Head Injury, Bleeds & Coma Flashcards
- Closed (concussional)
- or open (penetrating or blunt);
- acceleration, deceleration
- or rotational
What are these all types of?
Head injury!
Closed (concussional) or open (penetrating or blunt); acceleration, deceleration or rotational injury
What order incidence do these causes of head injuries with 1 being the top cause and 4 being the last –>.
Assault, falls, alcohol, RTA?
- Alcohol: 65%
- Assault: 30-50%,
- Falls: 22-45%
- RTA: 25% (more severe injuries),
What injury do these signs point to?
- haemotympanum,
- panda eyes (periorbital),
- CSF from ear/nose,
- Battle’s sign
SIGNS OF A BASAL SKULL FRACTURE
- Battle’s sign = bruising behind ears
- haemotympanum = blood in middle ear e.g. behind eardrum
What injuries type mostly occur to the scalp?
- simple penetrating injuries,
- debridement
- & suture
Damage to the anterior, middle and posterior fossa of the skull produce different symptoms.
Damage to which fossa produces these signs/symptoms?
- orbital haematoma,
- bleeding from the ear,
- CSF otorrhoea,
- CN 7,8 palsy including deafness
Middle fossa
- greater wing of sphenoid, temporal bone
Damage to the anterior, middle and posterior fossa of the skull produce different symptoms.
Damage to which fossa produces these signs/symptoms?
- nasal bleeding,
- orbital haematoma,
- CSF rhinorrhoea (rich in glucose, low mucin, +ve for tau protein),
- CN 1-6 palsy including anosmia,
- aerocele in paranasal sinuses
anterior fossa damage
- frontal, ethmoid, lesser wing of sphenoid
Damage to the anterior, middle and posterior fossa of the skull produce different symptoms.
Damage to which fossa produces these signs/symptoms?
- Battle’s sign (bruising behind ears)
- CN 9-12 palsy
- occipital
Posterior fossa!
How can you tell there is an orbital haematoma e.g. # of anterior and middle cranial fossa?
NB: it is hard to distinguish an orbital haematoma from a black eye…
- Subconjunctival haemorrhage (with no posterior limit)
- Absence of grazing of surrounding skin
- Confined to the margin of orbit (black eye involves surrounding cheek)
- Mild exophthalmos (anterior eye bulging)
- Degree of ophthalmoplegia
- Bilateral haematoma
A patient presents with nasal discharge that is
- Worse on bending forwards
- Doesn’t stiffen handkerchief’s/tissue
- Halo sign
- Can’t sniff it back up
What Ix should be done?
this is ?CSF rihinorrhoea
- Ix:
- Beta-2 transferrin level (gold standard)
- & glucose (bedside test) level (as after halo test e.g. just shows is CSF, glucose is also found in blood)
- –>Send to hospital
What is the worst type of shearing force and what does it cause?
rotational shearing forces (e.g. acel and decel) causes diffuse axonal injury
–> axon damage & rupture of small vessels
shearing through brainstem = fatal
How do you get “parenchymal contusion” of the brain define?
e.g. brain bruise
- this is focal rather than diffuse intra-axial problem
- e.g. parenchymal contusion = brain bruise
- –> focal injury can happen as brain hits the skull
-
get coup and contre-coup
- Coup: direct impact of brain on the skull at the site of injury e.g. frontal/ temporal lobes
- Contre-coup: injury from brain rebounding of opposite part of skull e.g. occipital lobe
- (e.g. as brain is like jelly in a solid box)
-
get coup and contre-coup
What can occur a spenoid ridge?
e.g. on sphenoid ridge can get:
Laceration within the skull -
- brain impinges on sharp of bony edge within the skull
Extra axial = lesions outside the brain
what can occur there for primary brain injury?
Bleeds!
- Cerebral oedema,
- ischaemia,
- infarction,
- herniation,
- hydrocephalus,
- SIADH
- cerebral salt wasting
are all types of what brain injury?
secondary brain inury!
- 1o brain injury occurs during initial insult e.g. intra- and extra-axial –> the displacement of physical structures of the brain
- vs
- 2o brain injury is NOT causes by by mechanical damage it –> it can result from 1o ijury or be independent of it… e.g.
