial infection.
purulent sputum, cloudy urine.
Promote good handwashing by staff Reduces risk of cross-contamination.
and patient.
Maintain aseptic technique for IV High glucose in the blood creates an excellent
insertion procedure, administration medium for bacterial growth.
of medications, and providing
maintenance/site care. Rotate IV
sites as indicated.
Provide catheter/perineal care. Minimizes risk of UTI. Comatose patient may be
Teach the female patient to clean at particular risk if urinary retention occurred
from front to back after elimination before hospitalization. Note: Elderly female
diabetic patients are especially prone to urinary
tract/vaginal yeast infections.
Provide conscientious skin care; Peripheral circulation may be impaired, placing
gently massage bony areas. Keep the patient at increased risk for skin
skin dry, linens dry and wrinkle- irritation/breakdown and infection.
free.
Auscultate breath sounds. Rhonchi indicate accumulation of secretions
possibly related to pneumonia/bronchitis (may
have precipitated the DKA). Pulmonary
congestion/edema (crackles) may result from
rapid fluid replacement/HF.
Place in semi-Fowler’s position. Facilitates lung expansion; reduces risk of
aspiration.
Reposition and encourage Aids in ventilating all lung areas and mobilizing
coughing/deep breathing if patient is secretions. Prevents stasis of secretions with
alert and cooperative. Otherwise, increased risk of infection.
suction airway, using sterile
 technique, as needed.
Provide tissues and trash bag in a Minimizes spread of infection.
convenient location for sputum and
other secretions. Instruct patient in
proper handling of secretions.
Encourage/assist with oral hygiene. Reduces risk of oral/gum disease.
Encourage adequate dietary and Decreases susceptibility to infection. Increased
fluid intake (approximately3000 urinary flow prevents stasis and aids in
mL/day if not contraindicated by maintaining urine pH/acidity, reducing bacteria
cardiac or renal dysfunction), growth and flushing organisms out of system.
including 8 oz of cranberry juice per Note: Use of cranberry juice can help prevent
day as appropriate. bacteria from adhering to the bladder wall,
reducing the risk of recurrent UTI.
Administer antibiotics as Early treatment may help prevent sepsis.
appropriate.
Nursing Diagnosis: Sensory Perception, risk for disturbed (specify)
Risk factors may include

 Endogenous chemical alteration: glucose/insulin and/or electrolyte imbalance

Desired Outcomes

 Maintain usual level of mentation.

 Recognize and compensate for existing sensory impairments.

Monitor vital signs and mental status. Provides a baseline from which to
compare abnormal findings, e.g., fever
may affect mentation.
Address patient by name; reorient as needed Decreases confusion and helps maintain
to place, person, and time. Give short contact with reality.
explanations, speaking slowly and
enunciating clearly.
Schedule nursing time to provide for Promotes restful sleep, reduces fatigue,
uninterrupted rest periods. and may improve cognition.
Keep patient’s routine as consistent as Helps keep patient in touch with reality
possible. Encourage participation in and maintain orientation to the
activities of daily living (ADLs) as able. environment.
Protect patient from injury (avoid/limit use Disoriented patient is prone to injury,
of restraints as able) when level of especially at night, and precautions need to
consciousness is impaired. Place bed in low be taken as indicated. Seizure precautions
position. Pad bed rails and provide soft need to be taken as appropriate to prevent
airway if patient is prone to seizures. physical injury, aspiration.
 Evaluate visual acuity as indicated. Retinal edema/detachment, hemorrhage,
presence of cataracts or temporary
paralysis of extraocular muscles may
impair vision, requiring corrective therapy
and/or supportive care.

Investigate reports of hyperesthesia, pain, or Peripheral neuropathies may result in

sensory loss in the feet/legs. Look for severe discomfort, lack of/distortion of
ulcers, reddened areas, pressure points, loss tactile sensation, potentiating risk of
of pedal pulses. dermal injury and impaired balance.
Provide bed cradle. Keep hands/feet warm, Reduces discomfort and potential for
avoiding exposure to cool drafts/hot water dermal injury.
or use of heating pad.
Assist with ambulation/position changes. Promotes patient safety, especially when
sense of balance is affected.
Monitor laboratory values, e.g., blood Imbalances can impair mentation. Note: If
glucose, serum osmolality, Hb/Hct, fluid is replaced too quickly, excess water
BUN/Cr. may enter brain cells and cause alteration
in the level of consciousness (water
intoxication).
Carry out prescribed regimen for correcting Alteration in thought processes/potential
DKA as indicated. for seizure activity is usually alleviated
once hyperosmolar state is corrected.

MULTIPLE CHOICE QUESTIONS:

1. The probable cause of Erythroblastosis fetalis can be (c)

(a) Bleeding
(b) Haemophilia
(c) Adjoining of RBC
(d) Diapedesis
2. This can help on the diagnosis of the genetic basis of a disorder(a)
(a) PCR
(b) ELISA
(c) ABO blood group
(d) NMR
3. This measure does not help to prevent diabetes complications(c)
(a) controlling blood lipids and blood pressure
(b) Prompt detection of diabetic eye and kidney disease
(c) Eliminating all carbohydrates from the diet
(d) controlling blood glucose
4. The disease as a result of prolonged clotting is due to lack of plasma thromboplastin
component (PTC) necessary to the formation of thromboplastin, is(c)
(a) Haemophilia
(b) Hypoprothrombinemia
(c) Christmas disease
(d) Stuart disease
5. This diabetes drug acts by decreasing the amount of glucose produced by the liver(c)
(a) Alpha-glucosidase inhibitors
(b) Sulfonylureas
(c) Biguanides
(d) Meglitinides
6. Presence of RBC in urine is known as(b)
(a) Proteinuria
(b) Hematuria
(c) Urolithiasis
(d) Nephritis