Ms. Blake is an older adult with diabetes and has been too ill to get out of bed for 2 days. She has had a severe cough and has been unable to eat or drink during this time. She has a history of Type I diabetes. On admission her laboratory values show: Sodium (Na+) 156 mEq/L Potassium (K+) 4.0 mEq/L Chloride (Cl–) 115 mEq/L Arterial blood gases   (ABGs) pH- 7.30; Pco2-40;   Po2-70; HCO3-20 Normal values Sodium (Na+) 136-146 mEq/L Potassium (K+) 3.5-5.1 mEq/L Chloride (Cl–) 98-106 mEq/L Arterial blood gases   (ABGs) pH- 7.35-7.45 Pco2- 35-45 mmHg Po2-80-100 mmHg HCO3–22-28 mEq/L 1. What is the etiology of Diabetic Ketoacidosis? 2. Describe the pathophysiological process of Diabetic Ketoacidosis 3. Identify the hallmark symptoms of Diabetic Ketoacidosis 4. Identify any abnormal lab results provided in the case and explain why these would be abnormal given the patient’s condition. 5. What teaching would you provide this patient to avoid heart failure symptoms? McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). (7th ed.) St. Louis, MO: Mosby)

1. The etiology of Diabetic Ketoacidosis (DKA) in Ms. Blake’s case can be attributed to her history of Type I diabetes. Type I diabetes is characterized by the body’s inability to produce insulin, which is essential for the utilization of glucose for energy. Without insulin, the body resorts to breaking down fat stores for energy, leading to an accumulation of ketone bodies. Increased levels of ketones in the bloodstream, along with high blood sugar levels, result in the development of DKA.

2. The pathophysiological process of DKA involves a combination of insulin deficiency, increased counter-regulatory hormone levels, and metabolic derangements. In Type I diabetes, insulin production is significantly reduced or absent, leading to decreased uptake of glucose by cells. As a result, blood glucose levels rise, causing hyperglycemia.

In response to hyperglycemia, the body releases counter-regulatory hormones such as glucagon, cortisol, and epinephrine. These hormones stimulate the breakdown of glycogen in the liver, further increasing blood glucose levels. Simultaneously, insulin deficiency prevents glucose uptake in peripheral tissues, causing a state of cellular starvation.

To compensate for the lack of glucose utilization, the body begins breaking down adipose tissue for energy. This process, known as lipolysis, results in the production of ketone bodies, including acetoacetate, beta-hydroxybutyrate, and acetone. The accumulation of these ketone bodies in the bloodstream leads to a condition called ketosis.

However, in DKA, the accumulation of ketones exceeds the body’s ability to metabolize and excrete them. This imbalance results in a further decrease in pH, leading to metabolic acidosis. As the pH decreases, compensatory mechanisms attempt to normalize it through increased respiratory rate and renal elimination of acids. This compensatory response is reflected in the laboratory values of the arterial blood gases provided in the case.

3. The hallmark symptoms of Diabetic Ketoacidosis include polyuria (excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger), weight loss, fatigue, and dehydration. These symptoms result from the body’s inability to utilize glucose as an energy source and the subsequent breakdown of fats for energy. The increased production of ketones in the bloodstream leads to an osmotic diuresis, causing excessive urination and thirst. The lack of glucose utilization also contributes to the loss of body weight and energy. Additionally, the metabolic derangements in DKA can cause electrolyte imbalances and fluid shifts, leading to dehydration and fatigue.

4. The abnormal lab results provided in the case include elevated sodium (Na+) levels, normal potassium (K+) levels, elevated chloride (Cl–) levels, and abnormal arterial blood gas values.

The elevated sodium levels (156 mEq/L) can be attributed to the hyperosmolar state induced by the presence of ketones in DKA. The high levels of ketones lead to an increase in the osmolarity of the blood, resulting in water shifting out of the cells and into the extracellular space. This movement of water dilutes the sodium concentration, leading to a relative increase in sodium levels.

The normal potassium levels (4.0 mEq/L) are expected in DKA, as insulin deficiency promotes potassium movement from the intracellular to the extracellular compartment. However, it is essential to monitor potassium levels closely, as insulin therapy given during DKA treatment can cause a rapid intracellular shift of potassium, leading to hypokalemia.

The elevated chloride levels (115 mEq/L) can be attributed to the ketone-driven metabolic acidosis in DKA. The accumulation of ketones leads to the release of hydrogen ions, which combine with chloride to form hydrochloric acid, resulting in an increase in the chloride levels.

The arterial blood gas values show a pH of 7.30 (below the normal range of 7.35-7.45), a Pco2 of 40 mmHg (within the normal range of 35-45 mmHg), a Po2 of 70 mmHg (below the normal range of 80-100 mmHg), and a HCO3- of 20 mEq/L (below the normal range of 22-28 mEq/L).

The decreased pH reflects the metabolic acidosis in DKA caused by the accumulation of ketones and the subsequent increase in hydrogen ions. The Pco2 within the normal range indicates adequate respiratory compensation through increased ventilation to eliminate excess carbon dioxide. The decreased Po2 values can be attributed to inadequate oxygenation due to the effects of DKA on pulmonary function. The decreased HCO3- levels reflect the primary metabolic acidosis caused by the accumulation of ketones and the resulting decrease in bicarbonate levels.