- Cerebral oedema, ischaemia, infarction, herniation, hydrocephalus, SAH and traumatic brain injury
What type of secondary head injury is blown pupils a sign of?
Herniation
(e.g. apparently from uncal herniation - The key clinical sign of uncal herniation is ipsilateral oculomotor nerve palsy with a fixed and dilated pupil due to compression by the medial temporal lobe.)
After an intra-cerebral / intra-axial bleed what 2o injury can you get?
hydrocephalus
What 2o injury can traumatic brain injury lead to?
syndrome of inappropriate ADH (or anterior hypopituitarism, rarely)
–> causes retention of too much water & hyponatraemia
- Hyponatraemia due to SIADH commonly occurs after TBI, but is usually mild and transient.
- Chronic (dilution) hyponatraemia due to SIADH following TBI is a rare but important complication.
- It likely results from damage to the pituitary stalk or posterior pituitary causing inappropriate non-osmotic hypersecretion of ADH.
- NB: ADH is secreted from hypothalamus
what complication can sub arachnoid haemorrhage (1o injury comp.) lead to?
Cerebral salt wasting
- hyponatraemia
- extracellular fluid depletion due to inappropirate sodium wasing in the urine
How is cerebral perfusion pressure (CPP) defined?
cerebral perfusion pressure =
mean arterial pressure (MAP) - intracranial pressure (ICP)
What is cushings reflex?
the opposite of sepsis so is reflex INCREASE in BP and dc in HR
from
↑ICP + hypotension –> ↓cerebral blood flow → detected by cardiorespiratory centres in floor of 4th ventricle → the Cushing’s reflex - reflex increase in BP & bradycardia
What can be used to treat post traumatic cerebral oedema?
- Also (as well as inc. ICP and hypotension decreaseing cerebral BF –> cushings reflex to inc BP and bradycardia)
- hypercapnia causes cerebral vasodilation,
- –> in the presence of oedema this may further raise ICP
- & exacerbate brain injury
therapeutic hyperventilation & hypocapnia is used to treat post-traumatic cerebral oedema
What are the signs of all brain bleeds
e.g. including extradural, subdural, subarachnoid and intracerebral?
Cushing’s reflex:
- raised intracranial pressure,
- hypertension (to over come the high Cerebral perfusion pressure)
- reflex bradycardia (terminal sign :( - neither due to high BP triggering aortic arch baroreceptors or compressing intracranial vagal nerve)
Signs of raised intracranial pressure:
- papilledema on fundoscopy,
- pupil dilation (surgical oculomotor nerve palsy - normally constricts pupil)
What is an AVM?
aka Arteriovenous malformation?
- A Tangle of abnormal vessels
- range from telangiectasia –> cavernous & venous malformations
- often with arteriovenous fistulae;
- common over the distribution of the MCA
What problems/complications can an arteriovenous malformation cause?
- focal epilepsy,
- headaches,
- slowly progressive paralysis,
- SAH/intracerebral bleed
- Bruit can be heard over the eye, skull vault or carotid arteries
- Sturge-Weber syndrome:
- Cortical malformations
AVM can cause sturge-weber syndrome
- what is this?
-
port-wine stain
- localized to one or more segments of the cutaneous distn of the trigeminal nerve (V1,V2,V3)
- with corresponding extensive venous angioma; m
- ay cause contralateral focal fits
How do you investigate AVM?
cerebral angiography
(uses x ray and contrast to show blockages/other abnormalities in brain if cerebral etc)
What is the Rx for AVM?
- surgery OR
-
stereotactic radiography (gamma Knife)
- e.g. non-surgical radiation therapy used to treat functional abnormalities and small tumors of the brain. It can deliver precisely-targeted radiation in fewer high-dose treatments than traditional therapy, which can help preserve healthy tissue
Brain injury can result in abnormal posturing via damage to one or both corticospinal tracts or to the upper brainstem (e.g. midbrain and pons).
If there is damage to one or both corticospinal tracts (cortex–>LMN in spinal cord) what abnormal posturing do you get?
