In this episode of Hospital Medicine Unplugged, we sprint through hyperosmolar hyperglycemic state (HHS)—spot early, rehydrate hard (safely), fix electrolytes, start insulin after fluids, and hunt the trigger.

We open with the do-firsts: ABCs, tele, frequent vitals, bedside neuro checks, and labs that matter—glucose, BMP with corrected Na⁺, calculated effective osmolality (>320 mOsm/kg), serum/urine ketones (minimal/absent), β-hydroxybutyrate, VBG/ABG, CBC, lactate, UA/cultures, CXR/ECG as indicated. Think precipitant early: infection (most common), meds (steroids, thiazides, antipsychotics), MI/stroke, nonadherence, undiagnosed DM.

Call the diagnosis when glucose >600 mg/dL, effective osmolality >320 mOsm/kg, minimal/absent ketosis, and marked dehydration. Mental status change is common but not required. Distinguish from DKA—no significant acidosis/ketosis and often older type 2 patients.

Risk reality check: mortality often >10%; danger flags include hypotension, AKI, corrected hypernatremia, severe hyperosmolality, infection, and altered mental status. Most patients need ICU.

Treatment—build the HHS bundle (sequence matters):
• Fluids first (cornerstone): start 0.9% saline to restore perfusion; target a gradual fall in osmolality (≤3 mOsm/kg/hr) and glucose drop ~50–75 mg/dL/hr. Switch to 0.45% saline if corrected Na⁺ is high and the patient is hemodynamically improved. Add D5 when glucose <300 mg/dL to prevent rapid osm shifts.
• Potassium next: total body K⁺ is depleted—start replacement once urine output is adequate; hold insulin if K⁺ <3.3 until corrected.
• Insulin after partial volume repletion: IV regular insulin 0.1 U/kg/hr (or 0.14 U/kg/hr without bolus). Titrate to keep glucose ~200–300 mg/dL until osmolality normalizes, then transition to subQ when eating and stable.
• Electrolytes/thiamine: replace Mg²⁺/PO₄³⁻ if severe/symptomatic; consider thiamine in malnourished to prevent Wernicke’s.
• Treat the trigger: early antibiotics if infection suspected; manage MI, stroke, pancreatitis, offending meds.

Monitoring that saves: strict I/O, weights, mental status, q1–2h glucose, q2–4h electrolytes/osmolality early, continuous cardiac monitoring (arrhythmias from K⁺/Mg²⁺ shifts). Avoid overcorrection—aim for steady, not speedy tonicity change.

If the backbone buckles: refractory hyperosmolality or hemodynamic fragility → slow down insulin, reassess fluids/Na⁺ strategy, check for occult infection, consider ICU protocols for glycemic variability reduction. Watch for cerebral edema (rare in adults; risk in children)—worsening headache, bradycardia, neuro decline → pause rapid correction, escalate care.

HHS vs DKA—management contrasts that matter:
• HHS = bigger fluid deficit (8–12 L), slower insulin start, tonicity-driven targets; DKA = earlier insulin, acidosis focus.
• Ketones minimal in HHS; bicarbonate rarely helpful (reserve for severe acidosis from another cause).

Medication pitfalls you don’t want to meet: insulin before K⁺ correction, missing corrected Na⁺, swinging osmolality too fast, skipping thiamine in high-risk patients, or undertreating infection.

We close with the system moves: an HHS pathway that (1) triages to ICU when altered or unstable; (2) defaults to fluids → K⁺ → insulin with nurse-driven titration; (3) embeds q2–4h labs and osmolality targets; (4) auto-orders trigger workup + early antibiotics; (5) flags anticoagulation/VTE prophylaxis; (6) standardizes electrolyte/PO₄³⁻/Mg²⁺/thiamine replacement; (7) transitions to basal–bolus insulin with diabetes education, sick-day rules, meter/CGM review, and follow-up.

Fast, protocolized, and osmolality-wise—fill the tank, fix the salts, then insulin; treat the cause and prevent the next hit.