All about Diabetes Mellitus and its complications

1. Mrs Dipali Dumbre
Msc Nursing
Medical Surgical Nursing
SCON

2. Definition
Diabetes mellitus is a chronic multisystem disease related
to abnormal insulin production, impaired insulin
utilization, or both.

3. Etiology
 Heredity
 Autoimmune
 Viral
 environmental factors (e.g., stress).
 Regardless of its cause, diabetes is primarily a disorder of
glucose metabolism related to absent or insufficient
insulin supplies and/or poor utilization of the insulin that
is available.

4. Classification
 The two most common types of diabetes are classified as
Type 1 diabetes mellitus
Type 2 diabetes mellitus
 Other classifications of diabetes commonly seen in
clinical practice
Gestational diabetes
Prediabetes
secondary diabetes

5. Type 1 diabetes mellitus
 Formerly known as “juvenile onset” or “insulin-
dependent” diabetes.
 Type 1 diabetes mellitus most often occurs in people who
are under 30 years of age, with a peak onset between ages
11 and 13, but it can occur at any age.
 Typically, it is seen in people with a lean body type,
although it can occur in people who are overweight.

6. Etiology
 Type 1 diabetes is the end result of a long-standing process
in which the body's own T cells attack and destroy
pancreatic beta (β) cells, which are the source of the
body's insulin.
 Autoantibodies to the islet cells cause a reduction of 80%
to 90% of normal β-cell function before hyperglycemia .
 A genetic predisposition and exposure to a virus are factors
that may contribute to the pathogenesis of immune-
related type 1 diabetes.

7.  Type 1 diabetes may be caused by nonimmune factors of
unknown (idiopathic) etiologies is known as type 1B
diabetes.
 When type 1 diabetes is caused by an immune
mechanism, the disease is known as type 1A.

8. Onset of Disease
 Type 1 diabetes is associated with a long preclinical period.
 The islet cell autoantibodies responsible for β-cell destruction
are present for months to years before the onset of symptoms.
 Manifestations of type 1 diabetes develop when the person's
pancreas can no longer produce insulin.
 The onset of symptoms is usually rapid, and the patient comes
to the emergency department with impending or acute
ketoacidosis.

9.  The patient usually has a history of recent and sudden weight
loss.
 The classic symptoms of
 Polydipsia (excessive thirst)
 Polyuria (frequent urination)
 Polyphagia (excessive hunger)
 The individual with type 1 diabetes requires a supply of insulin
from an outside source (exogenous insulin), such as an
injection, in order to sustain life.
 Without insulin, the patient will develop diabetic
ketoacidosis (DKA), a life-threatening condition resulting in
metabolic acidosis.

10.  Newly diagnosed patients with type 1 diabetes often experience
a remission, or “honeymoon period,” soon after treatment is
initiated.
 During this time, the patient requires very little injected
insulin because β-cell mass remains sufficient for glucose
control as the progressive destruction continues to occur.
 Eventually, as more β cells are destroyed, blood glucose levels
increase, more insulin is needed, and the honeymoon period
ends.
 The honeymoon period usually lasts 3 to 12 months, after
which the person will require insulin on a permanent basis.

11. Prediabetes
 Prediabetes, also known as impaired glucose tolerance
(IGT) or impaired fasting glucose, is a condition in which
blood glucose levels are higher than normal (>100 mg/dl but
<126 mg/dl [7.0 mmol/L] when fasting) but not high enough
for a diagnosis of diabetes .
 Most people with prediabetes are at increased risk for
developing type 2 diabetes, and if no preventive measures are
taken, they will usually develop it within 10 years.
 Long-term damage to the body, especially the heart and blood
vessels, may already be occurring in patients with prediabetes.

12.  People with prediabetes usually do not have symptoms.
 Individuals with prediabetes should test their blood
glucose regularly and watch for the symptoms of diabetes,
such as polyuria, polyphagia, or polydipsia.
 If action is taken to manage blood glucose, patients with
prediabetes can delay or prevent the development of type
2 diabetes.
 Maintaining a healthy weight, exercising regularly, and
eating a healthy diet have all been found to reduce the
risk of developing diabetes in people with prediabetes.

13. Gestational Diabetes
 Gestational diabetes develops during pregnancy .
 It is detected at 24 to 28 weeks of gestation.
 Women with gestational diabetes have a higher risk for
cesarean delivery, perinatal death, and neonatal
complications.
 Although most women with gestational diabetes will
have normal glucose levels within 6 weeks postpartum,
 Their risk for developing type 2 diabetes in 5 to 10 years is
increased.
 Nutritional therapy is considered to be the first-line
therapy.
 If nutritional therapy alone does not achieve desirable
fasting blood glucose levels, insulin therapy is usually
indicated.

