Hyperglycemic Hyperosmolar State

This week in #AMReport @wchospital we talked about type 2 diabetes and hyperosmolar hyperglycemic state (HHS). Along with Diabetic Ketoacidosis (DKA) and hypoglycemia, HHS is one of the most common diabetic crises we manage in internal medicine.

HHS is characterized by marked hyperglycemia (think sugars > 30 mmol/L), along with polyuria, (compensatory polydipsia), and profound dehydration due to osmotic diuresis. Although we are taught in medical school that hypoglycemia is more acutely dangerous than hyperglycemia, severe HHS can easily result in an altered mental status and coma (hyperosmolar hyperglycemic non-ketotic coma).

It is important to differentiate HHS from DKA (see table for distinguishing factors). The main difference that drives the pathophysiology and therefore the management is insulin. In DKA, there is no insulin to shut off ketogenesis, as well there is an abundance of free fatty acids that cannot be metabolized due to the lack of insulin. This feeds ongoing ketone production. HHS is a disorder of glucose, the pancreas is usually secreting at least some insulin throughout which is enough to keep ketone production down.  Even though DKA is commonly associated with Type 1 Diabetes, up to 50% of Hispanic and African American Patients who present with DKA end up having Type 2 Diabetes. This may be related to acute, transient beta cell failure.

Disease State DKA HHS
Glucose High VERY high
Serum sodium Normal-low ~130 mmol/L Normal-high ~140 mmol/L

*often appears low due to pseudohyponatremia

Potassium Spectrum – can be low or high


Falsely normal in acidosis

Usually normal
Bicarbonate Usually < 10 mmol/L Usually > 15 mmol/L
Serum ketones PRESENT ABSENT
Electrolyte Anomalies Potassium, magnesium, and phosphorus deficits are usually marked – masked by severe acidosis and dehydration Highly elevated serum osmolarity, and elevated BUN

Adapted From Canadiem (https://canadiem.org/crackcast-e126-diabetes-mellitus-disorders-glucose-homeostasis/)

Even patients with well controlled diabetes can present with HHS in the context of: non-adherence, infection, MI/ACS, substance use (e.g. stimulants, alcohol).  HHS can even be seen in patients without diabetes in the context of peritoneal dialysis, burns, corticosteroids, or parenteral feeding.

The onset of HHS is usually insidious, taking place over days to weeks. An important question to ask patients on history is if they track their own blood sugars.  Many glucose monitors will not read when the sugar is above 30 so if they haven’t recorded the values and you suspect HHS, ask if they have been getting error messages or “HIGH” when they try to check.

The management for HHS is:

  • Isotonic IV fluids (usually deficit of 4-8 L)
  • Subcutaneous insulin is usually sufficient
  • Monitoring of electrolytes
  • Identify and treat underlying triggers

The goal is not to normalize the blood sugar, but to manage the volume deficit, treat the underlying cause and to stop the osmotic diuresis by reducing the blood sugar. Frequently patients will need to be started on insulin but can sometimes be transitioned back to oral agents after a few months if there was an obvious, treatable trigger for their episode.

HHS is something that we manage in the AACU, especially when a patient has no alteration of mental status or hemodynamic instability. We can often get people home in few hours and avoid inpatient hospitalizations or emergency room visits and can bring them back for rapid follow up to ensure their sugars are in check.



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