Complications of DM

By: Julyn Marie Elnas Abad-Gallardo

 Insulin
administration
1. Subcutaneous injections and mixing insulin
-it must be injected SQ because it is a protein
that is destroyed in the digestive tract if taken orally.
-the primary form of insulin, identical to human
insulin (Humulin), synthesized by bacteria using
recombinant DNA techniques.
-it is standardized in units for SQ administration
2. Insulin pumps

- continuous SQ insulin infusion is administered

by an externally worn device that contains a syringe
attached to a long , thin, narrow-lumen tube with a
needle or Teflon catheter to the end.
 -the client inserts the needle or Teflon catheter
into the SQ tissue (usually on the abdomen) and
secures it with tape or a transparent dressing.
-the pump is worn on a belt or in a pocket.
-the needle or Teflon catheter is changed at least
every 2 to 3 days.
- a continuous basal rate of insulin infuses
- based on the blood glucose level, the
anticipated food intake, and activity level,
the client delivers a bolus of insulin before
each meal.
 - both rapid-acting and regular insulin (buffered
to prevent the precipitation of insulin crystals within
the catheter) are appropriate for use in these pumps.
3. Insulin pumps and a skin sensor
-a skin sensor device that monitors the
client’s blood glucose continuously
-the information is transmitted to the pump,
determines the need for insulin, and then the insulin is
injected.
 - the pump holds up to a 3-day supply of insulin
and can be easily disconnected for activities such as
bathing.
 4. Jet
injectors
-is a needleless device that delivers insulin
through the skin under pressure in an extremely fine
stream
-usually absorbs faster
-can cause bruising at the site of insulin delivery
 6. Pancreas
transplant
-the goal of pancreatic transplantation is to halt
or reverse the complications of DM
-transplantations are performed on a limited
number of clients (generally, these are clients who are
undergoing kidney transplantation simultaneously)
- Immunosuppressive therapy is prescribed to
prevent and treat rejection.
 Self-monitoring of blood glucose
1. level the client with the current
Self-monitoring provides
blood glucose level and information to maintain
good glycemic control
2. Monitoring requires a finger prick to obtain a drop
of blood for testing
3. Alternative site testing (obtaining blood from the
forearm, upper arm, abdomen, thigh, or calf) is now
available using specific measurement devices.

4. Tests must be used with caution in clients

with diabetic neuropathy.
Client instruction:

1. Use the proper procedure for obtaining the sample

for determining the blood glucose level
2. Perform the procedure precisely to obtain
accurate results
3. Follow the manufacturer’s instructions for the
glucometer
4. Wash hands before and after performing the procedure to
prevent infection

