5.1 Glycemic Emergencies: DKA, HHS & Glucose Control

5.1 Glycemic Emergencies: DKA, HHS & Glucose Control

Endocrine content is only 6% of the PCCN blueprint, but diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are among the most frequently tested emergencies because they combine acid-base, fluid, and electrolyte management into a single high-stakes scenario. Both are life-threatening complications of uncontrolled diabetes mellitus, but they differ enough in pathophysiology and presentation that the PCCN exam routinely asks you to tell them apart.

Diabetic Ketoacidosis (DKA)

DKA results from an absolute or relative insulin deficiency combined with excess counter-regulatory hormones (glucagon, cortisol, catecholamines, growth hormone). Without insulin to suppress lipolysis, fatty acids flood the liver and are converted to ketone bodies (beta-hydroxybutyrate and acetoacetate), producing a high-anion-gap metabolic acidosis. Simultaneously, reduced glucose uptake plus increased gluconeogenesis and glycogenolysis drive severe hyperglycemia, which causes an osmotic diuresis, dehydration, and major electrolyte losses.

Common triggers: infection (the most common precipitant), missed or inadequate insulin dosing, new-onset type 1 diabetes, myocardial infarction, pancreatitis, corticosteroid use, and SGLT2 inhibitors (which can cause "euglycemic DKA" with a near-normal glucose).

Classic presentation: polyuria and polydipsia, Kussmaul respirations (deep, rapid breathing that blows off CO2 to partially compensate for the metabolic acidosis), a fruity or acetone breath odor, nausea, vomiting, and abdominal pain that can mimic an acute surgical abdomen. Mental status ranges from alert to comatose depending on severity, and dehydration signs (tachycardia, hypotension, dry mucous membranes) are common.

Diagnostic criteria require all three: hyperglycemia (glucose ≥200 mg/dL or known diabetes), ketosis (beta-hydroxybutyrate ≥3.0 mmol/L or urine ketones ≥2+), and acidosis (pH <7.3 and/or bicarbonate <18 mEq/L). Severity is graded by pH and bicarbonate: mild (pH 7.25–7.30, bicarbonate 15–18), moderate (pH 7.00–7.24, bicarbonate 10 to <15), and severe (pH <7.00, bicarbonate <10).

Hyperosmolar Hyperglycemic State (HHS)

HHS typically occurs in older adults with type 2 diabetes, often triggered by infection, stroke, MI, or simple dehydration, and it develops over days rather than hours. Enough residual insulin remains to suppress significant ketogenesis, but not enough to control glucose, so the hallmark is profound hyperglycemia and hyperosmolality without significant acidosis.

Diagnostic criteria: glucose ≥600 mg/dL, effective serum osmolality >300 mOsm/kg (or total osmolality >320), minimal ketosis (beta-hydroxybutyrate <3.0 mmol/L), pH ≥7.30, and bicarbonate ≥15 mEq/L. Because acidosis is minimal, patients do not develop Kussmaul respirations or fruity breath. Presentation is dominated by neurologic findings — lethargy, confusion, focal deficits that can mimic stroke, seizures, or coma — correlating directly with the degree of hyperosmolality. Fluid deficits in HHS are typically larger than in DKA, often 8–10 liters.

Priorities of Care

1. Fluids first. Begin with isotonic 0.9% normal saline; the rate and total volume are guided by hydration status, hemodynamics, and cardiac/renal function. HHS patients generally need larger total volumes.
2. Potassium before, or with, insulin — a critical safety point. Insulin drives potassium intracellularly. Even though many DKA/HHS patients present with a normal or high serum potassium (acidosis shifts K+ out of cells), they are almost always total-body potassium depleted. If serum K+ is below 3.3 mEq/L, hold insulin and replace potassium first — starting an insulin infusion in a hypokalemic patient can precipitate life-threatening dysrhythmias and respiratory muscle weakness. If K+ is 3.3–5.3 mEq/L, start the insulin infusion (typically 0.1 units/kg/hr) while replacing potassium concurrently. If K+ is above 5.3 mEq/L, hold potassium replacement, start insulin, and recheck levels frequently.
3. Titrate the insulin infusion carefully. Check glucose hourly. As glucose approaches roughly 200–250 mg/dL in DKA (or 250–300 mg/dL in HHS), add dextrose-containing IV fluids and reduce — rather than stop — the insulin rate, because glucose normalizes faster than ketosis resolves and the infusion must continue until the anion gap closes.
4. Know the true resolution criteria for DKA: anion gap closure with bicarbonate ≥18 mEq/L and pH ≥7.3, not simply a normal glucose reading. Overlap the first dose of subcutaneous (basal) insulin with the IV infusion by 1–2 hours before discontinuing the drip to prevent rebound ketoacidosis.
5. Watch for complications: cerebral edema (rare in adults but a feared complication, particularly if fluids/glucose are corrected too rapidly), hypoglycemia and hypokalemia from over-aggressive insulin therapy, and — in HHS — gradual correction of osmolality to avoid abrupt fluid shifts into the brain.

Hyperglycemia and Hypoglycemia

Hypoglycemia thresholds per the American Diabetes Association: Level 1 (alert value) is glucose <70 mg/dL; Level 2 (clinically significant) is <54 mg/dL and requires immediate action; Level 3 (severe) is any hypoglycemia associated with altered mental status or physical function requiring assistance from another person, regardless of the glucose value. Adrenergic symptoms (tachycardia, diaphoresis, tremor, hunger, anxiety) typically appear before neuroglycopenic symptoms (confusion, slurred speech, seizure, coma) as glucose continues to fall — though this warning phase can be blunted by long-standing diabetes, autonomic neuropathy, or beta-blocker therapy ("hypoglycemia unawareness"). Treat a conscious patient who can swallow with 15–20 g of fast-acting carbohydrate, recheck in 15 minutes, and repeat if still below 70 mg/dL (the "rule of 15"). For an unconscious patient or one unable to swallow safely, give IV dextrose (D50W) or IM/intranasal glucagon if IV access is unavailable.