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Pathology and Surgery on head injuries Flashcards

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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
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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
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3
Q

Which skull fracture are you likely to get meningitis?

A

Basilar

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4
Q

Which skull fracture is a/w a particular haematoma?

A

general - epidural haematoma

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5
Q

Define contusion

A

bruising or the brain

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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.
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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

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8
Q

Define sylvian fissure?

A

The groove that sections off the temporal lobe

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9
Q

Define FRACTURE contusions

A

Pieces of bones/fractures of the skull become displaced and directly insult the brain tissue

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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

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11
Q

What is formed when a fracture contusion enters white matter

A

haematoma

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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

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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.

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14
Q

When does delayed traumatic intracerebral haematoma occur?

A

48 hrs after injury

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15
Q

What drug exacerbates contusional haemorrhage?

A

Mannitol can transiently increase cerebral blood flow and has been suggested to exacerbate delayed contusional haemorrhage.

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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

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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

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18
Q

What type of injury is EDH most associated with?

A

skull fracture - 98%

linear

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19
Q

Define EDH

A
  • blood in extradural space due to falls, RTAs, assaults (from most common to least)
  • two types: Arterial, venous EDH
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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

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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%

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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
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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

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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
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25
Q

Treatment for extradural haematoma

A

emergency craniotomy

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26
Q

Define subdural haematoma

A

collection of blood (mostly venous) in subdural space(between dura and arachanoid)
can be acute/chronic

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27
Q

Common causes of acute subdural haematoma

A

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

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28
Q

Prognosis of ASDH

A

high overall mortality; 30–50 % for ASDH and a good outcome in about 30–50 % of cases

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29
Q

What is the key factor in determining outcome of ASDH

A

Key factor in determining outcome is the extent of associated parenchymal pathology, particularly contusions and brain swelling.

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30
Q

Macro/Microscopic appearance of ASDH

A

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

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31
Q

Tx of ASDH

A

emergency craniotomy

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32
Q

What other conditions may cause SDH

A
  • 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
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33
Q

How does ASDH present on post mortem

A

as soon as dura is reflected ASDH pours out

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34
Q

What is a sequalae of ASDH

A
  • 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
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35
Q

Define chronic SDH

A
  • 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)
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36
Q

Risk factors for chronic SDH

A

coagulopathy, arachnoid cysts, neurosurgical shunts, metastatic carcinoma and long-term dialysis, therapeutic anticoagulation (major risk factor), alcoholism

37
Q

Treatment of chronic SDH

A

Early burr hole drainage in the presence of raised ICP or lateralising signs

38
Q

What are subarachanoid haemorrhages typically a/w?

A

contusions and lacerations which cause damage to cortical vessels mainly veins that cause bleeding in subarachanoid space

39
Q

Describe traumatic SAH

A

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
Q

Define traumatic intracerebral haemorrhage

A

parenchymal brain haematoma that does not extend through the cortical surface into the subarachnoid space.

41
Q

Pathogenesis of traumatic ICH

A

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
Q

What are common types of intracerebral haemorrhage?and how does it come about?

A

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
Q

What is a common condition that likely contributes to haemorrhage post traumatic injury?

A

cerebral amyloid angiopathy- makes vessels stiffer and more prone to bleed

44
Q

Tx of intracerebral haemorrhage

A

Usually conservative but evacuation of haematoma in the presence of raised ICP or marked midline shift

45
Q

What else is intracerebral haematoma a/w?

A

diffuse axonal injury
subdural haematoma
contusions?

46
Q

Describe features of diffuse axonal injury DAI

A

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
Q

How do you manage DAI?

A

conservation, decompressive craneiectomy

48
Q

Features of penetrating injuries

A

1/3 Have a vascular injury
1/3 Result In Infection
Universally fatal if crossing
midline

49
Q

Management of penetrating injuries

A

wound debridement
removal of foreign body
angiography

50
Q

Consequences of increased ICP ?

A

herniation

reduced cerebral perfusion

51
Q

How is cerebral perfusion pressure calculated?

A

CPP = MAP – ICP

MAP = diastolic + 1/3 pulse pressure

52
Q

What is normal ICP?

What pressure is a/w brain dysfunction? Fatal?

