Topic 21 -22 Traumatic brain Injury Flashcards

1
Q

Provide a classification for Head Injuries/Traumatic Brain Injuries (TBI)

A

◦ Concussion
◦ diffuse axonal damage- damage to white matter intense, no localisation

◦ Focal lesions (brain localised to the sites of impact-coup, contracoup)

  • Lacerations
  • Contusion
  • haemorrhage

• Skull fractures with associated brain damage (open head injury) penetrating

- Simple (linear or comminuted)
- Depressed (bone embedded into brain tissue)
 - Basilar (base of skull)
  • Closed head injury (No skull fracture) with diffuse neuronal damage(CHI)
  • Injury to blood vessels Haemorrhage/haematomas
    • Extradural/epidural haematoma
    • Subdural haematoma
    • Sub arachnoid hematoma
    • Intracerebral haematoma
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2
Q

Epidural (EDH) Hematoma

A

b/w dura and skull, Therefore can cross midline, but not past cranial sutures.

Rupture of the middle meningeal artery usually due to # temporal bone. Artery therefore rapidly expanding. Initially lucid period without signif. Neurosurgical emergency-

S&S rapidly increasing ICP, herniation and possibility death.

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3
Q

Subdural(SDH) Hematoma

A

b/w dura and arachnoid, rupture of the bridging veins.
Can’t cross midline due to falx. Due to rupture of bridging veins.

types:
Chronic SDH- usually seen in elderly population, shearing injury with min or no trauma.
Develops over wks/mths. Slow accommodation

S&S: H/a, confusion, unsteady gait.
Acute SDH- signif trauma. Poorer prognosis

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4
Q

Subarachnoid(SAH) Hemorrhage

A

b/w CSF filled arachnoid and pia which follows brain contours and contains major blood vessels of brain

Non Traumatic SAH-
Majority ruptured Saccular (berry) aneurysms (80-90%), less common AVM, cocaine abuse.
Castastrophic headache prior to neurological S&S.

Traumatic SAH
bleeding into CSF damaged blood vessels ass. with cerebral contusions
Complicated: -re bleeds -vasospamsischemic stroke –hydrocephalus

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5
Q

Intracerebral (ICH) Hemorrhage

A

• 2nd most common form of stroke (infarct most common).
Associated with H/T, drug use, tumour, AVM
• ICP and neuro stability
• Most common sites- BG, thalamus, cerebellar nuclei and brainstem (pons).
• Can be traumatic

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6
Q

Diffuse axonal Injury

A

Diffuse axonal Injury
Widespread ‘white matter’ or axonal damage due to shearing or tearing as a result of rotational or severe acceleration/deceleration forces. Usually occur in MVA, falls or in child abuse (‘shaken baby syndrome’)

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7
Q

• Describe the mechanism of brain damage in coup-contrecoup injuries

A

Occurs during blow to the head Site, opposite the initial impact, Widely recognized as having greater severity than coup , Often seen when moving skull impacts an immovable/external object

2 theories eg
The denser CSF moves toward the site of skull impact displacing the brain in the opposite direction, such that the initial impact of the brain parenchyma is at the contrecoup location. During the process of closed head injury, the brain parenchyma is initially displaced away from the site of skull impact and toward the contrecoup site resulting in the more severe brain contusion.

Head hits force, sudden deceleration of the skull. Brain continues to move forwards hits the front part of the skull and damages it Coup then bounces back and hits posterior aspect of skull contre coup injury.

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8
Q

Define herniation

list 4 types

A

Intracranial compartment separated into 3 compartments by 2 major dural structures- Falx cerebri and tentorium cerebelli. Herniation pushes brain tissue from one compartment to another.

  • Transtentorial-Uncal
  • Central
  • Subfalcine
  • Tonsillar
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9
Q

Uncal herniation what is it associated with?

A

Uncal herniation associated with clinical ’triad’- blown pupil, hemiplegia and coma

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10
Q

Subfalcine herniation

A

-Innermost portion of frontal lobe pushed under the falx cerebri. Less pressure on brainstem but may impact on anterior cerebral artery unilaterally or bilaterally. Can lead to central herniation and usually occurs in conjunction with uncal herniation. May present with abnormal posturing and coma.

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11
Q

Central herniation

A

-diencephalon and temporal lobes both hemispheres pushes down through notch of tentorium cerebelli.

