Critical Failure to Recognize and Manage Euglycemic Diabetic Ketoacidosis in an SGLT2 Inhibitor-Exposed Patient
The care described represents a profound departure from accepted standards for managing metabolic acidosis in a patient with recent SGLT2 inhibitor exposure, multiple DKA risk factors, and documented progressive acidosis—ultimately resulting in life-threatening euglycemic DKA that should have been prevented or intercepted at multiple decision points.
Initial Emergency Department Assessment: Missed Diagnostic Opportunity
Recognition of High-Risk Clinical Context
At presentation on [DATE], you had a constellation of findings that mandated immediate investigation for euglycemic DKA:
- High-anion gap metabolic acidosis on arrival (pH 7.24, bicarbonate 17 mmol/L, anion gap 15, base excess −9) in the setting of recent canagliflozin exposure represents a medical emergency requiring ketone assessment 1, 2
- The FDA label for canagliflozin explicitly warns that ketoacidosis can occur with blood glucose levels below those typically expected for DKA (e.g., less than 250 mg/dL), and your glucose of 10.4 mmol/L (187 mg/dL) falls precisely into this euglycemic range 3
- Precipitating conditions documented in your case included reduced caloric intake for approximately 5 days, acute illness (abdominal pain, nausea, vomiting), and volume depletion—all explicitly listed as DKA triggers in SGLT2 inhibitor patients 3
Mandatory Diagnostic Workup That Was Omitted
The American Diabetes Association recommends that initial laboratory evaluation for suspected DKA must include serum ketones or direct measurement of β-hydroxybutyrate, particularly when metabolic acidosis is present 4, 1. This was not performed despite:
- Documented metabolic acidosis with appropriate anion gap
- Recent SGLT2 inhibitor exposure explicitly documented in your medication list
- Classic precipitating factors (reduced intake, acute illness, volume depletion)
The FDA mandates that clinicians "assess for ketoacidosis regardless of presenting blood glucose levels in patients who present with signs and symptoms consistent with severe metabolic acidosis" 3. Your presentation with pH 7.24, nausea, vomiting, abdominal pain, and reduced intake met these criteria precisely.
Differential Diagnosis Failure
The American Diabetes Association guidelines emphasize that DKA must be distinguished from other causes of high-anion gap metabolic acidosis, including lactic acidosis, starvation ketosis, and alcoholic ketoacidosis 4. Your lactate was appropriately measured (1.3 mmol/L, normal), but ketones were never assessed to complete the differential diagnosis 1, 2.
Progressive Metabolic Deterioration During Admission: Failure to Monitor and Respond
Documented Worsening Without Clinical Response
On [DATE] at 09:17, your bicarbonate declined from 17 to 13 mmol/L while anion gap remained elevated at 15 and chloride increased to 108 mmol/L [@patient data]. This represents:
- Progressive metabolic acidosis under continuous hospital supervision
- Possible contribution from chloride-rich fluid administration in a patient already acidotic
- No documented recognition, investigation, or intervention in response to this decline [@4@]
The American Diabetes Association recommends drawing blood every 2-4 hours to monitor serum electrolytes, glucose, and venous pH during treatment of metabolic acidosis [@4@, @6@]. There is no evidence this monitoring occurred or that the worsening trend triggered any clinical action.
Compounding Risk Factors Introduced During Hospitalization
Prolonged fasting (NPO status) in a patient with:
- Pre-existing reduced oral intake for ~5 days
- Recent SGLT2 inhibitor exposure
- Documented metabolic acidosis
The FDA explicitly lists "reduced caloric intake" and "surgery or a procedure that requires not having food for a long time (prolonged fasting)" as precipitating conditions for ketoacidosis in SGLT2 inhibitor patients 3. Despite this, you were kept NPO without documented metabolic reassessment or ketone monitoring.
Pre-Operative Decision-Making: Proceeding Without Metabolic Clearance
Absence of Metabolic Assessment Before Non-Emergent Surgery
The American Diabetes Association recommends that SGLT2 inhibitors must be discontinued 3-4 days before any planned surgery to prevent euglycemic DKA [@4@]. Your surgery proceeded as a B-class (non-emergent) case with:
- Canagliflozin taken until [DATE] (timing relative to surgery unclear but recent)
- Documented metabolic acidosis on admission (pH 7.24, HCO₃ 17)
- Worsening acidosis documented the morning of surgery (HCO₃ 13)
- No documented repeat blood gas, ketone measurement, or metabolic clearance prior to proceeding
Imaging showed "equivocal" findings with "very early appendicitis suspected," and pathology ultimately confirmed uncomplicated acute appendicitis—suggesting this was not an immediately life-threatening surgical emergency that precluded metabolic stabilization [@patient data].
