Hyperglycemic Emergencies Study Guide: Diabetes Chapter 15

1. Definitions & Pathophysiology

Hyperglycemic emergencies are medical emergencies requiring immediate treatment. They are distinct but can overlap.

Diabetic Ketoacidosis (DKA):
- Mechanism: Severe insulin deficiency + elevated counter-regulatory hormones (glucagon, catecholamines) $\rightarrow$ hyperglycemia, lipolysis, and ketone production (acidosis).
- Population: Primarily Type 1 Diabetes, but can occur in Type 2 (especially “Ketosis-Prone Diabetes”).
- Main Feature: Ketoacidosis.
Hyperosmolar Hyperglycemic State (HHS):
- Mechanism: Relative insulin deficiency (enough to prevent ketosis but not hyperglycemia) $\rightarrow$ profound hyperglycemia + osmotic diuresis $\rightarrow$ severe dehydration (ECFV depletion).
- Population: Type 2 Diabetes, often elderly.
- Main Feature: Hyperosmolarity and dehydration.

Key Concepts:

Incidence: DKA is more common in Type 1, but Type 2 patients can experience it (approx. 0.32-2.0 per 1,000 patient-years). HHS is less common but has higher mortality (12-17%).
Ketosis-Prone Diabetes (KPD): A term for patients who present with DKA but lack typical Type 1 features (often have very little beta-cell function).
Euglycemic DKA: DKA presenting with normal or mildly elevated blood glucose, commonly associated with SGLT2 inhibitor use or pregnancy.

2. Clinical Presentation & Risk Factors

Feature	Diabetic Ketoacidosis (DKA)	Hyperosmolar Hyperglycemic State (HHS)
Onset	Rapid (hours to days)	Slow/Insidious (days to weeks)
Symptoms	Polyuria, polydipsia, weight loss, nausea, vomiting, abdominal pain, air hunger (Kussmaul breathing).	Polyuria, polydipsia, weakness, altered level of consciousness (confusion, coma, seizures).
Signs	Acetone breath (fruity odor), tachycardia, hypotension, Kussmaul respirations.	Profound dehydration (poor skin turgor, dry mucous membranes), neurological deficits (stroke-like state).
Precipitants	Insulin omission/reduction, new diagnosis, infection, pump failure, SGLT2 inhibitors, cocaine.	Infection (40-60% of cases), MI, stroke, diuretics, glucocorticoids, restricted fluid intake (elderly).

3. Diagnosis & Lab Findings

DKA Criteria:

Arterial pH: $\le 7.3$
Serum Bicarbonate: $\le 15$ mmol/L
Anion Gap: $> 12$ mmol/L
Ketones: Positive in serum and/or urine.
Glucose: Usually $\ge 14.0$ mmol/L (but can be lower in “Euglycemic DKA”).

HHS Criteria:

Plasma Osmolality: $> 320$ mOsm/kg
Glucose: Typically $\ge 34.0$ mmol/L
pH & Bicarbonate: Usually normal (minimal acid-base disturbance).

Beta-Hydroxybutyrate (beta-OHB): Measuring blood ketones (beta-OHB) is preferred over urine ketones. A level $> 1.5$ mmol/L warrants further testing for DKA.

Note: Negative urine ketones cannot rule out DKA (as they measure acetoacetate, not beta-OHB).

4. Management Algorithm

Management focuses on 4 pillars: Fluid resuscitation, Potassium correction, Insulin therapy, and Acidosis resolution.

Step 1: Fluid Resuscitation (ECFV Restoration)

Initial: 0.9% NaCl (Normal Saline).
- Shock: 1–2 L/h.
- No Shock: 500 mL/h for 4 hours, then 250 mL/h.
Maintenance: Once euvolemic, switch to 0.45% NaCl (half-normal saline) to match ongoing losses.
Preventing Hypoglycemia: Once Plasma Glucose reaches 14.0 mmol/L, add dextrose (D5W or D10W) to the IV fluids to maintain glucose between 12.0–14.0 mmol/L.
- CDE Pearl: Do not stop insulin when glucose drops; add dextrose instead to allow continued insulin for clearing ketones.

Step 2: Potassium ( $K^+$ ) Management

Hypokalemia ( $K^+ < 3.3$ mmol/L): HOLD INSULIN. Give $K^+$ (40 mmol/L) until $K^+ \ge 3.3$ mmol/L. Insulin drives K+ into cells and can cause fatal arrhythmias if started too early.
Normokalemia ( $3.3 - 5.5$ mmol/L): Give $K^+$ (10-40 mmol/L) with insulin to prevent drop
Hyperkalemia ( $> 5.5$ mmol/L): Do not give $K^+$ initially. Wait until it falls and diuresis begins

Step 3: Insulin Therapy

Standard Dose: IV short-acting insulin infusion at 0.1 units/kg/h.
Bolus? Not routinely recommended for adults; definitely avoided in children (risk of cerebral edema).
Target: Continue insulin infusion until the anion gap normalizes (resolution of ketoacidosis), not just until glucose is normal.

Step 4: Acidosis Management

Bicarbonate: Only recommended if pH is extremely low ( $\le 7.0$ ) or in severe shock. Routine use does not improve outcomes.

5. Sick Day Management (Prevention)

Educating patients on “Sick Day Rules” is a key CDE responsibility.

Medications:

S.A.D.M.A.N.S.: Hold Sulfonylureas, ACE inhibitors, Diuretics, Metformin, ARBs, NSAIDs, and SGLT2 inhibitors if dehydrated/vomiting.
Insulin: Never stop insulin completely (even if not eating) for Type 1 diabetes. Doses may need adjustment.

Monitoring: Check BG every 2–4 hours.

Ketones: If T1D and BG $> 14.0$ mmol/L (or symptoms present), check for ketones.

Hydration: Drink plenty of sugar-free fluids. If unable to retain fluids, go to ER.

6. Diabetes Canada Guidelines Recommendations

Protocol Use: All adults with DKA/HHS should be managed using a standard protocol focusing on fluid, potassium, insulin, and precipitating causes.
Screening: Use capillary beta-hydroxybutyrate (beta-OHB) to screen for DKA if BG $> 14.0$ mmol/L. Do not use negative urine ketones to rule out DKA.
Fluid Rate: For DKA, start 0.9% NaCl at 500 mL/h for 4 hours, then 250 mL/h (unless in shock).
Insulin Rate: Use 0.1 units/kg/h IV infusion. Maintain until anion gap normalizes.
Add Dextrose: Start IV dextrose when plasma glucose drops to 14.0 mmol/L to prevent hypoglycemia while continuing to treat acidosis.
SGLT2 Inhibitors: Suspect DKA in symptomatic patients on SGLT2 inhibitors even if BG is not elevated (Euglycemic DKA).

Reference:

Goguen J, Gilbert J. Hyperglycemic Emergencies in Adults. Canadian Journal of Diabetes. 2018;42:S109-S114. doi:10.1016/j.jcjd.2017.10.013