Topic 1: Neurological Brain herniation: displacement of the brain
tissue due to increased ICP
1: Traumatic Brain Injuries (TBI)
Infection
Traumatic brain injury is a non-degenerative, - Due to external becoming in contact with
non-congenital insult to the brain from an internal.
external mechanical force. Possibly leading to - Causes inflammation of the brain & possibly
permanent or temporary impairment of swelling. Seizure risk.
cognitive, physical, and psychosocial
functions, with an associated diminished or Increased ICP & Cushing’s Triad
altered state of consciousness. 2. Signs and symptoms of increased ICP.
Death due to TBI can occur @ 3 points after Signs & symptoms of increased ICP
injury: Changed LOC
- Immediately after Bradycardia.
- 2hrs after Irregular respirations (dyspnoea).
- ≈ 3 weeks Widening pulse pressure.
Weakness/lethargy,
TBI victims who survives often suffer from Headache.
physical, psycho-social & psychological disabilities Vomiting
after injury. Blurred vision.
Behaviour changes.
Primary & Secondary Brain Injury Decerebrate/decorticate posturing.
1. How does secondary injury occur in TBI Abnormal pupils.
patient?
3. What signs and symptoms would indicate
Primary brain injury: cerebral damage Cushing’s Triad?
due to trauma at the time of injury.
- Irreversible (cannot be prevented/reduced. Cushing’s triad: set of signs indicative of
- Can be diffuse or focal. increased intracranial pressure (ICP).
Signs include (BDWPP):
Secondary brain injury: injury developing Bradycardia
post-trauma, that may result in extended Dyspnoea.
damage & diminished neurological Widened pulse pressure.
outcome.
- Preventable (can be reduced with appropriate The change in pressure causes ↓ in cerebral
management strategies) perfusion pressure (CPP).
- Can be within seconds-minutes-days after
When ICP > MAP brain can no
injury. longer receive enough O2.
- Can result due to intracranial or extracranial
changes.
Causes of Secondary Brain Injury
Increased ICP (above 5-15mmHg)
- Causing ischaemia due to compressing blood
vessels.
- Compresses brain tissue, can even displace
brain tissue.
- Worst complication – hence focus of tx.
NS2882 definition Property Drug/Intervention ① ② ③ ④ ↓ ↑ ∴ ≈ 💡
, Preventing secondary TBI’s Drug is also used for other diuretic therapies.
E.g., to correct low plasma osmolality after
Focus of TBI tx. = Secondary injury prevention dialysis
- Begins @ time of accident & continues
through all stages of care. During infusion MONITOR:
- Fluid & electrolyte status.
Tx involves:
- Controlling ICP.
Hypertonic Saline
- Maintain cerebral perfusion & oxygenation.
- Promoting neuroprotection
3% Saline – Osmotic agent.
- Mitigate long-term neurological deficits.
- Increases plasma osmolality (salt).
- Shifting fluid into the blood vessel & excretes
it.
Monroe Kelly hypothesis - Known to work just as well as mannitol.
4. Explain the Monroe-Kelly hypothesis.
During infusion MONITOR:
Monroe-Kelly hypothesis states that if one - Blood pressure.
component of ICP increases, one of the other - Serum sodium levels.
components decreases to maintain a constant
pressure. Note: patients will have ↑ urine output with both
mannitol & hypertonic saline.
3 components of ICP include:
- Brain tissue
- Blood
- Cerebrospinal fluid.
When balance disrupted and/or compensatory
mechanisms fail --> increased ICP can result.
Primary TBI – Diffuse & Focal
Diffuse injury: a primary brain injury that
Treatment of increased ICP cannot be localised to one area.
- Includes mild concussion & diffuse axonal
Mannitol injury.
Mannitol:
Concussion
- Osmotic diuretic (draws water out of brain)
Def. Concussion: sudden alteration/
- Reduces intercranial pressure.
transient LOC - mild to moderate TBI.