14. Secondary Diabetes
Diabetes occurs because of another medical condition or
due to the treatment of a medical condition that causes
abnormal blood glucose levels.
Conditions that may cause secondary diabetes can result
from damage to, injury to, interference with, or destruction
of the pancreas.

15. These include Cushing syndrome, hyperthyroidism,
recurrent pancreatitis, and the use of parenteral
nutrition.
Commonly used medications that can induce diabetes
include corticosteroids (prednisone), thiazides,
phenytoin , and atypical antipsychotics .
Secondary diabetes usually resolves when the
underlying condition is treated.

16. Type 2 Diabetes Mellitus
Definition:
“The pancreas usually continues to produce some
endogenous (self-made) insulin, the insulin that is
produced is either insufficient for the needs of the body
and/or is poorly utilized by the tissues.”

17. • Type 2 diabetes mellitus is, by far, the most prevalent type
of diabetes, accounting for over 90% of patients with
diabetes.
• Type 2 diabetes usually occurs in people over 35 years of
age, and 80% to 90% of patients are overweight at the
time of diagnosis.

18. Etiology
 In type 2 diabetes the insulin that is produced is either
insufficient for the needs of the body and/or is poorly
utilized by the tissues.
Risk factor are:
 Obesity, specifically abdominal and visceral adiposity.
 Metabolic syndrome is a cluster of abnormalities that act
synergistically to greatly increase the risk for
cardiovascular disease and diabetes.

19.  Metabolic syndrome is characterized by
 Insulin resistance
Elevated insulin levels
 High levels of triglycerides (more than 150mg/dl)
 Decreased levels of high-density lipoproteins
(HDLs)
 Increased levels of low-density lipoproteins (LDLs)
Hypertension

20. Pathophysiology
 First Factor is Insulin resistance:
 Insulin resistance in glucose and lipid metabolism, which is a
condition in which body tissues do not respond to the action
of insulin.
 This is due to insulin receptors that are either unresponsive to
the action of insulin and/or insufficient in number.
 Most insulin receptors are located on skeletal muscle, fat, and
liver cells.
 When insulin is not properly used, the entry of glucose into
the cell is impeded, resulting in hyperglycemia.

21.  A second factor in the development of type 2 diabetes is
a marked decrease in the ability of the pancreas to
produce insulin, as the β cells become fatigued from the
compensatory overproduction of insulin or when β-cell
mass is lost.
 A third factor is inappropriate glucose production by the
liver. Instead of properly regulating the release of glucose
in response to blood levels, the liver does so in a
haphazard way that does not correspond to the body's
needs at the time.

22.  A fourth factor is alteration in the production of
hormones and cytokines by adipose tissue (adipokines).
Adipokines appear to play a role in glucose and fat
metabolism.

24. Onset of Disease
 Disease onset in type 2 diabetes is usually gradual.
 The person may go for many years with undetected
hyperglycemia that might produce few symptoms.
 If the patient with type 2 diabetes has marked
hyperglycemia a sufficient endogenous insulin supply may
prevent DKA from occurring.
 However, osmotic fluid and electrolyte loss related to
hyperglycemia may become severe and lead to
hyperosmolar coma.

25. Clinical Manifestation
 The clinical manifestations of type 2 diabetes are often
nonspecific.
 Fatigue
 Recurrent infections
 Prolonged wound healing
 Blurred vision
 Weight loss

26. Diagnostic studies
• Fasting plasma glucose level ≥126 mg/dl.
• Fasting is defined as no caloric intake for at least 8 hours.
 Random glucose measurement ≥200 mg/dl)
 Two-hour OGTT level ≥200 mg/dl (11.1 mmol/L), using a
glucose load of 75 g.
 When overt symptoms of hyperglycemia (polyuria,
polydipsia, and polyphagia) coexist with FPG levels of 126
mg/dl or greater, further testing using the OGTT may not
be necessary to make a diagnosis

27.  Measurement of glycosylated hemoglobin, also known as
the hemoglobin A1C (A1C) test.
 A1C tests are used by diabetic patients and health care
providers to monitor success of treatment and to make
changes in treatment modalities.
 It is not used as a diabetes diagnostic test.
 The test works by showing the amount of glucose that has
been attached to hemoglobin molecules over their life
span.

