Traumatic brain injury

Question 1

what is a TBI

Answer 1

An alteration in brain function, or other evidence of brain pathology,
caused by an external force”

Question 2

epidemiology

Answer 2

True incidence unknown (minor head injuries not reported)

Estimate of annual incidence of traumatic brain injury in Ireland = 13,444 (ESRI)

European estimate: 150 to 300 cases / 100,000 population

M:F 3:1

1 in 3 patients aged <25y

Major cause of death in people <45y

Mortality with neurosurgical admission = 12% (Phillips, 2009)

Question 3

classifying traumatic brain injury

Answer 3

diffuse or focal 
closed or open
penetrating injuries 
mild moderate or severe
multiple injuries

Question 4

anatomy

Answer 4

Brain is not directly anchored to the
skull so may move independently

During sudden, swift movements or high-energy impacts, shearing and stretching of the brain may occur

Damage is inflicted on the soft brain structure as it moves across the irregularities of the internal surface of the skull

Question 5

brain damage primary secondary

Answer 5

primary
Direct consequences of impact to the brain: bleed, contusions, diffuse axonal injuries

secondary
Physiological responses to trauma
Rosner’s conjecture – ischaemia caused by consequences of TBI – hypotension, hyperglycaemia, fever, brain swelling

Question 6

primary brain damage

Answer 6

Causes = EXTERNAL FORCES
Direct impact on the skull
Penetration through skull
Collision between brain substance and internal skull structure

Consequences
Diffuse axonal injury
Contusions
Haemorrhage
Skull fracture

Question 7

diffuse axonal injury

Answer 7

Cause: acceleration-deceleration and rotational
forces (commonly from RTC)
Affects long axonal tracts
Axons may be stretched or severed in myelin
sheaths causing Wallerian degeneration
Microscopic haemorrhage in white matter
Frequent cause of minimally conscious state
Clinical findings disproportionate to imaging

Common sites of injury: corpus callosum, internal capsules, brainstem and cerebellar peduncles

Question 8

contusions

Answer 8

Bruise” of the brain tissue

Multiple micro-haemorrhages

Most commonly occur on under-surface of frontal lobes and tips of temporal lobes due to bony ridges – regardless of initial site of injury

Coup / contre-coup injury: contusions at point of contact (coup) and at opposite side of skull (contre-coup)

Consequence: attention, emotional, and memory problems more common in TBI survivors than any other ABI

Risk factor for development of seizures

Question 9

intracranial haemorrhage

Answer 9

subarachnoid
Distinct from SAH caused by aneurysm rupture
Traumatic SAH = high velocity injuries

subdural haemorrhage
Rupture of veins in
subdural space
Acute (high velocity trauma) – active bleeding <24h
Acute on chronic – 2-
10 days post injury
Chronic – older people >10 days post injury (often minor)

extradural haemorrhage
Blood collects between skull and dura
Often with skull fracture
Middle meningeal
vessels torn
Rare in older people (dura more adherent to skull surface)
Prognosis depends on speed of evacuation of haemorrhage
Can present with mild symptoms but suddenly deteriorate as haemorrhage grows

Question 10

fractures

Answer 10

Think not just skull, but everywhere else.  Common sites:
Base of Skull (BOS)
Skull
Facial including orbital, zygomatic
Spinal
Long bone
Ribs
Lacerations / bruising… check deep lacerations  for depressed skull fracture
Clinical features of BOS fracture:
CSF rhinorrhoea or otorrhoea
Bilateral periorbital haematoma - “Raccoon
eyes”
Subconjunctival haemorrhage

Question 11

radiology

Answer 11

CT brain can show haemorrhage, contusions,
DAI only 20%

Basal cisterns effaced - sign of raised ICP with brain shift from expanding mass/swelling
Trauma protocol: CT and x-ray spines, x-ray
ribs, limbs

All traumas in Beaumont Hospital are treated with spinal precautions until actively moving all 4 limbs.

