Diabetic Ketoacidosis and HHS Flashcards

A 34-year-old woman with type 1 diabetes presents with DKA (pH 7.18, glucose 320 mg/dL, anion gap 24). She is started on an insulin drip and IV fluids. Six hours later, her glucose has normalized to 180 mg/dL, but her anion gap remains elevated at 20 and bicarbonate is 14 mEq/L. Which of the following is the most appropriate next step?

Answer: Continue the insulin drip and add dextrose to the IV fluids

DKA resolution is defined by anion gap normalization (7.0 in DKA, and increasing the insulin rate without glucose supplementation risks hypoglycemia without meaningfully accelerating ketone clearance.

A 72-year-old man with type 2 diabetes is brought in by his family after 5 days of polyuria and decreased oral intake. Labs: glucose 1,050 mg/dL, Na+ 128 mEq/L, BUN 68 mg/dL, Cr 2.1 mg/dL, pH 7.38, bicarbonate 24 mEq/L, osmolality 385 mOsm/kg. His corrected sodium is 149 mEq/L. What is the most critical consideration when initiating fluid resuscitation?

Answer: Avoid dropping serum osmolality by more than 3–4 mOsm/kg/hour to prevent cerebral edema

In HHS, the extreme hyperosmolarity causes profound intracellular dehydration, particularly in the brain. Rapid correction of osmolality (>3–4 mOsm/kg/hour) risks cerebral edema as water shifts rapidly into brain cells. This is more hazardous than the sodium correction rate itself in HHS. While sodium correction guidelines apply, osmolality rate of change is the primary safety parameter guiding HHS fluid management. Isotonic saline is used initially for hemodynamic stabilization, but hypotonic fluids are typically needed thereafter; colloids are not standard.

A 28-year-old man with type 1 diabetes and a history of alcohol use presents with DKA. Initial labs: glucose 210 mg/dL, pH 7.22, anion gap 26 mEq/L, beta-hydroxybutyrate elevated, phosphate 0.9 mg/dL. He is started on insulin and fluids. Which complication is he at highest risk for as treatment progresses?

Answer: Respiratory muscle weakness due to rebound hypophosphatemia

This patient already has severe hypophosphatemia (0.9 mg/dL) at presentation, which is exacerbated by insulin therapy — insulin drives phosphate intracellularly along with glucose and potassium. Profound hypophosphatemia (<1.0 mg/dL) can cause diaphragmatic weakness and respiratory failure, hemolytic anemia, and rhabdomyolysis. Phosphate replacement is warranted when levels fall below 1.0 mg/dL, especially in patients with baseline deficiency or who are at risk (e.g., alcohol users). Metformin-associated lactic acidosis would require metformin use, which is typically avoided in type 1 diabetes.

A 45-year-old woman with type 2 diabetes on an SGLT-2 inhibitor presents with nausea, vomiting, and fatigue. Labs: glucose 195 mg/dL, pH 7.21, bicarbonate 13 mEq/L, anion gap 22 mEq/L, beta-hydroxybutyrate 4.8 mmol/L. Urine dipstick shows 3+ ketones. Which statement best explains her presentation?

Answer: SGLT-2 inhibitors can cause euglycemic DKA by increasing glucagon-to-insulin ratio and promoting ketogenesis independent of hyperglycemia

SGLT-2 inhibitors can precipitate euglycemic DKA — a dangerous and underrecognized condition where DKA occurs despite near-normal glucose levels. The mechanism involves SGLT-2 inhibitor-mediated glucosuria (lowering glucose threshold), increased glucagon secretion relative to insulin, volume contraction, and a caloric-restriction state, all of which promote lipolysis and ketogenesis. Glucose levels may be 250 mg/dL does NOT apply in this setting. Euglycemic DKA from SGLT-2 inhibitors is a known FDA warning.

A 55-year-old man with type 2 diabetes in DKA (pH 7.10, K+ 5.8 mEq/L) is started on IV insulin. Thirty minutes later, his telemetry shows peaked T-waves and a widening QRS. A repeat potassium is 6.4 mEq/L. What is the most likely explanation and the most appropriate intervention?

Answer: Acidosis correction has been inadequate; administer calcium gluconate for cardiac membrane stabilization

In severe acidosis, insulin-mediated potassium uptake is blunted, and the transcellular shift may be insufficient to prevent dangerous hyperkalemia early in treatment. When EKG changes of hyperkalemia (peaked T-waves, widened QRS) are present at K+ ≥6.5 or with EKG changes at any level, calcium gluconate is immediately indicated to stabilize the cardiac membrane — it does not lower potassium but protects against lethal arrhythmia while other measures work. Doubling insulin without addressing the cardiac emergency is dangerous. Pseudohyperkalemia would not typically cause EKG changes, and the clinical scenario does not suggest it.

A 67-year-old woman with known type 2 diabetes is admitted for HHS (glucose 920 mg/dL, osmolality 378 mOsm/kg, Na+ 152 mEq/L, pH 7.36). She is treated with IV fluids and a low-dose insulin infusion. On day 2, she develops worsening consciousness despite glucose now at 380 mg/dL and osmolality 342 mOsm/kg. Brain MRI shows bilateral striatal restricted diffusion. Which mechanism best explains this complication?

Answer: Osmotic demyelination syndrome from excessively rapid correction of hyperosmolarity

Osmotic demyelination syndrome (ODS) — classically associated with rapid sodium correction — can also occur with excessively rapid correction of hyperosmolarity in HHS. When osmolality falls too quickly (>3–4 mOsm/kg/hour), the brain, which has generated idiogenic osmoles to compensate, undergoes osmotic injury. Striatal involvement (rather than the classic pontine pattern) is a recognized variant of ODS. In this case, osmolality dropped from 378 to 342 in ~24 hours, which may represent too rapid a correction. This underscores why HHS management mandates careful osmolality monitoring with gradual correction. Cerebral venous thrombosis is a real HHS complication but would not explain bilateral striatal DWI changes in this pattern.