Pathology and Surgery on head injuries Flashcards
(88 cards)
1
Q
Classify traumatic brain injuries
A
Focal
- scalp lacerations
- lacerations/contusions
- skull fracture - general, basilar,comminuted, linear,depressed
- intracranial haemorrhage
- focal lesions sec to raised intracranial pressure
Diffuse
- global ischaemic injury
- diffuse vasular injury
- traumatic axonal injury
- brain swelling
2
Q
Describe different types of skull fractures
A
General
-caused by a break in the bones in the skull due to HEAD INJURY
-a/w dissection of cerebral arteries
-fragments may cause
;bruising of brain(contusion)/
laceration
;damage to blood vessels
;intracranial haematomas
;epidural haematomas
Comminuted
multiple fragments of bone which can be driven into brain
Linear- 89% of pts - most common
;widely distributed forces
;growing fracture - brain
swelling
;diastatic features: sep of bones at sutures, wall trauma
Depressed - 11% , very serious
comminuted fractures ; thus bones displaced inwards can cause raised ICP and crushing of delicate tissue. Dura mater is torn- complex- surgery indicated
Basilar - rare CSF in eyes or nose CSF rhinorrhea, otohrrea battle's sign-blood clot behind ear raccoon eyes haemotympanum-blood in tympanic membrane cranial nerve palsy 1-10% ; entrapment of ocular nerve
3
Q
Which skull fracture are you likely to get meningitis?
A
Basilar
4
Q
Which skull fracture is a/w a particular haematoma?
A
general - epidural haematoma
5
Q
Define contusion
A
bruising or the brain
6
Q
What occurs in a contusion?
A
- damage to small blood vessels causing haemorrhage
- pia mater intact overlying contusions
- May become larger as a result of further haemorrhage; may cause rapid clinical deterioration in conscious patients in the absence of further haemorrhage.
7
Q
Typical areas a contusion occurs at?
A
frontal lobes and inferior aspect
temporal lobes and inferior and lateral aspect
cortex above and below Sylvian fissure
8
Q
Define sylvian fissure?
A
The groove that sections off the temporal lobe
9
Q
Define FRACTURE contusions
A
Pieces of bones/fractures of the skull become displaced and directly insult the brain tissue
10
Q
What are the typical areas involved in fracture contusions
A
Superficial injuries- apex of gyri this grey area is involved
Can go to white matter
11
Q
What is formed when a fracture contusion enters white matter
A
haematoma
12
Q
Define coup injury/contrecoup injury
A
When the contusion is as a result of impact (acceleration/deceleration) eg fall- injury may occur under pt of impact or distant to pt of impact
13
Q
What is the proposed mechanism of pts with contusions?
A
pts become coagulopathic post traumatic injury (45% pts) - further microvascular haemorrhage (delayed/continuous)
Frank rupture of vessels at time of injury occurs sec to forces initiating molecular change that causes structural change in vessels.
14
Q
When does delayed traumatic intracerebral haematoma occur?
A
48 hrs after injury
15
Q
What drug exacerbates contusional haemorrhage?
A
Mannitol can transiently increase cerebral blood flow and has been suggested to exacerbate delayed contusional haemorrhage.
16
Q
Classify intracranial haemorrhages
A
Intracranial haemorrhages are classified by anatomical location:
• Extradural /epidural (EDH), subdural (SDH), subarachnoid (SAH) or intracerebral (ICH)
a/w lucid interval in pts- clinical deterioration esp in EDH w/ minimal primary brain injury
17
Q
What are the factors that determine the clinical complications of a haematoma?
A
size/volume of the lesion, the anatomical location, and the rapidity with which the haematoma develops
18
Q
What type of injury is EDH most associated with?
A
skull fracture - 98%
linear
19
Q
Define EDH
A
- blood in extradural space due to falls, RTAs, assaults (from most common to least)
- two types: Arterial, venous EDH
20
Q
Which type of EDH shows symptoms first?
A
Arterial(middle meningeal artery) - develops over hours
(Venous EDH develops over hours to days)- middle meningeal vein
21
Q
What is a common mechanism that causes the damage to the a/ artery and vein in EDH
A
fracture of the squamous temporal bone that results in damage to the underlying middle meningeal artery or vein.- 50%
22
Q
What are the macroscopic/microscopic features of the EDH?
A
- Extradural bleeding strips the dura (periosteum) from the inner table of the skull, forming a circumscribed ovoid blood clot that progressively flattens and indents the adjacent brain.
- Biconvex due to attachment of dura to skull sutures
- focal ischaemic injury seen in most fatal cases
23
Q
What are some RARE, non traumatic causes of EDH?
