Skull And Head Injury Flashcards
What GCS corresponds to what head injury severity
Mild 14-15
Moderate 9-13
Severe 8 and lower
What skull fracture pattern would you expect in a motor vehicle incident involving a helmet wearer
Multiple linear fractures due to forces being spread out across the skull
What are the categories of traumatic head injury
Focal - haematoma and contusion
Diffuse - concussion and DAI
What is the most common base of skull fracture
Longitudinal fracture of the petrous part of the temporal bone
Describe the signs seen in base of skull fractures and relate them to the location
Anterior cranial fossa - racoon eyes, CSF rhinorrhoea, optic nerve damage
Middle cranial fossa - CSF ottorhoea, haemotympanum, Battles sign
Describe that pathophysiology of racoon eyes
Bleeding from venous sinuses tracks down but is stopped by the orbital septum leading to tarsal sparing
What is the pathway of CSF to leak out of the nose?
Leaks into the paranasal sinuses (particularly ethmoid) and from here to the nasal cavity
OR
Could be coming from the middle ear via the Eustachian tube
How do we test that “CSF” is in fact CSF
Look for Halo sign
Bedside test is glucose
Can also test for B2 transferin
What vessel damage leads to Battles sign?
Posterior auricular (branch of external carotid)
What is often the first base of skull fracture sign?
Haemotympanum
What other structures are you also worried about due to their association with base of skull fractures
C-spine
Vertebral arteries
How would you investigate a base of skull fracture
Non-contrast CT which will show a fracture and also pneumocephalus
CTA to assess for vascular injury
Compare a longitudinal vs transverse petrous temporal bone fracture in terms of incidence, nerve damage and hearing loss
Longitudinal occurs 80% of the time and is associate with conductive hearing loss (TM perforation)
Transverse occurs 20% of the time and can leads to facial nerve injury and sensorineural hearing loss (vestibulocochlear nerve injury)
What bones form the jugular foramen
Petrous part of the temporal bone
Occipital
What causes a jugular foramen fracture
Axial compression
What is the contents of the jugular foramen
Internal jugular vein
CN 9,10,11
How does a jugular foramen fracture present
Vernets syndrome which essentially describes damage to CN 9,10,11 so loss of gag reflex, hoarse voice, SCM and trapezius paralysis
What are the complications of a jugular foramen fracture
Internal jugular or dural venous sinus thrombosis
Compare the MOI, bleeding source, presentation and CT signs of extradural vs subdural haematoma s
Extradural: acceleration/deceleration or blow to pterion leads to an arterial bleed often from middle meningeal but can be DVS. Patient often has a lucid interval. CT shows a hyperdense bioconvex area (due to limitation of suture lines)
Subdural: acceleration/deceleration or blunt trauma leads to bleeding from cortical bridging veins which are more taught in the elderly and alcoholics so more prone to stretching and tearing. Presentation is often slower and can look like an evolving stroke. CT shows a hyperdense cresent
Describe the course of the middle meningeal artery
Arises from the first part of the maxillary artery (branch of external carotid) and travels through foramen spinosum.
The anterior division runs anterio-superiorly on the greater wing of sphenoid and under the pterion making a groove in the bone
The posterior division runs horizontally posterior
What do the cortical bridging veins connect?
Drain neural tissue into the dural venous sinuses therefore crossing the subdural space
What are the most common berry aneurysm locations
Junction of anterior cerebral and anterior communicating
Bifurcation of middle cerebral artery
Junction of internal carotid and posterior communicating
What are risk factors for berry aneurysm rupture
Cocaine, PKD, Ehlers-Danlos, HTN, hypercholestrolaemia
Describe the bleeding source, presentation and CT results for a SAH
Berry aneurysm rupture, AV malformation, direct traumatic damage to small arteries and veins
Thunderclap headache often occipital in location, meningism, Terson’s syndrome (vitreous haemorrhage)
CT shows hyperdense sulci and basal cisterns
State the cause of a posterior fossa bleed
Occipital fracture leading to dural venous sinus bleed
Describe the time frame of a posterior fossa bleed
Presentation can be delayed (normally a venous bleed)
But once it presents, patients often deteriorate quickly as the posterior fossa is enclosed and crowded so susceptible to RICP
How would a posterior fossa bleed present
Pons and medulla compressed = reduced GCS and ventilatory failure
4th ventricle compressed = hydrocephalus
Lower CN’s compressed = loss of gag reflex
Cerebellum compressed = DANISH
What is a cerebral contusion
Small vessel leakage and microhaemorrhages leading to oedema and RICP
The pia-arachnoid membranes are not torn
You get a coup (directly under the site of impact) and contrecoup (impact from the opposing surface as the brain bounces off) injury
What is the most common location of a cerebral contusion and why
Inferior surface of the frontal and temporal lobes as they sit on bony and ridgy surfaces
What is a cerebral laceration
Similar to a contusion other than that the pia-arachnoid membranes are torn
What is diffuse axonal injury