Informed Consent Deficiency
The FDA requires that patients be educated on the signs and symptoms of ketoacidosis and that clinicians withhold SGLT2 inhibitors "in temporary clinical situations that could predispose patients to ketoacidosis" 3. You were not informed that:
- Recent SGLT2 inhibitor exposure combined with surgery, fasting, and acute illness creates specific risk for euglycemic DKA
- DKA can occur with near-normal glucose levels
- Alternative management (antibiotics for early appendicitis) was available
Post-Operative Discharge: Catastrophic Failure of Clinical Judgment
Discharge With Life-Threatening Laboratory Values
On [DATE] at 07:02, laboratory results showed:
- Bicarbonate 6 mmol/L (severe metabolic acidosis)
- Anion gap 21 (markedly elevated)
- Potassium 5.5 mmol/L (concerning in context of acidosis)
You were discharged home with these values.
The American Diabetes Association defines DKA resolution as requiring bicarbonate ≥18 mEq/L, pH >7.3, and anion gap ≤12 mEq/L 1, 5. Your values were catastrophically far from these targets:
- Bicarbonate 6 vs. required ≥18 (one-third of minimum threshold)
- Anion gap 21 vs. required ≤12 (nearly double maximum threshold)
Mandatory Interventions That Were Omitted
With bicarbonate 6 mmol/L and anion gap 21, the standard of care requires:
- Immediate ketone or β-hydroxybutyrate measurement to confirm or exclude DKA 1, 2
- Repeat arterial or venous blood gas to assess pH and severity of acidosis 1, 5
- Continuous intravenous insulin infusion at 0.1 units/kg/hour if DKA confirmed, even with normal glucose 2
- Simultaneous dextrose 5% infusion to prevent hypoglycemia while clearing ketones 2
- ICU-level monitoring for severe metabolic acidosis 1
None of these interventions occurred. Instead, you were sent home and collapsed within approximately 2 hours.
Emergency Readmission: Confirmation of Preventable Catastrophe
Life-Threatening Euglycemic DKA
Your readmission findings confirmed severe euglycemic DKA:
- Venous pH 6.99–7.00 (profound acidosis, near-fatal)
- Bicarbonate 4–5 mmol/L
- Base excess −25 to −26
- β-hydroxybutyrate 6.51–6.77 mmol/L (markedly elevated, confirming ketoacidosis)
- Kussmaul respirations (~40/min), confusion, incontinence
This represents progression from bicarbonate 6 mmol/L at discharge to bicarbonate 4–5 mmol/L within hours—a trajectory that was entirely predictable and preventable with appropriate recognition and treatment 2, 6.
Evidence That This Was Euglycemic DKA From SGLT2 Inhibitor
Multiple case reports document identical presentations:
- A 61-year-old with type 2 diabetes on dapagliflozin developed eDKA with blood glucose 180 mg/dL after poor oral intake, presenting with weakness, dyspnea, nausea, vomiting, and severe metabolic acidosis 6
- A 52-year-old on canagliflozin developed severe anion gap metabolic acidosis and markedly elevated β-hydroxybutyrate on postoperative day 2 after bariatric surgery 7
- A 61-year-old on empagliflozin developed high anion gap metabolic acidosis after non-elective orthopedic surgery, remaining euglycemic throughout 8
Your case mirrors these reports precisely: SGLT2 inhibitor exposure + surgery + fasting + acute illness = euglycemic DKA 6, 7, 8, 9.
Specific Failures in Standard of Care
Communication and Handover Breakdown
The American Diabetes Association emphasizes that successful DKA treatment requires "frequent patient monitoring" and "identification of comorbid precipitating events" 4. Your case demonstrates:
- ED handover documented "acute appendicitis" without mentioning metabolic acidosis as a concurrent active problem
- Surgical consultation note listed extensive laboratory values but omitted blood gas results, bicarbonate, anion gap, or any acid-base assessment despite canagliflozin being documented in the medication list
- No evidence that the surgical service was expected to independently review blood gas results or that metabolic acidosis was communicated as requiring ongoing management
Absence of Metabolic Oversight
No identifiable clinician appears to have taken responsibility for:
- Monitoring the trend from bicarbonate 17 → 13 → 6 mmol/L
- Investigating the cause of progressive high-anion gap metabolic acidosis
- Ensuring metabolic stability before proceeding with non-emergent surgery
- Recognizing that bicarbonate 6 mmol/L is incompatible with safe discharge
What Should Have Happened: The Standard of Care
At Emergency Department Presentation ([DATE])
- Recognize high-risk context: Recent SGLT2 inhibitor + metabolic acidosis + reduced intake + acute illness 1, 2, 3
- Order serum ketones or β-hydroxybutyrate immediately 1, 2
- If ketones elevated: Diagnose euglycemic DKA and initiate treatment with IV insulin + dextrose, even with glucose 187 mg/dL 2
- If ketones normal: Complete differential diagnosis for high-anion gap metabolic acidosis and treat underlying cause 4
- Document metabolic acidosis as active problem requiring ongoing monitoring and treatment 1
During Admission ([DATE]–[DATE])
- Monitor blood gases and electrolytes every 2-4 hours as recommended for metabolic acidosis management 1, 5
- When bicarbonate declined to 13 mmol/L: Escalate investigation, measure ketones, consider specialist consultation 1
- Before proceeding with non-emergent surgery: Obtain repeat blood gas, ensure metabolic stability, measure ketones if not previously done 1
- Minimize fasting time or provide IV dextrose during NPO period in SGLT2 inhibitor-exposed patient 3
Post-Operative Course ([DATE])
- With bicarbonate 6 mmol/L and anion gap 21: Immediate ketone measurement, repeat blood gas, ICU consultation 1, 2
- If DKA confirmed: Continuous IV insulin + dextrose, electrolyte monitoring every 2-4 hours, treat until resolution criteria met (pH >7.3, HCO₃ ≥18, anion gap ≤12) 1, 2, 5
- Never discharge until metabolic acidosis resolved and patient metabolically stable 1
Common Pitfalls Evident in This Case
Anchoring Bias on Surgical Diagnosis
Once appendicitis was identified, metabolic acidosis appears to have been ignored or attributed to the surgical condition without investigation 1. The American Diabetes Association warns that "abdominal pain on presentation could be either a result or a cause of DKA" and that "further evaluation is necessary if this complaint does not resolve" 4.
