Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both. Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves. 1. Microvascular (due to damage to small blood vessels). 2. Macrovascular (due to damage to larger blood vessels).

1. COMPLICATIONS OF
DIABETES MELITUS
Mr. ANILKUMAR B R , M.sc Nursing( Assist
Professor)
Medical – Surgical Nursing

2. OVERVEIW
Diabetes mellitus (DM) has routinely been
described as a metabolic disorder characterized by
hyperglycemia that develops as a consequence of
defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations
of glucose in the blood, which in turn damage many
of the body's systems, in particular the blood vessels
and nerves.

3. COMPLICATIONS OF DIABETES MELITUS
1. Acute
Complications of
Diabetes
2. Long-Term
Complications of
Diabetes

4. ACUTE COMPLICATIONS OF DIABETES
There are three major acute complications of
diabetes related to short-term imbalances in
blood glucose levels:

5. LONG-TERM COMPLICATIONS OF DIABETES
Long-term complications are becoming more common
as more people live longer with diabetes. The long-term
complications of diabetes can affect almost every organ
system of the body.
Long-term complications are seen in both type 1 and
type 2 diabetes but usually do not occur within the first 5
to 10 years of the diagnosis.

6. COMPLICATIONS OF DIABETES MELITUS
Diabetes complications are divided into two categories.
1. Microvascular (due to damage to small blood
vessels).
2. Macrovascular (due to damage to larger blood
vessels).

8. MICROVASCULAR COMPLICATIONS
Microvascular complications include:
1. Damage to eyes (retinopathy) leading to
blindness
2. Damage to kidneys (nephropathy) leading to
renal failure ( chronic renal failure) .
3. Damage to nerves (neuropathy) leading to
impotence and diabetic foot disorders (which include
severe infections leading to amputation).

9. MACROVASCULAR COMPLICATIONS
 Macrovascular complications include:
1. HEART (Cardiovascular diseases such as heart
attacks (MI)
2. BRAIN ( strokes ( CVA) and insufficiency in blood
flow to legs ( Peripheral vascular disease).

11. ACUTE COMPLICATIONS OF DIABETES
 HYPOGLYCEMIA (INSULIN REACTIONS)
Hypoglycemia (abnormally low blood glucose level) occurs
when the blood glucose falls to less than 50 to 60 mg/dL (2.7
to 3.3 mmol/L).
It can be caused by too much insulin or oral hypoglycemic
agents, too little food, or excessive physical activity.
Hypoglycemia may occur at any time of the day or night. It
often occurs before meals, especially if meals are delayed or
snacks are omitted.

12. CLINICAL MANIFESTATIONS
The clinical manifestations of hypoglycemia may be
grouped into two categories:
Adrenergic
symptoms
Central nervous
system (CNS)
symptoms.

13. In mild hypoglycemia, as the blood glucose level
falls, the sympathetic nervous system is stimulated,
resulting in a surge of epinephrine and
norepinephrine.
This causes symptoms such as sweating, tremor,
tachycardia, palpitation, nervousness, and hunger.

14. IN MODERATE HYPOGLYCEMIA, THE FALL IN BLOOD GLUCOSE LEVEL DEPRIVES THE
BRAIN CELLS OF NEEDED FUEL FOR FUNCTIONING.
Signs of impaired function of the CNS may include
• Inability to concentrate
• Headache
• Lightheadedness
• Confusion memory lapses,
• Numbness of the lips and tongue
• Slurred speech
• Impaired coordination
• Emotional changes
• Irrational or combative behavior, double vision, and drowsiness.

15. IN SEVERE HYPOGLYCEMIA
 CNS function is so impaired that the patient needs
the assistance of another person for treatment of
hypoglycemia.
 Symptoms may include disoriented behavior,
seizures, difficulty arousing from sleep, or loss of
consciousness.

