NRNP 6537 Week 6 DKA Management Note Example

Euglycemic Diabetic Ketoacidosis After Surgery in a 57-Year-Old Man Taking an SGLT2 Inhibitor: A Problem-Oriented Management Note

Student Name

College of Nursing, Walden University

NRNP 6537: Advanced Nurse Practice in Adult/Gerontology Acute Care I

Instructor Name

Month Day, Year

Euglycemic Diabetic Ketoacidosis After Surgery in a 57-Year-Old Man Taking an SGLT2 Inhibitor: A Problem-Oriented Management Note

Presentation

The patient is a composite. B.N. is a 57-year-old electrician with type 2 diabetes for eleven years, treated with metformin and empagliflozin, admitted two days ago for an elective laparoscopic cholecystectomy. Since surgery he has eaten little because of nausea, and his insulin-free home regimen was continued, including empagliflozin, which was not held before the operation. On postoperative day two he reports worsening nausea, vomiting, vague abdominal pain, and fatigue. His nurse notes rapid, deep breathing. The medication history is the most important part of this presentation: an SGLT2 inhibitor, continued through surgery and poor intake, is the recognized setup for ketoacidosis with a near-normal glucose (Peters et al., 2015).

Examination

Temperature 98.9 F, heart rate 112, blood pressure 108/66, respiratory rate 28 with deep, regular breaths, oxygen saturation 98 percent on room air. He is alert but tired, with dry mucous membranes and a faint fruity odor on the breath. The abdomen is mildly and diffusely tender without guarding or rebound; the laparoscopic port sites are clean and dry. There is no jaundice. Capillary refill is three seconds. The combination of deep, rapid respirations and diffuse abdominal discomfort in a patient with diabetes should prompt a check for ketoacidosis regardless of the glucose reading, since both are common features of the condition.

Laboratory Findings, Interpreted Step by Step

Blood glucose 218 mg/dL, elevated but far below the levels usually associated with diabetic ketoacidosis. Venous pH 7.14, bicarbonate 9 mmol/L, sodium 136 mmol/L, chloride 104 mmol/L, potassium 4.9 mmol/L. Beta-hydroxybutyrate markedly elevated. Lactate normal. Creatinine mildly increased from baseline. Serum osmolality mildly elevated, with no osmolar gap. Lipase normal.

Step 1, the acid-base state: a low pH with a low bicarbonate is a metabolic acidosis. Step 2, the anion gap: sodium minus chloride and bicarbonate gives a gap of 23, well above normal, so this is an anion gap metabolic acidosis (Berend et al., 2014). Step 3, the cause of the gap: markedly elevated beta-hydroxybutyrate identifies ketoacidosis; a normal lactate and no osmolar gap argue against lactic acidosis and toxic alcohols. Step 4, respiratory compensation: his deep, rapid breathing is appropriate compensation. The glucose is only modestly elevated because SGLT2 inhibitors keep excreting glucose in the urine while lowering insulin secretion and increasing glucagon, which promotes ketone production.

Ranked Differential

1. Euglycemic diabetic ketoacidosis precipitated by an SGLT2 inhibitor, surgery, and reduced intake: anion gap acidosis with high ketones and glucose below the usual threshold in a patient taking this class.

2. Alcoholic ketoacidosis: retired because he has no history of heavy drinking or recent binge.

3. Starvation ketosis: two days of poor intake can produce ketosis, but not an acidosis of this depth; his bicarbonate is far lower than starvation alone explains.

4. Lactic acidosis: considered because of metformin and surgery; retired by a normal lactate.

5. Toxic ingestion: retired by the absence of an osmolar gap, normal mental status, and no exposure history.

Management

Management follows the structure of the consensus guidance for hyperglycemic crises: fluids, insulin, electrolytes, and the precipitating cause (Kitabchi et al., 2009; Umpierrez et al., 2024).

Fluids: isotonic fluid replacement for volume depletion from vomiting and osmotic diuresis, with the fluid choice and rate adjusted to his hemodynamic response, urine output, and sodium.

Insulin: a continuous insulin infusion to suppress ketone production. This is where euglycemic ketoacidosis differs from the usual picture: because his glucose is only modestly elevated, dextrose-containing fluid is started early alongside insulin, so that insulin can be continued long enough to clear the ketones without causing hypoglycemia. Glucose alone cannot steer insulin decisions here, since a normal glucose does not mean the ketoacidosis has resolved.

Electrolytes: potassium is checked before and throughout insulin therapy, because insulin moves potassium into cells and his total body potassium is likely depleted despite a normal serum level; replacement is started as levels fall. Phosphate and magnesium are monitored, and bicarbonate is not given, since his pH does not reach the level at which it is considered.

Precipitant: empagliflozin is stopped and will not be restarted until he is eating normally and has recovered; metformin is held during the acute illness. The surgical team is asked to rule out a postoperative complication such as a bile leak, though his abdominal findings and lipase are reassuring.

Why This Diagnosis Is Easy to Miss

On a surgical floor, a patient with nausea, vomiting, and abdominal pain on the second day after cholecystectomy invites a surgical explanation, and a glucose of 218 in a patient with diabetes looks unremarkable. Without a blood gas and a ketone measurement, this picture could have been attributed to postoperative ileus or opioid side effects, and the acidosis would have progressed. The protective habit is simple: in any patient taking an SGLT2 inhibitor who is unwell, particularly after surgery, fasting, or acute illness, check for ketones and acidosis rather than relying on the glucose. The perioperative lesson is also concrete. Current labeling and guidance advise stopping SGLT2 inhibitors several days before scheduled surgery, which did not happen here, and the case will be reviewed with the surgical service so that the preoperative medication instructions change for the next patient.

Monitoring and Resolution

Rechecked frequently: glucose, to guide the dextrose and avoid hypoglycemia; beta-hydroxybutyrate or the anion gap, because resolution of ketoacidosis is defined by closure of the gap and falling ketones, not by glucose; potassium, because of the shifts caused by insulin; and pH or bicarbonate, to confirm the acidosis is correcting. Resolution is declared when the acidosis has cleared and the anion gap has closed, and only then is he transitioned to subcutaneous insulin, overlapping with the infusion to prevent rebound ketosis. Before discharge he is taught sick-day rules: stop the SGLT2 inhibitor during illness, poor intake, or before planned surgery, and seek care for nausea or vomiting while taking it. Whether to restart the drug at all later is a shared decision with his primary care clinician, weighing its heart and kidney benefits against this event.

References

Berend, K., de Vries, A. P. J., & Gans, R. O. B. (2014). Physiological approach to assessment of acid-base disturbances. New England Journal of Medicine, 371(15), 1434-1445. https://doi.org/10.1056/NEJMra1003327

Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes Care, 32(7), 1335-1343. https://doi.org/10.2337/dc09-9032

Peters, A. L., Buschur, E. O., Buse, J. B., Cohan, P., Diner, J. C., & Hirsch, I. B. (2015). Euglycemic diabetic ketoacidosis: A potential complication of treatment with sodium-glucose cotransporter 2 inhibition. Diabetes Care, 38(9), 1687-1693. https://doi.org/10.2337/dc15-0843

Umpierrez, G. E., Davis, G. M., ElSayed, N. A., Fadini, G. P., Galindo, R. J., Hirsch, I. B., Klonoff, D. C., McCoy, R. G., Misra, S., Gabbay, R. A., Bannuru, R. R., & Dhatariya, K. K. (2024). Hyperglycemic crises in adults with diabetes: A consensus report. Diabetes Care, 47(8), 1257-1275. https://doi.org/10.2337/dci24-0032