Trauma and CSF Flashcards
uses of GCS
preduct coma or other prognosis
diagnosis of coma
3 classes within GCS and which is the most important
eye opening
verbal response
motor - most important
classification within eye opening - GCS
4 - Spontaneous
3 - Verbal
2 - To pain
1 - None
classification within verbal response - GCS
5 - orientated 4 - confused 3 - inappropriate words 2 - incomprehensible sounds 1 - nothing
classification within motor response - GCS
6 - obeys 5 - localises to pain 4 - withdrawal to pain 3 - decorticate motor response 2 - decerebrate motor response 1 - unresponsive
what is decorticate positioning
severe damage to cerebrum, internal capsule and thalamus but midbrain spared
abnormal arm flexion, hands clenched to fist and legs extended with feet inwards
disturbance to lateral CST and hence rubrospinal causes abnormal UL flexion and reticulospinal causes leg extension
what is decrebrate positioning
severe brainstem damage, below the red nucleus
head arched back and arms and legs extrended
rubrospinal and lateral CST are compromised
reticulospinal tract takes over to lead to full body extension
describe CSF production in the brain
produced in the choroid plexus of the ventricles
flows from lateral ventricles to third ventricle by foramen of munro
flows through cerebral acqueduct/sylvius to reach 4th ventricle
circulates to SA space by formamen of magendie and luschka and absorbed by arachnoid granulations back to venous blood
what is the normal ICP
5-15mmHg
describe how the monroe kellie hypothesis may be compromised by increased ICP
brain autoregulates cerebral blood flow and so as ICP rises autoregulation becomes compromised
this leads to ischaemia, swelling and herniation
possible causes raised ICP?
SOL - tumour, haemorrhage, haematoma cerebral oedema - ischaemia, liver failure, hypercarbia CSF obstruciton IIH raised venous pressure
features of raised ICP
headache nausea and vomiting papilloedema drowsy cushings triad
what is cushings triad
hypertension
bradycardia
decreased respiration
what is uncal herniation and how may it present
medial temporal lobe herniation through tensorium
pupillary dilatation due to CN III compression
can compress pyramidal tracts to lead to contralateral hemiparesis
what is subfalcine herniation and how may it present
herniation of cingulate gyrus below falx
can lead to LL weakness due to compression of ACA
what is transcalvarial herniation
herniation through the skull
what is central herniation
descent of the diencephalon and midbrain
can lead to VI palsy and brainstem dysfunction
what is tonsillar herniation
displacement of cerebellar tonsils through foramen magnum
can be posterior fossa lesion or arnold chiari
medullary compression, neck stiffness, abnormal neck posture
cheyne stokes breathing
coma
death
what is an epidural haematoma and what is the usual cause
bleeding between dura and skull
MMA damage, usually temporoparietal skull fracture leading to damage to pterion
clinical features of an epidural haematoma
often a young adult with closed head trauma
brief loss consciousness, lucid interval and then deterioration with headache, vomiting, contralateral hemiparesis or ipsilateral pupil dilatation
imaging for epidural haematoma
CT with lens shapes appearance not crossing suture lines
possible mass effect and herniation
management of an epidural haematoma
immediate surgical evacuation if neuro deficit
if small can be managed conservatively if small and no neuro deficit
what is a subdural haematoma
bleeding below dura and above arachnoid mater
describe the features of an acute SDH
immediately symptomatic, often following head trauma
cerebral blood flow may be reduced so there is cerebral oedema and ischaemia
in acute cases presentatiob is a severely decreased state of consciousness
causes of chronic SDH
brain atrophy - age, dementia, alcohol
anticoagulation
inflammation, previous head trauma
describe how brain atrophy leads to SDH
as atrophy occurs bridging veins are stretched leading to bleeding
leaky vessels accumulate blood into SD space and osmotic gradient causes pull into space
features of a chronic SDH
headache confusion urinary incontinence weakness seizure cognitive dysfunction gait abnormality
imaging of SDH
CT
crescent shaped hyperdense if acute and hypodense if chronic
what is normal pressure hydrocephalus and what are possible causes
build up of CSF due to impaired resorption at arachnoid granulations or overproduction of CSF
usually idiopathic but can be secondary to trauma, haemorrhage, meningitis
clinical features of normal pressure hydrocephalus
apraxia - shuffling gait
reversible dementia
urinary incontinence
imaging and management of normal pressure hydrocephalus
massively enlarged ventricles
VP shunt, reserved for ventriculomegaly with severe symptoms or after marked improvement with CSF removal