Shearing of the grey-white matter interface leading to Wallarian-degeneration distal to the axonal tear as well as a cascade of events including protein accumulation, transport interruption and the spread of cell death
What is the MOI causing DAI
Acceleration-deceleration leading to shearing forces
How does DAI present
Patients will initially appear fine before deteriorating later
Doesn’t show up on imaging
It is impossible to tell the difference between DAI and hypoxic damage
What is a concussion
Transient change to mental status and consciousness without structural damage following a closed head injury
In rotational forces on the brain, which areas are subjected to high strain
Due to the brains fixed attachments (neck, falx etc) this means that the corpus colosum, internal capsule and fornix are most at risk
What are some signs and symptoms of a concussion
Headache, memory loss, foggy head, cognitive slowing lasting for weeks to a month
What are the 2 types of posturing and the respective lesion location that causes them
Decorticate - lesion above the red nucleus
Decerebrate - lesion below the red nucleus
Red nucleus is located in the midbrain
Describe the pathophysiology behind the signs of decorticate posturing
Disinhibition of the rubrospinal tracts gives upper limb flexion with hands forming a fist
Disruption of lateral corticospinal tracts (supplying lower limb flexors) leads to unopposed extension of legs (done by vestibulospinal tracts)
Describe the pathophysiology leading to the signs of decerebrate posturing
Disruption of rubrospinal tracts leads to unopposed upper limb extension (reticulospinal tracts)
Disruption of corticospinal tracts (lower limb flexion) leads to unopposed lower limb extension (vestibulospinal tracts)
What would progression from decorticate to decerebrate posturing indicate
Uncal or tonsilar herniation
What would you include in a focussed neurological examination
GCS Pupils and extra-ocular movements Gross limb movements Breathing patterns Auscultation of carotids C-spine assessment
Describe the parts of GCS
Eyes 1) no eye opening 2) eye opening to pain 3) eye opening to voice 4) spontaneous eye opening Voice 1) non verbal 2)incomprehensible sounds 3) inappropriate words 4) confused 5) orientated Motor 1) no movement 2) extension to pain 3) flexion to pain 4) withdraws from pain 5) localising pain 6) obey commands
What are the indications for an adult head CT
GCS less than 13 on arrival
GCS less than 15 2 hours after the injury
Vomiting more than once
Seizure
Focal neurological deficit
Suspected base of, open or depressed skull fracture
What is a secondary brain injury and some examples
Evolving pathophysiological consequences of the primary injury due to a number of neurobiological cascades
Eg RICP, hypoxia, seizures, infection, hydrocephalus, hypercapnia
Why do seizures worsen RICP
High metabolic demand so increased blood flow so further RICP
Describe the Monro-Kellie hypothesis
Volume (x axis) vs pressure (y-axis)
The skull is a fixed space. As volume begins to rise, compensatory mechanisms can kick in such as compression of ventricles. However when volume reaches a certain point, these mechanisms are no longer enough and pressure begins to rise. This reduces cerebral perfusion pressure and causes ischaemia
How is cerebral perfusion pressure calculated
Mean arterial pressure - intracranial pressure
Briefly describe the 2 types of cerebral oedema
Cytotoxic (cellular) - movement is extracellular to intracellular
Vasogenic - movement is intravascular to interstitial
What is malignant MCA
Neurological deterioration due to cerebral oedema following a MCA territory stroke
How does malignant MCA present differently to the effects of normal cerebral oedema and why
Cerebral oedema consequences normally present on day 2-4
Malignant MCA presents within 24 hours (younger patients with less brain atrophy so less compensatory space)
Briefly describe the types of brain herniation syndromes
Subfalcine - cingulate gyrus pushed under the free edge of falx
Uncal - uncus of the temporal lobe pushed under the free edge of tentorium cerebelli
Tonsilar - cerebellar tonsils pushed through foramen magnum
How does a subfalcine herniation present
Contralateral leg weakness due to compression of the anterior cerebral artery
How does an uncal herniation present
Ipsilateral pupil dilated and eye in down and out position due to CN3 compression
Ipsilateral diplopia on horizontal gaze due to CN compression
Reduced GCS due to reticular formation compression
Contralateral homonomous hemianopia with macula sparing due to posterior cerebral artery compression
Ipsilateral hemiparesis due to compression of contralateral descending motor tracts
How does a tonsilar herniation present
Respiratory and cardiac depression due to compression of cardio-resp centres in the brainstem
Ataxia
Occipital headache
Why do you get vomiting in RICP
Compression of the chemoreceptor trigger zone in the medulla
Why do you get papilloedema in RICP
The optic nerve is covered in dura which is continuous with that of the brain so RICP communicates
Compression of veins in the sheath leads to reduced venous return and therefore oedema
What is cushings reflex and its pathophysiology
Pressure on the brainstem stimulates the sympathetics causing raised BP
Carotid sinus detects this and increases the vagal tone leading to reduced HR