A
paracranial infections, coagulopathies (both acquired and congenital), vascular malformations and neoplastic conditions, including metastatic disease
24
Q
Where else can EDH be seen and how does it present?
A
fire related deaths
- pink foamy lesions
- a/w heat related fissuring of skull
- mechanism unknown
25
Treatment for extradural haematoma
emergency craniotomy
26
Define subdural haematoma
collection of blood (mostly venous) in subdural space(between dura and arachanoid)
can be acute/chronic
27
Common causes of acute subdural haematoma
seen after falls/assaults
ASDH may be due to rupture of a bridging vein, the so-called ‘pure’ subdural haematoma, or secondary to contusions with damage to cortical veins or arteries and overlying leptomeninges
28
Prognosis of ASDH
high overall mortality; 30–50 % for ASDH and a good outcome in about 30–50 % of cases
29
What is the key factor in determining outcome of ASDH
Key factor in determining outcome is the extent of associated parenchymal pathology, particularly contusions and brain swelling.
30
Macro/Microscopic appearance of ASDH
covers entire cerebral surface
crescent shaped - With large lesions, there is deformation of the underlying cerebral hemisphere, often with accentuation of the gyral pattern on the same side as the haematoma, and flattening of the gyri on the contralateral side.
a/w parenchymal injury
31
Tx of ASDH
emergency craniotomy
32
What other conditions may cause SDH
- neurosurgical complications
- metabolic disorders-menkes disease, galactosaemia, glutaric aciduria
- perinatal-complication of labour
- coagulation-both inherited and acquired, haematological malignancies
- hypernatraemia/severe dehydration
- cardiac malformation
- cerebrovenous sinus thrombosis
33
How does ASDH present on post mortem
as soon as dura is reflected ASDH pours out
34
What is a sequalae of ASDH
- can become a subacute subdural haematoma due to organization and resorption of the haematoma
- by 12 months haematoma has resolved and resembles normal dura
- in children, resolves spontaneously
35
Define chronic SDH
- a separate entity
- refers to the formation of a thick-walled membrane encasing altered blood, prone to rebleeding and having a high incidence of recurrence
- often follows a relatively trivial head injury (and having risk factors)
36
Risk factors for chronic SDH
coagulopathy, arachnoid cysts, neurosurgical shunts, metastatic carcinoma and long-term dialysis, therapeutic anticoagulation (major risk factor), alcoholism
37
Treatment of chronic SDH
Early burr hole drainage in the presence of raised ICP or lateralising signs
38
What are subarachanoid haemorrhages typically a/w?
contusions and lacerations which cause damage to cortical vessels mainly veins that cause bleeding in subarachanoid space
39
Describe traumatic SAH
Traumatic SAH a/w higher ICP and worse clinical prognosis
massive basal tSAH related to vertebral artery damage (Caused by a blow in neck(Assault) in otherwise healthy male)
Mechanism: hyperextension of the neck + rise intra-arterial pressure due to blow
40
Define traumatic intracerebral haemorrhage
parenchymal brain haematoma that does not extend through the cortical surface into the subarachnoid space.
41
Pathogenesis of traumatic ICH
Pathogenesis unclear - rupture of a parenchymal blood vessel at the time of injury, with immediate haemorrhage
Excludes contusions and the haemorrhagic progression in contusions- severe outcome
42
What are common types of intracerebral haemorrhage?and how does it come about?
traumatic basal ganglia haematoma - happens due to RTAs commonly
- outcome poor; majority dying
traumatic intraventricular haemorrhage a/w (high energy impact) RTAS aka angular acceleration forces .
In some cases, it represented the extension of a parenchymal haematoma into the ventricle or retrograde spread of subarachnoid blood from the infratentorial structures.
haemorrhage could be form structures in the periventricular region aka fornix, septum pellucidum, subependymal veins in ventricular walls , choroid plexus or damaged corpus callosum
43
What is a common condition that likely contributes to haemorrhage post traumatic injury?
cerebral amyloid angiopathy- makes vessels stiffer and more prone to bleed
44
Tx of intracerebral haemorrhage
Usually conservative but evacuation of haematoma in the presence of raised ICP or marked midline shift
45
What else is intracerebral haematoma a/w?
diffuse axonal injury
subdural haematoma
contusions?
