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Hyperglycemia (HHS, DKA)

Hyperosmolar Hyperglycemic State (HHS) and Diabetic Ketoacidosis (DKA) are possible consequences of uncontrolled diabetes. Both are medical emergencies that require attention at an urgent care site. See below for more information and resources.

Definitions and Pathophysiology

Diabetic Ketoacidosis (DKA)

  • DKA happens when there is a lack of insulin and an increase in glucagon and other counterregulatory hormones. This results in reduced glucose uptake and utilization in the peripheral tissue, and an increase in glucose production and release from the liver; all leading to hyperglycemia.
    • Note that SGLT2 inhibitors may lower the threshold for developing DKA. People on these meds might develop DKA at lower glucose levels than expected. 
  • When the glucose level exceeds the renal threshold, glucose spills into the urine. This excess glucose in the urine acts as an osmotic diuretic, pulling fluid from the vascular space and causing rapid dehydration. 
  • Without sufficient insulin, fats are broken down as an alternate energy source. The end-products of fat breakdown are ketoacids. The accumulation of ketoacids in the bloodstream result in acidosis.
  • The lungs attempt to rid the body of this excess acid by hyperventilating (Kussmaul’s respirations). The labored breathing serves to excrete carbonic acid by venting carbon dioxide.
  • The body attempts to buffer the hydrogen ions in the cells with protein, phosphate and bicarbonate. As the hydrogen ions move into the cells, potassium is driven out of the cells into the extracellular space, in an ion exchange. The potassium may then be excreted in the urine with the ketoacids. As a result, the total body potassium is usually low, but the serum potassium level may be high, normal or low.
  • With deficient insulin supplies, the new glucose sources remain unavailable to the cells and blood glucose levels continue to rise.
  • As hyperglycemia worsens, serum osmolarity rises, worsening the diuresis. If the cycle of ketosis, acidosis, and tissue breakdown is not reversed by medical management, coma and death will occur.
  • The anion gap is measured and used by physicians to help in the determination of DKA. The anion gap is the difference between the cations (sodium Na+ and potassium K+) and the anions (chloride Cl- and bicarbonate HCO3-) in serum. In healthy individuals, the anion gap is typically 8 to16 mEq depending on the lab parameters. Above 20 mEq/L, the probability of a true anion gap acidosis exists. An increased AG in the setting of positive ketones is used to diagnose DKA.

DKA requires emergency treatment with fluids, insulin and most often potassium (K+) replacement. Precipitating factors are investigated and treated.

For patients on an SGLT2 inhibitor, surgery can be a precipitating factor leading to DKA. It’s recommended that SGLT2 medications be stopped 3 d prior to planned surgery, and re-started only after adequate oral intake is resumed. (Canadian Journal of Diabetes guideline is here.)

 

Hyperosmolar Hyperglycemic State (HHS)

Formerly called Hyperglycemic Hyperosmolar Non-ketotic Coma (HONK or HHNK). HHS is the preferred term, because the majority of people do not present in a coma.

  • This is a rare syndrome of marked hyperglycemia, and plasma hyperosmolarity which results in profound dehydration in those with type 2 diabetes. There is enough effective insulin on board to prevent the development of ketoacidosis. However, due to the severe dehydration, mental changes involving profound lethargy or coma may occur.
  • Precipitating factors might include infection, insulin omission, myocardial infarction and others.
  • HHS requires emergency treatment for fluid and insulin replacement. Precipitating factors are investigated and treated. Although HHS is rare, mortality rates have been found to be 12 to 17% (though a confounding variable in this statistic is the underlying precipitating event).

 

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