# Clinical context An adult taking empagliflozin develops fever, poor intake, vomiting, and deep rapid respirations during a urinary infection; glucose is 184 mg/dL, beta-hydroxybutyrate 5.2 mmol/L, bicarbonate 12 mEq/L, and venous pH 7.24, establishing euglycemic diabetic ketoacidosis. Highlight the current symptoms and laboratory findings that establish euglycemic diabetic ketoacidosis despite glucose below 250 mg/dL. Do not select medication exposure or unrelated normal findings.

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=522749&lang=en  
> language: en  
> subject: Adverse Effects/Contraindications/Interactions  
> category: PPT

## Question

Clinical context
An adult taking empagliflozin develops fever, poor intake, vomiting, and deep rapid respirations during a urinary infection; glucose is 184 mg/dL, beta-hydroxybutyrate 5.2 mmol/L, bicarbonate 12 mEq/L, and venous pH 7.24, establishing euglycemic diabetic ketoacidosis.

Highlight the current symptoms and laboratory findings that establish euglycemic diabetic ketoacidosis despite glucose below 250 mg/dL. Do not select medication exposure or unrelated normal findings.

Emergency Record\nThe client takes empagliflozin for type 2 diabetes. During two days of fever and minimal intake, the client developed repeated vomiting and deep rapid respirations. Results are glucose 184 mg/dL, bicarbonate 12 mEq/L, venous pH 7.24, and beta-hydroxybutyrate 5.2 mmol/L. The creatinine is 0.9 mg/dL, the lactate is 1.4 mmol/L, the oxygen saturation is 98% on room air, the abdomen is soft without guarding, the no recent alcohol intake is reported, and the last A1C was 7.2 percent.

## Explanation

Empagliflozin use, acute infection, minimal intake, vomiting, deep rapid respirations, bicarbonate 12 mEq/L, pH 7.24, and beta-hydroxybutyrate 5.2 mmol/L support euglycemic DKA despite a glucose of 184 mg/dL.

## In-depth explanation

Quick answer
Do not let near-normal glucose hide ketonemia and metabolic acidosis.

Why this is correct
SGLT2 inhibitors increase urinary glucose loss, so serious ketoacidosis may present without marked hyperglycemia. Infection, reduced caloric intake, vomiting, and dehydration add insulin deficiency and counterregulatory stress.

Easy analogy or mental picture
Build a medication safety chain: identify the cue cluster, connect it to the drug mechanism, stop preventable exposure, stabilize the client, and verify the response with measurable findings.

Memory hook
Cue cluster, medication mechanism, protective action, and measurable reassessment.

NCLEX decision rule
Choose the action that prevents the most immediate medication-related harm while preserving treatment for the underlying condition.

Why the other choices are wrong
Options that rely on one reassuring value, continue a suspect exposure, bypass monitoring, or delay escalation leave the medication hazard active.References
1FDA Drug Safety Communication: SGLT2 inhibitor ketoacidosisKetoacidosis can occur with lower-than-expected glucose during infection, reduced intake, surgery, dehydration, or insulin reduction
22024 Consensus Report: Hyperglycemic Crises in Adults With DiabetesEuglycemic DKA recognition, fluids, insulin, dextrose, potassium, precipitant treatment, and resolution criteria
3Surviving Sepsis Campaign International Guidelines 2021Prompt infection evaluation, cultures when appropriate, antimicrobials, fluids, perfusion, and serial reassessment

## Clinical scenario

Clinical context
An adult taking empagliflozin develops fever, poor intake, vomiting, and deep rapid respirations during a urinary infection; glucose is 184 mg/dL, beta-hydroxybutyrate 5.2 mmol/L, bicarbonate 12 mEq/L, and venous pH 7.24, establishing euglycemic diabetic ketoacidosis.

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