Glasgow Coma Scale Score 13-15 (15)

Loss of consciousness, confusion, disorientation, unsteadiness,

dizziness, headache, visual disturbances (16).

Mild TBI

Moderate TBI
Severe TBI

Criteria for Traumatic Brain Injury Diagnosis

Glasgow Coma Scale Score 8 or less(15)

Extended period of unconsciousness (coma) or amnesia after the injury (15)

Type of accident

Observational study investigating fluid and

electrolyte balances in TBI patients.
Looking at ApoE genotypes in children with
TBI to see if ApoE is associated neurocognitive
outcomes that may intensify or emeliorate secondary injury
to development interventional approaches.

Etiology

Two studies currently registered with clincialtrials.gov

Ongoing Investigations

Treat each case as the individual based on

history, severity, complications, feeding tolerance, and clinical condition (7).

Falls and motor vehicle accidents are the most common causes (2,6)

Most common form of TBI

Incidence: 3.5 million new cases per year in the US (5)

Greatest incidence in children under 4 and 14 to 19 years of age (5).
Men have twice the risk of women for MTBI and
the risk is greatest in teenagers and young adults (2).

Epidemiology

The weighted average mortality for STBI is 39% (20).

Traumatic Brain Injury

Treament

Metabolic Presentation

Hypermetabolism, Hypercatabolism, Glucose dysregulation (7)

Secondary Injury
Evidence-based treaments

Pathological processes initiated at the moment of injury with delayed presentation (4).
Excitotoxicity, ionic imbalances, inflammatory response, oxidative stress, apoptosis,
infectious complications and feeding related complications (7, 17).
The degree of secondary neuronal injury is proportional to the degree of the
primary injury based on the release of chemical mediators in the primary injury (18).

Hypermetabolism
Brain injury itself stimulates the release cytokines and counter regulatory hormones including cortisol, epinephrine, and glucagon.
These hormones increase cardiac output, metabolic rate, oxygen consumption, glycogenolysis
and gluconeogenesis. All of this leads to hyperglycemia, protein catabolism and muscle wasting. (22).
Resting energy expenditure has been estimated between 40 and 200% above that of a non-injured person (21).

Proposed treatments

Ischemia-like pattern caused by biomechanical trauma leads to

anaerobic glycolysis and increased membrane permeability resulting
in the accumulation of lactic acid (4). Due to ischemia, there is a lack of ATP production from oxidative phosphorylation.
Overall this is what leads to the hypermetabolic state.

Zinc
Improves protein metabolism, GSC scores, and neurological outcomes (26).
Ketogenic diet
In a glucose compromised state,
cerebral metabolism of ketones after TBI provide
histological and functional neuroprotection and improve outcome (5).

The primary insult/mechanical damage (4).

Any transient or permanent neurologic dysfunction resulting from a biomechanical force (16).
A focal area of the brain damaged by contact injury or biomechanical injury (4).

Primary Injury

Less than 70% of patients receive an adequate enteral caloric intake (25).

Generally, early nutrition was significantly associated with a

lower risk of infectious complications compared with delayed nutrition
per the most recent systematic review (7).
Supplementation of Insulin like Growth Factor
seems to lower blood glucose
and improve protein conservation (27).
BCAA
More than 2/3 of patients with severe TBI exited post traumatic vegetative or
minimally conscious state compared with none in the control group (29).

70%-90% are mTBI (1,2)

Leading cause of morbidity and mortality worldwide in individuals under 45 (4)

Conclusion

Indirect calorimetry is the current preferred method for estimating energy expenditure (19).
Based on EEE, patients are administered a standard formula to meet their caloric needs (7).
Providing 140% of calculated basal energy expenditure will likely meet the needs of most TBI patients.
Anything above will be based on additional injuries (19).
Ideally, full caloric replacement will be present by day 7 after injury (19).
It is advised to begin feeding below levels of requirement and increased gradually.
Patients must be constantly monitored to adjust caloric intake up or downward as needed (30).
Data revealed the immune modulating formula was
associated with a statistical significant reduction in infection rate in
contrast with the standard formula per the most recent systematic review (7).
Probiotics, arginine, glutamine, nucleotides, and omega-3 are included in the immune modulating formula.
Immune formulas that contain omega-3 have shown decreased risk of infection.

Glasgow Coma Scale Score 9-12 (15)

Metabolism Changes

Omega-3 Supplementation
Anti inflammatory effects to
mediate the immune response (7).

Decreased circulating BCAA.

It is hypothesized this is due to increased usage (6).

Protein

Early enteral nutrition (within 72 hours of injury)

Forestalls breakdown of protein and fat stores, blunts the innate inflammatory response,
promotes immune competence, decreases ICU infections and can improve neurological outcome(28).
Epinephrine, glucagon, and cortisol lead to gluconeogenesis and glycogenolysis,
leading to increased hepatic glucose output (31).
Ketogenesis provides ketone bodies to the brain as an energy source (31).

Epinephrine, glucagon, and cortisol lead to protein

catabolism and muscle wasting and the release of BCAA (31).

Liver

Tissues Affected

Catabolism of proteins due to gluconeogenesis (22).

Protein catabolism peaks 8-14 days after injury and appears to be related to the severity of injury (23).
Protein catabolism is reflected in the increase in N output (24).

Carbohydrate
Lipid
Glucose
Initial hypermetabolism followed by hypometabolism.

Muscle
Adipose

In the neuron:
Primary insult results in non-specific depolarization of neurons which causes increased release of glutamate.
Increased glutamate causes a massive efflux of potassium causes ionic imbalance.
In order to return to ionic homeostasis there is increased Na/K-ATPase, which increases the utilization of ATP.
Hyperglycolysis is induced in order to meet the demand of ATP usage. (16)

Glucose shunted to PPP

Epinephrine, glucagon, and cortisol lead to lipolysis and

the release of free fatty acids (31),

Increased calcium and sodium influx can lead to intracellular catabolic pathways.
Calcium influx leads to activation of phospho-lipases, proteases,
and lipid peroxidases which leads increased intracellular fatty acids and free radicals (4).