(in both of the damaged the ankles are plantarflexed and legs stiffly extended)
Decorticate
means flexors predominate in the upper limb
- arms are adducted, internally rotates and FLEXED to lie across chest
- wrist and fingers are flexed
- legs are stiffly extended
- ankles plantarflexed (pointed toes)
The lesion happening before the red nucleus = rubrospinal intact means flexors in upper limb predominate
Brain injury can result in abnormal posturing via damage to one or both corticospinal tracts or to the upper brainstem (e.g. midbrain and pons).
If there is damage to the upper brainstem e.g. midbrain and PONs what abnormal posturing do you get?
(in both of the damaged the ankles are plantarflexed and legs stiffly extended)
Decerebrate
(CENTRAL TEGMENTAL TRACT DAMAGE)
- damage to upper brain stem (midbrain, pons)
-
extensors predominate (vestibulospinal)
- Arms adducted, extended, internally rotated
- Wrists pronated & fingers flexed
- Legs stiffly extended
- Ankles plantar flexed
What should be asked in a head injury history?
- How? mechanism of injury,
- condition before/during/after/changes since
associated syx:
- headache,
- LOC,
- N&V,
- visual disturbance,
- seizures,
- amnesia
What can you check O/E for a head injury?
- ABC,
- GCS,
- c-spine,
- full CNS examination
- ? ipsilateral CN3 palsy + loss of light reflex (cerebral oedema)
- consensual reaction in tact initially but lost as compression increases -
- bilateral fixed & dilated pupils is a very late sign
- ? ipsilateral CN3 palsy + loss of light reflex (cerebral oedema)
What investigations should be done for ?head injury?
- ABCDE assessment
- Bloods - U&E look @hyponatriemia –> SIADH (following Trauma B.I. causing pituitary problems)
- XR - skull & c-spine
- CTH +/- CTA (if indicated)(CT angiography = stroke)
- LP –> MC&S, spectrophotometry, xanthochromia - (SAH) or traumatic tap
- Angiograph (DSA- digital subtraction angiography) for SAH
- referral to neurosurg
A patient experiencing any one of these is elidgible for what?
- GCS <13 at any point after injury, GCS <15 at 2hrs post-injury
- Suspected open or depressed skull fracture
- Any sign of basal skull fracture
- Post-traumatic seizure
- Focal neurological deficit
- >1 episode of vomiting
An immediate CT head
A patient experiencing any of these (below) is eligable for what?
- Amnesia for >30mins of events before impact
- Age ≥65yrs,
- coagulopathy/bleeding disorder/WARFARIN,
- dangerous mechanism of injury provided that some loss of consciousness or amnesia has been experienced
a CT head
within 8hrs of injury
A patient experiencing any of these symptoms (below) is eligable for what?
- Major intracranial injury (extradural haematoma, moderate/large subdural ICH)
- Progressive focal neurological signs
- Definite or suspected penetrating head injury
- CSF leak or base of skull fracture
- Persisting coma (GCS≤8) after initial resuscitation or deterioration in GCS score after admission
A referral to neurosurgery…
What should be written in a neurosurgery referral?
- Brief history and other injuries
- GCS
- Neurological examination
- Medical history
- Anticoagulation
- Scans – transferred and reported
In the management of head injury there are things you should watch out for (e.g. complications) things to observe (obs), conservative, medical and early/delayed indication for surgery.
What should be watched for when managing head injury e.g. to prevent complications?
- increasing cerebral oedema,
- ICH (extradural, subdural, intracerebral),
- hypoxia,
- infection,
- hydrocephalus,
- hyper-pyrexia,
- post-concussional syndrome weeks-months of headaches/dizziness)
- amnesia,
- epilepsy
In the management of head injury there are things you should watch out for (e.g. complications) things to observe (obs), conservative, medical and early/delayed indication for surgery.
What should be OBSERVED for when managing head injury? e.g. what observations do you do?
- GCS
- pupil size & responses
- vitals
- ICP monitoring via catheter placed within ventricles
What is the conservative Rx of head injury?
- MAINTAIN PHYSIOLOGY
- oxygenation,
- BP,
- anti-convulsant’s,
- fluid & electrolyte management
- +/- ICP monitoring (catheter placed within ventricles)
- ICP monitoring appropriate if GCS 3-8 and normal CT
- ICP monitoring mandatory if GCS 3-8 and abnormal CT scan
What is the medical management of head injury?