16. MANAGEMENT (IMMEDIATE TREATMENT MUST BE
GIVEN WHEN HYPOGLYCEMIA OCCURS )
The usual recommendation is for 15 g of a fast-acting
concentrated source of carbohydrate such as the following,
given orally:
• Three or four commercially prepared glucose tablets
• 4 to 6 oz of fruit juice or regular soda
• 6 to 10 Life Savers or other hard candies
• 2 to 3 teaspoons of sugar or honey

17.  The blood glucose level should be retested in 15 minutes
and retreated if it is less than 70 to 75 mg/dL (3.8 to 4
mmol/L).
 If the symptoms persist more than 10 to 15 minutes after
initial treatment, the treatment is repeated even if blood
glucose testing is not possible.
 Once the symptoms resolve, a snack containing protein
and starch (e.g., milk or cheese and crackers) is
recommended unless the patient plans to eat a regular
meal or snack within 30 to 60 minutes.

18. INITIATING EMERGENCY MEASURES
 For patients who are unconscious and cannot swallow, an
injection of glucagon 1 mg can be administered either
subcutaneously or intramuscularly.
 Glucagon is a hormone produced by the alpha cells of the
pancreas that stimulates the liver to release glucose (through
the breakdown of glycogen, the stored glucose)
 Injectable glucagon is packaged as a powder in 1-mg vials
and must be mixed with a diluent before being injected. After
injection of glucagon, it may take up to 20 minutes for the
patient to regain consciousness.

19. GLUCAGON INJECTABLE 1 MG ( 1 UNIT)
Glucagon is sold by prescription
only and should be part of the
emergency supplies kept
available by patients with
diabetes who require insulin.
Family members, neighbors, or
coworkers should be instructed
in the use of glucagon.

20.  In the hospital or emergency
department, patients who are
unconscious or cannot swallow
may be treated with 25 to 50 mL
50% dextrose in water (D50W)
administered intravenously.
 The effect is usually seen within
minutes.

22.  DKA is caused by an absence or markedly inadequate amount of
insulin. This deficit in available insulin results in disorders in the
metabolism of carbohydrate, protein, and fat.
 The three main clinical features of DKA are:
1. Hyperglycemia (abnormally low blood glucose level)
2. Dehydration and electrolyte loss
3. Acidosis

23. PATHOPHYSIOLOGY
This osmotic diuresis, which is characterized by excessive urination
(polyuria), leads to dehydration and marked electrolyte loss.
Both factors lead to hyperglycemia. In an attempt to rid the body of
the excess glucose, the kidneys excrete the glucose along with water
and electrolytes (eg, sodium and potassium).
Without insulin, the amount of glucose entering the cells is
reduced and the liver increases glucose production.

24. Three main causes of DKA are decreased or missed dose of
insulin, illness or infection, and undiagnosed and untreated
diabetes (DKA may be the initial manifestation of diabetes).
Other potential causes of decreased insulin include patient error in
drawing up or injecting insulin (especially in patients with visual
impairments), intentional skipping of insulin doses (especially in
adolescents with diabetes who are having difficulty coping with
diabetes or other aspects of their lives), or equipment problems
(e.g., occlusion of insulin pump tubing).

25.  Illness and infections are associated with insulin resistance.
 In response to physical (and emotional) stressors, there is an
increase in the level of “stress” hormones—glucagon, epinephrine,
norepinephrine, cortisol, and growth hormone.
 These hormones promote glucose production by the liver and
interfere with glucose utilization by muscle and fat tissue,
counteracting the effect of insulin.
 If insulin levels are not increased during times of illness and
infection, hyperglycemia may progress to DKA.

26. CLINICAL MANIFESTATIONS
 The hyperglycemia of DKA leads to polyuria and polydipsia
(increased thirst). In addition, patients may experience blurred
vision, weakness, and headache.
 Patients with marked intravascular volume depletion may have
orthostatic hypotension (drop in systolic blood pressure of 20 mm
Hg or more on standing).
 The ketosis and acidosis of DKA lead to GI symptoms such as
anorexia, nausea, vomiting, and abdominal pain.
 Patients may have acetone breath (a fruity odor), which occurs with
elevated ketone levels.

