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1. Describe the pathophysiologic changes in DKA.
Nurses Response: DKA results from when the body is no longer producing insulin. Our cells
need glucose and fatty acid to produce energy (ATP). In order to use glucose, it has to have
insulin. Glucose sits outside the cell and in order for glucose to get inside, it needs to have
insulin.. Without glucose, the cells breakdown fatty acids for its energy. Well, fatty acids leads to
acidosis, which as a result leads to hyperkalemia (high potassium), and elevated glucose level
because since glucose cannot get into the cell it is rising in our blood because it cannot get into
our cells to use it. So as the glucose rises, it leads to osmotic diuresis which forces pressure on
your kidneys leading to renal failure and increase creatinine. Two things are happening: We are
breaking down fatty acids which leads to acidosis and we are not using glucose that's leading to
hyperglycemia. So as a result Diabetic Ketoacidosis occurs.
2. What are commonly seen blood glucose levels?
Nurses Response: Normal blood glucose levels should range from 70- 110 mg/dL. When blood
glucose concentration exceeds 250- 300 mg/dl, generally, DKA has occurred.
3. What fluid and electrolyte disturbances commonly occur and why?
Nurses Response: Electrolytes are vital for the normal functioning of our body. They include
sodium, potassium calcium and bicarbonate. High blood sugar causes excessive urination and
spillage of sugar into the urine. This leads to loss of body water and dehydration as well as loss
of important electrolytes, including elevated sodium and potassium. The level of another
electrolyte, bicarbonate, also falls as the body tries to compensate for excessively acidic blood
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along with low Ph, acidosis. Normal Potassium (3.5-5.0), Sodium (135-145) Bicarbonate (22-28)
pH( 7.35-7.45)
4. What acid-base disturbances commonly occur and why ?
Nurses Response: Serum pH falls below 7.35 (acidosis). Bicarbonate level falls below
15mEq/L, resulting in Metabolic acidosis and hyperglycemia and Kussmauls respiration (deep
labored breathing).
5. Describe the medical management of a patient in DKA.
a. How is fluid status monitored in the acute stages of DKA?
Monitoring fluid volume status involves frequent measurements of vital signs, lung
assessment, and monitoring intake and output.
b. How is hypovolemia corrected? How rapidly is fluid volume replaced? Why?
Hypovolemia should be corrected by administer 1 L NS over 30-60 min and add a
second L if needed. Then 1/2NS should be administered. D5 1/2NS should be
administered when blood glucose exceeds 250 mg/dL or higher.
c. How are the complications of fluid replacement prevented?
Complications are prevented when 1 L NS is administered within 60 min.
d. How are blood glucose levels monitored? How often?
Blood glucose should be monitored by using an Accu-check, blood glucose monitor,
every hour.
e. How are elevated blood glucose levels corrected?
Blood glucose levels are corrected with insulin therapy if the accu-check monitor
shows the pts blood glucose is too high. Specific type, dose, and route of insulin are
given depending on the pt and their current condition.
f. How quickly is blood glucose corrected? Why?
Blood glucose must be corrected slowly in order to keep the pt from becoming
hypoglycemic. There are different ways and different types of insulin used to correct
blood glucose.
g. What electrolytes are monitored in the acute stage of DKA? Why?
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Potassium and sodium are the main electrolytes that are monitored in the acute
stages of DKA because potassium often leaves the intracellular space and sodium is
monitored because insulin may cause hypokalemia.
h. How are electrolyte imbalances corrected? How rapidly is this accomplished? Why?
How are complications of electrolyte replacement prevented?
Electrolyte imbalances are corrected by IV therapy with potassium chloride.
Potassium should be given 1-2 hours after insulin therapy starts.
i. How are acid-base disturbances monitored? How often?
Acid-base disturbances are monitored every hour by an ECG and by assessing ABGs.
j. How are acid-base disturbances corrected? How quickly is this accomplished? Why?
How are complications of acid-base correction prevented?
Acid-base disturbances are corrected by fluid replacement and also through insulin
therapy. This is accomplished slowly in order to prevent hypokalemia. Prevention
includes carefully assessing electrolyte levels, ABGs, and intake and output.
6. Define the following terms and describe how the results of each are used: anion gap,
serum osmolality and venous CO2.
Anion gap: the difference between electrolytes, cations anions = anion gap.
Serum osmolality measures the electrolytes, urea, and glucose in the blood to find fluid
and electrolyte imbalances in the body.
Venous CO2 is used to measure bicarbonate in the blood.