28.  When blood glucose is elevated over time, the amount of
glucose attached to the hemoglobin molecule increases
and remains attached to the red blood cell (RBC) for the
life of the cell (approximately 120 days).
 Therefore a glycosylated hemoglobin test indicates the
overall glucose control for the previous 90 to 120 days.
 All patients with diabetes should have regular
assessments of A1C done.
 For people with diabetes, the ideal A1C goal is 7.0% or less

30. Procedure for OGTT
 A zero time (baseline) blood sample is drawn.
 The patients is then given 75g of glucose solution to drink
within a 5 minute time frame.
 The blood is drawn as per the interval but usually 2 hours
interval is taken.

31. Collaborative care
 The goals of diabetes management are to reduce
symptoms, promote well-being, prevent acute
complications of hyperglycemia,.
 These goals are most likely to be met when the patient is
able to maintain blood glucose levels as near to normal as
possible.
 Diabetes is a chronic disease that requires daily decisions
about food intake, blood glucose testing, medication, and
exercise.

32.  Patient teaching, which enables the patient to become
the most active participant in his or her own care, is
essential for a successful treatment plan.
 Nutritional therapy, drug therapy, exercise, and self-
monitoring of blood glucose are the tools used in the
management of diabetes .

33. Drug Therapy
 Exogenous (injected) insulin is needed when a patient has
inadequate insulin to meet specific metabolic needs.
 People with type 1 diabetes require exogenous insulin to
survive and may need up to four to five injections per day
to adequately control blood glucose levels.
 People with type 2 diabetes, who are usually controlled
with diet, exercise, may require exogenous insulin
temporarily during periods of severe stress such as illness
or surgery.

34. Types of Insulin
 In the past, insulin was made from beef and pork
pancreas, but these forms of insulin are no longer
available.
 Today, only human insulin is used.
 Human insulin is not directly harvested from human
organs. Instead, it is prepared through the use of genetic
engineering. The insulin is derived from common bacteria
(e.g., Escherichia coli) or yeast cells using recombinant
DNA technology .

35.  Insulin differ in regard to onset, peak action, and duration and
are categorized as
 Rapid-acting,
 Short-acting,
 Intermediate-acting
 Long-acting insulin.
 The specific properties of each type of insulin are matched
with the patient's diet and activity.
 Various combinations of these insulin can be used to give
treatment to the patient's specific pattern of blood glucose
levels, lifestyle, eating, and activity patterns.

36. Insulin preparations showing onset, peak, and
duration of action

37. Types of Insulin
CLASSIFICATION EXAMPLES: CLARITY OF SOLUTION
Rapid-acting insulin Lispro (Humalog), clear
Aspart (NovoLog), clear
Glulisine (Apidra), clear
Short-acting insulin Regular (Humulin R, Novolin R, ReliOn R), clear
Intermediate-acting
insulin
NPH (Humulin N, Novolin N, ReliOn N), cloudy
Long-acting insulin Glargine (Lantus), clear
Detemir (Levemir), clear
Combination therapy
(premixed)
NPH/regular 70/30 (Humulin 70/30,
Novolin 70/30, ReliOn 70/30), cloudy
NPH/regular 50/50* (Humulin 50/50), cloudy

38.  Rapid acting insulin analog have an onset of action of
approximately 15 minute and should be injected 0 to 15
min before the meal.
 Short acting regular insulin has an onset of action 30 to
60 mintues and should be injected 30 to 45minute before
a meal to ensure that the onset of action coincides with
meal absorption.
 Long –acting insulins are released steadily and
continuously, they are used for once-daily .
 Short or rapid-acting insulin is often mixed with
intermediate –acting insulin to provide both mealtime
and basal coverage without having to administer two
separate injections

39. Insulin Regimens.
 The timing of insulin administration in relation to meal is very
important.
 Regular insulin is taken 30 to 45 minutes before meals to
ensure the onset of action in conjunction with meal
absorbtion.
 Ideally, regimens should be mutually selected by the patient
and the health care provider.
 The criteria for selection are based on the desired and feasible
levels of glycemic control and the patient's lifestyle.

41. Storage of insulin
 As a protein, insulin requires special storage
considerations.
 Heat and freezing alter the insulin molecule.
 Insulin vials that the patient is currently using may be left
at room temperature for up to 4 weeks unless the room
temperature is higher than 86° F (30° C) or below freezing
(less than 37° F [2° C]).
 Prolonged exposure to direct sunlight should be avoided.
 Extra insulin should be stored in the refrigerator.
 Prefilled syringes are stable for up to 30 days when stored
in the refrigerator.
 Syringes prefilled with a cloudy solution should be stored
in a vertical position with the needle pointed up to avoid
clumping of suspended insulin binders in the needle.