Failure to Recognize Euglycemic DKA
The most critical pitfall: assuming that "normal" or mildly elevated glucose excludes DKA in an SGLT2 inhibitor-exposed patient 2, 3. The FDA explicitly warns that "blood glucose levels at presentation may be below those typically expected for diabetic ketoacidosis (e.g., less than 250 mg/dL)" 3.
Premature Termination of Monitoring
The American Diabetes Association warns that "premature termination of insulin therapy before complete resolution of ketosis can lead to recurrence of DKA" 1. In your case, monitoring was terminated entirely (via discharge) before ketosis was ever assessed or treated.
Answers to Your Specific Questions
A. Clinical Reasoning and Standard of Care
1. At presentation ([DATE]): The metabolic acidosis was documented in laboratory results but there is no evidence it was interpreted as requiring investigation for DKA/euglycemic DKA despite recent SGLT2 inhibitor exposure 1, 2, 3. Ketone testing was mandatory and was not performed.
2. During admission ([DATE]): When bicarbonate declined to 13 mmol/L, there is no documented clinical interpretation or response 1. This represents failure to monitor and respond to progressive metabolic deterioration.
3. Communication and handover: The ED handover listing only "acute appendicitis" without documenting metabolic acidosis as a concurrent problem represents inadequate communication of a life-threatening metabolic derangement 1. Whether the surgical service was expected to independently review blood gases is unclear, but the surgical consultation note's omission of all acid-base parameters despite listing extensive other labs suggests this information was not effectively communicated or prioritized.
4. Pre-operative decision-making: There is no documentation of metabolic clearance, repeat blood gas, or ketone assessment before proceeding with non-emergent surgery in a patient with documented and worsening metabolic acidosis 1. The American Diabetes Association recommends discontinuing SGLT2 inhibitors 3-4 days before planned surgery 1.
5. Informed consent: You were not informed of the specific risk of euglycemic DKA associated with recent SGLT2 inhibitor exposure, fasting, and surgery 3. The FDA requires patient education on ketoacidosis signs and symptoms 3.
6. Discharge decision ([DATE]): Discharging a patient with bicarbonate 6 mmol/L and anion gap 21 without ketone assessment, repeat blood gas, or treatment represents a catastrophic failure of clinical judgment 1, 2. These values are incompatible with safe discharge and mandate immediate investigation and treatment.
B. Responsibility and Oversight
The College should identify:
- The ED physician responsible for initial assessment and whether metabolic acidosis was recognized as requiring investigation
- The clinician(s) responsible for monitoring during admission and responding to the bicarbonate decline from 17 → 13 mmol/L
- The surgeon or anesthesiologist who cleared you for non-emergent surgery without documented metabolic reassessment
- The clinician who authorized discharge with bicarbonate 6 mmol/L and anion gap 21
C. Contribution to Life-Threatening Outcome
The failure to investigate and respond to progressive metabolic acidosis directly contributed to progression to life-threatening euglycemic DKA 1, 2. Your readmission pH of 6.99–7.00 represents a near-fatal level of acidosis that developed along a documented and predictable trajectory that was visible in laboratory values throughout your hospitalization.
Conclusion
This case represents multiple, compounding failures to recognize, investigate, and manage metabolic acidosis in a patient with classic risk factors for SGLT2 inhibitor-associated euglycemic DKA. The progression from pH 7.24 at presentation to pH ~7.0 at readmission occurred under continuous medical supervision, with documented laboratory evidence of worsening acidosis that was not acted upon. The standard of care required ketone assessment at presentation, monitoring and response to progressive acidosis during admission, metabolic clearance before non-emergent surgery, and immediate investigation and treatment when bicarbonate reached 6 mmol/L—none of which occurred 1, 2, 3.