Head injury and hyperglycemia


I'm studying for a neuro test that I have Thursday, trying to figure out why patients who have head injuries (or really, any pathology that causes increased ICP) would have hyperglycemia. Is it related to the brain not getting enough oxygen, leading to anaerobic metabolism? But why would that cause increased glucose? I get that anaerobic metabolism causes acidosis, that it is inefficient, that it doesn't promote the energy needed to propagate an action potential - but why the hyperglycemia?


549 Posts

Has 1 years experience.

the liver makes stored glycogen available to the body in the form of glucose in times of trauma & stress. think about the fight or flight response... your pupils dilate, your heart rate increases, etc. glucose is released because it fuels your cells and the brain especially relies on it. so it's a compensatory mechanism. that's my educated guess.

Esme12, ASN, BSN, RN

4 Articles; 20,908 Posts

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma. Has 43 years experience.

Right on the nose.......The release of stress hormones (such as cortisol or norepinephrine) after a traumatic injury can induce stress hyperglycemia. Past research has shown that this state of elevated glucose has been related to increased medical complications and mortality rates. For a technical advanced explanation.

Hyperglycemia in acutely ill emergency patients Cause or effect? | Canadian Journal of Emergency Medicine Stress hyperglycemia results from the excessive release of counterregulatory hormones and cytokines, such as glucagon, epinephrine, cortisol, growth hormone and insulin-like growth factor, and from the overproduction of inflammatory mediators, such as tumour necrosis factor- alpha (TNF-α), interleukin-1 and interleukin-6.18

Inflammatory mediators initiate the metabolic response to injury and can precipitate MODS. During acute illness there is an increase in the systemic inflammatory response that is characterized by increased production of pro-inflammatory cytokines, such as interleukin-1, interleukin-6, TNF-α and macrophage inhibitory factor,19 and a decrease in the anti-inflammatory cytokines, interleukin-2, interleukin-4 and interleukin-10.20,21 Acute hyperglycemia further upregulates the production of several of these inflammatory cytokines.22

High levels of extracellular glucose inhibit G6PD (glucose-6-phosphate dehydrogenase) and impair oxygen radical production in activated neutrophils.23 In vivo, hyperglycemia could therefore impair microbial killing by neutrophils in a dose-dependent fashion. Neutrophil dysfunction24 and impaired intracellular bactericidal activity25 have been demonstrated when glucose concentrations are high. In an animal trauma model,26 maintenance of normoglycemia enhanced innate immunity by preserving phagocytosis and the monocyte oxidative burst function.27 These findings suggest that acute glucose control may lower the risk of infection that is so prevalent in our sickest patients.


19 Posts

Thanks! That makes the picture clearer. I get it, now! :up:

Esme12, ASN, BSN, RN

4 Articles; 20,908 Posts

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma. Has 43 years experience.