Hyperosmolar hyperglycemic state

Background

  • Prototypical patient is elderly with uncontrolled type II DM without adequate access to H2O
  • Occurs due to 3 factors:
    • Insulin resistance or deficiency
    • Increased hepatic gluconeogenesis and glycogenolysis
    • Osmotic diuresis and dehydration followed by impaired renal excretion of glucose
      • May result in TBW losses of 8-12L
  • Ketosis usually absent (may be mild)
  • Cerebral edema is uncommon complication (case reports)

Precipitants

Clinical Features

Differential Diagnosis

Hyperglycemia

Evaluation

Work Up

  • Chem
  • Serum Osm
  • Lactate
  • Serum ketones
  • CBC
  • Also consider:

Evaluation

  • Glucose >600
  • Osm >315
  • Bicarb >15
  • pH >7.3
  • Serum ketones negative or mildly positive

Management

  1. Fluid replacement
    • Average fluid deficit is 8-12L
      • 50% should be replaced over the initial 12hr
      • May have to replace slower if patient has cardiac/renal impairment
      • Aggressiveness of fluid replacement must be weighed against the risk of cerebral edema, which increases with younger age[1]
  2. Hypokalemia
    • Must treat aggressively
    • Once adequate urinary output has been established K+ replacement should begin
  3. Hyperglycemia
    • Do not start insulin until K > 3.3 and adequate urinary output has been established
  4. Hypomagnesemia
  5. Hypophosphatemia
    • Routine correction unnecessary unless phos <1.0

HHS.jpg

Disposition

  • Most patients require ICU admission

See Also

References

  1. Stoner GD. Hyperosmolar Hyperglycemic State. Am Fam Physician. 2005 May 1;71(9):1723-1730. http://www.aafp.org/afp/2005/0501/p1723.html