A

0-10 mmHg

> 40mmHg, >60 mmHg

53
Q

What the specific pathologies that occur with increased ICP sec to brain injury?

A
  • 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
Q

What is the body’s compensatory mechanism when there is an increase in ICP? What is the result when the mechanism fails?

A

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
Q

Discuss effects of blunt force injury / diffuse injury ischaemia

A

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
Q

Discuss diffuse traumatic axonal injury (DAI) to the brain

A

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
Q

Pathogenesis of traumatic diffuse axonal injury

A

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
Q

What is the best marker for identifying disruption in axonal flow?

How long does this marker take to present in children vs adults

A

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
Q

Causes of diffuse traumatic axonal injury

A

high velocity forces - rotational forces(Strong rotation of head) which can be due to RTAs, falls from heights and assaults

60
Q

Discuss the outcome of traumatic diffuse axonal injury

A

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
Q

What is rotational injury typically a./w?

A

haemorrhagic lesions; shearing of blood vessels causing perivascular haemorrhages

62
Q

What is the most common cause of death in traumatic brain injury?

A

increased ICP and brain swelling

63
Q

What is the mechanism for brain swelling ?

A
  • 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
Q

How is oedema described?

A

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
Q

Different types of brain swelling and a/ conditions

A

Focal=contusions, ICH

Diffuse (within one cerebral hemisphere)=ASDH

66
Q

What occurs after ASDH is removed surgically?

A

swelling may still be present - due to combo of non reactive vascular bed and local ischaemic injury

67
Q

Describe brain swelling seen on autopsy

A

flattening of the gyri, sulcal compression, ventricular compression and midline shift if the swelling is unilateral

68
Q

Describe brain stem injury
Causes
Main path finding

A

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
Q

What typically occurs in severe hyperextension?

A

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
Q

What predicts survival in a spinal cord injury

A

age of injury
neurological symptoms at time of injury
extent of injury

71
Q

Examples of spinal cord injuries (SCI)

A

spinal EDH
spinal SDH
cranial SDH that migrates to spine
closed SCI

72
Q

Non traumatic causes of spinal EDH and SDH

A

coagulopathy, neoplasms, vascular malformations and therapeutic procedures

73
Q

Describe closed SCI

A

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
Q

Define concussion

A

immediate, usually reversible episode of brain dysfunction after TBI, typically, but not always, with sudden brief impairment of consciousness and loss of memory.

75
Q

Describe spectrum of concussion

A

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
Q

What are the proposed pathogeneses a/w concussions

A

vascular, reticular, centripetal, pontine cholinergic and convulsive
Transient dysfunction of the neuron or may be associated with structural changes

77
Q

When are concussions typically seen?

A

Repetitive head injury is a particular concern within contact sports such as boxing, rugby, American football, Australian rules football and ice hockey

78
Q

Define second impact syndrome

A

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
Q

Pathology of second impact syndrome

A

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
Q

Long term consequence of brain injury

A
  • 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
Q

What causes vegetative state?

A

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
Q

How does chronic post concussion syndrome present?

A

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
Q

How does repetitive head injury present?

A

CTE and a/ symptoms
Neuropathology of repetitive head injury described Tau-immunoreactive neurofibrillary tangles and neuropil threads, particularly around blood vessels.

84
Q

What is seen in secondary brain injury?

A 
systemic effects
HYPOXIA
HYPOTENSION
HYPERCAPNIA
HYPERTHERMIA
POOR GLYCAEMIC CONTROL
intracranial effects
BRAIN SWELLING
BRAIN SHIFT & HERNIATION
RAISED ICP
POST - TRAUMATIC FITS
INTRACRANIAL INFECTION

prevention of sec brain injury can prevent death

85
Q

How do you assess/manage brain injuries initially?

A

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
Q

List the medical management of a brain injured pt

A

Head position - 30° head up

Mannitol

Frusemide

Hypertonic saline

87
Q

Anaethesia management?

A 
paralysis 
sedation
hyperventilation-temp mechanism to avoid herniation (lower oCo2 - cerebral vasoconstriction)
analgesia
hypothermia
88
Q

Surgical management of brain injured pt

A

ICP bolt

Removal of causative pathology – clot/tumour/swollen brain, etc

EVD-extra ventricular drain

Decompressive craniectomy

head injuries and brain tumors (2 decks)

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