Updated July 2026 · 10 min read · Educational reference, not a substitute for your unit's protocol
Part of the ICU Emergencies Hub — browse every related guide in one place.
Diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) are the two big hyperglycemic crises that land in the ICU. They share a lot of management — fluids, insulin, electrolytes, hunting the trigger — but they are not the same disease, and confusing them can cost you at the bedside. Here's how they differ, where they overlap, and the traps that catch nurses managing either one.
DKA is classically a type 1 (absolute insulin deficiency) problem, though it occurs in type 2 as well. With almost no insulin, the body burns fat for fuel, generating ketoacids and driving an anion-gap metabolic acidosis. HHS is a type 2 problem: there is some circulating insulin — enough to keep ketogenesis switched off — but not enough to control glucose, which drifts upward over days. The result is profound osmotic diuresis and dehydration without significant acidosis.
| Feature | DKA | HHS |
|---|---|---|
| Typical patient | Type 1 (or type 2); often younger | Type 2; often older, with a delayed presentation |
| Onset | Hours to a day or two | Days to weeks |
| Glucose | High (often >250 mg/dL), but can be moderate | Very high (often >600 mg/dL) |
| Ketones / acidosis | Present — anion-gap acidosis, low pH/bicarb | Minimal to none; pH near normal |
| Serum osmolality | Variable | Markedly elevated (often >320 mOsm/kg) |
| Mental status | Usually alert unless severe | Often obtunded; correlates with osmolality |
| Dehydration | Significant | Extreme — total-body water deficit is larger |
| Classic clues | Kussmaul breathing, fruity breath, abdominal pain | Profound dehydration, altered mentation, focal signs mimicking stroke |
Note the overlap: some patients present with mixed features, and glucose alone does not tell you which you are treating. It is the acidosis and ketones that define DKA, and the osmolality that defines HHS.
Despite the differences, the treatment scaffold is similar, and the sequence matters more than most new nurses expect.
Fluids first. Both are volume-depleted, HHS even more so. Isotonic crystalloid resuscitation is the opening move in both, and in HHS the fluid deficit is the main event — much of the glucose improvement comes from rehydration alone before insulin does its share.
Insulin, usually as a drip. A continuous IV insulin infusion closes the anion gap in DKA and lowers glucose in HHS. In DKA, the endpoint is closing the gap, not just normalizing glucose — which is why you don't stop insulin the moment sugar looks better.
Add dextrose before you stop insulin. When glucose falls to a threshold (commonly around 200 mg/dL in DKA, 250–300 in HHS), protocols add dextrose to the fluids so the insulin drip can keep running to clear ketones/osmolality without causing hypoglycemia. Stopping insulin too early in DKA lets the gap reopen. Our insulin drip / DKA guide walks the titration in detail.
Find and fix the trigger. Infection, missed insulin, MI, and new medications are common precipitants for both. Treating the crisis without treating the cause invites a bounce-back. Sepsis is a frequent driver — see the ICU sepsis guide.
Cerebral edema is the feared complication of overly rapid correction — classically emphasized in pediatric DKA, and a reason osmolality and sodium are corrected gradually rather than crashed. In HHS, correct slowly: the osmolality built up over days, and dropping it too fast risks fluid shifts into the brain. In DKA, don't chase the glucose number and forget the gap. And in HHS, the extreme dehydration raises thrombosis risk, so VTE prophylaxis is on the radar.
Related: Insulin drip & DKA guide · IV potassium replacement · ICU sepsis guide · CCRN exam guide
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