Diabetes Emergencies Nursing Guide 2026

⚕️ Medical Disclaimer: This content is for educational purposes only and is intended for licensed healthcare professionals. It does not constitute medical advice and should not replace clinical judgment, facility protocols, or physician orders. Always verify medications, doses, and procedures with your institution's guidelines.

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This article was created with AI assistance.

DKA vs. HHS comparison, insulin drip management, fluid resuscitation, potassium replacement rules, anion gap calculation, and hypoglycemia treatment for bedside nurses.

1. DKA vs. HHS Comparison

FeatureDKA (Diabetic Ketoacidosis)HHS (Hyperosmolar Hyperglycemic State)
Type of diabetesType 1 (primarily); also Type 2Type 2 (almost exclusively)
OnsetRapid (hours to 24 hr)Slow (days to weeks)
Blood glucose>250 mg/dL (can be lower in euglycemic DKA)>600 mg/dL (often 800–1200+)
pH<7.30 (metabolic acidosis)Normal or mildly low (>7.30)
Bicarbonate<18 mEq/L (often <10)>18 mEq/L (near normal)
KetonesPresent (serum + urine)Absent or minimal (some insulin present)
Anion gapElevated (>12)Normal or mildly elevated
Serum osmolalityVariable (may be <320)>320 mOsm/kg (often >350)
Mental statusAlert to confused; rarely comaSevere obtundation, coma (from hyperosmolality)
Fluid deficit3–6 liters8–12+ liters (profound dehydration)
Mortality<5% in adults10–20% (older, sicker patients)

2. DKA Pathophysiology

Insulin deficiency → cells cannot use glucose → starvation signal → counter-regulatory hormones (glucagon, cortisol, epinephrine) rise → lipolysis → fatty acid metabolism → KETONE BODIES (beta-hydroxybutyrate, acetoacetate, acetone)

Ketones are acids → high anion gap metabolic acidosis
Osmotic diuresis from hyperglycemia → polyuria, polydipsia, dehydration, electrolyte loss (K+, Na+, Cl-)

Classic presentation: Polyuria, polydipsia, polyphagia, nausea/vomiting, Kussmaul respirations (deep rapid breathing — body blowing off CO2 to compensate for acidosis), fruity/acetone breath, abdominal pain, dehydration

3. Anion Gap Calculation

Anion Gap = Na+ − (Cl- + HCO3-)
Normal: 8–12 mEq/L (some labs use 12–16 with albumin correction)
Elevated AG (>12) = MUDPILES: Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates

Corrected AG for hypoalbuminemia: Add 2.5 mEq/L for every 1 g/dL albumin below 4.0 (low albumin falsely lowers AG)

4. DKA Treatment Protocol

Step 1 — Fluids FIRST

Step 2 — Potassium Replacement (CRITICAL)

Check potassium BEFORE starting insulin.
Insulin drives K+ into cells → can cause life-threatening hypokalemia if K+ is already low.

Monitor K+ every 1–2 hours. Remember: patients are always total body K+ depleted even if serum K+ appears normal or high (acidosis shifts K+ out of cells).

Step 3 — Insulin

Standard DKA insulin protocol:
IV regular insulin infusion: start at 0.1 units/kg/hr (after K+ ≥3.3)
Some protocols: 0.1 units/kg IV bolus first, then 0.1 units/kg/hr

Goal glucose drop: 50–75 mg/dL per hour (not faster — cerebral edema risk, especially in children)
If glucose not dropping 50 mg/dL in first hour: double the insulin rate

When glucose reaches 200–250 mg/dL: reduce to 0.05 units/kg/hr; add dextrose to IV fluids; continue insulin until anion gap closed and bicarbonate >18

Do NOT stop insulin until: AG <12, pH >7.30, HCO3 >18, patient tolerating oral intake — then transition to subcutaneous insulin and overlap 2 hours before stopping drip

Step 4 — Bicarbonate?

Routine bicarbonate NOT recommended (even for severe acidosis) unless pH <6.9 — bicarbonate administration can worsen hypokalemia, cause paradoxical CNS acidosis, and may worsen cerebral edema. Fluids and insulin resolve the acidosis.

Step 5 — Phosphate

Replace if <1 mg/dL or symptomatic (respiratory muscle weakness); routine replacement not consistently shown to improve outcomes.

5. Cerebral Edema (DKA Complication)

Most dangerous complication, especially in pediatric DKA.
Risk factors: rapid correction of glucose/osmolality, too much fluid too fast, bicarbonate use, very young age

Signs: headache, change in mental status, vomiting, papilledema, bradycardia, hypertension (Cushing's triad) — may develop AFTER glucose is improving

Treatment: Mannitol 0.5–1 g/kg IV or 3% saline 5–10 mL/kg over 30 min; reduce IVF rate; call ICU

6. HHS Management

7. Hypoglycemia Management

ScenarioBlood GlucoseTreatment
Mild (awake, able to swallow)<70 mg/dL15-15 Rule: 15g fast-acting carbs (4 oz juice, 3–4 glucose tabs, 4 oz regular soda) → recheck in 15 minutes; repeat if still <70
Moderate (confused but conscious)<60 mg/dLOral glucose gel buccally OR if IV access: 25g D50W (1 amp = 50 mL of 50% dextrose) IV push
Severe (unconscious, no IV access)<40 mg/dLGlucagon 1 mg IM/SQ (glucagon kit); position lateral (vomiting risk after); establish IV access; then D50W when possible
ICU/continuous glucose monitoring<70 mg/dLD50W 1 amp IV; recheck q15 min; adjust insulin infusion; if on insulin drip — stop drip, treat, restart at lower rate
ICU Glucose Target: 140–180 mg/dL (not tight control — NICE-SUGAR trial showed tighter control increased mortality). Avoid hypoglycemia (<70 mg/dL) at all costs.
NCLEX High-Yield: Diabetes Emergencies

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