42. Administration of Insulin

43. Injection sites for insulin

44. Problems with Insulin Therapy
 Allergic Reactions.
Local inflammatory reactions to insulin may occur, such as
itching, erythema, and burning around the injection site.
 Local reactions may be self-limiting within 1 to 3 months
or may improve with a low dose of antihistamine.
 Lipodystrophy.
Lipodystrophy (atrophy of subcutaneous tissue) may occur if
the same injection sites are used frequently.
 It is best prevented by rotation of injection sites.
 Hypertrophy, a thickening of the subcutaneous tissue,
eventually regresses if the patient does not use the site for
at least 6 months.
 The use of hypertrophied sites may result in erratic insulin
absorption.

45.  Somogyi Effect and Dawn Phenomenon.
The Somogyi effect is a rebound effect in which an
overdose of insulin induces hypoglycemia.
 Usually occurring during the hours of sleep, the Somogyi
effect produces a decline in blood glucose level in
response to too much insulin.
Counterregulatory hormones are released, stimulating
lipolysis, gluconeogenesis, and glycogenolysis, which in
turn produce rebound hyperglycemia .
The danger of this effect is that when blood glucose levels
are measured in the morning, hyperglycemia is apparent
and the patient (or the health care professional) may
increase the insulin dose.
The patient may report headaches on awakening and may
recall night sweats or nightmares.

46. If the Somogyi effect is suspected as a cause for early
morning high blood glucose, the patient may be advised
to check blood glucose levels between 2:00 and 4:00 am to
determine if hypoglycemia is present at that time.
If it is, the insulin dosage affecting the early morning
blood glucose is reduced.
 Dawn phenomenon :
It is characterized by hyperglycemia that is present on
awakening in the morning due to the release of
counterregulatory hormones in the predawn hours.
It has been suggested that growth hormone and cortisol
are possible factors in this occurrence.
The dawn phenomenon affects the majority of people
with diabetes and tends to be most severe when growth
hormone is at its peak in adolescence and young
adulthood.

47. Drug Therapy: Oral Agents
 Oral agents (OAs) are not insulin, but they work to
improve the mechanisms by which insulin and glucose are
produced and used by the body.
 OAs work on the three defects of type 2 diabetes:
(1) insulin resistance
(2) decreased insulin production
(3) increased hepatic glucose production.
 OAs may be used in combination with agents from other
classes or with insulin to achieve blood glucose targets.

48. Nutritional Therapy
 The overall goal of nutritional therapy is to assist people with
diabetes in making healthy nutritional choices, eating a varied
diet, and maintaining exercise habits that will lead to
improved metabolic control.
 Maintain blood glucose levels to as near normal as safely
possible to prevent or reduce the risk for complications of
diabetes.
 Achieve lipid profiles and blood pressure levels that reduce the
risk for cardiovascular disease.
 Modify lifestyle as appropriate for the prevention and
treatment of obesity, dyslipidemia, cardiovascular disease, and
nephropathy.
 Improve health through healthy food choices and physical
activity.
 Address individual nutritional needs while taking into account
personal and cultural preferences and respecting the
individual's willingness to change.

49. Food Composition.
Carbohydrates.
 In the diabetic meal plan, carbohydrates and monounsaturated fats
should provide 45% to 65% of the total energy intake each day.
 Carbohydrates include sugars, starches, and fiber. Foods containing
carbohydrates from whole grains, fruits, vegetables, and low-fat milk
should be included as part of a healthy meal plan.21
 Glycemic index (GI) is the term used to describe the rise in blood
glucose levels after a person has consumed a carbohydrate-
containing food.
 A GI of 100 refers to the response of 50 g of glucose or white bread in
a normal person without diabetes.
 All other food with an equivalent carbohydrate value is measured
against this standard. For example, the GI of an apple is 52, regular
milk 27, baked potato 93, cornflake cereal 119, and baked beans 69.
 The GI of carbohydrates should be considered when choosing them
in a meal plan.
 Foods with a high GI (e.g., potatoes, white bread) will cause a sharp
rise in blood glucose, whereas those with a low GI (e.g., brown rice),
steadily increase blood glucose over a longer period of time.

50. Fats
 Fat should compose no more than 25% to 30% of the meal
plan's total calories, with less than 7% of calories from
saturated fats.
 Less than 300 mg/day of cholesterol and limited trans fats
are also recommended as part of a healthy meal plan.
 Decreasing fat and cholesterol intake assists in reducing
the risk for cardiovascular disease.
 Individuals with elevated LDL are advised to lower their
saturated fat intake to 7% and cholesterol to under 200
mg/day.

