Trauma - clinical aspects Flashcards
What are the treatment targets after TBI?
- Physical
- Behavioural
- Cognitive
- Emotional
- Personal and family-related functioning
- Environmental
What are examples of physical?
Speech
Movement
Sensation
Perception
What are examples of Cognitive?
Concentration
Memory
Executive function
Communication
What are examples of behavioural?
Initiation
Persistence
Flexibility
Impulse contol
What are examples of Emotional?
Management of anger
Iritability
Anxiety
Frustration
What are examples of personal and family-related functioning?
Employment
Socialisation
Schooling
What are examples of environmental?
Access to health-care
Transportation
Social support
What are examples of rehabilitation interventions?
- Restitutional
- Compensatory
- Adaptive
What is restitutional rehabilitation?
Repetition to relearn previously learned skills e.g. repeated exercise to restore cognition
What is compensatory rehabilitation?
Substitute intact strengths for impaired function e.g. assistive technology for memory impairment
What is adaptive rehabilitation?
Accommodation of disability via adjustment e.g. problem focused management of avoidance behaviours and other self-efficacy beliefs
What did 90% of admissions have?
Mild traumatic brain injury
What does TBI increase?
- Pyschiatric caseness
- Welfare recipiency
- Low educational attainment
- Homelessness
- offending
- Imprisonment
Reduces life expectancy
What is the effect of TBI increased/greater with?
Increased injury severity
Recurrence
Older age at first injury
What is retrospective estimation of single behavioural measured confounded by?
- Alcohol
- Drugs
- Sedation
- Analgaesia
- Metabolic factors
- Co-morbidiries
What does addition of radiological factors enable?
Retrospective classification of severity in the majority of cases of TBI
What is the mayo classification of moderate-severe TBI?
one or more of:
- Death due to this TBI
- GCS 3-8 (LoC) for 30 minutes or more
- Worst GCS in first 24 hours <13
- Post-traumatic amnesia for 24 hours or more
- One or more of the following imaging changes on acute CT: Extradural, subdural, subarachnoid blood or evidence of contusion, TAI or brainstem injury
What is the mayo classification of mild (probable) TBI?
If none of the cirteria A apply, and one or more of:
- Loss of consciousness if momentary to less than 30 minutes
- Post-traumatic amnesia if momentary to less than 24 hours
- Depressed, basilar or linear skull fracture (dura intact)
What is the mayo classification of symptomatic (possible) TBI?
If none of criteria A or B apply, and one or more of blurred vision, changes in mental state, dazed, dizzy, focal neurological symptoms, headache and nausea are present
Applies to majority of post-concussional injuries
What are examples of T(D)AI contusional injuries?
- Rotation (shear) (Traumatic axonal and micro-vascular injury)
- Translation (linear) - coup and contra-coup (haemorrhargic) contusions, & E/SDH)
- Impact and crush (E/SDH, couo)
What is increasing severity of disturbances in consciousness caused by?
Mechanically induced strain affecting the brain in a centripetal sequence of disruptive effect in function and structure
Where does the effect mechanics of primary injury in TBI begin and extend to?
Begins at the brain surface (Causing a syndrome of confusion with or without amnesia) and extend to affect the diencephalic/mesencephalic core at the most severe levels of trauma (coma and death)
What is ventricular dilatation?
Usually atrophic, secondary to TAI or contusional injury
Where is contusion located and what does it affect?
- Fronto-temporal
- Mobilise early but cognitive, affective and behavioural problems
- Poor judgement and planning, anxiety, irritability, impulsivity
Where does shear injury increase?
Centripetally with severity
What is used to prevent secondary injury after TBI?
Decompression due to brain herniation
What does depressed fracture after hammer assault cause?
Severe global cognitive impairment, low mood, PTSD
What is the natural history or PTA?
- E.D., A shepherd, aged 27, was admitted to hospital on May 3, 1931
- He was bleeding from the right ear and was tossing restlessly in bed. He made no attempt to speak and was in a deeply stuporose condition
- Owing to violent restlessnes he was transferred to ward for incidental delirium where had to be strapped in bed. He powerfully resisted any interference
- Fighting hard against the straps which held him down and calling out loudly without using any definite words
- Much of what he said was meaningless, but a few sentences were intelligible
- He was very talkative and emphasised all he said with powerful gestures
- After considerable persuasion he would respond to a simple request such as ‘‘put out your tongue’’
- He was quite changed. He remembered being troublesome in the ward and was now very apologetic
What is amnesia?
Disorder of memory
What is confusion?
Transient organic mental syndrome with acute onset characterised by a global impairment of cognitive functions with a concurrent disturbances of consciousness, attentional abnormalities, reduced or increased psychomotor activity and disrupted sleep/wake cycle
What is agitation?
excesses of behaviour, including a combination of aggression, restlessness, disinhibition, and/or lability
What is delirium?
Sometimes called acute confusional state
Disturbed consciousness, cogntive function or perception
Acute onset and fluctuating course
can be hypoactive, hyperactive or mixed…and can be restless, agitated and aggressive (or) withdrawn, quiet and sleepy…. caused by the direct physiological consequences of a general medical condition.”
Delirium
was first used by Celsus in the 1st century AD, prior to the rift between Neurology & Psychiatry, to describe mental disorders experienced during fever or head trauma
What does DSM-IV nor NICE delirium guideline mention?
TBI as a cause of delirium
What are the working model for time post-injury?
