A client is admitted to the intensive care unit (ICU) after a colon resection with the formation of a loop colostomy. The nurse determines the client's abdominal dressing is clean and dry. Vital signs are temperature 100° F (37.8° C) orally, heart rate 132 beats/minute, blood pressure 88/65 mm Hg, and urine output 10 mL/hour. Which intervention should the nurse implement?

A. White blood cell differential. Although infection is a common precipitating factor for DKA, an elevated WBC count is common in DKA due to stress, dehydration, and inflammation rather than infection itself. While a WBC differential may be done if infection is suspected, it is not a primary test for DKA management.
B. Hemoglobin A1C. Hemoglobin A1C (HbA1c) reflects long-term glucose control (past 2-3 months) but does not provide immediate information about the current metabolic status or severity of DKA. While it may be useful in assessing overall diabetes management, it is not essential for acute DKA treatment.
C. Serum electrolytes. Patients with DKA experience significant electrolyte imbalances, particularly potassium depletion due to osmotic diuresis and insulin deficiency. Monitoring serum sodium, potassium, and bicarbonate is crucial for guiding fluid and electrolyte replacement therapy. Potassium levels may appear normal or high initially due to acidosis but typically drop with insulin administration.
D. Urine culture. A urine culture is only indicated if a urinary tract infection (UTI) is suspected as a trigger for DKA. However, routine urine culture is not required in every case of DKA unless there are symptoms of infection such as fever, dysuria, or pyuria.
E. Anion gap. DKA is a form of high anion gap metabolic acidosis, caused by the accumulation of ketones. The anion gap (AG) is calculated as (Na⁺ - [Cl⁻ + HCO₃⁻]), with a value >12 mEq/L indicating metabolic acidosis. Monitoring the anion gap helps assess the severity of acidosis and guide treatment progress, as a decreasing anion gap suggests resolution of ketosis.
F. Urine ketones. Urine ketone testing helps confirm the presence of ketoacidosis, particularly in the initial stages of DKA diagnosis. While serum beta-hydroxybutyrate is a more accurate indicator of ketone levels, urine ketones remain useful for initial screening and monitoring treatment response as they decrease with appropriate management.

A. Promote oxygenation to tissues. Oxygenation is not a primary goal in DKA management unless there is a coexisting condition causing hypoxia. DKA primarily leads to metabolic acidosis and dehydration rather than respiratory failure, and oxygenation is typically maintained unless complications such as pneumonia or severe shock develop.
B. Reverse dehydration. Severe dehydration occurs in DKA due to osmotic diuresis caused by hyperglycemia. The priority is to restore intravascular volume with isotonic IV fluids such as 0.9% normal saline to improve circulation, support kidney function, and prevent shock. Fluid replacement is essential for stabilizing blood pressure and promoting glucose clearance.
C. Replace insulin. The lack of insulin is the primary cause of DKA, leading to unchecked lipolysis and ketone production. IV insulin therapy is necessary to suppress ketogenesis, lower blood glucose levels, and allow cells to use glucose for energy. Insulin must be administered cautiously with continuous monitoring to prevent hypoglycemia and electrolyte imbalances.
D. Correct electrolytes that are out of normal range. Electrolyte imbalances, particularly potassium depletion, are common in DKA due to osmotic losses and shifting caused by insulin therapy. Potassium replacement is required even if levels appear normal initially, as insulin will drive potassium into cells, leading to hypokalemia. Sodium and bicarbonate levels should also be monitored and corrected as needed.
E. Provide respiratory support. Respiratory support is not typically required unless the client experiences severe respiratory distress or altered mental status. Kussmaul respirations are a natural compensatory mechanism that helps the body exhale CO₂ and correct acidosis. Supplemental oxygen is only necessary if there is an underlying pulmonary condition or respiratory failure.
F. Prevent hyperventilation. Hyperventilation in the form of Kussmaul respirations is the body's way of compensating for metabolic acidosis. It should not be suppressed, as it plays a crucial role in reducing acid buildup. Treating the underlying cause of DKA with fluids, insulin, and electrolyte replacement will allow respiratory function to normalize.