Question

In the ER, A mother has brought in her 20-year-old daughter, C.J., who has type 1 diabetes mellitus (DM) and has just returned from a trip to Mexico. She has had a 3-day fever and diarrhea with nausea and vomiting (N/V). She has been unable to eat and has tolerated only sips of fluid. Because she was unable to eat, she did not take her insulin. Because C.J. is unsteady, you bring her to the examining room in a wheelchair. While assisting her onto the examining table, you note her skin is warm and flushed. Her respirations are deep and rapid, and her breath is fruity and sweet-smelling. C.J. is drowsy and unable to answer your questions. Her mother states, “She keeps telling me she's so thirsty, but she can't keep anything down.”

The mother also tells you the following:

“Blood glucose monitor has been reading ‘high.’ ”

“C.J. has had sips of ginger ale but that's all.”

“She has been vomiting about every other time she drinks.”

“When she first got home, she went [voided] a lot, but yesterday she hardly went at all, and I don't think she has gone today.”

“She went to bed early last night, and I could hardly wake her up this morning. That's why I brought her in.”

Vital Signs

Blood pressure 90/50 mm Hg

Heart rate 124 beats/min

Respiratory rate 36 and deep

Temperature 101.3° F (38.5° C) (tympanic)

Laboratory Test Values

Glucose 577 mg/dL

Potassium 5.8 mEq/L

After evaluating C.J., the ED physician admits the patient with DKA.

1.Describe the pathophysiology of diabetic ketoacidosis (DKA) and how it differs from hyperglycemic-hyperosmolar state (HHS).

2.Explain the rationale for C.J.'s presenting signs and symptoms.

3.What medical treatments are appropriate for this patient?

4.List five priority nursing interventions and the rationale for each.

5.The physician orders an insulin drip infusion at 4 units per hour. The label on the bag reads, “100 units regular (Humulin R) insulin in 250 mL of normal saline.” At how many milliliters per hour will you set the infusion pump?

Answer 1

1.

Diabetic ketoacidosis (DKA) is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. DKA usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counter-regulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). This type of hormonal imbalance enhances hepatic gluconeogenesis, glycogenolysis, and lipolysis.

Hepatic gluconeogenesis, glycogenolysis secondary to insulin deficiency, and counter-regulatory hormone excess result in severe hyperglycemia, while lipolysis increases serum free fatty acids. Hepatic metabolism of free fatty acids as an alternative energy source (ie, ketogenesis) results in accumulation of acidic intermediate and end metabolites (ie, ketones, ketoacids). Ketone bodies have generally included acetone, beta-hydroxybutyrate, and acetoacetate. It should be noted, however, that only acetone is a true ketone, while acetoacetic acid is true ketoacid and beta-hydroxybutyrate is a hydroxy acid.

Meanwhile, increased proteolysis and decreased protein synthesis as result of insulin deficiency add more gluconeogenic substrates to the gluconeogenesis process. In addition, the decreased glucose uptake by peripheral tissues due to insulin deficiency and increased counter regulatory hormones increases hyperglycemia.

Ketone bodies are produced from acetyl coenzyme A mainly in the mitochondria within hepatocytes when carbohydrate utilization is impaired because of relative or absolute insulin deficiency, such that energy must be obtained from fatty acid metabolism. High levels of acetyl coenzyme A present in the cell inhibit the pyruvate dehydrogenase complex, but pyruvate carboxylase is activated. Thus, the oxaloacetate generated enters gluconeogenesis rather than the citric acid cycle, as the latter is also inhibited by the elevated level of nicotinamide adenine dinucleotide (NADH) resulting from excessive beta-oxidation of fatty acids, another consequence of insulin resistance/insulin deficiency. The excess acetyl coenzyme A is therefore rerouted to ketogenesis.

Progressive rise of blood concentration of these acidic organic substances initially leads to a state of ketonemia, although extracellular and intracellular body buffers can limit ketonemia in its early stages, as reflected by a normal arterial pH associated with a base deficit and a mild anion gap.

When the accumulated ketones exceed the body's capacity to extract them, they overflow into urine (ie, ketonuria). If the situation is not treated promptly, a greater accumulation of organic acids leads to frank clinical metabolic acidosis (ie, ketoacidosis), with a significant drop in pH and bicarbonate ^[4] serum levels. Respiratory compensation for this acidotic condition results in Kussmaul respirations, ie, rapid, shallow breathing (sigh breathing) that, as the acidosis grows more severe, becomes slower, deeper, and labored (air hunger).

Ketones/ketoacids/hydroxy acids, in particular, beta-hydroxybutyrate, induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA. Moreover, acetone produces the fruity breath odor that is characteristic of ketotic patients.

Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. This loss is not mirrored in serum potassium levels, which may be low, within the reference range, or even high.

Potassium loss is caused by a shift of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis. Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis.

Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia. Sodium also is lost in the urine during the osmotic diuresis.

Typical overall electrolyte loss includes 200-500 mEq/L of potassium, 300-700 mEq/L of sodium, and 350-500 mEq/L of chloride. The combined effects of serum hyperosmolarity, dehydration, and acidosis result in increased osmolarity in brain cells that clinically manifests as an alteration in the level of consciousness.

Many of the underlying pathophysiologic disturbances in DKA are directly measurable by the clinician and need to be monitored throughout the course of treatment. Close attention to clinical laboratory data allows for tracking of the underlying acidosis and hyperglycemia, as well as prevention of common potentially lethal complications such as hypoglycemia, hyponatremia, and hypokalemia.

2. • Elevated blood glucose results from lack of insulin and probable infection.
• Warm, dry skin results from both the infection and worsening of ketosis.
• Fruity, acetone-smelling breath results from ketosis.
• Drowsiness results from depression of the central nervous system from acidosis.
• Hyperkalemia results from shifting of hydrogen ions intracellularly in an attempt to buffer the acidosis.

3.