Stress Hyperglycaemia

Elevated counter-regulatory hormones and pro-inflammatory cytokines stimulate gluconeogenesis and glycogenolysis in critical illness, producing stress hyperglycaemia even in patients without pre-existing diabetes. Counter-regulatory hormone release drives gluconeogenesis and glycogenolysis, leading to elevated admission blood glucose during critical illness. The pathophysiology linking SHR elevation to poor outcomes centres on activation of the HPA axis and the sympathetic adrenal system in response to severe physiological stress. Acute glycaemic elevation and fluctuations directly impair vascular function, induce endothelial dysfunction, and increase endothelial apoptosis, worsening prognosis through compounding organ damage.