Given IV. Caused by trauma induced ‘bouncing’ of
Stays in the blood vessel – molecules are too the brain in the skull.
large. Takes water to excretion also.
NS2882 definition Property Drug/Intervention ① ② ③ ④ ↓ ↑ ∴ ≈ 💡
, DOES have temporary LOC.
NO evidence of brain damage with
diagnostic imaging in mild TBI.
Diffuse Axonal Injury
Def. Diffuse axonal injury: Rotational
movement of brain within the cranial
cavity due to the impact. Coup-Contrecoup brain injury opposite side
of the brain also injured due to the
Causes widespread neuronal damage due to impact/rebound = multiple contusion sites.
shearing of axons from high impact rotational
Also known as a polar injury.
force
2: TBI –Deterioration
Focal injury: injury that can be localised to a
specific area. Can include: The most important neurological assessment you
- Lacerations can do is a Glasgow Coma Scale (GCS).
- Contusions
- Intracranial hematoma Glasgow Coma Scale (GCS)
- Cranial nerve injuries (12 nerves – clinical 5. Explore in detail the three (3) neurological
signs depend on cranial nerve injured. responses assessed, scores and actions
needed – score.
Brain Lacerations
Def. Brain Laceration: tearing of the brain
tissue.
Often caused by:
- Comminuted fracture – skull fragment
scratches brain
- Penetrating injury
e.g., bullet.
Contusion
Def. zx
Classification of Brain injury according to GCS
May contain areas of
haemorrhage, infarction,
Classification of TBI GCS
necrosis &/or oedema.
Mild 13-15
Can be localised – but often seen on opposite Moderate 9-12
pole also due to rebound impact of head 3-8
(Coup-Contrecoup) causing multiple Severe *<8 unable to
contusion sites. maintain airway
-Below GCS 8 – intubation is required.
-ANY DROP in GCS requires urgent medical
review.
NS2882 definition Property Drug/Intervention ① ② ③ ④ ↓ ↑ ∴ ≈ 💡
, Decorticate Decerebrate
Drop > 2 points = MET Call Origin @ cortex Origin @ brainstem
Arms bended Arms extended.
Complications after Stroke Damage to cortical Caused by lesion to
Posturing – Decorticate & Decerebrate white matter midbrain, pons, or
6. Compare and contrast decorticate and diencephalon
decerebrate posturing.
3: The Skull (not on study guide).
Due to neurological damage, normal postural
control & tone can be disrupted.
Skull fractures
DecortiCate Rigidity 1. Describe the types of skull fractures.
Decorticate posturing: damage to cerebral Skull fractures are categorised by:
hemispheres damaging corticospinal tracts - Appearance.
from cortex which are in control of voluntary - Location.
motor movement. - Degree of depression.
Presents as:
Arms folded in Linear: break is a thin line without
Hands clenched in flexion + turned distortion/splintering of the bone.
inwards.
Feet & legs extended out. Comminuted: skull bone shatters into
multiple pieces.
DecereBrate rigidity - Risk of fragment scratching the brain (brain
laceration)
Decerebrate posturing: damage to the brain
stem & extrapyramidal tracts. Interferes with Depression: denting / caving-in of the brain
voluntary motor messages being delivered to due to trauma.
all limbs.
Diastatic: fracture occurring along the suture
More common that decorticate rigidity but lines.
poorer prognosis & survival rate.
Basal: bones at the base of the skull break.
Presents as:
Arms & legs straight out in extension
Toes pointed downward.
Head and neck extended backward.
Hands clenched & internally rotated.
Ecchymosis: a skin discoloration due to
extravasation of blood (pooling).
Tear in the meninges can also cause:
- CSF rhinorrhoea (escape through nose)
- CSF otorrhoea (escapes through ear)
CSF leak indicates risk of meningitis is high.
