Running head: DIABETIC KETOACIDOSIS 1

Diabetic Ketoacidosis

Janie Rigsby

Mt. San Jacinto College

Advanced Medical Surgical Nursing

NURS 244

Wade Hagan, PhD, RN, PHN, CCRN

September 14, 2010

 Diabetic Ketoacidosis

This paper will discuss the factors that contribute to diabetic ketoacidosis (DKA).

Appropriate intervention strategies for the reversal of the resulting metabolic changes will also

be explored.

Factors contributing to Diabetic Ketoacidosis

Diabetic ketoacidosis occurs as a result of an excess of ketones in the blood (Ignatavicius

& Workman, 2010). When there is an absence of insulin, tissues such as fat and muscle are not

able to absorb glucose (Ignatavicius & Workman, 2010). “Counterregulatory hormones, such as

glucagon, growth hormone, and catecholamines, enhance triglyceride breakdown into free fatty

acids and gluconeogenesis, which is the main cause for the elevation in serum glucose level in

diabetic ketoacidosis” (Rucker, 2010, para. 3). Ketone bodies are produced due to the breakdown

of fat as opposed to the body breaking down carbohydrates for energy (Ignatavicius &

Workman, 2010). Metabolic acidosis follows as a result due to the depletion of cellular and

extracellular acid buffers (Rucker, 2010). The “hyperglycemia-induced osmotic diuresis depletes

sodium, potassium, phosphates, and water as well as ketones and glucose” (Rucker, 2010, para.

5). Patients will be dehydrated and will have electrolyte imbalances (Ignatavicius & Workman,

2010).

Ketoacidosis decreases the pH of the blood, stimulating the respiratory control areas of

the brain to buffer the effects of increasing acidosis (Ignatavicius & Workman, 2010). The rate

and depth of respiration are increased (Kussmaul respirations) in an attempt to excrete more

acids by exhalation (Ignatavicius & Workman, 2010). Then the lungs can no longer offset the

acidosis, the pH decreases below normal (Ignatavicius & Workman, 2010).

 Diabetic ketoacidosis is typically characterized by “hyperglycemia over 300 mg/dL, low

bicarbonate level (<15 mEq/L), and acidosis (pH <7.30)” with ketones in the blood and ketones

in the urine (Rucker, 2010, para. 2). While definitions vary, “moderate DKA can be categorized

by pH <7.2 and serum bicarbonate <10 mEq/L, whereas severe DKA has pH <7.1 and

bicarbonate <5 mEq/L. Mental status changes can be seen with mild-to-moderate DKA with

more severe deterioration in mental status typical with moderate-to-severe DKA” (Rucker, 2010,

para. 2).

Prevention is the best intervention strategy. Diabetics should have their blood glucose

controlled. Diabetic ketoacidosis is treated with insulin in an effort to aid the body in changing

from burning fat for energy to using carbohydrates (Ignatavicius & Workman, 2010). Insulin will

allow the tissues to take up glucose and reduce the production of ketone bodies (Porth, 2005).

Blood glucose should be monitored and care must be taken to avoid hypoglycemia (Ignatavicius

& Workman, 2010).

Fluid resuscitation is equally important to replace intravascular and extravascular

electrolytes and fluid volume (Ignatavicius & Workman, 2010). Fluids administered

intraveneously will also dilute the levels of counter-regulatory hormones as well as the glucose

level (Rucker, 2010). The intravenous solutions can be 0.9% normal saline for the first hour and

0.45% afterwards (Rucker, 2010). When glucose levels have dropped to under 250 mg/dL, the

fluid regime could change to D5 0.45% normal saline to “prevent hypoglycemia recognizing that

insulin is still needed to treat ketonemia” (Rucker, 2010, para. 15).

Potassium should be included in the initial fluid administration (Rucker, 2010). Prior to

giving potassium, insure that patient has urine output of at least 30 ml/hr (Ignatavicius &

Workman, 2010). The nurse should assess the potassium level after the start of insulin therapy as
hypokalemia may result (Ignatavicius & Workman, 2010). The nurse should assess electrolyte

levels for dehydration or fluid overload hourly as well as creatinine, BUN, and urine ketones.

Urine output should average 30 ml/hour (Ignatavicius & Workman, 2010).

Education is an integral part of diabetes management. The nurse must teach the patient

to check blood glucose levels every four to six hours as long as patient is symptomatic or the

blood glucose is over 250 mg/dL (Ignatavicius & Workman, 2010). Ketone levels should be

tested if glucose is greater than 300 mg/dL (Ignatavicius & Workman, 2010). Patient should

drink three liters of fluid a day and if vomiting, see the physician for treatment (Ignatavicius &

Workman, 2010). Patient should see a physician if they have a temperature of over 101.5 degrees

Fahrenheit or for any fever that lasts more than 24 hours (Ignatavicius & Workman, 2010).
 References

Ignatavicius, D., & Workman, M. (2010). Medical-surgical Nursing: Patient-centered

collaborative care (6th ed.). St. Louis: Saunders Elsevier.

Porth, C. (2005). Pathophysiology Concepts of altered health states (7th ed.). Philadelphia:

Lippincott.

Rucker, D. (2010). Diabetic Ketoacidosis. Retrieved from

http://emedicine.medscape.com/article/766275-overview