51. Protein.
 Protein should contribute less than 10% of the total energy
consumed in those with diabetes.
 Protein intake for the diabetic patient should be significantly lower
than the general population.
Alcohol.
 Alcohol is high in calories, has no nutritive value, and promotes
hypertriglyceridemia.
 The inhibitory effect of alcohol on glucose production by the liver
can cause severe hypoglycemia in patients on insulin or oral
hypoglycemic medications that increase insulin secretion.
 Patients should be cautioned to honestly discuss the use of alcohol
with their health care providers because its use can make blood
glucose more difficult to control.
 Moderate alcohol consumption can sometimes be safely
incorporated into the meal plan if blood glucose levels are well
controlled and if the patient is not on medications that will cause
adverse effects.
 Moderate consumption is defined as one drink per day for women
and two drinks per day for men.

52. Exercise for Patients with Diabetes Mellitus
1. Exercise does not have to be vigorous to be effective. The
blood glucose–reducing effects of exercise can be attained
with exercise such as brisk walking.
2. The exercises selected should be enjoyable to foster
regularity.
3. The exercise session should have a warm-up period and a
cool-down period. The exercise program should be started
gradually and increased slowly.
4. Exercise is best done after meals, when the blood glucose
level is rising.
5. Exercise plans should be individualized for each patient
and monitored by the health care provider.

53. 6. It is important to self-monitor blood glucose levels before,
during, and after exercise to determine the effect exercise has
on blood glucose level at particular times of the day.
 Before exercise, if blood glucose is less than 100 mg/dl, eat a
10-15 g carbohydrate snack. After 15 to 30 minutes, retest blood
glucose levels. Do not exercise if less than 100 mg/dl.
 Before exercise, if blood glucose is over 250 mg/dl, delay
exercise or if patient insists on exercising, reduce the intensity
and duration by half.
 Recheck blood glucose at the end of the exercise program.
7. Be alert to the possibility of delayed exercise-induced
hypoglycemia, which may occur several hours after the
completion of exercise.
8. Taking a glucose-lowering medication does not mean that
planned or spontaneous exercise cannot occur.
9. It is important to compensate for extensive planned and
spontaneous activity by monitoring blood glucose level to
make adjustments in the insulin dose (if taken) and food
intake.

54. Self-Monitoring of Blood Glucose (SMBG)
1. Wash hands in warm water. It is not necessary to clean the site
with alcohol, and it may interfere with test results. Finger
should be dry before puncturing it.
2. If it is difficult to obtain an adequate drop of blood for testing,
warm the hands in warm water or let the arms hang
dependently for a few minutes before the finger puncture is
made.
3. If the puncture is made on the finger, use the side of the finger
pad rather than near the center. Fewer nerve endings are along
the side of the finger pad.
4. The puncture should be only deep enough to obtain a
sufficiently large drop of blood. Unnecessarily deep punctures
may cause pain and bruising.
5. Follow monitor instructions for testing the blood.
6. Record results. Compare to personal target blood glucose
goals.

56. Complications of diabetes mellitus
 Acute complications:
 Ketoacidosis
 The hyperglycemic hyperosmolar nonketotic syndrome
 Hypoglycemia
 Chronic complications:
 Disorders of the microcirculation
 Neuropathies
 Nephropathies
 Retinopathies
 Macrovascular complications
 Foot ulcers

58. Definition
Diabetic ketoacidosis (DKA), also referred to as diabetic
acidosis and diabetic coma, is caused by a profound
deficiency of insulin and is characterized by
hyperglycemia, ketosis, acidosis, and dehydration.

59. Etiology
 Type 1 diabetes
 Type 2 diabetes in conditions of severe illness or stress
when the pancreas cannot meet the extra demand for
insulin.
 Precipitating factors include
Illness and infection
Inadequate insulin dosage
 Undiagnosed type 1 diabetes
 Poor self-management, and neglect.

60. Pathophysiology
 When the circulating supply of insulin is insufficient,
glucose cannot be properly used for energy so that the
body breaks down fat stores as a secondary source of fuel .
 Ketones are acidic by-products of fat metabolism that can
cause serious problems when they become excessive in
the blood.
 Ketosis alters the pH balance, causing metabolic acidosis .

61.  Ketonuria is a process that begins when ketone bodies are
excreted in the urine.
 During this process, electrolytes become depleted as
cations are eliminated along with the anionic ketones in an
attempt to maintain electrical neutrality.
 Insulin deficiency impairs protein synthesis and causes
excessive protein degradation.

