traumatic brain injury - rcp london

www.stgeorges.nhs.uk

Traumatic Brain Injury

Dr Colette Griffin

Consultant Neurologist


What is a TBI?

“Non degenerative, non congenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairments of cognitive, physical, and psychosocial functions with an associated diminished or altered state of consciousness”

(Dawodu, 2005)


Causes of TBI

RTAs - 25% of all TBIs

60% of deaths

Falls (22-43%)

Assaults (30-50%)

Work injuries

Sports injuries

Alcohol involved in 65%

70-88% of TBIs are male

(Head Injury; NICE Guidelines, 2007)

http://www.emedicine.com/cgi-bin/foxweb.exe/makezoom@/em/makezoom?picture=/websites/emedicine/med/images/Large/174Knife.jpg&template=izoom2


Why is this important?

Reconfiguration of trauma services pan UK

Major Trauma Centres developed

Trauma Units developed

NICE guidelines on head injury (2007)

NCEPOD “Trauma: who cares?” (2007)

Socially and economically catastrophic


TBI pathway

Referral straight to neurosurgery SPR 24 hours a day

Referral then straight to neurology / dedicated TBI SPR

Dedicated TBI MDT team

Head injury coordinator 8am daily e mail

Immediate availability of TBI MDT team

MDT screening tool

Follow up with consultant and psychologist


Why intervene early?

Intensive intervention leads to earlier gains Turner-Stokes L et al Cochrane

review 2005

Earlier rehabilitation improves functional outcome and lowers

rehabilitation and acute hospitalisation costs Cowen TD et al 1995


Neuroplasticity

Brain remodelling in response to external factors

Structural redundancies

Neural recovery

Neural compensation

Enlargement of dendrites and axons

Increase in neuronal density


Role of A&E

Trauma team

Imaging

Observation of patients overnight

Head injury booklet

Advice for GP follow up within one week (NICE)

Onward referral

Transfer to MTC as necessary


Imaging

NICE guidelines 2007

Canadian CT head rule

GCS <13 on presentation

GCS <15 two hours post trauma

Focal signs, vomiting, severe headaches

If intubated or GCS <13 also need spinal imaging

Spinal cord clearance


Discuss with neurosurgery

NICE guidelines 2007

Abnormal CT head

GCS 8 or below

Deteriorating GCS

Progressive neurology

Penetrating trauma

CSF leak


Classifications

Severity (mild/moderate/severe)

Isolated vs poly trauma

Mode of injury

Pathology


Classifications

90% of TBIs presenting to A&E have GCS 13-14 (mild TBI)

5% GCS 9-12 (moderate)

5% GCS 8 or below (severe)


Pathophysiology

Primary tissue disruption at the time of injury is generally

irreversible

Secondary insults over hours and days may well be reversible

Cellular ischaemia

Activation of inflammatory cascades

Neuronal and astrocytic swelling

Vasogenic oedema


White matter changes

Corpus callosum very vulnerable to shear and strain effects McAllister

et al 2012

Reduction in size and integrity of the corpus callosum, even in mild

TBI Aoki et al 2012

Loss of overall brain connectivity

TBI and dementia association may relate to selective white matter

damage and the role this plays in the expression of dementia via a

breakdown in neural connectivity


Chronic atrophy

Mechanical deformation

Axonal shearing

Focal lesional effects

Ischaemia

Pathological neuroexcitatory effects

Pathological neuroinflammatory reactions

Overlapping trauma induced neurodegenerative effects occur in the

same frontotemporolimbic areas associated with age related

neurodegenerative disorders


Erin D Bigler 2013


Common Presentations These can be many and varied

Confusion

Agitation

Aggression

Loss of memory

Hemiplegia

Poor problem solving

Inappropriate behaviour

Altered social skills Reduced insight

Reduced sensation

Emotional lability

Altered communication

Difficulty eating/drinking

Loss of balance

Altered level of consciousness

Fatigue


Post-Traumatic Amnesia

‘The period of post-traumatic amnesia is usually defined as

the time between receiving a head injury and the

resumption of normal continuous memory’

King et al 1997


Why is PTA important?.. Can assist in predicting the severity of TBI

Used along side GCS score to predict severity of injury (Teasdale and

Jennett, 1979)