Question 12

aims of management

Answer 12

Treat primary brain damage – if possible (neurosurgical unit): Evacuation of haemorrhage
Elevation of depressed skull fracture

Prevent secondary brain damage:
Maintenance of cerebral blood flow Cerebral factors
Systemic factors

Question 13

primary brain damage

Answer 13

Any expanding cranial mass needs urgent evacuation
Surgery also allows insertion of Intracranial Pressure (ICP) monitor
craniotomy - access to brain
burr hole evacuation for SDH
craniectomy R/o potion of skull to reduce ICP

Question 14

secondary brain damage = ischaemia

Answer 14

Ischaemia occurs due to:
Cerebral factors – brain swelling, ↑ ICP
Systemic factors – hypotension, hypoxaemia, pyrexia

Prevention of ischaemia depends on maintaining
cerebral blood flow (CBF)

Not possible to directly measure CBF
Cerebral Perfusion Pressure (CPP) is an indicator of CBF
Optimal range = 60 – 150 mmHg

Question 15

intracranial pressure

ICP

Answer 15

Monro-Kellie Doctrine: volume in rigid skull
cavity consists of 3 components: Brain (90%)
Blood CSF
None of these components is compressible
Increase in size of one of the components, or addition of pathologic component (e.g. tumour) means pressure will increase
Normal ICP = 0-10mmHg
Transient increases occur in normal life (e.g. coughing)
Sustained increases will cause ischaemia or compression

Question 16

principles of secondary brain damage prevention

Answer 16

systemic factors
Ventilate – prevent hypoxaemia
Infuse – hypotension normally due to hypovolaemia
Pump – if MAP <90 mmHg despite fluid resus, use inotropes (noradrenaline) to increase cardiac output

cerebral factors Control ICP
Maximise jugular venous return (30° head up, collar off)
Minimise cerebral metabolism

sedation Minimises cerebral metabolism, avoids stimulation to the brain → reduced cerebral metabolic demand → reduced oxygen consumption and anoxic effects
Morphine and midazolam
Propofol early on (can cause hypotension)

Question 17

management of elevated ICP

Answer 17

Physical:
Collar off
Keep PaCO2 slightly lowered (slightly high Resp Rate on ventilator)
– exploits chemoregulation effect
Avoid pyrexia.
1st line drug = Mannitol – reduces blood viscosity, reduces expanding  intravascular volume. Given early, then discontinued (risk of rebound  effect).
Third steps:
Decompressive craniectomy
Barbituates (thiopentone)

Question 18

decompressive craniectomy

Answer 18

Removal of bone flap to allow for expansion of skull contents for management of high ICP

Landmark study NEJM (Hutchinson et al, 2016): Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intracranial Pressure (RESCUEicp) trial to assess the effectiveness of craniectomy as a last-tier intervention in patients with TBI and refractory intracranial hypertension

Question 19

implications for physio

Answer 19

Physiotherapy is necessary in ICU to optimise respiratory function (avoid hypoxaemia), maintain muscle length and manage co-existing injuries from polytrauma
Heavy sedation → impaired cough, risk of pneumonia
If patient is fully sedated and has a labile ICP, be cautious: minimise interaction and handling, ask for bolus of sedation before respiratory intervention
Barbituate coma – complete cough suppression, long half-life (slow to
wean)
Know about significance of pupils assessment and Glasgow Coma Scale

Question 20

pupils assessment

Answer 20

Size: normal pupil size depends on the balance between sympathetic and
parasympathetic tone. Normal values vary 2-6mm.

Response to light stimulus: defined as normal, sluggish or absent. Tests CNII and CNIII function.

Normal pupil response to a bright light shone in the eye = pupillary light reflex:
Afferent impulse from retina sent along optic nerve CN II to Edinger- Westphal nucleus of oculomotor nerve CN III in midbrain
Efferent fibres leave CN III nucleus and pass via the ciliary ganglion to the constrictor fibres of the sphincter papillae muscle
Result: both pupils constrict at an equal rate and to a similar degree

Question 21

absent of pupil response

Answer 21

CNIII nerve function is the most useful indicator of an expanding cranial
lesion.