27. ASSESSMENT AND DIAGNOSTIC FINDINGS
Blood glucose levels may vary from 300 to 800
mg/dL (16.6 to 44.4 mmol/L). Some patients have
lower glucose values, and others have values of
1,000 mg/dL (55.5 mmol/L) or more (usually
depending on the degree of dehydration).

28. PREVENTION
For prevention of DKA related to illness, patients
must be taught “sick day” rules for managing their
diabetes when ill.
The most important issue to teach patients is not to
eliminate insulin doses when nausea and vomiting
occur.

29. PATIENT EDUCATION GUIDELINES TO FOLLOW DURING PERIODS
OF ILLNESS (“SICK DAY RULES”)
1. Take insulin or oral antidiabetic agents as usual.
2. Test blood glucose and test urine ketones every 3 to 4 hours.
3. Report elevated glucose levels (greater than 300 mg/dL [16.6
mmol/L] or as otherwise specified) or urine ketones to the
physician.
4. Insulin-requiring patients may need supplemental doses of
regular insulin every 3 to 4 hours.
5. If usual meal plan cannot be followed, substitute soft foods
(eg, 1⁄3 cup regular gelatin, 1 cup cream soup, 1⁄2 cup custard,
3 squares graham crackers) six to eight times per day.

30. PATIENT EDUCATION GUIDELINES TO FOLLOW DURING PERIODS
OF ILLNESS (“SICK DAY RULES”)
1. If vomiting, diarrhea, or fever persists, take liquids (eg,
1⁄2 cup regular cola or orange juice, 1⁄2 cup broth, 1
cup Gatorade) every 1⁄2 to 1 hour to prevent
dehydration and to provide calories.
2. Report nausea, vomiting, and diarrhea to the
physician, because extreme fluid loss may be
dangerous.
3. For patients with type 1 diabetes, inability to retain oral
fluids, may warrant hospitalization to avoid diabetic
ketoacidosis and possibly coma.

31. MEDICAL MANAGEMENT
In addition to treating hyperglycemia, management
of DKA is aimed at correcting dehydration,
electrolyte loss, and acidosis.

32. REHYDRATION
 In dehydrated patients, rehydration is important for maintaining tissue
perfusion. In addition, fluid replacement enhances the excretion of
excessive glucose by the kidneys.
 Patients may need up to 6 to 10 liters of IV fluid to replace fluid losses
caused by polyuria, hyperventilation, diarrhea, and vomiting. Initially,
0.9% sodium chloride (normal saline) solution is administered at a
rapid rate, usually 0.5 to 1 L per hour for 2 to 3 hours.
 Half-strength normal saline (0.45%) solution (also known as hypotonic
saline solution) may be used for patients with hypertension or
hypernatremia or those at risk for heart failure.

33. Monitoring fluid volume status involves frequent
measurements of vital signs (including monitoring
for orthostatic changes in blood pressure and heart
rate), lung assessment, and monitoring intake and
output.
Monitoring for signs of fluid overload is especially
important for older patients, those with renal
impairment, or those at risk for heart failure.

34. RESTORING ELECTROLYTES
 The major electrolyte of concern during treatment of DKA is potassium.
Although the initial plasma concentration of potassium may be low, normal,
or even high, there is a major loss of potassium from body stores and an
intracellular to extracellular shift of potassium.

35. REVERSING ACIDOSIS
Ketone bodies (acids) accumulate as a result of fat
breakdown.
The acidosis that occurs in DKA is reversed with
insulin, which inhibits fat breakdown, thereby
stopping acid buildup.
Insulin is usually infused intravenously at a slow,
continuous rate (e.g., 5 units per hour). Hourly
blood glucose values must be measured.