62.  Insulin deficiency also stimulates the production of
glucose from amino acids in the liver and leads to further
hyperglycemia.
 Because there is a deficiency of insulin, the additional
glucose cannot be used and the blood glucose level rises
further, adding to the osmotic diuresis.
 Untreated, this leads to severe depletion of sodium,
potassium, chloride, magnesium, and phosphate.
 Vomiting caused by the acidosis results in more fluid and
electrolyte losses.

63.  Eventually, hypovolemia followed by shock.
 Renal failure may eventually occur from hypovolemic
shock.
 This causes the retention of ketones and glucose, and the
acidosis progresses.
 Untreated, the patient becomes comatose as a result of
dehydration, electrolyte imbalance, and acidosis.
 If the condition is not treated, death is inevitable.

64. Clinical Manifestation
 Dehydration such as poor skin turgor,
 Dry mucous membranes,
 Tachycardia,
 Orthostatic hypotension.
 Lethargy and weakness.
 As the patient becomes severely dehydrated, the skin becomes
dry and loose, and the eyeballs become soft and sunken.
 Abdominal pain is another symptom of DKA that may be
accompanied by anorexia and vomiting.

65.  Finally, Kussmaul respirations (rapid, deep breathing
associated with dyspnea) are the body's attempt to reverse
metabolic acidosis through the exhalation of excess carbon
dioxide.
 Acetone is noted on the breath as a sweet, fruity odor.
 Laboratory findings include a blood glucose level above 300
mg/dl .
 arterial blood gas
 pH below 7.30,
 serum bicarbonate level less than 15 mEq/L (15 mmol/L),
 Ketones in the blood and urine.

66. Diagnostic Studies
 History and physical examination
 Blood studies, including immediate blood glucose,
complete blood count,
 Ketones,
 pH, electrolytes,
 Blood urea nitrogen
 Arterial blood gases
 Urinalysis, including specific gravity, pH, glucose, acetone

67. EMERGENCY MANAGEMENT:
 Etiology
Undiagnosed diabetes mellitus
• Inadequate treatment of existing diabetes mellitus
• Insulin not taken as prescribed
• Infection
• Change in diet, insulin, or exercise regimen
 Assessment findings
• Thirst
• Abdominal pain
• Nausea and vomiting
• Gradually increasing restlessness, confusion, lethargy

68. • Flushed, dry skin
• Eyes appear sunken
• Breath odor of ketones
• Rapid, weak pulse
• Labored breathing (Kussmaul respirations)
• Fever
• Urinary frequency
• Serum glucose 300 mg/dl (16.7 mmol/L)
• Glucosuria and ketonuria

69. Collaborative Management
 Administration of intravenous fluids
 Intravenous administration of rapid-acting insulin
 Electrolyte replacement
 Assessment of mental status
 Recording of intake and output
 Central venous pressure monitoring (if indicated)
 Assessment of blood glucose levels
 Assessment of blood and urine for ketones
 ECG monitoring
 Assessment of cardiovascular and respiratory status
 ECG, Electrocardiogram.

70.  Intervention:
Initial
• Ensure patent airway.
• Administer oxygen.
• Establish IV access with large-bore catheter.
• Begin fluid resuscitation with 0.9% NaCl solution 1 L/hr
until BP stabilized and urine output 30-60 ml/hr.
• Begin continuous regular insulin drip 0.1 U/kg/hr.
• Identify history of diabetes, time of last food, and
time/amount of last insulin injection.

71.  Ongoing Monitoring
• Monitor vital signs, level of consciousness, cardiac rhythm,
oxygen saturation, and urine output.
• Assess breath sounds for fluid overload.
• Monitor serum glucose and serum potassium.
• Administer potassium to correct hypokalemia.
• Administer sodium bicarbonate if severe acidosis (pH 7.0).

72. The hyperglycemic hyperosmolar nonketotic
(HHNK) syndrome
 Hyperosmolar hyperglycemic state (HHS) is a complication
of diabetes mellitus (predominantly type 2) in which high
blood sugars cause severe dehydration, increases in osmolality
 In hyperosmolar states, the increased serum osmolality has the
effect of pulling water out of body cells, including brain cells.
The condition may be complicated by thromboembolic events
arising because of the high serum osmolality.
 The most prominent manifestations are dehydration:
 Neurologic signs and symptoms:
 Seizures

73. • Muscle fasciculations
• Hyperthermia
• Nystagmus
• Visual hallucinations
• Excessive thirst
• The onset of HHNK syndrome often is insidious, and because it
occurs most frequently in older people, it may be mistaken for a
stroke.
• The main difference between HHS and DKA is that the patient
with HHS usually has enough circulating insulin so that
ketoacidosis does not occur.