3 signs of basal skull fracture:
NS2882 definition Property Drug/Intervention ① ② ③ ④ ↓ ↑ ∴ ≈ 💡
tissue due to increased ICP
1: Traumatic Brain Injuries (TBI)
Infection
Traumatic brain injury is a non-degenerative, - Due to external becoming in contact with
non-congenital insult to the brain from an internal.
external mechanical force. Possibly leading to - Causes inflammation of the brain & possibly
permanent or temporary impairment of swelling. Seizure risk.
cognitive, physical, and psychosocial
functions, with an associated diminished or Increased ICP & Cushing’s Triad
altered state of consciousness. 2. Signs and symptoms of increased ICP.
Death due to TBI can occur @ 3 points after Signs & symptoms of increased ICP
injury: Changed LOC
- Immediately after Bradycardia.
- 2hrs after Irregular respirations (dyspnoea).
- ≈ 3 weeks Widening pulse pressure.
Weakness/lethargy,
TBI victims who survives often suffer from Headache.
physical, psycho-social & psychological disabilities Vomiting
after injury. Blurred vision.
Behaviour changes.
Primary & Secondary Brain Injury Decerebrate/decorticate posturing.
1. How does secondary injury occur in TBI Abnormal pupils.
patient?
3. What signs and symptoms would indicate
Primary brain injury: cerebral damage Cushing’s Triad?
due to trauma at the time of injury.
- Irreversible (cannot be prevented/reduced. Cushing’s triad: set of signs indicative of
- Can be diffuse or focal. increased intracranial pressure (ICP).
Signs include (BDWPP):
Secondary brain injury: injury developing Bradycardia
post-trauma, that may result in extended Dyspnoea.
damage & diminished neurological Widened pulse pressure.
outcome.
- Preventable (can be reduced with appropriate The change in pressure causes ↓ in cerebral
management strategies) perfusion pressure (CPP).
- Can be within seconds-minutes-days after
When ICP > MAP brain can no
injury. longer receive enough O2.
- Can result due to intracranial or extracranial
changes.
Causes of Secondary Brain Injury
Increased ICP (above 5-15mmHg)
- Causing ischaemia due to compressing blood
vessels.
- Compresses brain tissue, can even displace
brain tissue.
- Worst complication – hence focus of tx.
NS2882 definition Property Drug/Intervention ① ② ③ ④ ↓ ↑ ∴ ≈ 💡
, Preventing secondary TBI’s Drug is also used for other diuretic therapies.
E.g., to correct low plasma osmolality after
Focus of TBI tx. = Secondary injury prevention dialysis
- Begins @ time of accident & continues
through all stages of care. During infusion MONITOR:
- Fluid & electrolyte status.
Tx involves:
- Controlling ICP.
Hypertonic Saline
- Maintain cerebral perfusion & oxygenation.
- Promoting neuroprotection
3% Saline – Osmotic agent.
- Mitigate long-term neurological deficits.
- Increases plasma osmolality (salt).
- Shifting fluid into the blood vessel & excretes
it.
Monroe Kelly hypothesis - Known to work just as well as mannitol.
4. Explain the Monroe-Kelly hypothesis.
During infusion MONITOR:
Monroe-Kelly hypothesis states that if one - Blood pressure.
component of ICP increases, one of the other - Serum sodium levels.
components decreases to maintain a constant
pressure. Note: patients will have ↑ urine output with both
mannitol & hypertonic saline.
3 components of ICP include:
- Brain tissue
- Blood
- Cerebrospinal fluid.
When balance disrupted and/or compensatory
mechanisms fail --> increased ICP can result.
Primary TBI – Diffuse & Focal
Diffuse injury: a primary brain injury that
Treatment of increased ICP cannot be localised to one area.
- Includes mild concussion & diffuse axonal
Mannitol injury.
Mannitol:
Concussion
- Osmotic diuretic (draws water out of brain)
Def. Concussion: sudden alteration/
- Reduces intercranial pressure.
transient LOC - mild to moderate TBI.
