CORE EM: Hyperglycemic Hyperosmolar Syndrome (HHS)

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Definition: An acute decompensated state in which patients manifest a change in mental status in the setting of hyperglycemia, hyperosmolarity and severe volume depletion. Altered mental status can present as focal neurologic defects or global encephalopathy.


  • Decreased activity of insulin leads to increased serum glucose via gluconeogenesis, glycogenolysis and decreased cellular glucose uptake
  • Resultant hyperglycemia leads to fluid shift from intracellular to extracellular space
  • Increased circulating glucose spills into urine resulting in osmotic diuresis
  • Decreased circulating volume leads to reduction in glomerular filtration rate (GFR) and hypotonic urine
  • Hypotonic diuresis produces dehydration and creates cycle of hyperglycemia, hypernatremia and increased osmolarity


  • Non-compliance with medications and/or diet
  • Inadequate access to fluids to counteract losses
  • Common acute conditions exacerbating chronic diabetes: infection (i.e. sepsis), myocardial ischemia/infarction, pulmonary embolism, trauma, burns, GI hemorrhage etc.

Clinical Manifestations

  • The development of HHS is typically prolonged in comparison to DKA
  • History
    • Polydipsia, polyuria, polyphagia
    • Weakness
    • Weight loss
    • Nausea/Vomiting
    • Confusion
    • 20% without a known history of DM II
    • Chronic renal insufficiency a common comorbid condition
  • Physical Examination
    • Hypotension
    • Tachycardia
    • Dehydration (dry mucous membranes, delayed capillary refill)
    • Neurologic Manifestations
      • Decreased level of consciousness
      • Seizures
      • Focal neurologic findings
      • Stroke-like syndromes

Diagnostic Testing

  • Blood glucose generally > 600 mg/dL
  • Serum osmolarity > 350 mOsm/L
  • Renal Function
    • Elevated BUN:Cr ratio common indicating pre-renal causes
    • Acute Kidney Injury (AKI) from hypoperfusion will often co-exist
  • Ketoacidosis generally absent (though starvation ketosis may be present)
  • Electrolyte disturbances
    • Profound hypokalemia secondary to osmotic diuresis
    • Hyponatremia often results from hyperglycemia and will correct without directed management on sodium
    • Phosphate and magnesium levels commonly low

Basics: ABCs, IV, Cardiac Monitor and 12-lead EKG

  • Establish at least 2 large-bore (16-18 gauge) peripheral IVs as patients may require multiple medications
  • Carefully consider underlying cause of decompensation and HHS

Initial Management

  • Intravenous fluids
    • Role
      • Replenish intravascular depletion resulting from osmotic diuresis
      • Correct increased serum osmolarity
      • Correct decreased GFR
    • Initial Fluid Dose
      • Patients with HHS frequently have concomitant comorbid conditions like CHF and chronic renal insufficiency
      • May not tolerate large volumes of fluid well
      • Consider smaller boluses (10 cc/kg) with repeat cardiac and lung assessment
    • 0.9% NaCl (Normal Saline)
      • Most commonly employed fluid
      • Problems
        • NS is far from “normal”
        • Large volume infusions (> 2-3 liters) can cause hyperchloremic metabolic acidosis (unclear impact on patient)
    • Lactated Ringers
      • Closer to physiologic solution
      • Does not cause hyperchloremic metabolic acidosis
    • Other options: balanced solutions (i.e. Plasma-Lyte)
  • Insulin therapy
    • Patients with HHS will typically have adequate basal insulin levels and additional insulin may not be necessary
  • Electrolyte Disorder Correction
    • Potassium
      • Aggressive repletion frequently necessary
        • Patients hundreds of mEq depleted
      • Supplementation (see hypokalemia post)
        • Oral: KCl 40 mEq every hour (if patient safe for oral route)
        • Intravenous: KCl 10-40 mEq in each liter of fluid (caution: infusion of > 10 mEq potassium/hour will cause burning in peripheral vein)
    • Sodium
      • Typically dilutional hyponatremia
      • Will correct without specific treatment
    • Magnesium
      • HypoK = HypoMg (Boyd 1984)
        • Both electrolytes lost during osmotic diuresis
        • Cannot replete intracellular potassium without magnesium
        • Serum magnesium level may not correlate with total body stores
      • Dose: 1-2 gm MgSO4
    • Phosphorous
      • If PO4 < 1.0 mEq, consider repletion with KPO4

Take Home Points

  • HHS is defined by hyperglycemia and hyperosmolarity due to volume depletion with resultant altered mental status
  • Profound hypokalemia is common as a result of osmotic diuresis. Replete aggressively
  • Hypokalemia = hypomagnesemia. Replete both of these electrolytes simultaneously
  • Fluid repletion is the key point in management but careful repletion is vital as patients may not tolerate aggressive administration
  • All patients should have an exhaustive investigation of the cause of their decompensation. Look for signs of infection, ischemia, trauma etc.

Read More

Cydulka RK, Maloney GE: Diabetes Mellitus and Disorders of Glucose Homeostasis; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 126: p 1652-1668.


Boyd JC et al. Relationship of potassium and magnesium concentrations in serum to cardiac arrhythmias. Clin Chem 1984; 30(5): 754-7. PMID: 6713638

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