Diabetic Ketoacidosis and HHS Flashcards

A 34-year-old woman with type 1 diabetes on an SGLT2 inhibitor presents with nausea, vomiting, and malaise. Blood glucose is 198 mg/dL, pH 7.18, bicarbonate 9 mEq/L, anion gap 24, serum ketones strongly positive, and urine ketones 4+. Which of the following best explains this presentation?

Answer: SGLT2 inhibitors promote renal glucose excretion, lowering blood glucose while allowing ketogenesis to continue, resulting in euglycemic DKA

SGLT2 inhibitors cause euglycemic DKA by promoting urinary glucose excretion (lowering serum glucose) while simultaneously increasing glucagon secretion and free fatty acid oxidation, driving ketogenesis. The result is significant ketoacidosis with only mildly elevated or even normal glucose — a dangerous presentation that can be missed if providers anchor on the glucose level. Standard DKA criteria require glucose >250 mg/dL, so euglycemic DKA is often underdiagnosed. Recognition requires a low threshold for checking ketones/pH in SGLT2i users who appear ill regardless of glucose.

A 72-year-old man with type 2 diabetes presents with altered mental status, serum glucose 1,140 mg/dL, plasma osmolality 382 mOsm/kg, pH 7.36, bicarbonate 22 mEq/L, and a small anion gap of 13. He is started on aggressive IV normal saline. Six hours later, his glucose has fallen to 600 mg/dL but his sodium has risen from 128 to 148 mEq/L. What is the most appropriate next step?

Answer: Switch IV fluid to 0.45% NaCl to provide free water and reduce the corrected sodium

In HHS, the initial fluid of choice is isotonic saline to restore intravascular volume, but once hemodynamic stability is achieved and the corrected sodium is rising (or already elevated), switching to 0.45% NaCl provides free water to correct the hyperosmolar state. Corrected sodium = measured Na + 1.6 × [(glucose − 100)/100]; a rising sodium during resuscitation signals that the free water deficit is not being adequately corrected. Overly rapid correction risks cerebral edema (though less common in adults than children), while under-correction perpetuates neurological impairment. Continuing isotonic saline in a patient with rising hypernatremia worsens the free water deficit.

A 28-year-old with type 1 diabetes is admitted in DKA (pH 6.98, bicarbonate 6 mEq/L, glucose 480 mg/dL, potassium 5.8 mEq/L). The team initiates IV fluids. When should insulin infusion be started?

Answer: After IV potassium supplementation has been given and serum potassium is confirmed ≥3.5 mEq/L

Although this patient is hyperkalemic (5.8 mEq/L), this is a falsely reassuring value — insulin drives potassium intracellularly, and the total body potassium in DKA is always depleted despite the apparent serum excess. The ADA protocol mandates holding insulin if K⁺ <3.5 mEq/L until potassium is repleted (risk of life-threatening hypokalemia and arrhythmia). With K⁺ ≥3.5 mEq/L, insulin can be started. This patient at 5.8 mEq/L should begin IV fluids and potassium monitoring; once K⁺ is confirmed ≥3.5 mEq/L (which it already is here), insulin infusion begins — but the key principle is never start insulin in hypokalemia. Bicarbonate is generally not indicated in DKA (except pH <6.9), and it does not need to precede insulin.

A 19-year-old with new-onset type 1 diabetes is admitted for DKA. After 10 hours of appropriate insulin infusion and IV fluids, his anion gap normalizes but his bicarbonate remains at 16 mEq/L. Arterial pH is 7.32. He has received 5 L of 0.9% normal saline. What is the most likely explanation for his persistent acidosis?

Answer: Hyperchloremic non-anion-gap metabolic acidosis from large-volume normal saline resuscitation

Large-volume resuscitation with 0.9% normal saline (chloride content 154 mEq/L) causes dilutional hyperchloremia, which produces a non-anion-gap (hyperchloremic) metabolic acidosis. As DKA resolves, ketoanions are metabolized and the anion gap closes, but the bicarbonate remains low because of the superimposed hyperchloremic acidosis from saline. This is a well-recognized phenomenon and does not represent treatment failure. Clinicians must distinguish between persistent ketoacidosis (rising or non-closing anion gap) and this benign iatrogenic acidosis (closed anion gap, elevated chloride). Using balanced crystalloids (e.g., lactated Ringer's or PlasmaLyte) reduces but does not eliminate this effect.

A 45-year-old with type 2 diabetes and a history of alcohol use disorder is found unresponsive. Labs: glucose 310 mg/dL, pH 7.24, bicarbonate 14 mEq/L, Na 138, Cl 96, anion gap 28. Serum lactate 1.1 mmol/L. Serum ethanol is undetectable. Urine is positive for ketones. Osmol gap is 22 mOsm/kg (normal <10). Which diagnosis best explains all findings?

Answer: Concurrent DKA and toxic alcohol ingestion (methanol or ethylene glycol) contributing to elevated osmol gap and anion gap

The combination of an elevated anion gap metabolic acidosis AND an elevated osmol gap strongly suggests toxic alcohol co-ingestion (methanol or ethylene glycol) in addition to DKA. DKA alone does not explain the osmol gap of 22 (normal <10). Toxic alcohols are metabolized to organic acids that close the osmol gap as they accumulate (early ingestion = high osmol gap/low anion gap; late ingestion = low osmol gap/high anion gap) — a mixed picture suggests intermediate timing. Undetectable serum ethanol does not exclude toxic alcohols. Emergent fomepizole, nephrology consultation, and ophthalmology evaluation (for methanol) are indicated while managing the DKA simultaneously. This is a life-threatening dual diagnosis that requires high clinical suspicion.

A 55-year-old woman with type 2 diabetes is recovering from DKA. On hospital day 2, glucose is 230 mg/dL and the anion gap has closed. She is tolerating oral intake. The team transitions her to subcutaneous insulin and discontinues the insulin infusion immediately. Two hours later, she develops nausea, glucose rises to 410 mg/dL, and repeat labs show pH 7.28 with recurrent ketonemia. What error in management caused this relapse?

Answer: The insulin infusion was discontinued without an adequate overlap period after the first subcutaneous dose, leading to a gap in insulin coverage

Subcutaneous insulin (especially basal insulin analogs) requires 1–2 hours to reach effective serum levels. If the IV insulin infusion is stopped simultaneously with — rather than 1–2 hours after — the first subcutaneous dose, there is a critical window of insulin deficiency. During this gap, counterregulatory hormones and free fatty acid oxidation resume ketogenesis, causing DKA relapse. The ADA transition protocol mandates giving the first subcutaneous dose 1–2 hours BEFORE stopping the insulin infusion to ensure seamless coverage. This is one of the most common and preventable errors in DKA management during the transition phase.