A nurse is administering a cleansing enema to a client who reports mild cramping during instillation of the solution. Which of the following actions should the nurse take?

• Check deep tendon reflexes: The client exhibits restlessness, diaphoresis, tachycardia, elevated temperature, and gastrointestinal symptoms, which are consistent with serotonin syndrome. Hyperreflexia and clonus are key neuromuscular findings associated with this condition. Assessing deep tendon reflexes helps confirm neuromuscular hyperactivity.
• Discontinue fluoxetine: Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) that increases serotonin levels and can precipitate serotonin syndrome. The client’s symptoms developed after initiating this medication, suggesting toxicity. Immediate discontinuation removes the source of excess serotonin.
• Administer citalopram: Citalopram is another SSRI that increases serotonin activity. Administering it while the client is experiencing serotonin toxicity would worsen the condition. Adding another serotonergic agent could intensify hyperthermia, autonomic instability, and neuromuscular symptoms.
• Administer phenelzine: Phenelzine is a monoamine oxidase inhibitor (MAOI) that significantly increases serotonin levels. Combining or switching to an MAOI in the setting of suspected serotonin syndrome is dangerous and can precipitate severe toxicity. MAOIs require a washout period after SSRIs due to fluoxetine’s long half-life.
• Administer propranolol: Propranolol may be used to manage autonomic instability such as tachycardia and hypertension associated with serotonin syndrome. The client’s elevated heart rate and blood pressure support this intervention. Controlling sympathetic overactivity reduces cardiovascular strain.

A. Negative urine ketones: Diabetic ketoacidosis (DKA) is characterized by increased production of ketone bodies due to insulin deficiency and enhanced lipolysis. Ketones accumulate in the blood and spill into the urine, producing positive urine ketone results. The absence of urine ketones does not support the presence of ketoacidosis, as ketosis is a defining metabolic feature.

B. Kussmaul respirations: Kussmaul respirations are deep, rapid breathing patterns that occur as a compensatory response to metabolic acidosis. In DKA, excess ketone production leads to accumulation of hydrogen ions and decreased serum bicarbonate. The respiratory system compensates by increasing ventilation to eliminate carbon dioxide.

C. Hypoglycemia: DKA is associated with hyperglycemia due to insufficient insulin, which prevents glucose from entering cells and leads to elevated serum glucose levels. Hypoglycemia involves low blood glucose and does not trigger the ketone overproduction seen in DKA. The pathophysiology of DKA centers on insulin deficiency and high circulating glucose.

D. Hypertension: Clients with DKA often experience osmotic diuresis from severe hyperglycemia, leading to dehydration and volume depletion. This intravascular fluid loss more commonly results in hypotension rather than elevated blood pressure. The hemodynamic changes in DKA are primarily related to dehydration and electrolyte imbalance.