NHD CPD eArticle NETWORK HEALTH DIGEST
Volume 8.16 - 8th November 2018
NEUROSCIENCES AND TRAUMA: THE CHALLENGES OF NUTRITION SUPPORT Hazel Clark Dietitian, Salford Royal NHS Foundation Trust Hazel is a rotational dietitian with experience in neurosurgery and neuro-rehab in a specialist neuro trauma centre.
Traumatic brain injury (TBI) is a physical injury to the brain tissue that temporarily, or permanently, impairs brain function. This occurs following trauma to the head, with the main causes of TBI being road traffic accidents (RTAs), assaults and falls.1 This article takes a look at the challenges associated with providing adequate nutrition support to prevent malnutrition and other associated risks in patients following ICU stepdown. In the UK, roughly 1.4 million patients per year attend hospital following a head injury.2 Whilst for some, the impacts of TBI can be minor, ranging from minor concussion and a period of post traumatic amnesia, for others, the impact is far more profound and can have life-changing consequences, with some studies reporting that 38% of patients with a severe head injury are deceased, or in a vegetative state at one year post injury.3 TBI is now one of the leading causes of mortality and disability among young individuals, particularly in high-income countries.1 Although traditionally TBI has been considered to be more prevalent within the young male population,4 it is predicted that in the future, due to the aging population, the elderly will comprise an increasingly significant proportion of the major trauma workload.5 The Glasgow Coma Scale (GCS) is used to classify the severity of TBI, by assessing coma and impaired consciousness. The scale is divided into three components: eye opening, verbal response and motor response and summed to give a total score ranging from 3-15. A severe head injury
is classified as GCS 3-8, moderate GCS 9-12 and mild GCS 13-15. It has been suggested that the severity of a head injury correlates to the degree of hypermetabolism exhibited by TBI patients.6 Studies show that patients with moderate to severe TBI demonstrate higher levels of hypermetabolism, increased energy expenditure and increased protein losses7 than those with mild head injuries. The metabolic changes observed in these patients in the acute phase are in part attributed to an increase in levels of cytokines and counter-regulatory hormones including cortisol, epinephrine, norepinephrine and glucagon,8 as well as the production of acute phase protein from the liver9 and increased cardiac output and hypertension leading to elevated CO2 production and O2 consumption.10 The increase in energy expenditure seen in severe head injuries is vital for synthesis of new tissue for healing and to meet the demands for the production of proteins for structural, transport, signalling, or immunologic functions. However, unless nutrition intake meets the increased demand for energy, the patient subsequently becomes
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