DKA vs HHS
Both DKA and HHS present with sky-high glucose, but picking the wrong distinguishing feature costs you the question. DKA kills with acidosis; HHS kills with dehydration and hyperosmolarity. The NCLEX expects you to match the right lab picture and clinical signs to the right emergency — fast.
Side-by-side comparison
Side-by-side2 compared
Dimension
DKA
HHS
Pathophysiology & risk
- Absolute insulin deficit → ketoacidosis
- Type 1 (or T2 under stress); onset hours–1–2 days
- Relative insulin deficit, enough to block ketosis
- Type 2, usually older adults
- Onset insidious — days to weeks
Signs & symptoms
- ★Kussmaul respirations (deep, rapid)
- Fruity breath; abdominal pain, N/V; alert→confused
- Profound dehydration (8–12 L deficit)
- Altered LOC, seizures, coma; NO Kussmaul/fruity
Diagnostics & labs
- ★Ketones positive; pH < 7.30, bicarb < 18
- Glucose > 250; anion gap elevated
- ★Serum osm > 320; ketones absent/trace
- Glucose > 600; pH > 7.30 (no acidosis)
Nursing priorities
- ★Insulin only after K⁺ ≥ 3.3 mEq/L
- IV 0.9% NS first; trend anion gap to closure
- ★Aggressive NS — fluids are top priority
- Insulin drip lower rate; monitor osm + neuro
Treatment & meds
- Regular insulin IV drip
- Add D5 when glucose ~200; replace K⁺/phos
- Transition to SubQ when gap closed + eating
- Regular insulin IV (slower titration)
- Treat precipitant (often infection)
- Replace K⁺ as fluids correct
Patient teaching
- Never stop insulin; sick-day rules
- Check ketones when ill or glucose > 240
- Hydrate + monitor glucose during illness
- Med adherence; infection is common trigger
Red flags — escalate
- Cerebral edema if glucose drops too fast
- Hypokalemia as insulin shifts K⁺ into cells
- Hypovolemic shock from severe dehydration
- Coma, thromboembolism (hyperviscosity)
Complications
- Mortality ~1–5%; cerebral edema (peds)
- Mortality ~10–20%; VTE, seizures
Pathophysiology & risk
DKA
- Absolute insulin deficit → ketoacidosis
- Type 1 (or T2 under stress); onset hours–1–2 days
HHS
- Relative insulin deficit, enough to block ketosis
- Type 2, usually older adults
- Onset insidious — days to weeks
Signs & symptoms
DKA
- ★Kussmaul respirations (deep, rapid)
- Fruity breath; abdominal pain, N/V; alert→confused
HHS
- Profound dehydration (8–12 L deficit)
- Altered LOC, seizures, coma; NO Kussmaul/fruity
Diagnostics & labs
DKA
- ★Ketones positive; pH < 7.30, bicarb < 18
- Glucose > 250; anion gap elevated
HHS
- ★Serum osm > 320; ketones absent/trace
- Glucose > 600; pH > 7.30 (no acidosis)
Nursing priorities
DKA
- ★Insulin only after K⁺ ≥ 3.3 mEq/L
- IV 0.9% NS first; trend anion gap to closure
HHS
- ★Aggressive NS — fluids are top priority
- Insulin drip lower rate; monitor osm + neuro
Treatment & meds
DKA
- Regular insulin IV drip
- Add D5 when glucose ~200; replace K⁺/phos
- Transition to SubQ when gap closed + eating
HHS
- Regular insulin IV (slower titration)
- Treat precipitant (often infection)
- Replace K⁺ as fluids correct
Patient teaching
DKA
- Never stop insulin; sick-day rules
- Check ketones when ill or glucose > 240
HHS
- Hydrate + monitor glucose during illness
- Med adherence; infection is common trigger
Red flags — escalate
DKA
- Cerebral edema if glucose drops too fast
- Hypokalemia as insulin shifts K⁺ into cells
HHS
- Hypovolemic shock from severe dehydration
- Coma, thromboembolism (hyperviscosity)
Complications
DKA
- Mortality ~1–5%; cerebral edema (peds)
HHS
- Mortality ~10–20%; VTE, seizures
★ marks the fact that sets a column apart.
Clinical Pearl
Ketones + Kussmaul + acidosis = DKA; extreme glucose + altered LOC + no ketones = HHS.
Play this as a game — free
Drill DKA vs HHS in Swipe Right & Speed Sort. 14-day free trial, no card required.