5. Calibrate the monitor as instructed by the manufacturer

6. Check the expiration date on the test strips

7. Is the blood glucose level results do not seem reasonable,

reread instructions, reassess technique, check the expiration
date of the test strips, and perform the procedure again to
verify results.
Urine testing
-Urine testing for glucose is not a reliable
indicator of the blood glucose level and is not used for
monitoring purposes
-instruct the client in the procedure for testing
for urine ketones
 -the presence of ketones may indicate
impending ketoacidosis
-urine ketone testing should be performed
during illness and whenever the client with type 1 Dm
has persistently elevated blood glucose levels (higher
than 240 mg/dL for two consecutive testing periods)
Complications of Insulin
Therapy
 1. Local allergic
reactions
a. Redness
b. Swelling
c. Tenderness
d. Induration or a wheal at the site if injection – 1 to
2 hours after administration
 -Reactions usually occurs during the early
stage of insulin therapy.
Instruct the client to cleanse the skin with
alcohol before injection.
 2. Insulin
Lipodysthropy
Lipoatrophy - is a loss of subcutaneous fat and
appears as slight dimpling or more serious pitting of SQ
fat
- the use of human insulin helps prevent this
complication
Lipohypertrophy – is the development of fibrous
fatty masses at the injection site
- is caused by repeated use of an injection site
Nursing Management:
-instruct the client to avoid injecting insulin into
affected sites
-instruct the client about the importance of rotating
insulin injection at one anatomical site
 3. Insulin
resistance
-the client receiving insulin develops immune
antibodies that binds the insulin, thereby decreasing
the insulin available for the use in the body.
-is also the term used for lack of tissue sensitivity
to the insulin from the body, which results in
hyperglycemia.
Treatment
: - administering a purer insulin preparation
4. Dawn Phenomenon
-results from reduced tissue sensitivity to insulin
that usually develops between 5 and 8 am
(prebreakfast hyperglycemia occurs)
-it may be caused by nocturnal release of growth
hormone.
Treatment:
- administering an evening dose (or increasing the
amount of a current dose) of intermediate-acting
insulin at about 10 pm.
5. Somogyi phenomenon
-normal or elevated blood glucose levels are
present at bedtime
-hypoglycemia occurs at about 2 to 3 am, which
causes an increase in the production of
counterregulatory hormones.
 - by about 7 am, in response to the
counterregulatory hormones, the blood glucose
rebounds significantly to the hyperglycemic range.
Treatment:
- decreasing the evening (predinner or bedtime) dose
of intermediate-acting insulin or increasing the
bedtime snack.
Acute complications of
DM
 Hypoglycemia (Insulin
Shock)
-occurs when the blood glucose level falls below
70 mg/dL or when the blood glucose level drops rapidly
from an elevated level.
-it usually occurs in Type 1 DM, following
strenuous exercise, an error in dosage, vomiting, or
skipping a meal after insulin administration.
• The lack of glucose quickly affects the nervous
system – because neurons cannot use fats or
proteins as an energy source.
• It can be life-threatening or can cause brain
damage if it is not treated promptly.
Assessment
• One group of signs is related to impaired
neurologic function resulting from the lack of
glucose.
a. Poor concentration
b. Slurred speech
c. Lack of coordination
d. Staggering gait
- They are sometimes assumed to be intoxicated with
alcohol.
• The second group of signs is related to the
hypoglycemic state stimulating the sympathetic
nervous system (SNS).
a. Increased pulse
b. Pale moist skin
c. Anxiety
d. Tremors
- If untreated , loss of consciousness, seizure and death
will result.
A. Mild hypoglycemia

-the client remains fully awake but displays

adrenergic symptoms.
-blood glucose level: lower than 60 mg/dL.
• Hunger
• Nervousness
• Palpitations
• Sweating
• Tachycardia
• Tremor
Interventions:
1. Give 10 to 15 g of a fast-acting simple carbohydrates
a. commercially prepared glucose tablets
b. 6 to 10 Life Savers or hard candy
c. 4 tsp of sugar
d. 4 sugar cubes
e. 1 tbsp. of honey or syrup
f. ½ cup of fruit juice ore regular (nondiet) soft
drinks
g. 8 oz low-fat milk
h. 6 saltine crackers
i. 3 graham crackers
2.Retest the blood sugar level in 15 mins, and repeat the
treatment of symptoms do not resolve, a snack
containing protein and carbohydrates is recommended
unless the client plans to eat a regular meal within 60
mins.
a. low-fat milk
b. cheese
c. crackers
 B. Moderate
hypoglycemia
-the client displays symptoms of worsening
hypoglycemia.
-blood glucose level: lower than 40 mg/dL.
• Confusion • Inability to concentrate
• Double vision • Irrational or combative
• Drowsiness behavior
• Emotional changes • Light-headedness
• Headache • Numbness of the lips and
• Impaired tongue
coordination • Slurred speech
Interventions:

1. Administer 15 to 30 g of a fast-acting simple

carbohydrate.
2. Administer additional food after 10 to 15 mins such
as:
a. low-fat milk
b. cheese
c. crackers
 C. Severe
hypoglycemia
-the client displays severe neuroglycopenic
symptoms.
-blood sugar level: lower than 20 mg/dL
• Difficulty arousing
• Disoriented behavior
• Loss of consciousness
• Seizure
Interventions:
1. If the client is unconscious and cannot swallow,
an injection of glucagon is administered SQ or IM.
2. Administer a second dose in 10 mins. if the client
remains unconscious
3. Give nothing my mouth.
4. A small meal is given to the client when the client
awakens as long as the client is not nauseated
 4. The physician is notified if a severe hypoglycemic
reaction occurs.

