Hypermetabolism and nutritional management in

traumatic brain injury

Lisa Carrigg, Tiffany Craig, Rebecca Oshiro, Jason Park, Lisa Shelton

Introduction
Traumatic Brain Injury (TBI) is
damage to the brain as a result of
internal or external forces (Giza, 2001)

Results

Results

TBI Induced Hypermetabolism

Standard Treatment (Cook, 2008)
Early feeding within 72 hours

Primary insult affects neurological

tissue (Werner, 2007)

Use indirect calorimetry to determine

caloric needs

Secondary insult results in systemic

effects (Werner, 2007)

140% of calculated caloric needs will meet

the demands of most TBI patients

Hypermetabolism and
hypercatabolism in acute phase

Begin feeding at an amount lower than

whats calculated and gradually increase
Reassess energy requirement regularly

Annual Number of TBIs

Close monitoring of health status overall

The most recent systematic

review concluded:
Immune-enhancing formula containing
arginine, glutamine, probiotics, and
omega-3 fatty acids was associated with a
significant reduction in infection in
contrast with the standard formula (CI,
0.35-0.82; P<0.05) (Wang et al., 2013)
Figure 1. Reported number of TBI cases in the United States.
(CDC, 2010).

The aim of this review was to

examine changes in metabolism, and
identify the effective nutritional
form(s) of treatment in TBI

Methods
How is metabolism altered and what
specific tissues are affected?
What treatment is typically applied?
What are possible supplemental
treatments?

Conclusions
Our analysis of the current literature
concludes that there is variation for
treatment in each TBI patient, directly
related to the severity of the injury
Individual variability can be extreme
but managing the hypermetabolic state
is critical in restoring cognitive
function
Although proposed nutritional
treatments with valid mechanisms have
been identified, there is not sufficient
evidence at this point to recommend
their use
Refer to Fig. 3 for the evidence-based
treatment protocol

Nutritional Protocol to Meet

TBI Needs

Other proposed supplemental

treatments:
Figure 2. Metabolic pathways observed in TBI patients and
tissues affected.

Ketogenic diet (Greco, 2013)

As shown in Fig. 2, glucose metabolism in the

neuron is impaired, affecting metabolism in
peripheral tissues (Giza, 2001)

High protein and fat diet and low

carbohydrates to induce a fasting state
and the use of ketone bodies as fuel

The brain is in a hypermetabolic state and uses

glucose rapidly to meet ATP demands (Giza, 2001)

Metabolism of ketone bodies can

decrease production of reactive oxygen
species, produce antioxidant, antiinflammatory, and anti-apoptotic effects

Abrupt depolarization due to the initial insult of the

membrane leads to a sequence of ionic imbalances
and there is accelerated use of ATP to restore ionic
homeostasis (Giza, 2001)
Other contributing factors to decreased ATP
production (Greco, 2013)
Ischemia and hypoxia force the brain to go into
anaerobic glycolysis
Stress hormones are released at the time of
injury, initiating catabolic pathways
Release of cytokines trigger an immune
response

Branched Chain Amino Acid

Supplementation (Aquilani, 2008)
Improving protein synthesis
Prevention of further muscle wasting
Alternative fuel source

Figure 3. Our recommended nutritional treatment plan for

TBI patients, based on a comprehensive literature review.