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12
Q

Infratentorial herniation

A

posterior fossa structures herniate upwards through the tentorium in the direction of the midbrain ◦ posterior fossa structures herniate downwards through the foramen magnum (cerebellar cone, tonsillar hernia)

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13
Q

List the major pathological sequelae (complications) to head injury, including;

A
  • Haemorrhages, DONE
  • Cerebral oedema: Excessive fluid in the extracellular or intracellular space of the brain.
  • Hydrocephalus: Abnormal increase in CSF volume in any part or all of the ventricular system.
  • Herniation DONE
  • Increased intracranial pressure
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14
Q

Describe the factors that may cause an increase in Intracranial pressure (ICP)

A

<15mmHg is normal intracranial pressure
Causes:
·Localised mass lesions- neoplasms
·Cerebral blood volume( haemorrhage ) Major venous sinus disruption
· brain & intracellular water( cerebral oedema, tumor)
· CSF( hydrocephalus)

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15
Q

Effect of increased ICP

A
◦ Secondary cell death 
◦ Herniation ◦ Death
Disrupt cerebral blood flow
Destroy brain cells
Displace brain tissue (herniation)
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16
Q

Clinical Features of Raised ICP

A
  • Headache- throbbing and worse am
  • Papilloedema
  • Vomiting
  • Deteriorating conscious level
  • Pupillary dilatation
  • Bilateral ptosis
  • Impaired upgaze
  • Extension to pain
  • Respiratory irregularity
17
Q

Mechanisms of Brain Injury

A
◦ Brain damage occurs as a result of:
 1. Effects of hypoxia and ischaemia
2. Excitatory amino acid injury
3. Increased intracranial pressure
 	◦ cerebral oedema
 	◦ haematoma/haemorrhag e
   	◦ hydrocephalus (increased CSF)
  	◦ herniation
18
Q

Traumatic brain injury cascade

Phase 1 & Phase 2

A

Phase one- Primary Injury/insult - direct tissue damage, altered BF & impaired metabolic activity

  • Direct tissue damage- contusion, haemorrhage and lacerations, shearing and/or compression
  • Impaired cerebral blood flow
  • Metabolic imbalances

Phase two- Secondary injury/insult secondary cell death

  • Neuronal disruption resulting in depolarization
  • Release of excitatory neurotransmitters
  • Intracellular breakdown
  • Free radical generation
  • Apoptosis
  • necrosis
19
Q

Define consciousness

What are the 2 aspects of conciousness?

A

Consciousness implies an awareness of self and the environment and being able to respond appropriately to new stimuli.

There are two aspects to consciousness:
◦ Arousal and wakefulness
◦ Content and cognition

20
Q

Define alert

A

Alert: appropriately attentive to environment, orientated to time, place and person, able to carry on appropriate conversation

21
Q

Define drowsy

A

Drowsy: asleep most of the time, responds appropriately (usually verbally) to verbal command or sensory input

22
Q

Define stuperosed

A

Stuperosed: appears asleep most of the time, BUT only responds to a painful stimulus. The response is purposeful (ie. withdraws the part of the body appropriately or tries to push stimulus away).

23
Q

Define deeply stuperosed

A

Deeply Stuperosed: appears asleep most of the time, BUT only responds to a painful stimulus. The response is reflexive (increase in abnormal posturing eg flexor or extensor patterns of the limbs).

Coma : no response to any stimulus

24
Q

List 4 criteria that may be used to diagnose brain death

A
  • Absence of brain reflex responses to all stimuli including pain
  • Absence of brain-stem reflexes
  • Complete absence of any breathing efforts even when the patient is not connected to the mechanical ventilator for much longer that anyone would be able to hold their breath.
  • Significant damage on brain scans, normal temperature, BP, absence of metabolic disorders, sedation, intact LMN.
25
Q

Describe the Decorticate posture and explain where a lesion would present to display this

Describe decerebrate posture and explain where a lesion would present to display this

A

Decorticate posture
◦ Decorticate posturing seen with forebrain to midbrain damage
- Upper extremity flexion with adduction, internal rotation, pronation.
-Lower extremity extension with adduction and internal rotation

Decerebrate posture
◦ Decerebrate posturing seen with damage in caudal midbrain ( rostral pons) to rostral medulla

Extension with adduction, internal rotation of the upper and lower extremities