DKA

Question 1

What population of diabetics is DKA most likely to occur?

Answer 1

Type I diabetes who are dependent on insulin

Question 2

What are the diagnostic criteria for DKA?

Answer 2

blood glucose > 250 mg/dl

pH

Question 3

What is glucagon?

Answer 3

Glucagon raises the blood glucose by converting glycogen to glucose
Glucagon is released from the liver and its release is stimulated when insulin is ineffective in providing the cells with glucose for energy

Question 4

What effect does DKA have on osmolality?

Answer 4

Hyperglycemia increases plasma osmolality and the blood becomes more hyperosmolar

Question 5

Glycogen?

Answer 5

Glucagon raises the blood glucose by converting glycogen to glucose
Glucagon is released from the liver and its release is stimulated when insulin is ineffective in providing the cells with glucose for energy

Question 6

What ABG changes would you expect to see in a DKA patient? Why?

Answer 6

Metabolic acidosis – acid ketones dissociate and yield hydrogen ions, which accumulate and precipitate a fall in serum pH and the level of bicarbonate decreases

Question 7

Why does a DKA patient have Kussmaul’s respirations?

Answer 7

Kussmaul respirations are when breathing becomes deep and fast. This is to release carbonic acid in the form of carbon dioxide.

Question 8

Why is the DKA patient at risk for dehydration? What is meant by osmotic diuresis? How does the dehydrated DKA patient present?

Answer 8

In an attempt to rid the body of the excess glucose during DKA, the kidneys excrete the glucose along with water and electrolytes - this happens by osmotic diuresis
Polyuria, increased BUN, creatinine, and hematocrit,

Question 9

What is hyperglycemia hyperosmolar state?

Answer 9

Hyperglycemia hyperosmaolar state is a severe, sustained elevation of blood glucose that leads to a serum hyperosmolality. If this is left untreated it progresses towards cellular dehydration, coma, and death

Question 10

What are later signs and symptoms of the DKA patient?

Answer 10

Nausea, vomiting, extreme fatigue, weight loss, dehydration, CNS depression, decreased LOC, progressing to coma and death

Question 11

The physician orders 1 liter of normal saline to be infused immediately in a patient admitted for DKA? Why?

Answer 11

It is infused to replenish the vascular deficit and to reverse hypotension

Question 12

Why might 20 to 30 mEq of potassium be added to the liter of normal saline if the patient has normal kidney function?

Answer 12

It is important if the potassium needs replacement to give it before administering the insulin bolos. Also rehydration leads to increased urinary excretion of potassium

Question 13

After the DKA patient’s serum glucose level decreases to 200 mg/dL, normal saline is changed to a 50/50 mix of hypotonic saline and 5% dextrose. Why is the DKA patient given dextrose at this point?

Answer 13

Dextrose is added to replenish depleted cellular glucose as the circulating serum glucose decreases to 200mg/mL. Dextrose also prevents unexpected hypoglycemia when insulin is continued and the patient is not able to take in an adequate amount of carbohydrates.

Question 14

What type of insulin is administered to the DKA patient? How is it given?

Answer 14

An initial IV bolus of regular insulin at 0.1 unit for each kilogram of weight is administered. Then a continuous infusion of regular insulin at 0.1/kg/hr is infused simultaneously with IV fluid replacement.

Question 15

How often are blood glucose levels checked in the DKA patient?

Answer 15

At first blood glucose tests are performed every hour then decreases to every 2-4 hours as the patient’s blood sugar returns to normal

Question 16

As insulin is administered and metabolic acidosis is reversed, what may happen to serum potassium?

Answer 16

The patient can become hypokalemic because the serum potassium follows the insulin into the cells.

Question 17

How fast should blood glucose levels fall in the treatment of the DKA patient?

Answer 17

50-70mg/dL per hour

Question 18

What are ketones?

Answer 18

Broken down fatty acids from the liver.
Used for energy when glucose is not available due to no carbohydrate intake (Atkin’s diet)
Ketones are a product of fatty acid metabolism. In insulin deficiency states, fat is rapidly converted into glucose (gluconeogenesis).
Ketones are formed when the cells must use free fatty acids for energy because all of the glucose is in the bloodstream.

Question 19

Early Signs of DKA pt?

Answer 19

Early:

• Malaise
• H/A
• polyuria (excessive urination)
• polydipsia (excessive thirst)
• polyphagia (excessive hunger)
• Dry mouth
• Dehydration
• dry skin
• hypotension
• weakness

Question 20

Late Signs of DKA pt?

Answer 20

Late:

• N/V
• Fatigue
• Dehydration
• weight loss
• CNS depression
• decreased LOC progressing to coma and death
• Ketoacidosis
• air hunger
• acetone breath odor
• respirations deep and rapid

Question 21

What lab changes would you expect in a DKA patient and why? Look at blood glucose level, potassium, ABG’s, serum osmolality?

Answer 21

Hyperglycemia
Ketones
ABGs: Uncompensated metabolic acidosis (pH and HCO3)
Decreased CO2
Elevated anion gap
Low sodium: due to movement of water from intracellular to extracellular
Normal potassium: if low, it suggests significant potassium deficiency
Metabolic acidosis
If serum osmolality is elevated the K+ will help carry the insulin into the cells, decreasing the serum glucose level

Question 22

What are immediate treatments for the patient in DKA?

Answer 22

Goal: Reverse dehydration, replace insulin, reverse ketoacidosis, replenish electrolytes.

Reverse dehydration: 1. 0.9% NaCl (Isotonic NS): Replenishes vascular deficit
Reverse hypotension

		2. 1L NS:			For severe dehydration
		3. 0.45 (Hypotonic NaCl):	For hypernatremia
		4. Include 20-30 mEq of potassium per liter in infusion

After glucose decreases to 200: change infusion to 50/50 hypotonic saline and 5% dextrose (dextrose is added to replenish depleted cellular glucose, also prevents unexpected hypoglycemia)

Hydration assessment: hourly intake, BP changes (orthostatic hypotension, pulse pressure, pulse rate, character, rhythm), neck vein filling, skin turgor, skin moisture, body weight, central venous pressure (CVP), pulmonary arterial occlusion pressure (PAOP), hourly output, increased thirst

Replace insulin: 1. Check potassium in not

Question 23

Key nursing interventions?

Answer 23

Make sure the patient is npo until the hyperglycemia is under control.
When bg levels fall to 200mg/dl 5%dextrose with 0.45%NaCl is given to stop hypoglycemia.
you want to monitor I&O measurements must be maintained to monitor reveral of dehydration.
Watch HR, BP, and CVP to determine if fluid replacement was good.
Watch for fluid volume overload (neck vein engorgement, dyspnea, and pulmonary crackles), hypoglycemia (unexpected behavior, decreased LOC, diaphoresis, and tremors), hypokalemia and hyperkalemia (large peaked t wave, flattened p wave, and widened qrs), hyponatremia (abdominal cramping, postural hypotension, and behavior change), risk for cerebral edema (confusion, and sudden headache), risk for infection, dehydration, hypovolemia, and hypophosphatemia, assess bony prominences, oral care, strict sterile technique).

Question 24

What happens to stored protein and fat when glucagon is released into the blood?

Answer 24

Glucagon converts fat and protein into new glucose (gluconeogenesis)