74. Pathophysiology

75. Treatment
 HHS constitutes a medical emergency and has a high mortality
rate.
 Therapy is similar to that for the treatment of DKA and includes
immediate IV administration of either 0.9% or 0.45% NaCl .
 Regular insulin is given by IV bolus, followed by an infusion after
fluid replacement therapy is instituted to aid in reducing the
hyperglycemia.
 When blood glucose levels fall to approximately 250 mg/dl (13.9
mmol/L), IV fluids containing glucose are administered to prevent
hypoglycemia.
 Electrolytes are monitored and replaced as needed.
 Vital signs, intake and output, tissue turgor, laboratory values, and
cardiac monitoring are assessed to monitor the efficacy of fluid and
electrolyte replacement.
 Patients with renal or cardiac compromise require special
monitoring to avoid fluid overload during fluid replacement.
 This includes monitoring of serum osmolality and frequent
assessment of cardiac, renal, and mental status.

76. Hypoglycemia
 Hypoglycemia occurs from a relative excess of insulin in the blood and is
characterized by below-normal blood glucose levels.
 It occurs most commonly in people treated with insulin injections, but
prolonged hypoglycemia also can result from some oral hypoglycemic
agents.

77.  Many factors precipitate an insulin reaction in a person with type 1
diabetes, including:
 Error in insulin dose
 Failure to eat
 Increased exercise
 Decreased insulin need after removal of a stress situation
 Medication changes and a change in insulin site
 Alcohol decreases liver gluconeogenesis, and people with diabetes
need to be cautioned about its potential for causing hypoglycemia.

78.  Because the brain relies on blood glucose as its main energy source,
hypoglycemia produces behaviors related to altered cerebral function:
 Headache
 Difficulty in problem solving
 Disturbed or altered behavior
 Coma
 Seizures
 At the onset of the hypoglycemic episode, activation of the parasympathetic
nervous system often causes hunger.
 The initial parasympathetic response is followed by activation of the
sympathetic nervous system; this causes anxiety, tachycardia, sweating, and
constriction of the skin vessels (i.e., the skin is cool and clammy).

79. Treatment
 The most effective treatment of an insulin reaction is the
immediate ingestion of a concentrated carbohydrate source,
such as sugar, honey, candy, or orange juice.
 Alternative methods for increasing blood glucose may be
required when the person having the reaction is unconscious or
unable to swallow:
 Glucagon may be given intramuscularly or subcutaneously.
 In situations of severe or life-threatening hypoglycemia, it
may be necessary to administer glucose intravenously.

80. Macrovascular complications
Macrovascular complications are diseases of the large and medium-size
blood vessels that occur with greater frequency and with an earlier onset
in people with diabetes.
 Diabetes mellitus is a major risk factor for coronary artery disease,
cerebrovascular disease, and peripheral vascular disease.
 Multiple risk factors for vascular disease, including obesity,
hypertension, hyperglycemia, hyperlipidemia, altered platelet
function, are found in people with diabetes.
 In people with type 2 diabetes, macrovascular disease may be present
at the time of diagnosis.
 In type 1 diabetes, the attained age and the duration of diabetes appear
to correlate with the degree of macrovascular disease.

81. MICROVASCULAR
COMPLICATIONS
“Microvascular complications result from thickening of the
vessel membranes in the capillaries and arterioles in response
to conditions of chronic hyperglycemia.’”

82. Peripheral neuropathies
 Diabetic neuropathy is nerve damage that occurs because of the
metabolic derangements associated with diabetes mellitus.
 About 60% to 70% of patients with diabetes have some degree of
neuropathy, with neurologic complications occurring equally in type 1 and
type 2 diabetes.
 The most common type of neuropathy affecting persons with diabetes is
sensory neuropathy.
 This can lead to the loss of protective sensation in the lower extremities
and complications that result in a lower limb amputation.

83. Classification
 The two major categories of diabetic neuropathy are sensory
neuropathy, which affects the peripheral nervous system, and
autonomic neuropathy. Each of these types can take on several
forms.
1.Sensory Neuropathy
 The most common form of sensory neuropathy is distal
symmetric neuropathy, which affects the hands and/or feet
bilaterally.
 Characteristics of distal symmetric neuropathy include
 loss of sensation,
 abnormal sensations,
 pain, and paresthesias.
 The pain, which is often described as burning, cramping,
crushing, or tearing, is usually worse at night and may occur
only at that time.

