The pathophysiology of Hyperosmolar Hyperglycaemic State (HHS) remains incompletely understood.
Notably, the measurable insulin secretions surpass those observed in Diabetic Ketoacidosis (DKA). These high levels of insulin secretion effectively inhibit ketogenesis, it proves insufficient to adequately regulate hepatic glucose production.
Concurrently, an elevation in counter-regulatory hormones such as glucagon, cortisol, and catecholamines contributes to the described metabolic disturbances.