36. HYPERGLYCEMIC
HYPEROSMOLAR
NONKETOTIC SYNDROME
(HHNS)

37. Hyperosmolar Hyperglycemic Nonketotic
Syndrome (HHNS), also known as Hyperosmolar
Hyperglycaemic State (HHS) is a dangerous
condition resulting from very high blood glucose
levels.
This condition occurs most often in older people (ages 50
to 70) with no known history of diabetes or with mild type

38. Clinical Manifestations
 The clinical picture of HHNS is one of
1. Hypotension
2. profound dehydration (dry mucous membranes, poor
skin turgor),
3. tachycardia, and variable neurologic signs (eg, alteration
of sensorium, seizures, hemiparesis). The mortality rate
ranges from 10% to 40%, usually related to an
underlying illness.

39. ASSESSMENT AND DIAGNOSTIC FINDINGS DIAGNOSTIC
 Assessment includes a range of laboratory tests including:
1. Blood glucose
2. Serum electrolytes
3. BUN
4. complete blood count
5. serum osmolality, and arterial blood gas analysis. The
blood glucose level is usually 600 to 1,200 mg/dL

40. MEDICAL MANAGEMENT
 The overall approach to the treatment of HHNS is similar to that
of DKA:
1. fluid replacement, correction of electrolyte imbalances, and
insulin administration. Because of the older age of the typical
patient with HHNS, close monitoring of volume and electrolyte
status is important for prevention of fluid overload, heart
failure, and cardiac dysrhythmias.
2. Fluid treatment is started with 0.9% or 0.45% NS, depending on
the patient’s sodium level and the severity of volume depletion.

41. NURSING MANAGEMENT
 Nursing care of the patient with HHNS includes close monitoring of vital signs,
fluid status, and laboratory values. In addition, strategies are implemented to
maintain safety and prevent injury related to changes in the patient’s
sensorium secondary to HHNS. Fluid status and urine output are closely
monitored because of the high risk for renal failure secondary to severe
dehydration.

42. COMPLICATIONS OF HHNS
 Fluid overload
 pulmonary edema
 heart failure
 Hypokalemia
 Hyperglycemia and ketoacidosis
 Hypoglycemia
 Cerebral edema

43. LONG-TERM
COMPLICATIONS OF
DIABETES

44. COMPLICATIONS OF DIABETES MELITUS
Diabetes complications are divided into two categories.
1. Microvascular (due to damage to small blood
vessels).
2. Macrovascular (due to damage to larger blood
vessels).

45. MICROVASCULAR COMPLICATIONS
Diabetic retinopathy (eye disease)

46. DIABETIC RETINOPATHY (EYE DISEASE)
Diabetic retinopathy is a leading cause of
blindness and visual disability.
 It is caused by small blood vessel damage to the
back layer of the eye, the retina, leading to
progressive loss of vision, even blindness.

47.  Symptoms
 Usually Retinopathy is a painless process. In nonproliferative
and preproliferative retinopathy, blurry vision secondary to
macular edema occurs in some patients, although many
patients are asymptomaticthe patient complains of blurred
vision, although other visual symptoms may also be present.
 Diagnosis
 Diagnosis of early changes in the blood vessels of the retina
can be made through regular eye examinations.

48. TREATMENT
 Good metabolic control can delay the onset and progression of
diabetic retinopathy. As well, early detection and treatment of
vision-threatening retinopathy can prevent or delay blindness.
 This involves regular eye examinations and timely
intervention.
1. Control of hypertension
2. Control of blood glucose
3. Cessation of smoking

49. NEPHROPATHY (KIDNEY
DISEASE)

50. NEPHROPATHY (KIDNEY DISEASE)
 Nephropathy, or renal disease secondary to diabetic microvascular
changes in the kidney, is a common complication of diabetes.
 People with diabetes account for nearly half of new cases of end
stage renal disease (ESRD).
 Etiology
 Diabetic kidney disease is also caused by damage to small blood
vessels in the kidneys. This can cause kidney failure, and eventually
lead to death. In developed countries, this is a leading cause of
dialysis and kidney transplant.

51. Patients with type 1 diabetes frequently show
initial signs of renal disease after 10 to 15
years, whereas patients with type 2 diabetes
develop renal disease within 10 years of the
diagnosis of diabetes.

