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PHTY300 > Week 6- Acquired Brain Injury > Flashcards

Week 6- Acquired Brain Injury Flashcards

0
Q

Where is the centre for respiratory

A

Brainstem

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1
Q

Ventricles and CSF

A

Cushioning within bony ridges
Responses to pressure changes
pH of CSF influences pulmonary drive

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2
Q

What does the medulla do to respiration

A

Inspiration centre (dorsal and respiratory groups of nuclei)

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3
Q

What does the pons do

A

Apneustic and pneumotaxic centres

Apneustic breathing

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4
Q

How do chemoreceptors control respiration

A

Within medulla respond to changes in pH of CSF

Within carotid and aortic bodies respond to 02 and C02 blood concentrations

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5
Q

How do mechanoreceptors control respiration

A

Within chest wall, airways and lung parenchyma (feedback loop)

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6
Q

What happens to pH of CSF with increased levels of C02.

What does this result in

A

pH of CSF becomes more acidic with increases levels of c02

Triggers chemoreceptors
Initiates hyperventilation to maintain homeostasis

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7
Q

Influence of pH of CSF

A

Influences pulmonary drive and cerebral blood flow

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8
Q

What does the blood brain barrier do

A

Maintains micro environment of brain tissue

Tight endothelial junctions regulate passage of molecules from blood to brain tissue

Brain injury has the potential to disrupt the BBB and therefore homeostasis

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9
Q

What is auto regulation

A

The process whereby cerebral blood flow is maintained at constant levels

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10
Q

Mean arterial pressure cerebral blood flow

A

60-150 mmHh

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11
Q

What does decreased P02 to do cerebral bold flow?

A

Cerebral dilation

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12
Q

What does decreased PC02 to do cerebral bold flow?

A

Cerebral vasoconstriction

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13
Q

What is normal intercranial pressure

A

7-15 mmHg

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14
Q

What is intercranial pressure

A

Balance of pressures exerted by the contents of the skull

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15
Q

Volume of brain, CSF and blood

A

1400 mL, CSF 150 mL, blood 150 mL

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16
Q

What is the Monroe-kellie doctrine

A

As volume of any of these content (brain, CSF, blood) increases to maintain a constant pressure the volume of another must decrease

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17
Q

What is cerebral perfusion pressure.

CPP =

A

Pressure gradient across the brain

CPP = MAP - ICP

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18
Q

What is cerebral pressure gradient normally

A

70-90 mmHg

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19
Q

What is a primary injury

A

Mechanical, physiological or anatomical insult that occurs at the time of head trauma

Occurs at the time of injury and is not reversible

Permanent

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20
Q

What is a secondary injury

A

Systemic or local changes which increase tissue damage resulting from the primary injury

Post injury inflammatory sequlae

Clinical picture represents the combination of the primary and secondary injury (can’t separate the two clinically)

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21
Q

Mechanisms of brain injuries (traumatic)

A

Closed/blunt force (acceleration/deceleration)

Blast injury (thermal, mechanical, electromagnetic forces)

Penetrating injury

Skull fractures - linear or depressed

22
Q

Mechanisms of brain injury (non traumatic)

A

Hypoxic injury (eg near drowning)
CVA
Infection - abscess, meningitis
Tumour, bleeding into tunours

23
Q

GCS mild TBI

A

13-15

Patient may be awake, confused, drowsy but can communicate and follow commands

24
Q

GCS moderate TBI

A

9-12

Drowsy to obtunded. Open eyes and localise to pain. High risk of deterioration

25
Q

GCS severe TBI

A

3-8
Do not follow commands, decerebrate or decorticate posturing. Significant injury high risk for further deterioration and secondary injury. High morbidity and mortality

26
Q

Cause of extra dural haematoma (EDH)

A

Direct impacted

Associated with skull fracture

27
Q

Physiology and treatment of extra dural haematoma (EDH)

A

Blood on the surface of the brain, below the skull but above the dura level
•Volume predicts outcome
•Craniotomy and evacuation (drainage)

(on scan: loss of volume in ventricle)

28
Q

What is a subdural haematoma (SDH)

A
  • Tearing of the bridging veins
  • Collection of blood below the dura
  • Rapid acceleration or deceleration
  • Acute
  • Sub-acute 1-2 weeks post
  • Chronic > 2 weeks post incident
  • Acute on chronic

(midline shift on scan))

29
Q

What is a subarachnoid haemorrahage (SAH)

A

Bleed into the subarachnoid space (Bleed directly into brain tissue)
•Bleed can come from trauma, aneurysm, or arteriovenous malformation
•Traumatic or spontaneous

30
Q

Result of subarachnoid haemorrahage (SAH) and symptons

A

•Poorer outcome
•Hydrocephalus
•Aneurysmal clipping
•Endovascular coiling (coil embolization)
•High risk of vasospasm
photophobia, don’t like walking, don’t like noise

31
Q

What is an Intraventricular Haemorrhage IVH

A
  • Bleeding into the ventricles post trauma
  • Associated with acute hydrocephalus
  • Often in conjunction with other bleeds
  • Insertion of Extraventricular Drain - EVD
32
Q

What is a contusion

A
  • Parenchymal haemorrhage (brain bruising)

* Typically frontal or temporal lobes

33
Q

What is a coup injury?

