Hyperosmolar Hyperglycemic State (HHS)

Fix it before you operate - HHS is an ICU resuscitation with endocrine and intensive care involved, not something you carry into an elective case. Postpone elective surgery until volume and osmolality are corrected.

Volume first, insulin second - Isotonic fluid, 15 to 20 mL/kg bolus then 200 to 250 mL/hr in adults, about twice maintenance in children. Hydration alone drops glucose 75 to 100 mg/hr and blunts counterregulatory hormone release. Starting an insulin drip early is what causes a precipitous glucose fall.

The glucose target is not normal - Check glucose hourly and hold it around 300 mg/dL. Cerebral edema from rapid osmolar correction is the feared complication, and the risk is higher in HHS than DKA and highest in children - in peds, spread rehydration and electrolyte correction over 48 hours.

Potassium will fool you - Serum potassium can look normal or high from the extracellular shift while total body stores are depleted. Start replacement once serum potassium is 4 to 4.5 mmol/L, and recheck often after insulin starts, since insulin drives potassium intracellularly and untreated hypokalemia leads to ventricular arrhythmia.

Correct the sodium before you read it - Measured sodium is falsely low. Corrected Na = measured Na + 1.6 x ((glucose - 100)/100). Trend the corrected value, not the reported one.

Airway follows mental status - Obtundation comes from hyperosmolality and reduced cerebral perfusion. Secure the airway if the GCS is under 8.

Expect hypotension on induction - Deficits are profound. Elevated BUN and creatinine reflect prerenal azotemia and an elevated hemoglobin and hematocrit reflect hemoconcentration. Elderly patients presenting with coma and hypotension do worst.

Find the trigger - Infection accounts for 50 to 60 percent of cases. Send a CBC, and blood cultures, urine culture, and chest X-ray if the white count is up. Review the med list for thiazides, beta-blockers, glucocorticoids, and atypical antipsychotics, and get an ECG, since MI and stroke also precipitate HHS.

Trend labs, don't sample once - Electrolytes and ABG every 2 to 3 hours. pH is usually 7.30 or above with a near-normal anion gap; a widened gap in HHS means lactate from tissue hypoperfusion, not ketones.

Magnesium and phosphate - Magnesium is often low. Phosphate can be high on presentation, especially with rhabdomyolysis, then falls once insulin and fluid drive it intracellularly and renal perfusion improves - recheck both after treatment starts.

Hyperosmolar hyperglycemic state (HHS) is the type 2 diabetes crisis that sits opposite diabetic ketoacidosis (DKA). Enough endogenous insulin remains to suppress ketogenesis, but not enough to move glucose into peripheral tissue, so counterregulatory hormones - glucagon, cortisol, growth hormone, catecholamines - drive gluconeogenesis and glycogenolysis unopposed. Glucose typically climbs above 600 mg/dL with effective serum osmolality over 320 mOsm/L and no significant ketoacidosis.

The resulting osmotic diuresis strips free water and electrolytes. Dehydration is more severe than in DKA and cardiovascular collapse is more likely. The brain defends its volume by generating idiogenic osmoles, which is why dropping osmolality too fast causes cerebral edema. Infection precipitates 50 to 60 percent of cases; thiazides, beta-blockers, glucocorticoids, atypical antipsychotics, MI, and stroke account for much of the rest. Mortality reaches 20 percent, roughly ten times DKA.