5. Family members need to be instructed about the

administration of glucagon.
 DO NOT attempt to administer oral food or fluids
to the client experiencing a severe hypoglycemic
reaction who is semiconscious or unconscious and is
unable to swallow.

RISK FOR
ASPIRATION!
In hospital setting:

- the client may be treated with an IV injection of

25-50 mL of 50% dextrose in water (D50W) – bolus.
 Diabetic Ketoacidosis
(DKA)
-is a life-threatening complication of Type 1 DM that
develops when severe insulin deficiency occurs.
-the main clinical manifestations include:
a.hyperglycemia
b.dehydration
c.ketosis
d.acidosis
• It is more common in Type 1 DM patients.
• It usually develops over a few days and may be
initiated by an infection or stress, which increases
the demand for insulin in the body.
• It may also result from an error in dosage or
overindulgence in food or alcohol.
Manifestation
s
• Ketosis
a. Kussmaul’s respiration – rapid and deep
-compensation
b. nausea
c. “acetone” breath-results
fruity, from smell – acetone
sweetelectrolyte
expired

d. abdominal pain imbalances of Na, K,

Ch
• Dehydration or electrolyte loss
a. polyuria –osmotic diuresis due to glucosuria
b. polydipsia – response to water loss
c. weight loss - loss of fluid and lack of glucose to
d. cells
dry skin decreased interstitial
e. sunken fluid
eyes indicates depression of the CNS owing
f. lethargy - to
g. coma - acidosis and decreased blood flow
• Metabolic acidosis develops as ketoacids bind with
bicarbonate ions in the buffer, leading to decreased
serum bicarbonate levels and decreased serum pH.
• As dehydration progresses,
renal compensation is reduced, acidosis becomes
decompensated, and serum pH falls, resulting in
loss of consciousness.
• Actual serum values of electrolytes may be
misleading – because the proportion of water lost
can affect the serum level even though the
electrolytes were lost in the urine.
• Serum sodium is often low, but the potassium
concentration may be elevated because of
acidosis.
• Oliguria (decreased UO) – indicates that
compensation mechanisms to conserve fluid in the
body are taking place.
• If the condition remains untreated, CNS depression
develops owing to the acidosis and dehydration,
leading to coma.
Note: DKA and hypoglycemia both causes loss of
consciousness. The Emergency treatment for DKA
is insulin, fluid, ad sodium bicarbonate.
Assessment should differentiate the cause.
Interventions
• Restore circulating blood volume and protect
against cerebral, coronary, and renal
hypoperfusion.
• Treat dehydration with rapid IV infusions of 0.9% or
0.45% normal saline (NS) as prescribed
• Dextrose is added to IV fluids (D5NS, or 5% dextrose
in 0.45% saline) when the blood glucose level
reaches 250 to 300 mg/dL
• Treat hyperglycemia with regular insulin
administered intravenously as prescribed.

Regular insulin is the ONLY insulin that can be

administered IV. Used in emergency treatment for
DKA
• Correct electrolyte imbalances (potassium level may
be elevated as a result of dehydration and acidosis).