Research suggests it can be used to predict rehab outcomes

PTA duration Severity of Injury

< 5 mins Very mild

5-60 mins Mild

1-24 hours Moderate

1-7 days Severe

1-4 weeks Very severe

>4 weeks Extremely severe

Jennett, 1976

Russell and Smith, 1961


Neuropsychiatric Management

Drug treatment of the neurobehavioural sequelae of TBI is common practice

There is limited evidence to guide drug treatment choices

Guidelines are based on consensus and some common principles between disorders

Presentation based on time course and common symptoms/disorders

See Chew & Zafonte 2009; Warden et al. 2006


Post Traumatic Amnesia

Avoid typical antipsychotics and/or Benzodiazepines

• May delay recovery and neuroplasticity Arcienegas & Silver,

2006

Atypical antipsychotics as effective as Haloperidol

• Less interference with dopaminergic function and may

normalise cholinergic function

• Have fewer adverse effects Arcienegas & McAllister, 2008


Management of PTA

Limit no. of visitors and their length of stay

Avoid restraints, consider one to one nursing

Allow patients to wander on ward with supervision

Try and keep patients in the same bed for orientation

Provide external structure (e.g. timetable, routine)

Allow frequent rest breaks

Keep instructions simple


KEEP CALM

AND

BE NICE (EVEN IF YOU DON’T FEEL LIKE IT)


PTA & Capacity

A patient is deemed NOT to have capacity when they are in PTA

Implications for the treating team:

Cannot be discharged

Have to ensure that patient stays on the ward

If a patient absconds they need to be brought back

Not ready for rehabilitation (historically)


The Absconding Patient

Mental Capacity Act – MDT approach

Deprivation of Liberties - the least restrictive method of restraint must be used

Use of family / friends

Usually gentle guidance, explanation of risks and effective communication help

Use of pictorial and other external aids


Key “take home” points

Reduce stimulation

Limit visitors to two at a time

Quiet environment

Stay calm with the person

Reassure them

Orientate them

Don’t encourage/allow any negative behaviour – whole team must have a consistent approach


Seizures

Early post traumatic (<one week later): 25% develop epilepsy

Late post traumatic (>one week later): 80% develop epilepsy

65% of bullet induced TBIs develop seizures

20% of closed TBIs develop seizures

Over 35% of patients who have at least two neurosurgical

procedures post TBI develop late onset seizures

Immediate provoked single seizure: no AEDs

Seizure within first week: rapid titration and withdrawal

Late seizures: Lamotrigine or Levitiracetam

Epilepsy information and referral to epilepsy services


Endocrinology

SIADH

Cerebral salt wasting

Chronic changes: hypopituitarism

Testing more useful at a later point in time

Most patients do not need replacement therapy


VTE

TBI is a prothrombotic state

Patients are often totally immobile

Local trust VTE policies

“Individual patient based decision making”

Haemorrhage is a contra-indication

Heparin and TEDs

Personal experience


Herb A Phelan Pharmacologic Venous Thromboembolism Prophylaxis

after Traumatic Brain Injury: A Critical Literature Review J Neurotrauma

2012;29(10):1821-1828


Headaches

Should usually settle with time

Do not use Paracetamol or Codeine containing products

Ibuprofen is typically contra-indicated

Personal experience

Associated loss of sleep-wake cycle: use of Melatonin


Vertigo

Can be problematic clinically

Again should settle with time

Vestibular physiotherapy is often very helpful


Pre-hospital neurosurgery…………..


TBI Top tips

These patients are not a new invention

There will already be a fair number in the trust

They can be managed within a Trauma Unit or District General

Hospital setting

The hub and spoke model is the correct model of care

SGH service can be replicated elsewhere


TBI Top tips

The first planned Trauma Unit TBI pilot will be Frimley Park

Hospital

Patient cohorting within the Trauma Unit is critical

Acute Stroke Unit model of care

No funding……………….

Rearrangement of services

Consultant responsible for service

Alteration in distribution of AHPs


TBI Top tips

These are NICE and NCEPOD targets from almost a decade

ago…………………

Current care is not ideal

Patient care has to be utmost priority

The days of playing “pass the parcel” are over


Kamp MA et al. Traumatic Brain Injuries in illustrated literature:

experience from a series of over 700 head injuries in the Asterix comic

books. Acta Neurochir (Wein) 2011;153(6):1351-1355


Risk factors for TBI

Roman nationality (TBIs caused by Gauls)

Lost helmet

Ingestion of the “magic potion”

Forgot to call for help


References

NICE guideline CG56. Triage, assessment, investigation and early

management of head injury in infants, children and adults. 2007

NCEPOD Trauma; who cares? 2007

Turner-Stokes L et al. Multi-disciplinary rehabilitation for acquired

brain injury in adults of working age. Cochrane Database Sys Rev

2005;(3):CD004170

Cowen TD et al. Influence of early variables in traumatic brain

injury on functional independence measure scores and

rehabilitation length of stay and charges. Arch Phys Med Rehabil

1995;76:797-803


References

Teasdale GM et al. Analysing outcome of treatment of severe head

injury: a review and update on advancing the use of the Glasgow

Outcome Scale. J Neurotrauma 1998;15:587-97

Erin D Bigler. Traumatic brain injury, neuroimaging and

neurodegeneration. Frontiers In Human Neuroscience 2013


Thank you

traumatic brain injury - rcp london

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