Traumatic brain injuries Flashcards
Which patients are at highest risk of morbidity and mortality from traumatic brain injury?
- The elderly (risk of falls, cerebral atrophy)
- Infants (large head size, compressible skull, risk of non-accidental injury)
- Patients with a bleeding diathesis (e.g. on warfarin)
- Chronic alcoholics (at risk of falls and assaults, cerebral atrophy, coagulopathy due to chronic liver disease)
How is the severity of traumatic brain injury classified on initial assesment?
Assesment using the glasgow coma scale
- Minor = GCS 13-15
- Moderate = GCS 9-12
- Severe = GCS <8
What are the two types of brain injury and define each
Primary injury
- occurs at the time of the initial traumatic event, and may be focal or diffuse.
- Focal injuries include hematomas, contusions and lacerations resulting from blunt or penetrating trauma.
- Diffuse injuries typically result from acceleration-deceleration forces and affect the whole brain resulting in axonal shearing or concussion.
Secondary injury
- is potentially preventable and reversible, and occurs after the time injury.
- Mechanisms of injury include oedema, hypoxia, hypotension, and metabolic disturbanc
What is the monro-kellie doctrine ?
The Monro-Kellie doctrine holds that the brain lies within a rigid box (the cranium). In addition to brain, within the rigid box there is blood and cerebrospinal fluid (CSF). As a result, expansion of the volume of any of the components must be offset by an equal decrease in volume of the others or intracranial pressure will increase.
The compensatory capacity within the non-compliant cranium is limited. The capacity for CSF to displace into the spinal theca and into the venous system via arachnoid granules, and intracranial blood to redistribute peripherally is easily overcome. This usually occurs with mass lesions of about 100 to 120 Mls, and when it does intracranial pressure increases linearly.
Implications for treatment of TBI?
The implication for management of traumatic brain injury is that space is at a premium, and aggressive treatment to control the volume of intracranial contents is essential to prevent raised intracranial pressure which can lead to compression of vital brain structures, impaired blood flow to the brain and ultimately death.
Name the types of brain herniation on this diagram
- Subfalcine herniation - thick sheet of dura mater separates right and left hemispheres. Singulates gyrus herniates loops underneath falx cerebri and brings one of the lateral ventricles with it and is shown as midline shift on CT. Leads to traction and tension on the circle of willis –> could present as stroke syndrome
- Trans tentorial herniation - See next card
- Tonsilar herniation/ Coning - the posterior cranial fossa can run out of space really quickly. Medial and inferior section of cerebellum is known as the tonsil. Herniation of the tonsil causes pressure on the medulla (through foramen magnum) which contains cardiac and respiratory centre. Patient can die very quickly
Trans tentorial herniation signs
- tentorium cerebelli covers over posterior cranial fossa separating the cerebellum on the bottom and the cerebral hemispheres on top.
- Brainstem runs through the middle. When ICP is raised occulomotor nerve is squeezed and pupil will be dilated. Parasympatheic part lies on the outside of the nerve so they are affected first as somatic motor fibres are on the inside. therefore, Pupil involvement before eye movement issues.
- Pressure on corticospinal tracts results in contralateral hemiparesis
What is cerebral perfusion pressure and how does raised intracranial pressure impair blood flow to the brain?
Cerebral prefusion pressure = mean arterial pressure- intracranial pressure
CPP= MAP - ICP
Blood, flows from high to low pressure. Hence raised ICP decreases the pressure gradient favouring blood flow to the brain. Hence CPP is used as a surrogate marker of cerebral blood flow. It also follows that to maintain blood flow to the brain in the presence of raised intracranial pressure, and increased driving pressure (i,e mean arterial pressure) is required.
How is the concept of cerebral autoregulation relevant to traumatic brain injury?
- cerebral blood flow should increased with increased MAP
- this is not the case because of cerebral autoregulation
- the normal brain used compensatory mechansism to preserve constant cerebral flow over a range of tolerable MAPS (60-150mmhg)
- CBF will fall when the MAP is below the range of autoregulation, and rise when the MAP is above the range of autoregulation
- the injured brain is unable to perform cerebral autoregulation
- as a result CBF is directly dependent on MAP resulting in the dashed linear curve shown above.
- Thus optimize of MAP is critically important in the management of STBI
What are the common indications for a head CT in TBI
- GCS <13
- GCS <15 post-injury
- Age >65 years
- Bleeding diathesis or on anticoagulants or antiplatelet agents
- Focal neurology
- Suspected open or depressed skull fracture
- Evidence of basal skull fracture
- Vomiting > 1 episode
- Retrograde amnesia >30 minutes
- Dangerous mechanism (e.g. pedestrian versus vehicle, fall >1m or 5 stairs, ejected from motor vehicle)
What is the name of the CT clinical decision rules for TBI?
Canadian CT head rules
- used in patients with a GCS 13-15 with witnessed LOC, amnesia to the head injury event or confusion
- High risk
- GCS <15 at 2 hours post injury
- suspected open or depressed skull fracture
- any sign of basilar skull fracture
- >2 episodes of vomitting
- Age >65
- medium risk
- retrografe amesia to the event >30 mins
- dangeous mechanism (pediestrian struck by motor vehicle. occupant ejected from motor vehicle, fall from >3 feet or 5 stairs
rule not appicalble if
- non trauma cases
- GCS <13
- <16 years
- bleeding disorder
- obvious open skull fracture
management of patient with severe TBI in ED
- activate the trauma team
- remove patient from a rigid spine board as soon as possible by transferring to trauma bed
primary survey and resuscitaiton (ABCDE)
Airway
- intubate - if GCS <8
- avoid nasopharyngeal airways due to risk of intracranial passage
- maintain cervical spine precautions
Breathing
- high flow oxygen 15 litres via a non-rebreather mask
circulation with haemorrhage protocol
- target MAP of 70mmHg to maintain adequate CPP
- avoid permissive hypotension
Disability
- assess GCS, pupils, motor and sensory functions inall limbs prior to sedation or intubaition
- suspect critically raised intracranial pressure if: Cushings response (bradycardia, hypertension, apneas), fixed and dilated [upils, hemiparesis
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Clinical signs of basal skull fracture
- haemotympanum
- racoon eyes - bruising around the eyes
- battles sign- bruising of the mastoid process of the temporal bone
- CSF otor+/- rhinorrhea
History key points
- mechanism of injury
- time of injury
- LOC/amnesia
- subsequent symptoms - headache, nausea, vomitting, limb weakness, parasthesia, diplopliia, rhinorrhoea, otorrhoea
- PMH- particularly those that might of caused the head injury (cardiac arrhythmias, epilepsy, diabetes), remember to ask about previous head ijury
- DH - recent alcohol and drug injestion, anticoagulants
- SH - before contemplating discharge there needs to be a responsible adult at home
- tetanus status - if there is any wounds consider need for tetanus prophylaxis
head inuury examination
- cervical spine injury
- glasgow coma scale
- vital signs - BP, pulse, and respiratory rate
- BMG
- alcohol
- eye signs - pupil size, and reaction to light. Unilaterally pupillary dilation - raised ICP. Eye movements and the presence of diploplia or nystagmus.
