Nurses Notes on Diabetic Ketoacidosis

Diabetic Ketoacidosis (DKA)

Develops when there is an absolute deficiency of insulin and an increase in the insulin counterregulatory hormones. Glucose production by the liver increases, peripheral glucose use decreases, fat mobilization increases, and ketogenesis (ketone formation) is stimulated. Increased glucagon levels activate the gluconeogenic and ketogenic pathways in the liver. In the presence of insulin deficiency, hepatic overproduction of beta- hydroxybutyrate and acetoacetic acids (ketone bodies) causes increased ketone concentrations and an increased release of free fatty acids. As a result of a loss bicarbonate (which occurs when the ketone is formed), bicarbonate buffering does not occur, and a metabolic acidosis occurs, called DKA.

DKA involves four metabolic problems:

·         Hyperosmolarity from hyperglycemia and dehydration

·         Metabolic acidosis from an accumulation of ketoacids

·         Extrracellular volume depletion from osmotic dieresis

·         Electrolyte imbalances (such as loss of potassium and sodium) from osmotic dieresis

  

Risk Factors:

·         Infection such as diarrhea, vomiting, and/or high fever (40%),

·         missed or inadequate insulin (25%)

·         newly diagnosed or previously unknown diabetes (15%).

·         heart attack

·          stroke

·          trauma

·          stress,

·         alcohol abuse,

·         drug abuse, and surgery

·         Approximately 5% to 10% of cases have no identifiable cause

Signs and Symptoms

ü       Dehydration (from hyperglycemia)

·                  Thirst

·                  Warm, dry skin with poor turgor

·                  Soft eyeballs

·                  Dry mucous membranes

·                  Weakness

·                  Malaise

·                  Rapid, weak pulse

·                  Hypotension

ü  Metabolic Acidosis (from ketosis)

·                  Nausea and vomiting

·                  Ketone (fruity, alcohol – like)

·                  Breath odor

·                  Lethargy

·                  Coma

ü  Other Manifestations

·         Abdominal Pain (cause unknown)

·         Kussmaul’s respirations (increased rate and depth of respirations, with a longer expiration; a compensatory response to prevent a further decrease in pH)

Management:

a) When teaching the diabetic client about foot care, the nurse should instruct the client to avoid walking barefooted.

b) Blood Glucose Monitoring should be done to detect hypoglycemia and hyperglycemia. It also  helps the client with diabetes reach a desired level of glycemic control.

c) During blood glucose monitoring, the nurse must collect a blood sample from the side of the finger (adult); Outer aspect of the heel (infant).

d) Blood sugar monitoring must be done early monitoring before breakfast.

Diagnostic Tests to Monitor Diabetes Management 

·         Fasting blood glucose (FBG). This test is often ordered, especially if the client is experiencing symptoms of hypoglycemia and hyperglycemia. In most people, the normal range is 70 to 110 mg/ dL.

·         Glycosylated hemoglobin. This test determines the average blood glucose level over approximately the previous 2 to 3 months. When glucose is elevated or control of glucose is erratic, glucose attaches to the hemoglobin molecule and remains attached for the life of the hemoglobin, which is about 120 days. The normal level depends on the type of assay done, but values above 7% to 9% are considered elevated.

·         Urine Glucose and ketone levels. These are not as accurate in monitoring changes in blood glucose as blood levels. The presence of glucose in the urine indicates hyperglycemia. Most people have a renal threshold for glucose exceeds 180 mg/dL; that is, when the blood glucose exceeds 180 mg/ dL, glucose is not reabsorbed by the kidneys and spills over into the urine. This number varies highly, however.

·         Urine test for the presence of protein as albumin (albuminuria). If albuminuria is present, a 24- hour urine test for creatinine clearance is used to detect the early onset of nephropathy.

·         Serum cholesterol and triglyceride levels. These are indicators of atherosclerosis and an increased risk of cardiovascular impairments.

·         Serum electrolytes. Levels are measured in clients who have DKA or HHS to determine imbalances.

Treatment of DKA

·         Alterations in level of consciousness, acidosis, and vomiting are common necessitating intravenous fluid placement. The initial fluid replacement may be accomplished by administering 0.9% saline solution at a rate of 500 to 1,000 mL/h. After 2- 3 hours (or when blood pressure is returning to normal), the administration of 0.45% saline at 200- 500 mL/h may continue for several more hours. When the blood glucose levels reach 250 mg/dL, dextrose is added to prevent rapid decrease in glucose; hypoglycemia could result in fatal cerebral edema.

·         Regular insulin is used in the management of DKA and may be given by various routes, depending on the severity of the condition. Mild ketosis may be treated with subcutaneous insulin, whereas severe ketosis requires intravenous insulin infusion.

·         Potassium replacement is begun early in the course of treatment, usually by adding potassium to the rehydration fluids.