HYPERGLYCEMIA AND DIABETIC KETOACIDOSIS

Hyperglycemia –is a result when glucose cannot be transferred to the cells because of lack of
insulin. Without available carbohydrates for cellular fuel, the liver converts its glycogen stores back to
glucose (glycogenolysis) and increases biosynthesis of glucose (gluconeogenesis). These responses
worsen the situation by raising the glucose level even higher.

In type I diabetes mellitus, as the need for cellular fuel grows, the body begins to draw fat and
protein stores for energy. Excessive amounts of fatty acids are mobilized from adipose tissue cells and
transported to the liver. The liver then accelerates the rate which produces ketone bodies (ketogenesis)
for catabolism by other body tissues, especially muscle. As fat metabolism increases, the liver may
produce too many ketone bodies. Ketone bodies accumulate in the blood (ketosis) and are excreted in
the urine (ketonuria).

Diabetic ketoacidosis – is a condition when metabolic acidosis develops from the acidic effect of the
ketones acetoacetate and beta-hydroxybuterate.

Diabetic coma – severe acidosis may cause diabetic client to lose consciousness.

ETIOLOGY AND RISK FACTORS

o Taking too little insulin

o Skipping doses of insulin
o Inability to meet an increased need for insulin created by surgery, trauma, pregnancy, stress,
puberty or infection.
o Developing insulin resistance through the presence of insulin antibodies

PATHOPHYSIOLOGY

Infection; Stress Missed insulin dose

New onset diabetes

Excess secretion of
glycogen and other Inadequate insulin
counter regulatory
hormones Decrease glucose
Glycogenolysis and uptake
gluconeogenesis
Increased lipolysis of adipose
by the liver
tissue Hyperglycemia

Ketogenesis
Osmotic diuresis

Ketosis Potassium loss

Vomiting

Acidosis
Dehydration

Three pathologic events of DKA:

o Ketosis and acidosis

 o Dehydration
o Electrolye imbalance

CLINICAL MANIFESTATIONS

o Abdominal Pain
o Anorexia
o Dehydration
o Fruity odor of ketones on breath
o Kussmaul’s respiration
o Hypotension
o Impaired level of consciousness or coma
o Nausea and vomiting
o Polyuria
o Somnolence
o Tachycardia
o Thirst
o Visual disturbance
o Warm and dry skin
o Weakness
o Weight loss

MEDICAL MANAGEMENT

Rehydrate

 IV rehydration is required for clients who are vomiting, unable to drink and have acidosis
 Start Isotonic or normal saline solutions
 1000ml of isotonic solution during 1st hour (10-20ml/kg)
 Additional 2000-8000ml over the next 24 hours.
 Slower IV fluid replacement for client’s with cardiovascular disorder
 Nasogastric tube for clients who are comatose or vomiting
 Frequent oral care for dry mouth
 Assess bowel sound for changes
 Encourage intake of fluids if the client can tolerate
 Drink salted broth to replenish needed sodium
 Record I and O especially with urinary catheter
 Report UO of less than 0.5ml/kg/hour
 Aseptic catheter care to prevent infection

Reverse Shock

 Physician may order blood, albumin or other plasma volume expander such as dextran, to be
administered alternately with normal saline solution.
 Combination of colloids and saline solution administration may raise serum levels both sodium
chloride and plasma protein.

Restore Potassium Balance

 Frequently assess and measure urine output ; don’t give to clients with decreased urine output
(less than 0.5 ml/kg/hour)
 Assess for hyperkalemia (bradycardia, cardiac arrest, weakness, flaccid paralysis, oliguria) or
hypokalemia (weakness, paralytic ileus, flaccid paralysis, cardiac arrest)
  Replacement of potassium
 Plan to begin potassium administration within 1-2 hours after starting insulin therapy and after
adequate urine output is ensured.
 If recovered, give foods high in potassium (bananas, orange juice)
 Monitor sodium chloride and phosphate levels

Correct pH and Administer Insulin

 Check calcium level before giving phosphate

 Administer sodium bicarbonate if blood pH is less than 7.1
 Low- dosage insulin therapy (5-10 units/hour)
 Initial Regular Insulin IV bolus (0.15 unit/kg)
 Don’t give insulin subcutaneously (Subq tissues are dehydrated and poorly perfused)
 Monitor blood glucose levels every 30 mins. If blood glucose is 25 mg/dL, insulin infusion should
be reduced and 5% dextrose is added.
 Monitor client’s level of consciousness; faster correction of hyperglycemia can lead to cerebral
edema.

Prevent Recurrence

 Take insulin appropriately (dose and time)

 Monitor blood glucose level frequently at least before each meal or bedtime
 Monitor urine ketone levels when blood glucose levels increased to greater than 250 mg/dL
 Schedule regular appointments to health care provider
 Seek consult if symptoms of DKA are felt
 Emphasize that the greatest weapons against DKA are regular, daily SMBG; adherence to DM
management program and early recognition and intervention in mild ketosis.