The Importance of Recognizing Diabetic Emergencies
While chronic complications of diabetes (like kidney failure, blindness, and neuropathy) develop gradually, acute diabetic emergencies can occur suddenly and are often fatal if not treated quickly. Two of the most critical are:
- Diabetic Ketoacidosis (DKA) – common in Type 1 diabetes, triggered by insulin deficiency.
- Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) – more common in Type 2 diabetes, associated with extreme hyperglycemia and dehydration.
Both conditions require urgent recognition and management in hospital settings.
Pathophysiology and Causes
Diabetic Ketoacidosis (DKA)
Occurs mostly in Type 1 diabetes.
Triggered by lack of insulin, leading to fat breakdown and ketone production.
Causes:
- Infection (most common)
- Stress (surgery, trauma, illness)
- Missed insulin doses
- Stomach viruses or flu
Mnemonic: “D = DKA = D comes first in alphabet → Type 1, faster, younger onset.”
Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS)
Occurs mostly in Type 2 diabetes.
Triggered by very high blood sugar leading to severe dehydration but without ketone production.
Causes:
- Illness or infection
- Older age
- Poor compliance with diabetes medications
Mnemonic: “H = HHNS = H comes second → Type 2, slower, older onset.”
Signs and Symptoms
DKA
- D – Dry & High sugar: Blood glucose 250–500+ mg/dL
- K – Ketones & Kussmaul respirations (deep, rapid breathing with fruity breath odor)
- A – Abdominal pain (often mistaken for surgical abdomen)
- A – Acidosis: Blood pH < 7.35 (metabolic acidosis)
- High Potassium (K⁺): Hyperkalemia often seen initially
HHNS
- H – Highest sugar: Blood glucose over 600 mg/dL
- H – Higher dehydration: Severe fluid loss, extreme thirst, dry skin, poor turgor
- N – Neurological changes: Confusion, seizures, altered consciousness
- N – No ketones, No acidosis: Unlike DKA, no fruity breath or abdominal pain
- S – Slower onset: Develops over days to weeks
Key Diagnostic Differences Between DKA and HHNS
Feature | DKA | HHNS |
---|---|---|
Diabetes type | Type 1 | Type 2 |
Onset | Rapid (hours to days) | Slow (days to weeks) |
Blood Glucose | 250–500 mg/dL | >600 mg/dL |
Ketones | Present (positive urine/blood ketones) | Absent |
Breathing | Kussmaul respirations, fruity breath | Normal respiration |
pH (acidosis) | < 7.35 (metabolic acidosis) | Normal |
Dehydration | Moderate | Severe |
Neurological symptoms | Mild to moderate | Severe (seizures, confusion, coma) |
Treatment of DKA
The mnemonic D-K-A summarizes treatment steps:
1. D – Dehydration (First):
- Administer IV fluids (0.9% Normal Saline initially).
- Restore circulation and prevent shock.
2. K – Kill the sugar (Slowly):
- Give IV regular insulin only (NEVER rapid-acting IV except in DKA emergencies).
- Lower glucose gradually to prevent cerebral edema.
- Switch to D5W IV when glucose < 200 mg/dL.
3. A – Add Potassium (K⁺):
- Insulin drives potassium into cells, risking hypokalemia.
- Always check K⁺ before starting insulin.
- Replace potassium if <3.5 mEq/L.
Re-assessment and Monitoring
- Check blood glucose hourly.
- Monitor blood pressure, capillary refill, urine output, mental status.
- Watch for hypokalemia (muscle weakness, arrhythmias).
Treatment of HHNS
1. H – Hydration:
- Aggressive fluid replacement (start with 0.9% NS, then hypotonic solutions).
- Correct dehydration slowly.
2. S – Stabilize Sugars:
- IV insulin (regular only).
- Methods: bolus, titration, IV drip, or SQ insulin.
- Goal: reduce glucose gradually.
Key Point: HHNS patients usually die from hypovolemia (shock), while DKA patients die from hypokalemia.
Potassium Management in DKA and HHNS
Potassium plays a central role in both conditions:
- Normal K⁺ = 3.5–5.0 mEq/L
- High K⁺ (>5.0): Risk of arrhythmias → peaked T waves, ST elevation.
- Low K⁺ (<3.5): Risk of weak contraction → flat T wave, ST depression, U wave.
Clinical Rule:
- Never give potassium IV push (fatal).
- Always use a pump, slow infusion.
- Continuous cardiac monitoring required.
Nursing & Clinical Considerations
DKA in Children: Even if nauseous and not eating, insulin should still be given because stress increases blood glucose during illness.DKA vs HHNS:
- DKA → more GI symptoms (abdominal pain, fruity breath).
- HHNS → more neurological symptoms (confusion, seizures).
Rehydration Signs: Stable BP, warm skin, urine output >30 mL/hr.
NCLEX Tip: In emergencies, regular insulin IV is the only insulin used.Complications if Untreated
- DKA: Severe acidosis, cerebral edema, arrhythmias from hypokalemia, death.
- HHNS: Extreme dehydration, seizures, coma, death.
- Both require ICU-level care with close electrolyte and glucose monitoring.
Table: Quick Reference Summary of DKA vs HHNS
Feature | DKA | HHNS |
---|---|---|
Onset | Fast (Type 1, younger) | Slow (Type 2, older) |
Glucose | 250–500+ | 600+ |
Ketones | Present | Absent |
Acidosis | Yes (pH <7.35) | No |
Breath | Fruity, Kussmaul | Normal |
Main Risk | Hypokalemia (K⁺ shift) | Hypovolemia (dehydration) |
Treatment Focus | Fluids, insulin, K⁺ replacement | Fluids, insulin, neuro monitoring |
FAQs on DKA and HHNS
1. What is the main difference between DKA and HHNS?
DKA is characterized by ketones and acidosis (Type 1), while HHNS involves severe hyperglycemia and dehydration without ketones (Type 2).
2. Why do patients in DKA have fruity-smelling breath?
The fruity odor is due to acetone, a byproduct of ketone metabolism.
3. Can Type 2 diabetics develop DKA?
Yes, but it’s rare. DKA is much more common in Type 1 diabetes.
4. What kills patients with DKA and HHNS?
- DKA → death from hypokalemia (arrhythmias, cardiac arrest).
- HHNS → death from hypovolemia (shock).
5. Can DKA occur even if the patient is not eating?
Yes. Illness and infection raise blood sugar levels, so insulin is still needed.