Diabetic Ketoacidosis and HHS Flashcards

A 52-year-old woman with type 2 diabetes on empagliflozin, metformin, and lisinopril presents with 2 days of vomiting and decreased oral intake. She is tachypneic with Kussmaul breathing. Labs: glucose 181 mg/dL, Na 138, Cl 102, HCO₃ 9 mEq/L, pH 7.16, beta-hydroxybutyrate 4.4 mmol/L. Which mechanism best explains her ketoacidosis despite a near-normal glucose?

Answer: Relative insulin deficiency with glucagon excess driving ketogenesis, while SGLT2 inhibition promotes urinary glucose excretion and lowers the renal threshold for glycosuria

SGLT2 inhibitors can cause euglycemic DKA (euDKA) by increasing the glucagon-to-insulin ratio (promoting ketogenesis) while simultaneously lowering the renal threshold for glucose excretion. Blood glucose remains near-normal despite true DKA because glucosuria is markedly enhanced. Clinicians must maintain a high index of suspicion for euDKA in patients on SGLT2 inhibitors, especially during fasting, surgery, or intercurrent illness. Metformin-associated lactic acidosis is possible but would show an elevated lactate rather than elevated ketones. Type 4 RTA causes a non-anion gap hyperchloremic acidosis.

A 61-year-old man with alcoholic cirrhosis (albumin 1.8 g/dL) and type 1 diabetes presents with 3 days of vomiting. Labs: Na 136, Cl 104, HCO₃ 18 mEq/L, glucose 415 mg/dL, pH 7.29, large urinary ketones. A resident calculates an anion gap of 14 mEq/L and concludes the acidosis is non-gap and DKA is unlikely. Which response best corrects this reasoning?

Answer: The albumin-corrected anion gap is approximately 19.5 mEq/L, revealing a masked elevated anion gap consistent with DKA

Albumin is the principal unmeasured anion contributing to the normal anion gap. When albumin is low, the baseline anion gap falls, masking an elevated anion gap acidosis. The correction formula is: corrected AG = calculated AG + 2.5 × (4 − patient albumin g/dL). Here: 14 + 2.5 × (4 − 1.8) = 14 + 5.5 = 19.5 mEq/L — clearly elevated and consistent with DKA. Failing to correct the AG in hypoalbuminemic patients (common in cirrhosis, malnutrition, nephrotic syndrome) is a high-yield pitfall on the ITE.

A 74-year-old man with poorly controlled type 2 diabetes is brought in confused and lethargic. Labs: Na 148 mEq/L, glucose 978 mg/dL, BUN 66 mg/dL, creatinine 2.2 mg/dL, HCO₃ 22 mEq/L, pH 7.38. Measured serum osmolality is 374 mOsm/kg. Which value most accurately reflects the tonicity responsible for his neurological symptoms?

Answer: Effective osmolality of approximately 350 mOsm/kg, calculated as 2[Na] + glucose/18, because urea is an ineffective osmole that freely crosses cell membranes

Effective (or tonicity) osmolality = 2[Na] + glucose (mg/dL)/18. In this patient: 2(148) + 978/18 ≈ 296 + 54 = 350 mOsm/kg. Urea is excluded because it is an ineffective osmole — it crosses cell membranes freely and does not generate an osmotic gradient across cells. Including urea in the osmolality falsely inflates the value without contributing to tonicity. The neurological manifestations of HHS correlate with effective osmolality; the diagnostic threshold is ≥ 320 mOsm/kg. A corrected sodium helps adjust for hyperglycemia but does not directly yield an osmolality value.

A 29-year-old woman with type 1 diabetes presents with severe DKA: arterial pH 6.86, HCO₃ 3 mEq/L, serum potassium 2.8 mEq/L, glucose 540 mg/dL. IV fluids and aggressive potassium replacement are initiated. Which approach to bicarbonate administration is most consistent with current evidence-based guidelines?

Answer: Bicarbonate may be considered given pH < 6.9, but should be withheld until potassium is repleted to ≥ 3.5 mEq/L, as correction of acidosis will drive potassium intracellularly and risk life-threatening hypokalemia

ADA guidelines acknowledge that bicarbonate may be considered for adults with pH < 6.9, but it must never be given before potassium is safely above 3.5 mEq/L. As acidosis resolves (whether from insulin or bicarbonate), H⁺ moves out of cells and K⁺ moves back in — with a potassium of 2.8, this shift could precipitate fatal arrhythmias. Insulin therapy should also be withheld until K⁺ ≥ 3.5 mEq/L for the same reason. Rapid bicarbonate infusion is always contraindicated (risk of paradoxical CNS acidosis, osmotic shift). The absolute contraindication framing in choice C is too extreme — guidelines do allow consideration at pH < 6.9.

A 38-year-old man with type 1 diabetes is recovering from DKA. After 10 hours of insulin infusion, his glucose is 198 mg/dL, anion gap is 10 mEq/L, bicarbonate is 19 mEq/L, and he is eating a meal. The team decides to transition to subcutaneous insulin. He has never been on insulin before. Which transition strategy is most appropriate?

Answer: Administer subcutaneous basal insulin and maintain the insulin infusion concurrently for a minimum of 2 hours before discontinuing the drip

IV regular insulin has an extremely short half-life (approximately 4–5 minutes). Abrupt discontinuation without adequate subcutaneous overlap results in rapid loss of insulin action, quickly leading to DKA recurrence — a preventable and dangerous complication. The correct strategy is to give subcutaneous basal insulin and continue the IV infusion for at least 2 hours (some protocols recommend longer) to allow subcutaneous absorption to reach therapeutic levels before the drip is stopped. The transition criteria used here (anion gap closure, tolerating PO intake) are appropriate; it is the overlap step that is critical and frequently missed. Basal insulin is chosen because this patient has no prior regimen to resume.

A 47-year-old woman with type 1 diabetes is 8 hours into treatment for DKA. Her admission phosphate was 2.6 mg/dL. Repeat labs now show phosphate 1.1 mg/dL, potassium 3.7 mEq/L, glucose 220 mg/dL. She is asymptomatic with no respiratory distress, normal cardiac rhythm, and no signs of hemolysis. Which statement most accurately describes the role of phosphate replacement in her management?

Answer: Routine phosphate replacement has not demonstrated clinical benefit in RCTs; replacement may be considered for severe hypophosphatemia (< 1.0–1.5 mg/dL) complicated by cardiac dysfunction, respiratory muscle weakness, or hemolytic anemia

Phosphate levels fall during DKA treatment as insulin drives phosphate intracellularly. However, randomized controlled trials have consistently failed to show that routine phosphate replacement improves clinical outcomes. The ADA therefore does not recommend routine replacement. The exception is severe hypophosphatemia (generally < 1.0–1.5 mg/dL) in the presence of specific complications where it becomes clinically relevant: cardiac dysfunction (phosphate-dependent myocardial contractility), respiratory muscle weakness (risk of ventilatory failure), or hemolytic anemia. At 1.1 mg/dL without symptoms or organ dysfunction, this patient is borderline but does not yet meet the threshold for mandatory replacement. Hypocalcemia is a real concern with phosphate infusion but is not an absolute contraindication.