NHD CPD eArticle Vol 8.16 by NH Publishing Ltd

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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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NHD CPD eArticle catabolic11 and can begin to break down muscle as an energy source.12 A systematic review by Foley et al13 found that the mean energy expenditure can range from 75% to 200% during the first 30 days following the TBI. Anecdotal evidence from practice has demonstrated that a number of patients can remain hypermetabolic post the acute phase of the injury, lasting weeks or months. The hypermetabolic state following TBI can result in malnutrition with further complications of hyperglycaemia, impaired wound healing and increased risk of infection and multiple organ failure.10 A recent Cochrane review7 states that, particularly in TBI, early feeding may be associated with better overall outcomes. It is, therefore, essential to ensure that adequate nutrition support is provided to patients with TBI. However, within this patient group, there are a number of barriers which impede the provision of optimal nutrition support, particularly following step down from the critical care environment. This has been discussed below, along with suggested management strategies to optimise nutritional status. AGITATION

Post traumatic agitation is a common issue following TBI.14 This is often difficult to treat using medication15 and, therefore, has to be managed at a ward level. Agitation can lead to difficulty in implementing dietetic plans as it can be challenging to site enteral tubes and ensure they are kept in situ. Management strategies: • Liaise with the medical team to ensure medical treatment for agitation is optimised. • Be aware of local policies on ‘specialing’ and 1:1 supervision. • Following local protocol, consider if mittens can be utilised. The Deprivation of Liberty Safeguards (DoLS) may need to be in place. • Liaise with therapy/neuropsychology for management strategies to help reduce agitation levels. ACCESS ISSUES

Within an ICU setting, patients with moderate to severe TBI may require mechanical ventilation

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and/or sedation, which removes the possibility of oral intake. Therefore, many TBI patients require alternative means of feeding. TBIs often occur alongside additional injuries, including: basal skull fractures, facial fractures and abdominal injuries. These can all lead to access issues for enteral nutrition (EN) and subsequently lead to a delay in feeding. Associated abdominal injuries from the initial trauma can preclude the use of gastrostomy/ jejunostomy placement for an extended period of time, meaning increased risk of tube displacement with nasogastric tubes (NGT). Management strategies: • ENT input may be required to assist with placing a NGT. • Depending on prognosis and expected requirements for longer-term feeding, discuss with the multidisciplinary team (MDT) if early placement of gastrostomy should be considered when NGT is unable to be placed or is frequently dislodged. • Utilise the provision of parenteral nutrition (PN) when EN cannot be supported, or nutritional goals have not been reached by EN by one week post-injury.16 GAPS IN FEEDING

Patients with TBI often have other injuries which require multiple operations and thus the patient may have periods of being placed nil by mouth in preparation for surgery. Due to agitation, the patient can often have recurrent NGT displacements which may require x-ray confirmation once replaced, leading to delay in feeding and the patient not receiving the full amount of feed. The patient’s feed may regularly be put on hold if they are experiencing tolerance issues. Ileus may be propagated by repeated and prolonged periods where patients are not fed. Management strategies: • Consider aiming to meet full nutritional requirements (NRQs) within a shorter time period by utilising a higher calorie feed and/or increasing rate of feed. • Consider feeding outside of work hours, so gaps are not caused by therapy sessions. • Where tolerance is not an issue, catch-up feeding can be utilised, based on local policy.

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Low mood, shock, depression, fatigue and pain related to the initial injury, as well as medication effects can also lead to reduced appetite . . . FEEDING INTOLERANCES

Impaired gastrointestinal function has been reported in up to 80% of TBI patients with a GCS < 12.17 Neurogenic bowel can occur in this patient group and can result in: diarrhoea, constipation, urgency and incontinence. Management strategies: • Ensure that the patient’s head of bed is elevated 30-40 degrees during feeding. • Consider use of alternative feeds (e.g. fibre free/tolerance feeds). • Liaise with the medical team to ensure tolerance issues are medically optimised. • Liaise with the medical team and Nutrition Support Team to consider post pyloric feeding. • Consider the use of bridging PN. • Discuss with palliative care for symptom management advice as sometimes sickness cannot be resolved although treatment has been optimised. FLUID AND SODIUM DISTURBANCES

