Week 4 Flashcards
Definition of TBI
nondegenerative, noncongenital insult to the brain from an external force mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical and psychosocial functions with an associated diminished or altered state of consciousness
what is the most common cause of death under the age of 35 in most developed countries
TBI
What is the most common cause of accidental death
TBI
TBI is most commonly the result of
road accidents
industrial and sporting accidents
attempted suicides
interpersonal violence
M vs F TBI
males outnumber females 2:1
What is the second leading type of ABI in australia
TBI, following stroke
Mild compared to moderate or severe TBIs
20% moderate or severe
80% mild
increasing number of elderly people sustaining TBI’s, why?
falls
Risk factors of TBI
young adults : 66% M>F Fall: 40% Transport (MVA: 33% Assault 25% substance abuse risk taking behaviour psychiatric disorder limited educational attainment unstable work history
sequelae =
complications
complications associated with TBI include
dependant on severity
physical and cognitive impairments - vary as a consequence of the lesion severity and location as well as the nature of brain damage and complications
can have devastating impact on lifestyle/future aspirations, creating general health and social problems causing disruption for family members and marital strain, affecting role relationships and fostering economic hardship
Individuals confront their disability for decades in a society which most commonly associates disability with the elderly or those with congenital intellectual disabilities
Common health issues in TBI include
seizures (early and late) Somatic complaints - headaches dizziness - pain - sleep disturbances
Post concussion syndrome Mental health issues - depression - anxiety - schizophrenia
What are ways to prevent TBIs
protective laws and recommendations have resulted in a reduced incidence (and reduced severity) of TBI
use of helmets by cyclists, motorcyclists
protective headache in sport
automobile seatbelts
automobile child restraints/rearfacing car seats
enforcement of drink driving laws
falls prevention strategies for those at risk of falls
MOI for TBI
neuropathological evidence suggests that there are several mechanisms of brain injury, some operating at the moment of impact and others as a consequence of secondary complications
Types of MOIs
direct - blunt/penetrating
indirect
Direct MOI is
direct blow to the head
indirect MOI is
impact from other parts of the body
Blunt direct MOI is
acceleration-deceleration injury commonly resulting in multiple body injuries and widespread brain damage; may cause scalp injuries, skull deformation +/- fractures and depressed fractures +/- perforated dura mater and brain
penetrating direct MOI
open head injury in which the dura mater is breached; may be caused by external objects or bone fragments from a skull fracture
Primary brain damage involves
occurs at the time of injury
effects are largely immediate
Neuropathic processes of primary brain damage
hypoxia
hypotension
cerebral metabolic flow uncoupling
impairments of CV autoregulation - important for maintaining ICP
Secondary brain damage cause
primary injury initiates cascade of neuropathological processes resulting in more severe and widespread brain damage
Neuropathic processes involved in secondary brain damage
excitotoxicity
impaired calcium homeostasis
oxygen free radicals
inflammatory processes
intracranial mechanisms in primary and secondary brain damage
primary
- diffuse
- -diffuse axonal injury
- focal
- laceration
- contusion
- -haemorrhage (subdural, epidural, subarachnoid, intraventricular)
Secondary
- brain swelling (vasogenic oedema, cytotoxic oedema )
- cerebral blood vessel constriction
Extracranial mechanisms
hypoxia
hypotension
predictors of outcome for TBI include
period of confusion (PTA) - immediate loss or impairment of consciousness
indices of severity of predictors of outcome
-depth of coma
-duration of coma
- length of post-traumatic amnesia (PTA)
depth of coma provides the best clinical picture of a patient’s current neurological status
Duration of coma and length of PTA appear to be better predictors of functional outcomes
Depth of coma
the GCS defines severity of a TBI within 48h of injury
most widely used measure of severity of coma
- severe =GCS less than or equal to 8
Moderate = 9-12
Mild =13-15
If a patient is intubated and therefore cannot give a verbal response for a GCS, what do you do
add the suffix T indicates intubation
therefore
maximum score = 10T
minimum score = 2T
Duration of coma is determined by
different definitions , they include
- time from injury to spontaneous eye opening
the following of commands
and scoring >/=8 on GCS
Severity of trauma using the duration of coma are
Severe= >6h Moderate = 20m - 6h Mild = <20m
Length of PTA
PTA is the period of impaired consciousness that extends from the initial injury until continuous memory for ongoing events is restored
Criteria for classification of severity using duration of PTA =
extremely severe = >4 weeks
Very severe= 1-4 weeks
Severe= 1-7 days
Moderate =1-24h
Mild =<1hour
Recovery from TBI includes
most exhibit a range of ongoing sensorimotor, cognitive and behavioural sequelae, which vary widely in their nature and severity
mechanism of recovery poorly understood
considerable variability in patterns of recovery
types of recovery
spontaneous recovery
- resolution of temporary physiological changes
regenerative neuronal changes
- limited potential, especially with severe injuries
neuroplasticity/cortical reorganisation
- capacity decreases with severe injuries
- presence of intact tissue enables reorganisation
Recovery from mild TBI
expected to recover quickly, how ever some will have psychological consequences that require management
