Hyperglycemic Hyperosmolar State — HHS

Blood glucose hits 1,200 mg/dL but there are no ketones and no Kussmaul respirations — the patient is obtunded and profoundly dehydrated. Missing HHS kills faster than DKA.

Hyperosmolar Hyperglycemic State occurs almost exclusively in type 2 diabetes because the pancreas still produces enough insulin to prevent lipolysis and ketone formation — but not enough to control glucose. Without ketoacidosis driving early nausea and vomiting, hyperglycemia builds silently over days to weeks, often triggered by infection, stroke, or medication non-adherence. Blood glucose typically exceeds 600 mg/dL and serum osmolality rises above 320 mOsm/kg, pulling water from cells and causing severe intracellular dehydration. Fluid deficits average 8–12 liters. Neurological changes — lethargy, seizures, focal deficits, coma — dominate the presentation and correlate with osmolality, not glucose alone. Mortality is 10–20%, roughly five times higher than DKA. Nursing priorities center on aggressive isotonic fluid resuscitation (normal saline initially), careful monitoring of serum sodium and osmolality trends, low-dose IV insulin only after fluid replacement is underway, strict I&O, and frequent neurological assessment. Rapid glucose correction risks cerebral edema, so glucose should not drop faster than 50–75 mg/dL per hour.

Key Distinctions

Don't confuse HHS with DKA: HHS has no significant ketones, no Kussmaul breathing, no fruity breath — neurological decline is the hallmark instead. Students assume higher glucose means worse DKA, but extreme hyperglycemia (>600) with absent ketosis points to HHS. Fluids come first in HHS; insulin alone without volume replacement worsens hypotension and can trigger cardiovascular collapse.

Clinical Pearl

No ketones, sky-high glucose, altered mental status — think HHS. Fluids before insulin. You're filling the tank before you open the drain.