84.  The paresthesias may be associated with tingling,
burning, and itching sensations.
 The patient may report a feeling of walking on pillows
or numb feet.
 At times the skin becomes so sensitive (hyperesthesia)
that even light pressure from bedsheets cannot be
tolerated.
 Complete or partial loss of sensitivity to touch and
temperature is common.
 Foot injury and ulcerations can occur without the
patient ever having pain .
 Neuropathy can also cause atrophy of the small
muscles of the hands and feet, causing deformity and
limiting fine movement.

85. 2. Autonomic Neuropathy.
 Autonomic neuropathy can affect nearly all body systems
and lead to hypoglycemic unawareness, bowel
incontinence and diarrhea, and urinary retention.
 Delayed gastric emptying (gastroparesis) is a complication
of autonomic neuropathy that can produce anorexia,
nausea, vomiting, gastroesophageal reflux, and persistent
feelings of fullness.
 Gastroparesis can trigger hypoglycemia by delaying food
absorption.
 Cardiovascular abnormalities associated with autonomic
neuropathy are postural hypotension, resting tachycardia,
and painless myocardial infarction.
 A patient with postural hypotension should be instructed
to change from a lying or sitting position slowly.

86. Diabetic nephropathy
 Diabetic nephropathy is the leading cause of end-stage renal disease,
accounting for 40% of new cases.
 The term diabetic nephropathy is used to describe the combination of
lesions that often occur concurrently in the diabetic kidney. The most
common kidney lesions in people with diabetes are those that affect
the glomeruli.
 Various glomerular changes may occur, including capillary basement
membrane thickening, diffuse glomerular sclerosis, and nodular
glomerulosclerosis.
 Among the suggested risk factors for diabetic nephropathy are:
 Genetic and familial predisposition
 Elevated blood pressure
 Poor glycemic control
 Smoking

87. Pathogenesis
 Three major histologic changes occur in the glomeruli of persons with
diabetic nephropathy.
 First, mesangial expansion is directly induced by hyperglycemia.
 Second, GBM (glomerular basement membrane) thickening occurs.
 Third, glomerular sclerosis is caused by intraglomerular
hypertension (induced by renal vasodilatation
The exact cause of diabetic nephropathy is unknown, but various
postulated mechanisms are:
 Hyperglycemia (causing hyperfiltration and renal injury)
 Activation of cytokines

88. Retinopathies
 Although people with diabetes are at increased risk for the
development of cataracts and glaucoma, retinopathy is the most
common pattern of eye disease.
 Diabetic retinopathy is characterized by abnormal retinal vascular
permeability, microaneurysm formation, neovascularization
( formation of network with red blood cell ) and associated hemorrhage,
scarring, and retinal detachment.
 Among the suggested risk factors associated with diabetic retinopathy
are poor glycemic control, elevated blood pressure, and
hyperlipidemia.
 Because of the risk of retinopathy, it is important that people with
diabetes have regular dilated eye examinations.
 Some people develop a condition called macular edema. It occurs when
the damaged blood vessels leak fluid and lipids onto the macula, the
part of the retina that lets us see detail. The fluid makes the macula
swell, which blurs vision.

89. Pathogenesis
 Diabetic retinopathy is the result of microvascular retinal changes.
 Hyperglycemia-induced thickening of the basement membrane lead to
incompetence of the vascular walls.
 These damages change the formation of the blood-retinal barrier and
also make the retinal blood vessels become more permeable.
 The lack of oxygen in the retina causes fragile, new, blood vessels to
grow along the retina and in the clear, gel-like vitreous humour that
fills the inside of the eye.
 Without timely treatment, these new blood vessels can bleed, cloud
vision, and destroy the retina.

90. Diabetic foot ulcers
 Foot problems are common among people with diabetes and may
become severe enough to cause ulceration and infection, eventually
resulting in amputation.
 Approximately 60% to 70% of people with diabetic foot ulcers have
neuropathy without vascular disease, 15% to 20% have vascular disease,
and 15% to 20% have neuropathy and vascular disease.
 Distal symmetric neuropathy is a major risk factor for foot ulcers.
 People with sensory neuropathies have impaired pain sensation and
often are unaware of the constant trauma to the feet caused by poorly
fitting shoes, improper weight bearing or infections.
 Motor neuropathy with weakness of the intrinsic muscles of the foot
may result in foot deformities, which lead to focal areas of high
pressure. When the abnormal focus of pressure is coupled with loss of
sensation, a foot ulcer can occur.
 Common sites of trauma are the back of the heel, the plantar
metatarsal area, or the great toe, where weight is borne during walking.