A

Coup injury – direct transmission of force to underlying tissue

34
Q

What is a countre coup injury

A

•Countre Coup injury – indirect forces contralateral to the impact forces

35
Q

What is a diffuse axonal injury DAI

A
  • Widespread axonal damage from shear and tensile forces
  • Heavy Trauma
  • Damaged axons swell disrupting cortical physiology and microanatomy in the white matter and brain stem
36
Q

What colour should CSF and how does it influence extra ventricular drain?

A

CSF should be clear or straw coloured. Drain stays in until it starts draining clear fluid

37
Q

Outcome diffuse axonal injury?

A

Long time impaired consciousness
Long time ventilation and weaning
May require permanent trache

38
Q

How does HDU differ to ICU

A

1 to 2 pt nursing
no ventilation
NIV

39
Q

Dysautonomia

A
  • Inc. HR, Inc. BP, Inc. temperature, rigidity and posturing, diaphoresis
  • Poorer neurological recovery
  • Very difficult to manage
  • Respiratory implications
  • Aka sympathetic storming, neurostorming, acute midbrain syndrome, central dysregulation
40
Q

Acute head injury management

A

-Prevent secondary brain injury (cerebral protecton)
Ventilation
Sedation
Paralysis (makes more likelly for critical illness polyneuropathy)
Monitoring (ICP monitor, end tidal C02 monitor)
Neurosurgical intervention
Nutrition

Consideration and stabilsation of concomitant injuries - pulmonary contusion/chest fracture/SCI/ pre-existing conditions eg COPD

41
Q

Respiratory sequalae after head injury

A
  • Long term decreased level of consciousness (long term depressed resp. system)
  • Airway protection lost – high risk for aspiration and pneumonia
  • Depression of respiration cortically
  • Decreased ability to manage secretions (dysphagia)
  • Prolonged weaning
  • Tracheostomy – may be permanent
42
Q

Physiotherapy intervention after TBI

A

•Optimise respiratory function thereby limiting secondary brain damage
•Avoid weaning delay
•Preserve the integrity of the musculoskeletal system
•Guide neurological recovery and functional re-education
Physiotherapy Intervention
•Knowledge of MOI and other relevant injuries/conditions
•Relevant protocols and proceedures
•Review of available images
•Regular intensive care/respiratory assessment
•Neurological assessment

43
Q

Considerations for physio management after TBI

A

–Weigh up potential risks and benefits
–Liaise with medical team/senior physiotherapist
–Previous response to interventions

44
Q

Preparation for physio interventions after TBI

A

–Use medication prior to, and if necessary during, treatment
–Adequately prepare patient for interventions, eg. medications, hyper-oxygenation
–Open or close EVD
•Timing
–Treat when CPP is not low / ICP is not high
–Time treatment with other interventions, eg. washing, turning
–Keep treatment short and frequent

45
Q

Assessment and monitoring during physio interventions after TBi

A 
–ABG (SpO2)
–End Tidal CO2
–Blood pressure MAP
–Central venous pressure
–Neurological parameters
•GCS
•ICP
•Cerebral perfusion pressure
46
Q

Positioning of patient after TBI

A 
–Turning in severe head injury
•Supine to side lying  ICP  88%
•Cervical flexion / extension during turning   ICP
–Head down   ICP Contraindicated
–Do not lie on bone flap defect
47
Q

Manual techniques after TBI

A 
•Shorter bursts
•Application whilst ventilated
•Percussion
–(in isolation)   ICP
–11 minutes of percussion, manual hyperinflation, vibrations & suction   ICP
Paratz & Burns (1993)
•Vibrations, shaking, rib springing
–In isolation, these techniques do not  ICP
48
Q

When can you not use BiPAP, CPAP, BIRD, cough assist in TBI

A

Contraindicated in base of skull fracture due to risk of pneumocephaly

49
Q

MHI after TBI

A 
Inc. intrathoracic pressure = Inc. ICP
•MHI can Dec. ICP by Dec. CO2
•Rebound vasodilation
•Short Rx
•Rate similar to ventilator or spontaneous rate
•MUST MONITOR
50
Q

Suctioning after TBI. When to use it and how.

A
  • Necessary procedure required at a frequency sufficient to maintain a patent airway and clear secretions
  • Must be used with extreme caution if ICP is elevated or erratic
  • Duration of catheter insertion 10-15 seconds
  • Hyperoxygenate pre and post suction
  • Maximise treatment interventions prior
  • Minimise interventions post
  • Note the quality of stimulated cough
  • Guedel suction with caution – gag and high risk for aspiration
51
Q

When is nasopharyngeal suction contraindicated?

A

•Nasopharyngeal suction is contraindicated for those with BOS fracture, dural tears (CSF leak) and facial injuries.

52
Q

When does rehab after TBI begin?

A

Day 1

PHTY300 (14 decks)

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