46
Describe features of diffuse axonal injury DAI
Account For 35 % Of All Fatal Head Injuries
Prolonged Unconsciousness In The Absence Of A Mass Lesion
Petechial haemorrhage
Basal cisterns effaced
Ventricles compressed
Sulci invisible
Loss of grey/white differentiation
47
How do you manage DAI?
conservation, decompressive craneiectomy
48
Features of penetrating injuries
1/3 Have a vascular injury
1/3 Result In Infection
Universally fatal if crossing
midline
49
Management of penetrating injuries
wound debridement
removal of foreign body
angiography
50
Consequences of increased ICP ?
herniation
| reduced cerebral perfusion
51
How is cerebral perfusion pressure calculated?
CPP = MAP – ICP
MAP = diastolic + 1/3 pulse pressure
52
What is normal ICP?
| What pressure is a/w brain dysfunction? Fatal?
0-10 mmHg
>40mmHg, >60 mmHg
53
What the specific pathologies that occur with increased ICP sec to brain injury?
- subfalcine herniation- most common where cingulate gyrus herniates into falx cerebri
- tentorial herniation
- diffuse TAI
- axial/ caudal displacement
- tonsillar herniation
- reverse herniation
- diencephalic and pituitary injury
54
What is the body's compensatory mechanism when there is an increase in ICP? What is the result when the mechanism fails?
increase in systolic blood pressure to maintain cerebral perfusion pressure (CPP) . however when compensatory mechanism is exhausted- increase in ICP, decrease in CPP which causes a stop in cerebral blood flow - tissue hypoxia - increase in pCO2 and decrease in Ph- cerebral vasodilation and oedema
55
Discuss effects of blunt force injury / diffuse injury ischaemia
This causes ischaemia of the brain- reduced blood flow relative to demand- causing decreased energy for neuronal population. This injures the neurons and also other cells (glial,smooth muscle and endothelial)-> pan necrosis aka infarction
Histologically necrosis seen as cytoplasmic eosinophila and change requires a survival of several hours
56
Discuss diffuse traumatic axonal injury (DAI) to the brain
DAI occurs secondary to trauma, metabolic encephalopathies like hypoglycaemic encephalopathies,MS, ischaemia or infection
-major cause of vegetative state and severe disability after TBI
It is a/w TBI w/o ischaemia, mass lesion and immediate loss of consciousness that lasts for more than a brief period
TBI classified by loss of consciousness
mild - 6-24 hrs unconscious
mod and severe- >24hrs
severe also shows -motor and posturing deficits
57
Pathogenesis of traumatic diffuse axonal injury
Trauma disrupts the normal axonal flow - axonal swelling = axonal varicosities = axonal ‘retraction’ bulb
15-18 hrs axonal bulbs can be identified
The axonal pathology evolves over at least 24 hrs and then plateaus, remaining easily identifiable for about 10–14 days after injury, after
58
What is the best marker for identifying disruption in axonal flow?
How long does this marker take to present in children vs adults
beta-APP
β-APP accumulation in paediatric cases 35–45 mins after TBI and 35 mins after TBI in adults
by 3–4 weeks after injury β-APP immunoreactivity is difficult to identify.
59
Causes of diffuse traumatic axonal injury
high velocity forces - rotational forces(Strong rotation of head) which can be due to RTAs, falls from heights and assaults
60
Discuss the outcome of traumatic diffuse axonal injury
Only a minority of axons undergo primary axotomy (cutting of axon); majority damaged as a consequence of focal axolemmal perturbations (axonal plasma membrane rupture) and degenerating over a period of time after the initial insult.
Most of the axonal damage is secondary and delayed.
61
What is rotational injury typically a./w?
haemorrhagic lesions; shearing of blood vessels causing perivascular haemorrhages
62
What is the most common cause of death in traumatic brain injury?
increased ICP and brain swelling
63
What is the mechanism for brain swelling ?
- oedema
- congestion
Focal or diffuse and is mostly due to oedema, an increase in the water content of the brain tissue, and congestion, an increase in the cerebral blood volume, with oedema accounting for most brain swelling
64
How is oedema described?
cytotoxic - abnormal water retention by injured cells
vasogenic-blood–brain barrier (BBB) breakdown leads to the passage of plasma proteins and water into the extracellular compartment
hydrocephalic(or interstitial) - increased intraventricular pressure, CSF is forced from the ventricle into the periventricular extracellular space
65
Different types of brain swelling and a/ conditions
Focal=contusions, ICH
| Diffuse (within one cerebral hemisphere)=ASDH
66
What occurs after ASDH is removed surgically?
swelling may still be present - due to combo of non reactive vascular bed and local ischaemic injury
67
Describe brain swelling seen on autopsy
flattening of the gyri, sulcal compression, ventricular compression and midline shift if the swelling is unilateral
68
Describe brain stem injury
Causes
Main path finding
Brain stem lesions are common, being seen in 60% of patients with severe TBI in one MRI study.