• Monitor potassium level closely because when the

client receives treatment for the dehydration and
acidosis, the serum potassium level will decrease and
potassium replacement may be required.
 Insulin IV
administration
• Use regular insulin only
• An IV bolus dose of regular insulin (usually 5 to 10
units) may be prescribed before a continuous
infusion is begun).
• Mix the prescribed IV dose of regular insulin for
continuous infusion with 0.9 % or 0.45% NS as
prescribed
• Flush insulin solution through the entire IV infusion
set and discard the first 50 to 100 mL of solution
before connecting and administering it to the client
(insulin molecules adhere to the plastic of IV infusion
sets)
• Always place the insulin infusion on an IV infusion
controller.
• Insulin is infused continuously until SQ
administration resumes to prevent a rebound of
the blood glucose level.
• Monitor vital signs
• Monitor urinary output and for signs of fluid
overload
• Monitor potassium and glucose levels and for signs
of increased intracranial pressure.
• The potassium level will fall rapidly within the first
hour of treatment as the dehydration and the
acidosis are treated
• Potassium is administered IV in a diluted solution as
prescribed when the potassium reaches normal level
to prevent hypokalemia.
• Ensure adequate renal function before
administering potassium.
• Monitor the client being treated for DKA closely for
signs of increased intracranial pressure.
• If the blood glucose level falls too far or too fast
before the brain has time to equilibrate, water is
pulled form the blood to the cerebrospinal fluid and
the brain, causing cerebral edema and increased
ICP.
 Client
education
Guidelines during illness
•Take insulin or oral antidiabetic medications as
prescribed
•Test blood glucose level and test the urine for
ketones every 3 to 4 hours
•If the usual meal plan cannot be followed, substitute
soft foods six to eight times a day.
• If vomiting, diarrhea, or fever occurs, consume liquids every
30 to 60 mins. to prevent dehydration and to provide calories.
• Notify the physician if:
a. vomiting, diarrhea, or fever persists
b. if blood glucose levels are higher than 250 to 300
mg/dL,
c. when ketonuria is present for more than 24 hours
d. When unable to take food or fluids for a period of 4
hours
e. or when illess persists for more than 2 days
Hyperglycemic hyperosmolar non-
ketotic syndrome (HHNS)

- life-threatening complication
- extreme hyperglycemia occurs without ketosis
or acidosis

Hyper osmolarity – because there’s a very

concentrated blood due to high blood glucose
in the body
• The syndrome occurs more often in individuals with
Type 2 DM
• Often the patient is an older person with infection or
one who has overindulged in carbohydrates, thereby
using more insulin than anticipated.
• In these case, hyperglycemia and dehydration develop
because of the relative insulin deficit, but sufficient
insulin is available to prevent ketoacidosis.
The Major Difference

• The major difference between HHNS and DKA is that

ketosis and acidosis do not occur with HHNS;
enough insulin is present with HHNS to prevent
breakdown of fats for energy, thus preventing
ketosis.
Manifestation
s
• Altered central nervous system function with neurologic
symptoms
• Dehydration or electrolyte loss: same as DKA
a. polyuria
b. polydipsia
c. weight loss
d. dry skin
e. sunken eyes
f. lethargy
g. coma
Interventions

• Treatments is similar to that for DKA, includes:

a. fluid replacement – in older adult client must be
done very carefully because of the potential of heart
failure.
- rehydration alone may decrease glucose levels.
b. correction of electrolyte imbalances
c. insulin administration – insulin plays a less
critical role in treatment of HHNS that it does
for the treatment of DKA because ketosis and
acidosis do not occur.
Chronic complications of
DM
Microangiopath
y
- where the capillary basement membrane
becomes thick and hard, causes obstruction or rupture
of capillaries and small arteries and results in tissue
necrosis and loss of function
 Diabetic
Retinopathy
-chronic and progressive impairment of the
retinal circulation that eventually causes hemorrhage
-permanent vision changes and leading cause of
blindness
-the client has difficulty with carrying out the
daily tasks of blood glucose testing and insulin
injections.
Assessment

• A change in vision – is caused by the rupture of

small microneurysms in the retinal blood vessels
• Blurred vision – results from macula edema
• Sudden loss of vision – results from retinal
detachment.
• Cataracts – results from lens opacity
Interventions

• Maintain safety
• Early prevention via the control of hypertension and
blood glucose level
• Photocoagulation (laser therapy) may be done to
remove hemorrhagic tissue to decrease scarring and
prevent progression of the disease process
• Vitrectomy may be done to remove vitreous
hemorrhages and thus decrease tension on the
retina, preventing detachment
• Cataract removal with lens implantation
improve vision
 Diabetic
nephropathy
-vascular degeneration in the kidney glomeruli,
eventually leading to chronic renal failure.
-it is responsible for 40% of patients in
end- stage renal failure.
Assessment
• Microalbuminuria
• Thirsts
• Fatigue
• Anemia
• Weight loss
• Signs of malnutrition
• Frequent UTI
• Signs of neurogenic
bladder
Interventions

