FACULTY OF PHARMACY, NURSING AND HEALTH

PROFESSIONS
ADULT HEALTH 2 – NURS 251

DIABETIC KETOACIDOSIS (DKA)

Students:
Reem Abedrabo – 1170079
Hisham Shahin - 1153334

Instructor:
Jihad Aljamal.
• DIABETIC KETOACIDOSIS:
Acute life-threatening condition of uncontrolled diabetes characterized by
hyperglycemia, ketosis and metabolic acidosis associated with dehydration and
electrolyte loss. DKA primarily affects persons with DM type 1 but may also occur with
type 2 when severe stress occurs such as trauma, sepsis, insufficient insulin… or it may
be a previous undiagnosed type 1diabetes.

• GLUCOSE AND BICARBONATE LEVELS:

Definitive diagnosis of DKA consists of hyperglycemia > 250 mg/dL. Low serum
bicarbonate, low arterial pH, positive serum and urine ketones. DKA can be subdivided
into:

1. Mild DKA:
HCO₃: 15 – 18 mEq/dL
pH: 7.25 – 7.30

2. Moderate DKA:
HCO₃: 10 - <15 mEq/dL
pH: 7.00 – 7.24

3. Severe DKA:
HCO₃: < 10 mEq/dL
pH: < 7.00

• CAUSES OF DKA:
- Decreased or missed dose of insulin.
- Illness or infection.
- Undiagnosed or untreated DM.

An insulin deficiency may result of an insufficient dosage of insulin prescribed or

insufficient insulin being given by the patient. Errors in insulin dosage may be made by
patients who are ill and who assume that if they are eating less or if they are vomiting,
they must decrease their insulin doses. (Because illness, especially infections, can cause
increased blood glucose levels, the patient does not need to decrease the insulin dose to
compensate for decreased food intake when ill and may even need to increase the insulin
dose.)
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).
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.

• MANAGEMENT:
In addition to treating hyperglycemia, DKA management focuses on managing
dehydration, electrolyte loss, and acidosis before correcting elevated blood glucose with
insulin.

1. Rehydration: rehydration is important in order to maintain tissue perfusion,

enhance the kidneys to excrete excessive glucose. The patient needs from 6 – 10L
of fluid to replace fluid losses caused by polyuria, hyperventilation, diarrhea and
vomiting. Initially, 0.9 NS is administered at a rapid rate (0.5 – 1 L/hr) for the first
3 hours. Measurements of V/S should be monitored in addition to lung sounds,
I&O and signs of fluid overload.

2. Restoring electrolytes: the major electrolyte that should be corrected is potassium

that most commonly tends to be high in DKA because of acidosis so serum
potassium levels must be monitored frequently. Rehydration process should be
considerable when correcting potassium (potassium dilution and increased urinary
excretion of the potassium). Therefore, insulin administration enhances potassium
movement back into cells. ECGs and laboratory tests should be measured q2-4
hours for the first 8 hours. Potassium replacement must be stopped when
hyperkalemia is present or when the patient is not urinating.
3. Reversing acidosis: acidosis is reversed by the administration of insulin to inhibit
fat breakdown and therefore inhibit the formation of ketones. Insulin is usually
administered as IV infusion at a low continuous rate (5units/hr) and blood glucose
levels should be measured hourly. IV fluids with high concentration of glucose
should be given when blood glucose levels reach 250 – 300 mg/dL to avoid the
rapid drop of glucose during the treatment. Insulin must be infused continuously
until subcutaneous administration can be resumed. Any interruption in the
treatment can result in the re-accumulation of ketone bodies and worsening
acidosis.