Causes: Severe form of the diffuse traumatic axonal injury – FTBSI - complex fall from height, accelerated fall, assault or severe impact on the top of the head.•Contusions and lacerations of the brain stem may be seen as a consequence of skull fractures around the foramen magnum, sometimes seen in the setting of extreme hyperextension
•Main pathological finding = haemorrhage in the brain stem.
69
What typically occurs in severe hyperextension?
In severe hyperextension of the neck, partial or complete pontomedullary or cervicomedullary avulsion can occur. They are mostly related to road traffic accidents, and are seen particularly in pedestrians rather than in those in the vehicle, or in motorcyclists involved in accidents. Die immediately
70
What predicts survival in a spinal cord injury
age of injury
neurological symptoms at time of injury
extent of injury
71
Examples of spinal cord injuries (SCI)
spinal EDH
spinal SDH
cranial SDH that migrates to spine
closed SCI
72
Non traumatic causes of spinal EDH and SDH
coagulopathy, neoplasms, vascular malformations and therapeutic procedures
73
Describe closed SCI
most common
due to hyperflexion/hyperextension , rotational movement(causes fracture dislocations a/w thoracocolumbar lesions) , compressive forces(eg fall from height landing on top of skull)
74
Define concussion
immediate, usually reversible episode of brain dysfunction after TBI, typically, but not always, with sudden brief impairment of consciousness and loss of memory.
75
Describe spectrum of concussion
Mildest form of TBI, part of a clinical spectrum ranging from mild concussion, in which consciousness is often preserved, to severe diffuse TAI resulting in the vegetative state.
76
What are the proposed pathogeneses a/w concussions
vascular, reticular, centripetal, pontine cholinergic and convulsive
Transient dysfunction of the neuron or may be associated with structural changes
77
When are concussions typically seen?
Repetitive head injury is a particular concern within contact sports such as boxing, rugby, American football, Australian rules football and ice hockey
78
Define second impact syndrome
rare, but fatal
complication of mTBI in young athletes who have a second impact before the effects of an initial impact have fully resolved
79
Pathology of second impact syndrome
Pathology includes thin-film ASDH and ‘malignant’ brain swelling possibly due to cerebral blood flow dysautoregulation and massive hyperaemia and, in some cases, a combination of both
80
Long term consequence of brain injury
* Vegetative State
* Loss of meaningful cognitive function and awareness in patients who retain spontaneous breathing and periods of wakefulness
* repetitive injury a/w neurodegeneration
* chronic post concussion syndrome
* post traumatic epilepsy -Incidence higher if post-traumatic amnesia>24 hours, intracranial haematoma, depressed skull fracture, penetrating injury
81
What causes vegetative state?
Damage to the thalamic nuclei and/or the afferent and efferent white matter pathways of the thalamus appear to play a major role in the genesis of the vegetative state after head injury
82
How does chronic post concussion syndrome present?
impaired attention, poor memory, and irritability persisting for years after mTB and chronic traumatic encephalopathy (CTE), a presumed neurodegenerative condition with behavioural, cognitive and/or motor symptoms
a/w premorbid anxiety and depression
RARE
83
How does repetitive head injury present?
CTE and a/ symptoms
Neuropathology of repetitive head injury described Tau-immunoreactive neurofibrillary tangles and neuropil threads, particularly around blood vessels.
84
What is seen in secondary brain injury?
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systemic effects
HYPOXIA
HYPOTENSION
HYPERCAPNIA
HYPERTHERMIA
POOR GLYCAEMIC CONTROL
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intracranial effects
BRAIN SWELLING
BRAIN SHIFT & HERNIATION
RAISED ICP
POST - TRAUMATIC FITS
INTRACRANIAL INFECTION
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prevention of sec brain injury can prevent death
85
How do you assess/manage brain injuries initially?
ABC
5-10% have associated c-spine injury
Early anaesthetic involvement
Rapid transfer to NSU
Glasglow Coma score - assessment of coma and impaired consciousness
(best eye response,best verbal response, best motor response)
86
List the medical management of a brain injured pt
Head position - 30° head up
Mannitol
Frusemide
Hypertonic saline
87
Anaethesia management?
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paralysis
sedation
hyperventilation-temp mechanism to avoid herniation (lower oCo2 - cerebral vasoconstriction)
analgesia
hypothermia
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88
Surgical management of brain injured pt
ICP bolt
Removal of causative pathology – clot/tumour/swollen brain, etc
EVD-extra ventricular drain
Decompressive craniectomy
