Week 6- Acquired Brain Injury Flashcards
Where is the centre for respiratory
Brainstem
Ventricles and CSF
Cushioning within bony ridges
Responses to pressure changes
pH of CSF influences pulmonary drive
What does the medulla do to respiration
Inspiration centre (dorsal and respiratory groups of nuclei)
What does the pons do
Apneustic and pneumotaxic centres
Apneustic breathing
How do chemoreceptors control respiration
Within medulla respond to changes in pH of CSF
Within carotid and aortic bodies respond to 02 and C02 blood concentrations
How do mechanoreceptors control respiration
Within chest wall, airways and lung parenchyma (feedback loop)
What happens to pH of CSF with increased levels of C02.
What does this result in
pH of CSF becomes more acidic with increases levels of c02
Triggers chemoreceptors
Initiates hyperventilation to maintain homeostasis
Influence of pH of CSF
Influences pulmonary drive and cerebral blood flow
What does the blood brain barrier do
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
What is auto regulation
The process whereby cerebral blood flow is maintained at constant levels
Mean arterial pressure cerebral blood flow
60-150 mmHh
What does decreased P02 to do cerebral bold flow?
Cerebral dilation
What does decreased PC02 to do cerebral bold flow?
Cerebral vasoconstriction
What is normal intercranial pressure
7-15 mmHg
What is intercranial pressure
Balance of pressures exerted by the contents of the skull
Volume of brain, CSF and blood
1400 mL, CSF 150 mL, blood 150 mL
What is the Monroe-kellie doctrine
As volume of any of these content (brain, CSF, blood) increases to maintain a constant pressure the volume of another must decrease
What is cerebral perfusion pressure.
CPP =
Pressure gradient across the brain
CPP = MAP - ICP
What is cerebral pressure gradient normally
70-90 mmHg
What is a primary injury
Mechanical, physiological or anatomical insult that occurs at the time of head trauma
Occurs at the time of injury and is not reversible
Permanent
What is a secondary injury
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)
Mechanisms of brain injuries (traumatic)
Closed/blunt force (acceleration/deceleration)
Blast injury (thermal, mechanical, electromagnetic forces)
Penetrating injury
Skull fractures - linear or depressed
Mechanisms of brain injury (non traumatic)
Hypoxic injury (eg near drowning)
CVA
Infection - abscess, meningitis
Tumour, bleeding into tunours
GCS mild TBI
13-15
Patient may be awake, confused, drowsy but can communicate and follow commands
GCS moderate TBI
9-12
Drowsy to obtunded. Open eyes and localise to pain. High risk of deterioration
GCS severe TBI
3-8
Do not follow commands, decerebrate or decorticate posturing. Significant injury high risk for further deterioration and secondary injury. High morbidity and mortality
Cause of extra dural haematoma (EDH)
Direct impacted
Associated with skull fracture
Physiology and treatment of extra dural haematoma (EDH)
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)
What is a subdural haematoma (SDH)
- 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))
What is a subarachnoid haemorrahage (SAH)
Bleed into the subarachnoid space (Bleed directly into brain tissue)
•Bleed can come from trauma, aneurysm, or arteriovenous malformation
•Traumatic or spontaneous
Result of subarachnoid haemorrahage (SAH) and symptons
•Poorer outcome
•Hydrocephalus
•Aneurysmal clipping
•Endovascular coiling (coil embolization)
•High risk of vasospasm
photophobia, don’t like walking, don’t like noise
What is an Intraventricular Haemorrhage IVH
- Bleeding into the ventricles post trauma
- Associated with acute hydrocephalus
- Often in conjunction with other bleeds
- Insertion of Extraventricular Drain - EVD
What is a contusion
- Parenchymal haemorrhage (brain bruising)
* Typically frontal or temporal lobes
What is a coup injury?
Coup injury – direct transmission of force to underlying tissue
What is a countre coup injury
•Countre Coup injury – indirect forces contralateral to the impact forces
What is a diffuse axonal injury DAI
- 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
What colour should CSF and how does it influence extra ventricular drain?
CSF should be clear or straw coloured. Drain stays in until it starts draining clear fluid
Outcome diffuse axonal injury?
Long time impaired consciousness
Long time ventilation and weaning
May require permanent trache
How does HDU differ to ICU
1 to 2 pt nursing
no ventilation
NIV
Dysautonomia
- 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
Acute head injury management
-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
Respiratory sequalae after head injury
- 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
Physiotherapy intervention after TBI
•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
Considerations for physio management after TBI
–Weigh up potential risks and benefits
–Liaise with medical team/senior physiotherapist
–Previous response to interventions
Preparation for physio interventions after TBI
–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
Assessment and monitoring during physio interventions after TBi
–ABG (SpO2) –End Tidal CO2 –Blood pressure MAP –Central venous pressure –Neurological parameters •GCS •ICP •Cerebral perfusion pressure
Positioning of patient after TBI
–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
Manual techniques after TBI
•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
When can you not use BiPAP, CPAP, BIRD, cough assist in TBI
Contraindicated in base of skull fracture due to risk of pneumocephaly
MHI after TBI
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
Suctioning after TBI. When to use it and how.
- 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
When is nasopharyngeal suction contraindicated?
•Nasopharyngeal suction is contraindicated for those with BOS fracture, dural tears (CSF leak) and facial injuries.
When does rehab after TBI begin?
Day 1