what is communicating hydrocephalus
excess CSF in ventricles leading to enlarged ventricular system with no flow obstruction
impaired resorption by arachnoid granulations
what is non communicating hydrocephalus
excess CSF in ventricles due to obstruction of flow
usually determined as 4th ventricle is smaller than 3rd and lateral
causes are colloid cyst, stenosis of acqueduct, tumour
common causes of congenital hydrocephalus
acqueductal stenosis
spina bifida or arnold chiari
common causes of acquired hydrocephalus
tumour
infection
trauma
presentation of congenital hydrocephalus
fail to thrive dilated scalp veins increased head circumference sunsetting gaze impaired upgaze diplopia vomiting macewen sign
presentation of acquired hydrocephalus
headache - mostly morning vomiting diplopia impaired upgaze papilloedema drowsy incontinence gait anomaly
investigation of congenital hydrocephalus
detailed hx and antenatal hx with milestones
head circumference, full ophthalamic exam
palpate ant fontanelle
MRI is best but CT more available
management of hydrocephalus
CSF diversion
VP shunt or endoscopic third ventriculostomy - needs functional CSF absorption as drains to basal cistern so only for non-comms hydrocephalus
what is a Chiari I malformation
most common and least severe malformation
caudally displaced cerebellar tonsils below foramen magnum
signs and symptoms of a chiari I malformation
headache, esp on cough and neck extension and suboccipital pain
downbeat nystagmus
central cord symptoms - sensory loss of pain and temp and progressive paralysis starting with UL
ataxic gait
what is a chiari II malformation and what is it associated with
less common and more severe
more frequent in children and clear association with spina bifida
can lead to hydrocephalus
caudal displacemnt of cerebellum and medulla below foramen magnum with herniation of the 4th ventricle
signs and symptoms of chiari II malformation
severe brainstem dysfunction - apnoea, stridor, nystagmus, dysphagia
weakness progressingt o quadriplegia
management of chiari malformations
non surgical
operative depending on imaging or symptoms
suboccipital craniotomy and upper cervical laminectomy to decompress
what is IIH
raised ICP in absence of any SOL or hydrocephalus
more common in obese and female
presentation of IIH
headache worst in morning and relief by standing
moderate to gross bilateral papilloedema
nausea and vomiting
VI nerve palsy
investigation of IIH
CT/MRI may show slit like ventricles
visual field testing and fundoscopy
LP if not contraindicated
management of IIH
weight loss
LP shunt potentially
azetazolamide
head injury severity scale on GCS - mild
14/15
head injury severity scale on GCS - moderate
9-13
head injury severity scale on GCS - severe
<8
when to have a CT within an hour
GCS <13 GCS <15 post 2hr suspected open or depressed skull fracture signs of basal skull fracture post trauma seizure focal neuro deficit >1 episode vomiting NAI
when to have an immediate head CT
Loss of consciousness or amnesia and one of the following
>65, dangerous mechanism injury or coagulopathic
what is an intracerebral haematoma
bleeding in the brain substance
what is the coup/contracoup effect
head strikes a solid object but brain continues to move and strikes skull at the opposite side
what is a diffuse axonal injury
appears as small hyperdense areas at grey/white matter interface, brainstem or corpus callosum
shearing force damaging axon
LOC,
medical management of raised ICP
sedate max venous drainage Lower Co2 on intubation osmotic diuretica CSF release last ditch
sedatives for raised ICP
propofol
BZD
barbiturates
venous drainage options for raised ICP
cervical collar
head of bed tilt
loosen ETT ties
osmotic diuretics for raised ICP
mannitol
hypertonic saline
CSF release or last ditch options for raised ICP
external drain
hemicraniectomy
bifrontal craniectomy
describe the features of brainstem death on exam and requirements for it to be carried out
no drugs, hypothermia or metabolic disturbance
no pupil response, corneal reflex
no motor response
no vestubulo-ocular response
no gag or cough
no respiration
tested twice by two doctors and one must be a consultant
calculation of CPP
MAP-ICP
calculation of cerebral blood flow
CPP/vascular resistance
describe cerebral blood flow autoregulation
remainst constant under changing BP
regulation of vascular resistance
arterioles dilate in presence of lactate or CO2
pressure constriction/dilatation as needed
early features raised ICP
decreased consciousness headache pupil dysfunction ±papilloedema change in vision N&V
late features raised ICP
coma fixed and dilated pupils, unilateral then bilateral hemiplegia bradycardia, hypertension hyperthermia reduced urine output
who often gets normal pressure hydrocephalus
the elderly
