Traumatic Brain Injuries Flashcards
What is the definition of a head injury?
TBI is a non-degenerative, non-congenital insult to the brain from an external mechanical force, possibly leading to temporary or permanent impairment of cognitive, physical and psychosocial function
What are the high risk groups for a TBI?
Young men Elderly Previous head injuries Residents of inner cities Alcohol and drug abuse Low-income
What are the mechanisms of injury for a TBI?
Assault Falls RTCs Sports OVER HALF DUE TO ALCOHOL
When are the peaks in head injury in deaths?
Initially within the 1st hour
Around 7 hrs due to secondary effects
3rd peak later on due to medical complications such as pneumonia, DVT, PEs
What is ATLS?
Airway with C-spine control
Breathing
Circulation
What are the categories for GCS?
Eye opening
Motor
Verbal
What are the different levels within eye opening of GCS?
Open spontaneously = 4 points
Eyes open to verbal command, speech or shout = 3 points
Eyes open to pain = 2 points
No eye opening = 1 point
What are the different levels within verbal response of GCS?
Oriented = 5 points Confused = 4 points Inappropriate responses, words discernible = 3 Incomprehensible sounds = 2 No verbal response = 1
What are the different levels within motor response of GCS?
Obeys commands = 6
Purposeful movement to painful stimuli/localising = 5
Withdraws from pain/ flexing = 4
Abnormal (spastic) flexion, decorticate = 3
Extensor (rigid) response, decerebrate = 2
No motor response = 1
Which section of the GCS scale is MOST important?
Motor
Describe the head injury severity scale
Mild: 14/15, brief LOC
Mod: 9-13
Severe: 3-8
What are the nice guidelines for CT scanning?
GCS under 13 on initial assessment GCS under 15 at 2 hours after injury Suspected open or depressed skull fracture Any sign of basal skull fracture Post traumatic seizure Focal neurological deficit More than 1 episode of vomiting Suspicion of NAI Age over 65 Coagulopathy Dangerous mechanism of injury
What are signs of a basilar skull fracture?
Lacunar eyes
Battle’s sign (bruising over mastoid)
Any blood of CSF leakage from ear canal
What are the different types of traumatic haematomas?
Extradural haematoma
Subdural haematoma
Intracerebral haematoma
Will an extradural haematoma cross the suture lines?
No - lens shape or biconvex shape
What is the classic presentation for an extradural haematoma?
Injury with LOC
Recovery “lucid interval”
Rapidly progressing neurological symptoms; deteriorating GCS, hemiparesis, unilateral fixed and dilated pupil then ultimately apnoea and death
Who is likely to get an acute subdural haematoma?
Elderly patients due to atrophy of brain
Bridging veins rupture
What is the differences on CT scan from an acute and a chronic subdural haematoma?
Acute; hyperdense
Chronic; hypodense
What is the management of a diffuse axonal injury?
Medical management to control ICP as there is nothing surgical to remove
What secondary insults do neurosurgeons aim to prevent?
Hypoxia
Hypotension
Mass lesions
Control ICP and CCP
How is CCP calculated?
MAP - ICP
THEREFORE
If you keep MAP up and ICP down you will have good cerebral perfusion
What occurs if the ICP gets too high?
Herniation; subfalcine, uncal or tonsillar
What is the medical management of a raised ICP?
Sedation; propofol, benzodiazepines or barbiturates
Venous drainage; tilt head, remove any compression of the neck e.g. cervical collars or ET tube ties
CO2 control
Osmotic diuretics (mannitol, hypertonic saline)
CSF release - external ventricular drain
What pCO2 do you aim for post TBI?
4.5; not too high as to increase ICP further but not so low as to reduce blood flow to the brain
What head position should all patients post TBI be placed at?
30 degrees
What is the last option in increased ICP if there is no surgical management and everything has been done to manage it medically?
Decompressive craniectomy
What is the consequence of loss of autoregulation of BP seen in TBI?
Direct changes in BP will directly influence the cerebral blood flow
What is every 10 kcal/kg decrease in caloric intake associated with in TBI?
30-40% increase in mortality rate
What are the different mechanisms of DAI?
Stretched axon
Sheared axon
Twisted axon
Compressed axon
What are the toxic effects of DAI?
Excitotoxicity
Apoptosis
Inflammatory mediator release
Where is DAI most likely to happen?
Grey/ white interface
What is the basic pathogenesis of excitotoxicity?
Increased glutamate release
Activates NMDA receptors
Calcium mediated activation of proteases and lipases
Secondary cell death
Which interleukin is released in TBI?
6- acute phase and fever
What should you ensure before attempting to carry out a brainstem assessment?
No drugs that will alter consciousness
Normothermic; cannot perform on a hypothermic patient, need to be warm
No severe metabolic or endocrine disrutbances
What is carried out in a brainstem death assessment?
No pupillary response No corneal reflex No gag reflex No VOR No motor response No respiration
How is respiration assessed in brainstem death?
Pre-oxygenate
Look for a change in pCO2 levels
Must rise to 6 pKa for it to be a positive test of lack of respiration
How many doctors need to carry out a brainstem death assessment?
2 - at least one a consultant
When is time of death recorded in brainstem death?
1st set of tests positive
2nd set is confirmatory
