The<unk>  hyperglycemic<unk>  (HHS) is the result of relative insulin deficiency and excess of counter-regulatory hormones like glucagon, growth hormone, catecholamine, and cortisol. The decrease in insulin-to-glucagon ratio puts the body in the catabolic<unk>  and leads to hyperglycemic and<unk><unk> . The hyperglycemia is secondary to activation of gluconeogenesis, glycogenolysis and decreased peripheral utilization of glucose. The increase in plasma osmolality is secondary to osmotic diuresis and dehydration. Advanced age and other underlying comorbidities such as congestive heart failure or chronic kidney disease, decrease in fluid intake and osmotic diuresis leading to activation of renal angiotensin aldosterone system (RAAS) further aggravate the increase in plasma osmolality. There is enough endogenous insulin secretion in the hyperglycemic<unk><unk>  (HHS) to prevent unrestrained ketosis but not enough to prevent hyperglycemia.
Hyperosmolar hyperglycemic state pathophysiology
Hyperosmolar hyperglycemic state epidemiology and demographics
Hyperosmolar hyperglycemic state risk factors
Diabetic ketoacidosis pathophysiology
Hyponatremia pathophysiology
Hypernatremia pathophysiology
Diabetes insipidus pathophysiology
Hypoglycemia pathophysiology