- Post-traumatic amnesia
- Post-traumatic confusion
- Acute confusional state or delirium
- Agitated confusion or Hyperactive delirium
- Rancho level IV
- Rancho level V
When does agitation resolve?
Before PTA ends
When does agitation, confusion and amnesia tend to increase?
During the day with fatigue, lack of structure and increased external stimuli
What are the management of post-traumatic amnesia, agitation and confusion?
- Avoid patient/carer/staff injury by managing risk
2. Use environmental modification, with drugs if needed, as treatment modalities
What are environmental management?
- Tolerate restlessness and agitation
- Use 1:1 supervision and a side-room +/- a matressed floor 3. Avoid excessive handling, stimulation and visiting
- Provide predictability, familarity, clarity and reality
- Involve/educate the family
- Use of safe vest or dry-suit rarely needed
What is the drug management?
Reduce hypervigilance rather than produce sedation
What are the management of post-traumatic agitation and confusion flow chart?
- Exclude other causes of agitation e.g. urinary retention
- Continue behavioural interventions
- Oral Lorazepam 1-2mg
- IM lorazepam 2mg and/or phenelzine 25059mg
- Repeat 6 hourly pm
- Add oral olanzapine 2.5-10mg (elderly 2.5-5mg)
- Tail over days or weeks
What does duration of PTA or coma enable?
Early prediction of ceilings to functional outcome later after moderate/severe TBI and faciliates goal setting
What is PTA?
An early behavioural marker of severity
What are (Neuro)physical consequences of severe TBI?
- Hydrocephalus and intracranial hypotension
- Asymmetric spastic-ataxic quadriparesis tremor
- Hemiparesis, ipsi-lesional or contralesional or both
- Imbalance commonest residual physical problem
- Thalamic pain
- Bulbar problems and incontinence
- Autonomic storms, & hypothalamuc and hypothalamic-pituitary axis dysfunction
- Syndrome of trephined
- Cranial neuropathies
- Incidental carotid/vertebral dissection, hyperextension myelopathies, traumatic plexopathies, compression mononeuropathies
- Heterotopic ossification
- Post-traumatic epilepsy
What does the guidelines address?
- Who to test?
- When to test?
- How to test?
- Why to treat?
What are the management of low awareness states after ABI?
- Rating scales
- Prevent avoidable complications (disability management)
- Causes of death
- Future options
Rating scale (ABI)
JFK Coma Recovery Scale - Revised (CRS-R)
Sensory Modality Assessment and Treatment Technique (SMART)
Rappaport coma/near-coma scale
Wessex Head Injury Matrix
Prevent avoidable complication (disability management)
24 hour posture and positioning, PEG/PEG-J
Intrathecal baclofen often avoided or delayed too long; good for storming
Longest survival in PVS >40 years
Possible costs per annum per patient: first year £6M; late £600,000
What are the causes of death?
- Sepsis
- Pulmonary Emboli
- Falls and fractures
- Fits
What are future options?
- Diagnostic functional imaging to identify covert awareness
- Drugs
- DBS or NIBS
- Neural restoration
- cultural change
What are the diagnosis based on behaviour influenced by?
- Medical instability
- Nutritional state
- Medication e.g. AEDs
- Altered sleep/wake cycle
- Severe physical impairment
- Positioning masking ability
- Repetitive movement
- Sensory impairment, particularly deafness and blindness
- Communication and behavioural problem
- Fluctuating attention and responsiveness
- Environmental problems
- New/inexperienced assessor
- Possibility of covert awarenss
How can later independence and QoL improved?
The preventable long term complications of not only physical but affective, behavioural and cognitive deficit must be avoided
What are examples of Affective, Behavioural, Cognitive deficits?
- Social isolation and loneliness
- Homelessnes
- Increased contact with mental heath and forensic services
What do the deficit particularly involve?
- Impaired executive function
- Social cognition
- Emotional processing and insight
- Damaged central control processes
- Repeated failure to cope with unexpected
- Prevented by emotional support
Damaged central control processes
(eg. the ‘supervisory attentional system’) dealing with novelty failing to formulate, implement, monitor and correct goal-directed behaviour and adaptive living strategies ‘in the moment
Repeated failure
to cope with the unexpected, leading to ‘catastrophising’ anxiety, aggression, low mood, depression, ritualised behaviours and ‘goal neglect’, which can be
Why is the importance of establishing the nature of impairments after TBI ignored?
- The pathology appears to be a fait accompli at the scene
- The subsequent impairments are often cognitive, affective and behavioural, rather than physical, and concealed or difficult to define
- They are more responsive to training rather than medical treatment
What is depression associated with?
Social isolation and lack of initiation - result of PTSD rather than abulia
What is 4 years after injury attributed to?
severe brain damage” or “a degenerative
neurological disorder”, rather than being functional in origin and psychologically mediated
largely as a result initially of a severe peripheral vestibulopathy.
What does lack of patient insight threaten?
professional insight, and may lead to a
failure to plan and support suitable rehabilitation and adjustment,
and risk work and financial loss, family disintegration and shortened
life expectancy.
What are trans-diagnostic therapeutics?
Treatments aimed at a disrupted brain function or network, that leads to similar symptoms or phenotypes across diseases, regardless of the conventional diagnostic labels or pathologies
For post-acute TBI, where is attentional difficulties seen?”|
both ADHD and TBI have led to trials of stimulants, most often Methylphenidate* but also Lisdexamfetamine#, Guanfacine@ and Atomoxetine+.
Where are significant functional gains in?
- Independence in personal care
- Functional mobility
- Self-organisation skills
- Psychological well being
