DKA vs Hyperosmolar hyperglycemic state (HHS)

[Oh_Gee]

why is plasma osmolarity (Posm) always high in HHS, whereas DKA Posm is variable?

Pathogenesis of DKA and HHS are discussed in the same article in uptodate but the Posm difference between the 2 is not clearly explained (at least to my feeble mind).

uptodate says "
The increase in plasma osmolality created by hyperglycemia pulls water out of the cells, expands the ECF, and thereby reduces the plasma sodium (Na) concentration. If a patient with normal serum electrolytes (Na = 140 mEq/L) rapidly developed a glucose concentration of 1000 mg/100 mL, and no urine was made, then that patient’s serum Na would fall to value between 119 and 126 mEq/L and the osmolality would increase to a level between 294 and 308 mosm/L. However, the osmolality usually increases to a greater degree because a large volume of relatively electrolyte-deficient urine is excreted during the evolution of the hyperglycemic state. The loss of this electrolyte-free water further raises the osmolality . In patients with ketoacidosis, high plasma acetone levels also contribute to the elevated osmolality."


according to the pathogenesis flowchart (see figure 1) in this article (Hyperglycemic Crises in Adult Patients With Diabetes), there is no real difference in the pathogenesis to HHS

first aid does mention than HHS is classically seen in elderly T2DM w/ limited ability to drink. is that the sole reason than HHS has hyperosmolarity?

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[Oh_Gee]

why is plasma osmolarity (Posm) always high in HHS, whereas DKA Posm is variable?

Pathogenesis of DKA and HHS are discussed in the same article in uptodate but the Posm difference between the 2 is not clearly explained (at least to my feeble mind).

uptodate says "
The increase in plasma osmolality created by hyperglycemia pulls water out of the cells, expands the ECF, and thereby reduces the plasma sodium (Na) concentration. If a patient with normal serum electrolytes (Na = 140 mEq/L) rapidly developed a glucose concentration of 1000 mg/100 mL, and no urine was made, then that patient’s serum Na would fall to value between 119 and 126 mEq/L and the osmolality would increase to a level between 294 and 308 mosm/L. However, the osmolality usually increases to a greater degree because a large volume of relatively electrolyte-deficient urine is excreted during the evolution of the hyperglycemic state. The loss of this electrolyte-free water further raises the osmolality . In patients with ketoacidosis, high plasma acetone levels also contribute to the elevated osmolality."

why is DKA Posm variable?

 

[coffeeclothesaddict]

the sugar is way higher in HHS >600 vs DKA which is >300, so thats why the osmolality is so high in HHS and also the patients present much later in HHS and have more severe dehydration on presentation, vs DKA which is more of an acute process

 

[Oh_Gee]

the sugar is way higher in HHS >600 vs DKA which is >300, so thats why the osmolality is so high in HHS and also the patients present much later in HHS and have more severe dehydration on presentation, vs DKA which is more of an acute process

is the sugar way higher in HHS b/c T2DM patients have so much insulin resistance? whereas T1DM patients don't have insulin resistance

 

[coffeeclothesaddict]

is the sugar way higher in HHS b/c T2DM patients have so much insulin resistance? whereas T1DM patients don't have insulin resistance

T1DM is insulin dependent because they dont produce insulin at all, whereras T2DM has insulin resistance but produces insulin still, therefore the way i look at HHS as a more insidious onset disorder whereas T1DM and DKA is more likely to be acute because they produce ketones since they have no insulin at all. Idk if that helps or if its exactly the pathogenesis for HHS but it helps me to remember it anyway