IV mannitol/frusemide
(mannitol = decrease pressure in eyes and to lower raised ICP)
What type of indication for neurosurgery of a head injury are these?
scalp lacerations, surgical toilet of a compound #, decompression & evacuation of haematoma
early indication for neurosurgery:
- scalp lacerations,
- surgical toilet of a compound # e.g. cleaning, irrigation and debridement,
- decompression &
- evacuation of haematoma
What type of indication for neurosurgery are these?
repair of dural tear with CSF rhinorrhoea, late repair of skull defects, late plastic surgery for deforming facial injuries
delayed indication of neursurgery
- repair of dural tear with CSF rhinorrhoea,
- late repair of skull defects,
- late plastic surgery for deforming facial injuries
What kind of brain bleed can a blunt head trauma causing arterial bleeding cause?
e.g. RTA, falls, assault
the majority of these blunt head traumas occuring with associated skull # and scalp haematomas
Extra-dural
brain bleed
What symptoms can a
- Blunt head trauma causing arterial bleeding e.g. middle meningeal artery
- Road traffic accidents, falls, assault
- The majority occur with associated skull fractures and scalp haematomas
- —-> e.g. extradural bleed
cause?
Symptoms:
- -“Talk & die” – a brief loss of consciousness after injury followed by a lucid period
- -headache
- -vomiting
- -confusion
- -seizures
- -focal neurology
Signs:
- -boggy scalp haematoma
- -dilated pupils
- –> death can result from rapidly rising intra-cranial pressure
What does this CT scan show?
- Extradural haematoma
- Convex pool of bright white acute blood which does not cross the suture lines
- Can cause substantial midline shift
If you saw this CT what is the managment?
- NEUROSURGICAL EMERGENCY –> Mannitol IVI whole being transferred
- bone flap or burr-hole over suspected site,
- evacuate clot,
- control bleeding
- diathermy,
- silver clips,
- under-running
What kind of brain bleed can be caused by acute or chronic trauma e.g.
- Acute – trauma causing shearing of bridging veins
- e.g. acceleration/ deceleration of road traffic accidents, falls, assaults
- Chronic – trivial injury in elderly,
- patients on anticoagulation or alcoholic patients months or weeks before causing a small tear in a cerebral vein (low-pressure venous bleed)
- *paeds shaken baby syndrome (fragile bridging veins)
sub-dural brain bleed!
(e.g. between dura and arachnoid)
What kind of symptoms would you get after a trauma such as:
Acute – trauma causing shearing of bridging veins e.g. acceleration/ deceleration of road traffic accidents, falls, assaults
Chronic – trivial injury in elderly, patients on anticoagulation or alcoholic patients months or weeks before causing a small tear in a cerebral vein (low-pressure venous bleed)
*paeds shaken baby syndrome (fragile bridging veins)
e.g. subdural (dura-arachnoid) brain bleed?
-
Slowly progressive & fluctuating symptoms
- also delayed in chronic subdural bleeds:
- progressive mental deterioration
- drowsiness progressing to coma
- focal neurology (e.g. hemiplegia)
- headache
- vomiting
- also delayed in chronic subdural bleeds:
What does this CT scan show?
Subdural haematoma!
- Semilunar, crescentic collection
- bright white if acute blood – hypERdense,
- dark if chronic blood – hypOdense
- Blood can cross suture lines and cause midline shift
- NB: unlike extradural which cannot cross suture lines
You see a patient with this on their CTH, what is your management?
- Acute -
- release of clot through craniotomy but outcome poor due to severity of underlying brain trauma
- Chronic - (e.g. from elderly pt/anti coag small cerebral vein tear)
- release of clot or fluid collection through burr-holes
What kind of brain bleed can be caused by trauma or non trauma (see below)?
- Traumatic –
- trauma,
- skull fractures,
- Traumatic brain injury
- Non-traumatic -
- Arterial aneurysm rupture
- Acomm > Pcomm > MCA/carotid siphon
- Congenital “weak area”, atherosclerosis, local high flow, trauma, infection (mycotic aneurysms)
- Associations: PKD, Ehler’s-Danlos, CoA
- AVM, arterial dissection, vasculitis, pituitary apoplexy, idiopathic (peri-mesencephalic)
- Arterial aneurysm rupture
subarachnoid bleeds
CSF in is in the subarachnoid space between arachnoid-pia
What presentation/ signs/symptoms do you expect with this presentation?