Given IV. Caused by trauma induced ‘bouncing’ of
Stays in the blood vessel – molecules are too the brain in the skull.
large. Takes water to excretion also.
NS2882 definition Property Drug/Intervention ① ② ③ ④ ↓ ↑ ∴ ≈ 💡
, DOES have temporary LOC.
NO evidence of brain damage with
diagnostic imaging in mild TBI.
Diffuse Axonal Injury
Def. Diffuse axonal injury: Rotational
movement of brain within the cranial
cavity due to the impact. Coup-Contrecoup brain injury opposite side
of the brain also injured due to the
Causes widespread neuronal damage due to impact/rebound = multiple contusion sites.
shearing of axons from high impact rotational
Also known as a polar injury.
force
2: TBI –Deterioration
Focal injury: injury that can be localised to a
specific area. Can include: The most important neurological assessment you
- Lacerations can do is a Glasgow Coma Scale (GCS).
- Contusions
- Intracranial hematoma Glasgow Coma Scale (GCS)
- Cranial nerve injuries (12 nerves – clinical 5. Explore in detail the three (3) neurological
signs depend on cranial nerve injured. responses assessed, scores and actions
needed – score.
Brain Lacerations
Def. Brain Laceration: tearing of the brain
tissue.
Often caused by:
- Comminuted fracture – skull fragment
scratches brain
- Penetrating injury
e.g., bullet.
Contusion
Def. zx
Classification of Brain injury according to GCS
May contain areas of
haemorrhage, infarction,
Classification of TBI GCS
necrosis &/or oedema.
Mild 13-15
Can be localised – but often seen on opposite Moderate 9-12
pole also due to rebound impact of head 3-8
(Coup-Contrecoup) causing multiple Severe *<8 unable to
contusion sites. maintain airway
-Below GCS 8 – intubation is required.
-ANY DROP in GCS requires urgent medical
review.
NS2882 definition Property Drug/Intervention ① ② ③ ④ ↓ ↑ ∴ ≈ 💡
, Decorticate Decerebrate
Drop > 2 points = MET Call Origin @ cortex Origin @ brainstem
Arms bended Arms extended.
Complications after Stroke Damage to cortical Caused by lesion to
Posturing – Decorticate & Decerebrate white matter midbrain, pons, or
6. Compare and contrast decorticate and diencephalon
decerebrate posturing.
3: The Skull (not on study guide).
Due to neurological damage, normal postural
control & tone can be disrupted.
Skull fractures
DecortiCate Rigidity 1. Describe the types of skull fractures.
Decorticate posturing: damage to cerebral Skull fractures are categorised by:
hemispheres damaging corticospinal tracts - Appearance.
from cortex which are in control of voluntary - Location.
motor movement. - Degree of depression.
Presents as:
Arms folded in Linear: break is a thin line without
Hands clenched in flexion + turned distortion/splintering of the bone.
inwards.
Feet & legs extended out. Comminuted: skull bone shatters into
multiple pieces.
DecereBrate rigidity - Risk of fragment scratching the brain (brain
laceration)
Decerebrate posturing: damage to the brain
stem & extrapyramidal tracts. Interferes with Depression: denting / caving-in of the brain
voluntary motor messages being delivered to due to trauma.
all limbs.
Diastatic: fracture occurring along the suture
More common that decorticate rigidity but lines.
poorer prognosis & survival rate.
Basal: bones at the base of the skull break.
Presents as:
Arms & legs straight out in extension
Toes pointed downward.
Head and neck extended backward.
Hands clenched & internally rotated.
Ecchymosis: a skin discoloration due to
extravasation of blood (pooling).
Tear in the meninges can also cause:
- CSF rhinorrhoea (escape through nose)
- CSF otorrhoea (escapes through ear)
CSF leak indicates risk of meningitis is high.
3 signs of basal skull fracture:
NS2882 definition Property Drug/Intervention ① ② ③ ④ ↓ ↑ ∴ ≈ 💡