52. Symptoms
Patients usually have no symptoms early on, but as the
disease progresses, they may feel tired, become anemic,
not think clearly, and even develop dangerous
electrolyte imbalances.
Diagnosis
One of the most important blood proteins that leaks
into the urine is albumin.
Early diagnosis can be made by a simple urine test for
protein as well as a blood test for kidney function.

53. MEDICAL MANAGEMENT
 In addition to achieving and maintaining near-normal blood glucose levels,
management for all patients with diabetes should include careful attention to the
following:
1. Control of hypertension (the use of angiotensin-converting enzyme
[ACE] inhibitors, such as captopril, because control of hypertension may
also decrease or delay the onset of early proteinuria)
2. Prevention or vigorous treatment of urinary tract infections
3. Avoidance of nephrotoxic substances
4. Adjustment of medications as renal function changes
5. Low-sodium diet
6. Low-protein diet

54. DIABETIC
NEUROPATHIES

55. DIABETIC NEUROPATHY
 Diabetic neuropathy refers to a group of diseases that affect all
types of nerves, including peripheral (sensorimotor), autonomic,
and spinal nerves.
 Etiology
 Diabetes causes nerve damage through different mechanisms,
including direct damage by the hyperglycemia and decreased blood
flow to nerves by damaging small blood vessels. This nerve damage
can lead to sensory loss, damage to limbs, and impotence in
diabetic men.
 It is the most common complication of diabetes.

56. SYMPTOMS
The symptoms are many, depending on which
nerves are affected: for example, numbness in
extremities, pain in extremities, and impotence.
Decreased sensation to feet can lead to patients not
recognizing cuts and developing foot infections.
If not treated early, these can lead to amputation
(more about diabetic foot disease below).

57. SEXUAL DYSFUNCTION
 Sexual dysfunction, especially impotence in men, is a complication
of diabetes. The effects of autonomic neuropathy on female sexual
functioning are not well documented.
 Reduced vaginal lubrication has been mentioned as a possible
neuropathic effect; other possible changes in sexual function in
women with diabetes include decreased libido and lack of orgasm.
 Vaginal infection, increased in incidence in women with diabetes,
may be associated with decreased lubrication and vaginal itching
and tenderness. Urinary tract infections and vaginitis may also
affect sexual function.

58. DIABETIC FOOT DISEASE
From 50% to 75% of lower extremity amputations
are performed on people with diabetes.
More than 50% of these amputations are thought
to be preventable, provided patients are taught foot
care measures and practice them on a daily basis.

59. DIABETIC FOOT DISEASE
 Diabetic foot disease, due to changes in blood vessels and
nerves, often leads to ulceration and subsequent limb
amputation.
 It is one of the most costly complications of diabetes,
especially in communities with inadequate footwear.
 It results from both vascular and neurological disease
processes. Regular inspection and good care of the foot
can prevent amputations. Comprehensive foot programs
can reduce amputation rates by 45-85%.

60. DIABETIC FOOT DISEASE

61. MANAGEMENT
Foot assessment and foot care instructions are most
important when caring for patients who are at high risk
for developing foot infections.
Teaching patients proper foot care is a nursing
intervention that can prevent costly, painful, and
debilitating complications. Preventive foot care begins
with careful daily assessment of the feet.

62. The feet must be inspected on a daily basis for any
redness, blisters, fissures, calluses, ulcerations,
changes in skin temperature, and the development
of foot deformities (i.e., hammer toes, bunions).

63. MACROVASCULAR
COMPLICATIONS

64. Diabetic macrovascular complications result from
changes in the medium to large blood vessels.
Blood vessel walls thicken, sclerose, and become
occluded by plaque that adheres to the vessel walls.
Eventually, blood flow is blocked.

65. These atherosclerotic changes are indistinguishable
from atherosclerotic changes in people without
diabetes, but they tend to occur more often and at
an earlier age in diabetes.
Coronary artery disease, cerebrovascular disease,
and peripheral vascular disease are the three main
types of macrovascular complications that occur
more frequently in the diabetic population.