Syndrome of inappropriate diuretic hormone secretion (SIADH) may require patients to have a fluid restriction leading to difficulties in meeting their elevated NRQs. Diabetes insipidus and cerebral salt wasting can occur following TBI. Management strategies: • With SIADH, consider utilising a high energy/low volume feed. • Where diabetes insipidus has occurred, consider a low sodium feed if persistently raised sodium levels. • There is little nutritional change to consider with cerebral salt wasting; this is medically managed. REDUCED ORAL INTAKE

Altered levels of consciousness and cognition can result in memory issues and confusion, which

can lead to difficulty in feeding and reduced oral intake. Low mood, shock, depression, fatigue and pain related to the initial injury, as well as medication effects can also lead to reduced appetite and poor oral intake. Communication issues and confusion may lead to patients being unable to communicate what their preferred foods or dietetic treatment plan would be. Taste fatigue can occur within this patient group due to long hospital stays, resulting in the patient becoming bored with the hospital menu or nutritional supplement drinks. Reduced ability for the patient to feed themselves can occur following injury. Dysphagia can be a common consequence of TBI, with as many as 61% of patients experiencing it.13 This may lead to reduced oral intake due to dislike of the textured foods and reduced variety available, as well as poor hydration with thickened fluids. Management strategies: • Consider if adaptive cutlery or assistance with all dietary and fluid intake is required – the patient’s family may be happy to assist with this.

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• Liaise with catering to provide the patient with alternative menu options. • It is important to keep enteral access for supplementary top-up feeding/ hydration/medication until oral intake is fully established and can be consistently maintained. • Longer-term EN may be needed in dysphagic patients due to poor oral intake and limited variety of high calorie supplements.

Management strategies: • Utilise high calorie feeds. • If the patient is able to eat orally, consider overnight NGT feeding alongside oral intake to assist with meeting the patient’s full NRQs. • Be cautious not to overfeed on protein if energy requirements are high and body weight is low; consider using high calorielow protein supplement (e.g. Vitajoule, ProCal Shot, Calogen etc.).

ELEVATED NUTRITIONAL REQUIREMENTS

Regular weights are essential to ensure metabolic demands are being met; however, this can often be difficult due to agitation or patient injuries requiring bed rest. Due to immobility, weight gain in this patient group tends to lead to an increase in fat stores, often making it more difficult to establish a ‘target weight’, as a healthy BMI in this patient group may constitute a larger proportion of fat than a mobile patient. In the rehab phase, a TBI patient’s metabolism can change suddenly, leading to excessive weight gain.

Anecdotal evidence from practice has demonstrated that often young males with TBI require in excess of 3000kcal/day. Paroxysmal sympathetic hyperactivity (PSH) is an excessive and uncontrolled increased activity of the sympathetic nervous system, which increases the patient’s fluid and energy needs. A report of indirect calorimetry in a 14-year-old with hypoxic brain injury and PSH revealed resting energy expenditure during an autonomic storm of 309% of the patient’s predicted resting energy expenditure.18

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NHD CPD eArticle Management strategies: • Ensure patients are weighed at least twice weekly (where possible) to ensure appropriate monitoring of their nutritional status. • When patients are unable to be weighed using hoist/chair scales, bed scales can be used where available. • Alternative measurements (e.g. midupper arm circumference) should be taken early in admission and regularly thereafter to allow monitoring of nutritional status, for those patients who are difficult to weigh. • Where available, bioimpedence can be utilised to monitor change in the patient’s body composition and to prevent excessive gain in fat stores. UNDERSTANDING

Patients with cognitive impairment may lack understanding of their elevated NRQs and/ or may forget discussions with the dietitian, therefore, compliance with dietetic care plans may be poor. There may be a lack of knowledge within medical teams regarding elevated NRQs in TBI patients, which can lead to premature removal of feeding tubes once oral intake is commenced. Management strategies: • Consider liaising with the patient’s family who may have more regular contact with the patient, as they may be able to encourage

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and remind them of the importance of following a dietetic care plan. • Liaise with the medical team regarding your concerns of the patient’s nutritional status; educate them on the nutritional challenges in this patient group. ETHICAL ISSUES

Depending on the extent of their injury, the patient may lack capacity to make decisions around treatment (e.g. feeding tube placement). Management strategies: • The medical team should ensure a capacity assessment is carried out. • If the patient lacks capacity, act in their best interest and endeavour to attend bestinterest meetings. • Where appropriate include the patient’s family in the decision-making process. CONCLUSION

The provision of adequate nutrition support for patients with TBI has been a clinical challenge for decades. The unique metabolic derangements, along with accompanying challenges of providing adequate nutrition support, means that this patient group is at particularly high risk of malnutrition. To help ensure the best outcome for the patient, in my experience, early dietetic input and an MDT approach to treating malnutrition is essential, as this can be a highly vulnerable and complex group of patients to manage.