• Early prevention measures – includes the control

of hypertension and blood glucose levels
• Assess vital signs
• Monitor intake and output
• Monitor the Blood urea nitrogen (BUN) and
creatinine and urine albumin (BUA) levels
• Restrict dietary protein, sodium, and potassium
intake as prescribed
• Avoid nephrotoxic medications
• Prepare the client for dialysis procedure if planned
• Prepare the client for kidney or pancreas transplant
if planned
Macroangopath
y
- affects the large arteries, thus leading to a high
incidence of heart attacks, strokes, and peripheral
vascular disease in diabetes.
 Diabetic
neuropathy
-General deterioration of the nervous system
throughout the body.
-complications include:
a.development of non-healing ulcers of the feet
b.gastric paresis
c.erectile dysfunction
Classifications

• Focal neuropathy or mononeuropathy

- involves a single nerve or group of nerves, most
frequently cranial nerves III (oculomotor) and VI
(abducens), resulting in diplopia.
• Sensory or peripheral neuropathy
- affects distal portions of nerves, most
frequently in the lower extremities
• Autonomic neuropathy
- symptoms vary according to organ system
involved
• Cardiovascular
-cardiac denervation syndrome (heart rate does
not respond to changes in oxygenation needs)
-orthostatic hypotension occurs
• Pupillary
- pupils does not dilate in response to decreased
light
• Gastric
- decreased gastric emptying (gastroparesis)
• Urinary
- neurogenic bladder
• Sudomotor
- decreased sweating
• Adrenal
- hypoglycemic unawareness
• Reproductive
- impotence (male), painful intercourse
(female)
Assessment

• Paresthesia
• Decreased or absent reflexes
• Decreased sensation to vibration or light touch
• Pain, aching, and burning in the lower extremities
• Poor peripheral pulses
• Skin breakdown and signs of infection
• Weakness or loss of sensation in cranial nerves
III (oculomotor), IV (trochlear), V (trigeminal), VI
(abducens)
• Dizziness and postural hypotension
• Nausea and vomiting
• Diarrhea or constipation
• Incontinence
• Dyspareunia
• Impotence
• Hypoglycemic unawareness
Interventions

• Early prevention measures include the control

of hypertension and blood glucose levels

• Careful foot care is required to prevent trauma

Preventive foot care instructions
1.Provide meticulous skin care and proper foot care
2.Inspect feet daily and monitor feet for redness,
swelling, or break in skin integrity
- Notify physician if this occur
3.Avoid thermal injuries from hot water, heating pads and
baths
-Wash feet with warm (not hot) water and dry
thoroughly (avoid foot soaks)
4.Avoid treating corns, blisters, or ingrown toenails
5.Apply moisturizing lotion to the feet but not between the
toes
-prevent moisture from accumulating between toes.
 6. Wear loose socks and well-fitting (not tight) shoes,
and instruct client not to go barefoot
- wear clean cotton socks to keep the feet
warm and change the socks daily
7. Avoid wearing the same pair of shoes 2 days in a row
-avoid wearing open-toe or shoes with strap that
goes between the toes
-check shoes for cracks or tears in the lining and
for foreign objects before putting them on
-break in new shoes gradually
8. Cut toenails straight across and smooth nails with an
emery board
9. Avoid smoking
 Interventions
cont’n
• Administer medications as prescribed for pain relief
• Initiate bladder training programs
• Instruct in the use of estrogen-containing lubricants
for women with dyspareunia
• Prepare the male client with impotence for penile
injections for possible treatment options as prescribed
• Prepare for surgical decompression of compression
lesions related to the cranial nerves as prescribed
Infections
-are more common and tend to be more severe in
diabetic – because of vascular impairment, which
decreases tissue resistance.
-delay in healing because of insulin deficit, and the
increased glucose levels in the body fluids that supports
infection
-wound healing is slow, predisposing to infection in
case of trauma or surgery.
• Susceptible for:
a. Tuberculosis
b. Fungal infections - Candida
c. UTI – if bladder function is compromised which
predisposes to cystitis and pyelonephritis
d. Periodontal disease (infection in the tissue around the
teeth)
e. Dental caries
Thank you for
listening!