Surgery Must Be Delayed for Metabolic Stabilization
This patient has euglycemic diabetic ketoacidosis (DKA) from canagliflozin with worsening metabolic acidosis (pH 7.24 dropping after chloride-rich fluids), and proceeding to surgery now would be catastrophic—immediate stabilization with insulin infusion, balanced crystalloids, and bicarbonate therapy is mandatory before any elective procedure. 1, 2
Critical Problem: SGLT2 Inhibitor-Induced Euglycemic DKA
Canagliflozin causes euglycemic DKA, defined as pH <7.3, bicarbonate <18 mEq/L (patient has 17, now 13), and elevated ketones despite normal glucose—this patient's 5-day history of poor oral intake, nausea, and abdominal pain are classic triggers. 1, 3
The metabolic acidosis is worsening (bicarbonate dropped from 17 to 13 after chloride-rich fluids), with pH 7.24, base excess -9, and anion gap 15—this represents ongoing ketoacidosis that will deteriorate further under surgical stress. 2, 3, 4
Canagliflozin should have been stopped 3-4 days before any planned surgery to prevent this exact complication, but the patient is now presenting with established DKA requiring urgent medical management before surgical intervention. 1
Why Surgery Cannot Proceed Now
Metabolic acidosis with pH <7.2 or base deficit >8 represents the "lethal triad" (acidosis, hypothermia, coagulopathy) that mandates abbreviated surgery or delay—this patient has pH 7.24 with BE -9, approaching these critical thresholds. 2, 5
Induction of anesthesia in an acidotic, volume-depleted patient causes hemodynamic collapse due to loss of compensatory mechanisms and catecholamine receptor resistance—the patient needs resuscitation first to prevent cardiovascular arrest on induction. 1, 2
The chloride-rich fluids worsened the acidosis (hyperchloremic metabolic acidosis), demonstrating improper resuscitation strategy—switching to balanced crystalloids is essential before proceeding. 2, 6
Immediate Stabilization Protocol
Stop the Offending Agent
- Discontinue canagliflozin immediately (should have been stopped 3-4 days pre-surgery)—note that glucosuria can persist for >10 days after stopping SGLT2 inhibitors, requiring ongoing monitoring. 1, 7
Correct the Ketoacidosis
Start continuous insulin infusion (5-10 units/hour) with dextrose-containing fluids once glucose normalizes to suppress ketogenesis—this is the definitive treatment for euglycemic DKA. 3, 4, 8
Administer sodium bicarbonate for pH <7.15—while not routinely recommended for lactic acidosis, bicarbonate is indicated when pH drops below 7.15 due to catecholamine receptor resistance causing refractory hypotension. 1, 2
Check beta-hydroxybutyrate levels to confirm ketoacidosis and monitor response to therapy—levels should decrease with insulin therapy. 3, 4, 7
Optimize Fluid Resuscitation
Switch immediately to balanced crystalloids (lactated Ringer's or Plasma-Lyte)—normal saline contains supraphysiological chloride that worsens hyperchloremic acidosis and impairs renal/gastric perfusion. 2, 6
Target MAP ≥65 mmHg, CVP 8-12 mmHg, and ScvO2 ≥70% within 6 hours—failure to achieve these goals within 6 hours in abdominal pathology with septic shock results in 0% survival. 1, 2
Monitor lactate clearance (current lactate 1.3 is reassuring but needs serial monitoring)—persistent or rising lactate despite resuscitation suggests ongoing tissue hypoperfusion or unrecognized pathology. 2
Address Electrolyte Abnormalities
Monitor and replace potassium aggressively—DKA causes total body potassium depletion despite normal serum levels, and insulin therapy will drive potassium intracellularly causing dangerous hypokalemia. 2, 3
Check renal function closely (current creatinine 53 μmol/L, eGFR 112 is acceptable)—metformin should have been stopped preoperatively and cannot be restarted until 48 hours post-surgery with confirmed eGFR ≥60. 1, 6
Timeline for Surgery
Delay surgery for 24-48 hours minimum until pH >7.30, bicarbonate >18 mEq/L, anion gap normalizes, and ketones clear—attempting surgery before metabolic normalization risks intraoperative cardiovascular collapse. 2, 3, 8
Serial arterial blood gases every 2-4 hours to document improvement—if acidosis worsens despite aggressive therapy, consider undiagnosed surgical pathology (bowel ischemia, perforation) requiring damage control approach. 2, 5
If this is truly emergent surgery (perforation, ischemic bowel), then proceed with damage control principles: abbreviated laparotomy for source control only, temporary abdominal closure, ICU resuscitation, and return for definitive repair after physiologic normalization. 1, 2, 5
Common Pitfalls to Avoid
Do not use normal saline for resuscitation—this patient's bicarbonate dropped from 17 to 13 after chloride-rich fluids, demonstrating iatrogenic worsening of acidosis. 2, 6
Do not assume normal glucose excludes DKA—euglycemic DKA is the hallmark complication of SGLT2 inhibitors and requires high clinical suspicion in patients with acidosis and poor oral intake. 1, 3, 4
Do not restart canagliflozin postoperatively—SGLT2 inhibitors should not be restarted until the patient is clinically stable, eating normally, and all metabolic derangements have resolved. 1
Do not delay surgical intervention if peritonitis or bowel ischemia is confirmed—in that scenario, surgical source control takes priority over complete metabolic correction, using damage control principles. 1, 2