References 1 Maas A, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neuro. 2008; 7: 728–41 2 National Institute for Health and Clinical Excellence: Guidance. Head injury: triage, assessment, investigation and early management of head injury in children, young people and adults. London: National Institute for Health and Care Excellence (UK), 2014 3 Thornhill S, Teasdale G, Murray G, McEwen J, Roy C, Penny K. Disability in young people and adults one year after head injury: prospective cohort study. BMJ. 2000; 17; 320(7250): 1631 4 Frost R, Farrer J, Primosch M, Hedges W. Prevalence of traumatic brain injury in the general adult population: a meta-analysis. Neuroepidemiology. 2013; 40(3): 154-9 5 Thompson H, McCormick W, Kagan S. Traumatic Brain Injury in Older Adults: Epidemiology, Outcomes, and Future Implications. Journal of the American Geriatrics Society. 2006 Oct; 54(10): 1590-1595 6 Fruin A, Taylon C, Pettis M. Caloric requirements in patients with severe head injuries. Surgical Neurology. 1986; 25: 25-8 7 Perel P, Yanagawa T, Bunn F, Roberts IG, Wentz R. Nutritional support for head-injured patients (Review). The Cochrane Library. 2008, Issue 4 8 Yanko J, Mitcho K. Acute care management of severe traumatic brain injuries. Crit Care Nurs Q 2001; 23: 1-23 9 Charrueau et al. Metabolic Response and Nutritional Support in Traumatic Brain Injury: Evidence for Resistance to Renutrition. Journal of Neurotrauma. 2009; 26(11): 1911-20 10 Vizzinni A, Aranda-Michel J. Nutritional support in head injury. Nutrition. 2011; 27: 129-132 11 Durr D, Hunt D, Rowlands B et al. Energy supply and demand following head injury - balancing the metabolic budget. JPEN J Parenter Enteral Nutr. 1987; 11: 5S 12 Rajpal V, Johnston J. Nutrition Management of Traumatic Brain Injury Patients. Support Line. 2009; Volume 31, No 1 13 Foley N, Marshall S, Pikul J, Salter K, Teasell R. Hypermetabolism following moderate to severe traumatic acute brain injury: a systematic review. Journal of neurotrauma. 2008; 25(12), 1415-1431 14 McNett M, Sarver W, Wilczewski P. The prevalence, treatment and outcomes of agitation among patients with brain injury admitted to acute care units. Brain Injury. 2012; 26(9): 1155-62 15 Fleminger S, Greenwood R, Oliver D. Pharmacological management for agitation and aggression in people with acquired brain injury. Cochrane Database Syst Rev. 2003; (1): CD003299 16 Cook A, Peppard A, Magnuson B. Nutrition Considerations in Traumatic Brain Injury. Nutrition in Clinical Practice. 2008; 23: 608 17 Kao C, ChangLai S, Chieng P, Yen T. Gastric emptying in head-injured patients. American Journal of Gastroenterology. 1998; 93: 1108-1112 18 Mehta B and Nejdl W. Unsupervised strategies for shilling detection and robust collaborative filtering. User Modelling and User-Adapted Interaction. 2009; 19: 65 Copyright © 2018 NH Publishing Ltd - All rights reserved. Available for printing and sharing for the use of CPD activities for personal use. Not for reproduction for publishing purposes without written permission from NH Publishing Ltd.

NHD CPD eArticle NETWORK HEALTH DIGEST

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Questions relating to: Neurosciences and trauma: the challenges of nutrition support Type your answers below, download and save or print for your records, or print and complete by hand. Q.1

Explain how the Glasgow Coma Scale is used to classify traumatic brain injury (TBI) severity.

Q.2

What are the metabolic changes shown in patients with moderate to severe TBI?

Q.3

Why is nutrition support vital for patients in this group?

Q.4

Outline three management strategies for post traumatic agitation common in TBI patients.

Q.5

What access issues can occur for enteral nutrition and nasogastric tube feeding?

Q.6

Describe the management strategies to aid gaps in feeding.

Q.7

Provide information on the consequences of TBI leading to reduced oral intake.

Q.8

When elevated nutrition is required, how can this be managed?

Q.9

Describe why weight measurements are important in TBI patients, giving examples of the measurement strategies required.

Please type additional notes here . . .