Herniation of the medial temporal lobe through the temporal hiatus directly damages the efferent CNIII fibres resulting in pupil dilatation with impaired or absent reaction to light.

The pupil dilates on the side of the expanding lesion – an important localising sign.

As ICP ↑ bilateral CNIII palsies occur

Question 22

papilloedema

Answer 22

Occurs in a proportion of patients with high ICP

Increased CSF pressure in the optic nerve sheath impedes venous drainage and axoplasmic flow in optic neurons.

Swelling of the optic disc and retinal and disc haemorrhages result.

Vision only at risk if severe or prolonged

Question 23

GCS

Answer 23

Developed by Teasdale & Jennett, 1974
Vague terms such as “semicoma” and “deep coma” disregarded
Conscious level described instead in terms of Eye opening (E)
Verbal response (V)
Motor response (M)
E, V and M measure different functions => report them separately (total score is of little clinical value)
High inter-rater reliability
Correlates well with outcomes following TBI

Question 24

scoring GCS

Answer 24

Where two limbs produce different motor responses, use the BEST
response

Use upper limbs for motor response as lower limb responses tend to be inconsistent, often arising from spinal and not cerebral origin

Standard for pain: supraorbital pressure or neck pinch to distinguish flexion vs. localising

Score less than 8 historically classified as “coma

Question 25

GCS limitations

Answer 25

External factors which alter the patient’s level of consciousness interfere with the scale’s ability to accurately reflect the severity of a traumatic brain injury, e.g. metabolic disturbances

Verbal response invalid patients who cannot speak (intubated /
tracheostomy)

Orbital trauma may make eye opening impossible

Spinal cord injury invalidates the motor scale for the limbs (unless patient is obeying commands – then use tongue)

Question 26

implications for physio (sedated)

Answer 26

Always check neurological observations in nursing notes before
assessing your patient with TBI
If fully sedated, pupils assessment only. Abnormal pupil response → warrants medical or neurosurgical intervention, may contraindicate physiotherapy management
GCS scores are important as patient emerges from sedation
Once sedation is weaned, progress as tolerated:
Respiratory: ventilator weaning – deep breathing, active cough
Active / active assisted exercise – Letto, therapist or family-assisted
Introduce anti-gravity activity, sitting over edge of bed, standing, sitting out
Positioning for pressure relief, minimise contracture risk

Question 27

classification of head injury severity

Answer 27

According to GCS:
13 – 15: Mild
9 – 12: Moderate
3 – 8: Severe
According to duration of post-traumatic amnesia – length of time from injury
to restoration of continuous memory, period of confused state:
< 1 hour: Mild
1 – 24 hours: Moderate
> 24 hours: Severe

Question 28

mortality following TBI

Answer 28

Herniation or ischaemia → Brain stem death

Systemic complications – respiratory, cardiovascular

Question 29

brain stem death

Answer 29

Irreversible structural brain damage, incompatible with life
Criteria:
Diagnosis compatible with brain stem death
Outrule other causes of reduced brain stem activity (barbituates, sedatives, hypothermia, endocrine)
Pupillary response absent
Corneal reflex absent
Vestibulo-ocular reflex absent
Gag reflex absent
Motor response absent
No spontaneous respiratory effort (movement and ABGs)

Question 30

minimally conscious state

Answer 30

Severe bilateral hemisphere damage may result in a state in which the
patient has no apparent awareness of themselves or their environment.

Important to distinguish from “locked-in syndrome”

Periods of eye-opening and closing may occur, suggesting sleep-wake cycles, and there may be spontaneous movements of face, trunk or limbs, but the patient does not communicate or interact with others in any way.

Becomes “permanent” when irreversibility can be established with a high
degree of certainty, e.g. 12 months after TBI.

One month after trauma, up to 33% of patients will show improvement in the subsequent year.