most people experiencing mild TBI recover fully within days to months, but a small percentage (1-20%) continue to experience symptoms three months after injury
Recovery from moderate - severe TBI
negatively accelerating curve, with recovery being most rapid in the first 3-6 months
may continue for several years
Rehabilitation includes
acute care stabilisation
recovery after TBI often exceeds expectations
rehabilitation routinely offered to patients who have some level of responsiveness to maximise potential for recovery
Physiotherapy assessment of the TBI patient
for patients with TBI, the standard neurological subjective/objective assessment should be performed
assessment may need to be modified based on patient’s presentation (eg. cognitive deficit, concurrent injuries)
Cranial nerves
all cranial nerves should be assessed by the MDT (with physio to focus on CN III< IV, VI and others if they have not been assessed)
Shoulder pain
prevalence of 62%
limited evidence in TBI population
implement assessment and management strategies with demonstrated efficacy in stroke patients
Remember decordicate
decerebrate
slide 31
common variations to standard neurological assessment with regards to extracranial injuries
fractures
soft tissue injuries
effect on outcome controversial
important in determining mortality and functional outcomes
contraindications, precautions and considerations for physio management
Acute medical management includes
ventilation evacuation of space occupying haematoma management of scalp lacerations and skull fractures correction of hypovolaemia provision of anticonvulsants monitoring of - ICP BP CPP -cerebral perfusion pressure -provision of brain protective agents
Physiotherapy management of a patient with TBI
physiotherapy can hold a major role in the management of a patient following a TBI. Management is as indicated based on the patient’s presentation (based on assessment)
physios are generally responsible for
- providing respiratory care (improve respiratory function ; prevent/manage respiratory complications)
Optimising MSK integrity (prevent/minimise /manage secondary adaptive changes in soft tissue)
Promoting the restoration of motor function
Evidence for physio management
no verifiable evidence of the efficacy of sensory stimulation programs
More intensive rehab programmes lead to early functional skills
- no ceiling effect identified for more intensive therapy
improvement in PROM after serial casts or orthosis
reduced spasticity after serial casts or orthosis
no verifiable clinical improvement after night splints in functional position
improvement in CV fitness after strength training
further evidence regarding physio management
There is good evidence for the efficacy of intensive task oriented training programmes
• Gait training with partial weight bearing is not superior to physiotherapeutic gait training
• Proof of efficacy for functional arm training
• Overall, it is important to analyse the immediate primary concerns of the patient through the process of clinical reasoning and to select and modify treatment methods appropriately
Benefits of CV training in these patients
Improves cardiovascular fitness
• Improves general health
• Reduces depression
• No evidence for transfer of the improvements to the functional level
• Evidence demonstrates that fitness often ignored in rehabilitation, particularly for patients with a FIM >4 for locomotion
• The treadmill is not ideally suited to functional gait training but it is superior to conventional gait training in terms of endurance and fitness
Functional training in patients with TBI
- Efficacy for upper limb and lower limb functional training • Evidence for CIMT in later/ chronic stage of TBI
- Influenced by patient compliance, criteria to participate in CIMT and strength and lack of evidence for acute management of TBI
- In contrast to stroke research, no proof of superiority for treadmill training with partial body weight support.• Practice walking on different surfaces, uneven ground, up and down slopes and over obstacles.
- Practice walking with selective head control but without loss of postural stability, walking under different lighting conditions and walking in crowds.
Treatment considerations for acute sever TBI
• Respiratory treatment should be provided with the patient in a maximally sedated state (bolus sedation)
• Treat when ICP is low (<20mmHg if possible)
• Maintain neck strictly midline throughout treatment as rotation will block CSF drainage and venous blood low with consequent increase in ICP
• Nurse with head 30°to optimise cerebral oedema drainage
• MHI can be used but with caution as it can increase ICP.
• If ICP is high, small rapid volume breaths will reduce ICP by removal of CO2 to allow intermittent MHI breaths
If positioning is required, perform slowly
• Turning may be better tolerated following a bolus of sedation
• Manual respiratory techniques can be performed with caution, ensuring obs are monitored closely
• Pre-oxygenate prior to suctioning
• Lightening of sedation required prior to mobilisation/ training
management of impairments includes
- Joint flexibility/ tone/ spasticity: PROM exs, positioning, stretching, serial casting, botulinum toxin
- Shoulder pain: PROM exs, positioning, electrical stimulation, specific retraining of shoulder motor function
- Respiratory: positioning, MHI, manual techniques to facilitate inspiratory effort
Management of activity limitations includes
- Bridging
- Supine to side-lying (rolling)
- Side-lying to sitting over edge of bed • Sitting to standing
- Standing to sitting
- Sitting balance
- Standing balance
- Gait
- Tilt table, physiotherapeutic functional retraining, aid prescription (e.g. wheelchair)