- Traumatic –
- trauma,
- skull fractures,
- Traumatic brain injury
- Non-traumatic - Arterial aneurysm rupture
- Acomm > Pcomm > MCA/carotid siphon
- Congenital “weak area”, atherosclerosis, local high flow, trauma, infection (mycotic aneurysms)
- Associations: PKD, Ehler’s-Danlos, CoA
- AVM, arterial dissection, vasculitis, pituitary apoplexy, idiopathic (peri-mesencephalic)
From a subarachnoid haemorrhage:
- -Acute onset thunderclap headache (occipital or unilateral)
- -LOC then wake (arterial rupture but when ICP > systolic BP bleeding is tamponaded) –> coma
- N&V
- seizures
- Meningism (headache, nuchal rigidity/neck stiffness, photophobia - haemosiderin is an irritant)
- positive Kernig’s sign (flexion of hip with extension of leg causes pain - meningeal irritation)
- focal neurology (e.g. caused by aneurysm)
- SAH –> cerebral salt wasting –> hyponatraemia
What does this CT scan show?
What Ix should be done?
- Bright white acute blood in the subarachnoid space,
- sulci and cisterns
- Often see hydrocephalus and some blood in the ventricles.
If there is Blood in ventricles & sulci – do LP 12hrs after onset if CT clear → xanthochromia (blood in CSF has yellow tinge)
What is the management of this CT?
(if aneurysm?)
(depends on cause of the SAH - AVM, dissection, vasculitis etc)
Until treated, strict bed rest, well controlled BP & avoid straining
- Intracranial aneurysms –> coil (minority require a craniotomy & clipping)
Main goal of surgery is to prevent re-bleeds:
-
Vasospasm prevention –> 21-day course of nimodipine 60mg 4hrly oral/ng (calcium channel blocker),
- also to prevent vasospasm = dont want hypervolaemia, induced-hypertension and haemodilution
- Hydrocephalus –> external ventricular drain or LT VP shunt
Rx hyponatraemia with fluid restriction
*re-bleeding is most worrying complication
What brain bleed type is caused by these (see below)?
- HTN damage to blood vessels e.g. perforating lenticulostriate arteries,
- Cerebral Amyloid Arthropathy (amyloid build up in brain artery walls), micro-aneurysms, anticoagulation, bleeding disorder, tumours, trauma or no underlying cause
intracerebral
(lobar, thalamic, pontine, cerebellar etc)
What symptoms do you expect to see from bleed by those causes below?
- HTN damage to blood vessels e.g. perforating lenticulostriate arteries,
- Cerebral Amyloid Arthropathy (amyloid build up in brain artery walls), micro-aneurysms, anticoagulation, bleeding disorder, tumours, trauma or no underlying cause
- Progression over minutes to hours:
- -impaired consciousness (the others dont have these)
- -focal neurology (e.g. hemiplegia)
- -headache
- -nausea and vomiting
What does this CTH show?
intracerebral haemorrhage
- Patches of bright white acute blood within the cortex
- which are well demarcated and odd shapes
- Can see intraventricular extension of bleeds
A pt has this CT head and presents with
Progression of syx over minutes to hours: impaired consciousness, focal neurology (e.g. hemiplegia), headache, nausea and vomiting . What is the Rx?
for intracerebral bleed: Optimise physiology –>
Surgical Rx: young, superficial bleeds, // critically raised ICP, major deficit
- CBM - brainstem compression, hydrocephalus - SURGERY, pts do well :)
- Lobar -surgery SIMPLER
- :( –>
- Brainstem - very bad will probably will die anyway
- Basal Ganglia –> too much eloquent brain to go through
Central nervous system problems are a common cause of coma. What specifically about the CNS can cause coma?
- Trauma
- Disease e.g.
- CerebroVascularAccident,
- epilepsy,
- SAH,
- tumour,
- abscess,
- meningitis
Central nervous system problems & drugs/toxins are a common cause of coma.
What drugs/toxins can cause coma?
- Alcohol
- Carbon monoxide
- Medical ones:
- Barbiturates,
- aspirin,
- opiates etc.
are all drugs/toxins that can cause coma.