Multidisciplinary management
RAMP Principles: Maintain and Prevent
Liaise with OT regarding seating
Tone management: splinting, passive exercise (active / passive cycle  ergometer – Letto), positioning (see Lecture 6)
Family involvement
NRH “SMART” programme
Sensory stimulation

Question 31

post traumatic amnesia

Answer 31

Post-traumatic amnesia (PTA) is the time after a period of unconsciousness when the injured person is conscious and awake, but is behaving or talking in a bizarre or uncharacteristic manner
PTA = cannot remember injury or time afterwards
Symptoms of PTA include confusion, agitation, distress or anxiety
Uncharacteristic behaviours may include violence or aggression, both
physical and verbal, swearing, shouting and disinhibition
If the person is mobile, difficulties may be experienced in preventing wandering
Increased risk of falls and orthopaedic complications

Question 32

physio Ax TBI

Answer 32

resp 
tone and ROM
strength
mobility / function
balance 
cerebellum
vestibular 
pain

Question 33

physio management TBI

Answer 33

PTA / cognitive impairment: focus, concentration, attention will be poor
→ not the time for task-specific training, intense practice of difficult
motor skills

Don’t expect the patient to remember exercises or instructions at first

Engage in automatic tasks that patient understands and can see a point
to it, e.g. walking, cycling, even football (with handling belt)

Carefully choose the amount of stimulation: quiet times in the physio
gym, time with visitors / family

Be mindful of safety awareness, educate team and family

Motor learning: practice, practice, practice

Question 34

rehab importance

Answer 34

Irish pathway: acute hospital → neurosurgical unit → acute hospital →
specialist rehabilitation (NRH) → long term care or home.
People with TBI can have significant unmet rehabilitation needs
Rehabilitation improves outcomes and saves costs (Turner-Stokes et al, 2016)
TBI should be conceptualised as a chronic health condition (Wilson et
al, 2017)
Similar to SCI, plan for long-term mitigation of effects of physical inactivity

Question 35

later outcomes

Answer 35

Sufferers of TBI have a reduced life expectancy, even after surviving
the acute injury
Diminished mobility is known to be a powerful predictor of increased mortality for patients with TBI, spinal cord injury, and many other conditions (Shavelle et al, 2001)
Recovery of ambulation post TBI (Katz et al, 2004)
82% of patients who achieved independent ambulation did so at 2 months post injury
95% were independently mobile at 3 months
For the remainder, only 9% recovered ambulation if they had not already done so at 3-4 months
Shavelle et al (2001): Standardised mortality ratios in TBI survivors –
16.4 in immobile survivors, 4.5 in survivors with impaired mobility (mobilised >20ft +/- assistance), 1.5 in those able to climb stairs independently.

Question 36

post traumatic epilepsy

Answer 36

Seizure occurrence is a recognized complication of TBI

Associated with poorer functional outcome after TBI (Asikainen et al, 1998)

The reported overall incidence of late PTS or PTE has a range of 13–50%,
depending on the population studied and the follow-up time

Highest incidence noted in studies of war veterans, who have the highest incidence of penetrating TBI (Englander et al., 2003)

Can experience either early or late onset post-traumatic epilepsy or seizure activity

Question 37

concussion

Answer 37

May include some or all of the following after a known blow to the head:
symptoms: somatic (e.g. headache), cognitive (e.g. feeling like in a fog)
and/or emotional symptoms (e.g. lability)
physical signs (e.g. loss of consciousness, amnesia)
behavioral changes (e.g. irritablity)
cognitive impairment (e.g. slowed reaction times)
sleep disturbance (e.g. drowsiness).

Question 38

TBI and neuro-degenerative changes

Answer 38

Topical issue in sports (see “Concussion” movie), but it has a long
history….
Martland (1928) first investigated the association of chronic progressive neuro-degeneration from observation of boxers, when the term “punch drunk syndrome” was first used to describe a progressive dementing disorder in participants of the sport
TBI in a number of other sports, such as American Football, can result in increased rates of late-life cognitive impairment (Guskiewicz et al., 2005)
History of just a single TBI is a risk factor for the later development of clinical syndromes of cognitive impairment such as Alzheimer’s Disease (Fleminger et al, 2003)