Ischaemia of respiratory centres leads to bradypnoea
What are duret haemorrhages
Due to stretching of the pontine arteries following herniation syndromes
How is RICP managed
Raise the head of the bed to 30
Hyperventilate to blow off CO2 leading to vasoconstriction
Mannitol
Manage pain, glucose, sodium and temperature
Why don’t Burr holes tend to work
Consistency of blood is clotted so won’t come out via the small hole
What causes venous sinus thrombosis in trauma
Skull fracture that extends to the DVS
Haemoatoma or oedema compressing the sinus
Endothelial injury activating the clotting cascade
Extension of a thrombus from injured emissary veins
How does cavernous sinus thrombosis present
Ophthalmoplegia (6 first then 3 ad 4) Proptosis Chemosis Sensory loss in V1/2 distribution Horners syndrome - sympathetics hitchhike of ICA and abducens
What is commotio medularis
Sudden death of an intoxicated patient following a mild-moderate blunt force head injury due to ethanol’s effects on the cardioresp centres
What 2 mechanisms can leads to a carotid artery dissection and what are the 2 possible outcomes
Direct trauma to the neck or neck hyperextension (deceleration incident) leading to a stretching of the ICA over vertebrae
Leads to an intimal tear with blood entering the space
The haematoma narrows the actual lumen leading to occlusion and ischaemia or there is clot formation with an emboli breaking free and causing an infarct
How does a carotid artery dissection present
Often asymptomatic until the cerebrovacsular ischaemia but can have
Neck pain
Ipsilateral horners syndrome (sympathetics hitchike)
Pulsatile tinnitus
Syncope
What are the causes of pupil dilation in trauma
Herniation leading to CN3 compression
Brainstem ischaemia due to reduced blood flow
Anoxia
Describe the types of skull fracture
Linear
Depressed
Ping pong - no fracture just a depression
Diastatic - along the suture lines
Growing - non healing fracture widens and brain herniates
Why is paediatric head injury more serious
Lack of fully developed paranasal sinuses so less buffering
Thinner bones
Larger head to torso ratio
Inability to maintain body temperature
Why are extradural haematomas rare in children
Dura is tightly attached to periosteum
Describe the location of the fluid in caput secundum, subgaleal haemorrhage and cephalhaematoma
Caput - soft puffy swelling between skin and aponeurosis
Subgaleal - blood between aponeurosis and periosteum
Cephalhaematoma - blood between periosteum and boney skull
Describe the features of an anterior cerebral artery stroke
Hemiparesis affecting the leg more
Incontinence
Split brain
Memory, motivation and empathy affected due to cingulate cortex
Describe the features of a middle cerebral artery stroke
Hemiparesis affecting the arm more
Aphasia (broca or wernike depending if frontal or temporal lobe)
Contralateral homonomous hemianopia
Hemispatial neglect
Describe the features of a posterior cerebral artery stroke
CN3 affected due to oedema post stroke! (WB)
Contralateral homonomous hemianopia with macula sparing
Hemisensory loss due to thalamus involvement
Brainstem or cerebellar syndrome
Describe the features of a vertebral artery stroke
DANISH
Which side does a stroke commonly cause aphasia
Left sided stroke
Damage to where causes a conductive aphasia
Arcuate fasiculus
Gold standard imaging for a stroke
Non-contrast CT
What is the management of a stroke
Thrombolyse with Alteplase within 4.5 hours
Aspirin 300mg for 2 weeks
Clopidogrel 75mg for life
What are the layers of the scalp
Skin, connective tissue, aponeurosis, loose areolar connective tissue, periosteum
Which direction of scalp laceration is more severe and why?
Coronal - the two bellies of the occipitofrontalis muscle contract and full apart the aponeurosis
Why do scalp lacerations bleed profusely?
Many anastamoses
Vessels tightly adhered to dense CT so can’t vasoconstrict
Opposing pull of occipitalis and frontalis
Rich blood supply in order to nourish hair follicles
What is a complication of a scalp laceration and how does this occur?
Cavernous sinus thrombosis due to infection spreading from the angular vein via valveless ophthalmic veins to the sinus
What is the blood supply to the scalp
From external carotid: occipital, posterior auricular and superficial temporal
From internal carotid: supratrochlea and supraorbital branch of ophthalmic
Where does the anterior meningeal artery originate
Internal carotid - ophthalmic - ethmoid
Where does the middle meningeal artery originate
External carotid - maxillary
+ accessory meningeal artery also branches off maxillary but travels through foramen ovale not spinosum
Where does the posterior meningeal artery originate
External carotid - ascending pharyngeal (through jugular foramen)
+ 3 branches from ascending pharyngeal (through hypoglossal canal), occipital (through jugular foramen) and vertebral (through foramen magnum)
Describe the passage of CSF though the ventricles
Lateral - interventricular foramen - 3rd - cerebral aqueduct - 4th
What is an arachnoid villi/granulation
Protrusion of arachnoid mater into the DVS allowing CSF to exit the subarachnoid space and drain into the DVS
What are the funtions of the ventricular system and CSF
Shock absorber
Decrease the weight of the brain
Waste removal, nourishment and chemical signalling
How much CSF is produced per day
450ml