Central nervous system problems, drugs/toxins & diabetes are a common cause of coma.
How can diabetes cause coma?
- hyperglycaemia
- hypoglycaemia
Central nervous system problems, drugs/toxins, diabetes are a common cause of coma.
What else in general can cause coma?
- Uraemia
- Hepatic failure
- Hypertensive encephalopathy
- Profound toxaemia
- Hysteria (old-fashioned term for a psychological disorder characterized by conversion of psychological stress into physical symptoms)
(so these + drugs/toxins, diabetes and CNS problems)
What is the definition of brain death?
After how long of asystole can it be defined & what needs to be absent?
Death of whole brain, including the brain stem i.e. loss of all brainstem reflexes & spontaneous respiration
Death can be diagnosed after 5 minutes of continuous asystole; all brain-stem reflexes should be absent
In order to diagnose brain death you need to exclude what other causes/differentials? e.g. reversible things that could improve brain function
- hypothermia,
- intoxication,
- sedative drugs,
- NMJ blocking drugs,
- severe electrolyte & acid-base abnormalities
In order to diagnose brain death you need to exclude:
hypothermia, intoxication, sedative drugs, NMJ blocking drugs, severe electrolyte & acid-base abnormalities
what evidence do you need to look at in order to exclude these?
-
Hypothermia
- Core temperature >34oc
-
Intoxication, sedative drugs
- Sufficient time since ingestion/drug withdrawal
-
Exclusion of neuromuscular block or injury
- Tendon reflexes present, or electrically confirmed
-
Severe electrolyte or endocrine abnormality (mmol/L)
- Sodium 115-160, potassium >3, phosphate & magnesium 0.5-3.0, glucose 3-20
-
Severe acid-base or respiratory disturbance
- pH normal, PaCO2 <6, PaO2 >10
-
Hypotension
- Mean arterial BP >60mmHg
Once you have excluded causes for coma, to be able to diagnose brain death you need to check the brain stem reflexes are absent (after death can be dx after 5m of continuous asystole).
What reflexes/responses need to be looked at?
What needs to be included in you Ix for brain death?
Include: a clearly identified cause of death (EEG, CTH, LP)
Brain injury is suspected to have caused irreversible loss of capacity for consciousness, and for respiration
- Deep coma of known aetiology
- Reversible causes excluded
- No sedation
- Normal electrolytes
Pt in a coma on a ventilator (brain death testing only possible in patients who are on mechanical ventilation)
- No respiratory movements when patient disconnected from mechanical ventilator (for long enough for PCO2 to be above stimulating threshold, >6.65kPa)
Reflexes
- Pupils fixed & dilated
- No corneal reflex
- No vestibulo-occular (dolls eye) reflexes - when head is passively turned, the eyes remain fixed relative to head
- No caloric reflexes - slow injection of 20mL ice-cold water into each ear, if no eye movements considered +ve
- No motor responses within cranial nerve distribution elicited by adequate stimulation
- No gag reflex - suction catheter passed down trachea
Formal brainstem testing involves checking:
- absent brainstem reflexes,
- absent motor response,
- absent respiratory effort
- apnoea testing (ensure no spontaneous effort to breathe e.g. otherwise would mean brainstem is alive)
THEN repeat a second time after enough time has passed for blood gases & baseline parameters to have got back to normal after first apnoea test (if the person were alive)
How do you check absent brainstem reflexes/motor response/absent respiratory effort?
- Pupils fixed & dilated, unresponsive to light
- Absent VOR (50mls ice cold water to either ear)
- No motor response to supra-orbital pressure
- Absent corneal reflex
- No gag or cough reflex
Formal brainstem testing involves checking:
- absent brainstem reflexes,
- absent motor response,
- absent respiratory effort
- apnoea testing (ensure no spontaneous effort to breathe e.g. otherwise would mean brainstem is alive)
- THEN repeat a second time after enough time has passed for blood gases & baseline parameters to have got back to normal after first apnoea test (if the person were alive)
How do you conduct apnoea testing (to ensure no spontaneous effort to breathe)?
- Well oxygenated (100%)
- Stable starting Ph & PaCO2 <6
- Reduced RR to allow CO2 to rise >6.5
- Disconnect from ventilator
- Maintain oxygenation
- Wait for 5mins
