TBI and Spinal Cord Injury Flashcards
Direct TBI
Occurs when the head is directly struck or its motion suddenly arrested by motion.
Indirect TBI
Cranial content are set into motion by forces other than direct contact. Eg. coup and counter coup
Primary TBI
Mechanical damage that occurs at the time of head trauma.
Eg. brain lacerations, haemorrhages, contusions, avulsions
Secondary TBI
- A facade if events proceeding primary TBI at the cellular and molecular level that continues for hours to days after the primary injury.
- Contributes to further brain injury including hypoxia, hypotension, hyperpyrexia, hyper/hypocarbia and anaemia.
Pathophysiology of brain injury
- brain injury as a result of trauma, cerebral oedema, hydrocephalus, space occupying lesion,
spontaneous bleed > increased ICP > decreased cerebral perfusion = hypoxia > ATP production > Na+/K+ pump fail > Na+ retained in cells causes cell swelling and cerebral oedema = further increase in ICP - brain needs O2 therefore patient needs increased ventilation and perfusion pressure but increased ventilation leads to decreased CO2 which causes vasoconstriction = decreased CPP > hypoxia develops > increased CO2 > increased ICP = further damage to brain
Patient presentation of TBI
- N/V
- Lacerations/contusion/haematomas to scalp
- Visible fractures or indentations to skull
- Racoon eyes
- CSF in nose/ears
- Unresponsiveness
- Confusion/disorientation
- Unequal puipls/fixed dilated
- Amnesia
- Combativeness/aggression
- numbness/tingling in extremities
- Loss of sensation/motor function
- Seizure
- Dizziness
- Visual disturbances
- Decorticate/decerebrate
- Cushings triad
Preventing secondary head injury
- Maintain SpO2 >94% using non-rebreather
- EtCO2 35-40mmHg
- Maintain MAP >80mmHg for cerebral perfusion
- Head tilt 30 degrees
- Pain management (fentanyl)
- Antiemetic
- Seizure management
- Prevention of hypothermia
Diffuse axonal injury
Axonal stretching leading to axolemmal disruption, ionic flux, neurofilament compaction, and microtubule disassembly, resulting in formation of retraction balls, axonal swelling and disconnection.
Cerebral herniation
Occurs with increased ICP due to increased volume overwhelming neuronal compensatory mechanisms of the CNS.
- Cushings triad
Other symptoms:
- sluggish pupils/fixed or dilated, bounding HR, altered LOC.
Cushings triad
- Hypertension or widening pulse pressure
- Bradycardia
- Irregular respiratory pattern (chyene-stokes) - alternating between hyperventilation and apnoea
Monroe-Kelly Hypothesis
- A pressure-volume relation between ICP and CCP regarding skull contents: CSF, brain and blood.
In case of injury where haemorrhage occurs, increasing fixed space within cranium, ICP is raised and CPP decreased. Arteries constrict to decrease intracranial volume = decreased perfusion and increased CO2 causes vasodilation. Further increase in ICP, compressed venous circulation, poor cerebral perfusion, increased swelling = brain tissue displacement and compression of brian stem.
Decorticate posturing
- Injury above midbrain
- Flextion of upper extremities and extension of lower extremities
Decerebrate posturing
- Arms extend abnormally and become adducted
- Clenched teeth
- Legs internally rotated
TBI Signs and symptoms (MIND CRUSHED)
- Mental status change
- Irregular breathing
- Nerve changes to optic/occular motor (pupils)
- Decorticate/decrebrate posturing
- Cushings triad
- Reflex sensitivity
- Unconscious
- Seizures
- Headache
- Emesis
- Deteriorating motor function
Intracranial pressure (ICP)
- Normal 5-15mmHg
- Influencing factors: CO2, O2, temp, body posturing, arterial.venous pressure
Cerebral perfusion pressure (CPP)
Pressure that pushes blood into the brain
- normal = 60-100mmHg
- CPP = MAP -ICP
Describe key management for TBI
- Airway management depending on level on conscious state (suctioning, OPA/NPA, LMA.
- Oxygenation (SpO2>94%) and EtCO2 (35-40mmHg).
- Fluid resusitation: Maintain MAP > 80mmHg as per inadequate perfusion CPG (SCI 500ml NaCl bolus only); 20ml/kg NaCl for isolated tachycardia, and tachycardia and hypotension.
- Analgesia as may have unrecognised pain
- Midazolam for seizures (0.1mg/kg)
- Glucose management if hypoglycaemic.
- Head tilt 30 degrees.
Describe autoregulation and effects on cerebral blood flow
- In response to decreasing CPP, auto regulation increases ICP to increase cerebral blood flow due to cerebral vasodilation.
- Autoregulation is efficient with a MAP of 50-150mmHg - if falls below 50mmHg cerebral blood flow becomes severely compromised and if above 150mmHg causes overstretching of cerebral blood vessels.
Metabolic factors affecting cerebral blood flow
CO2 concentration (vasoconstriction)
H+ concentration
O2 concentration (vasodilation)
Anatomy of spine: how many and types of vertebrae.
33 vertebrae:
- 7 cervical
- 12 thoracic
- 5 lumbar
- 5 sacral (fused)
- 4 coccygeal
Primary SCI
Injury which occurs as a direct result from trauma at the time of the incident.
Secondary SCI
- Injuries which occur due to cascade events following injury.
Impacted by hypoxia, hypotension, hyperthermia and hypoglycaemia.
Complete SCI
No motor/sensory function below level of injury
Incomplete SCI
Motor/sensory function are both or partially present below level of injury
Neurogenic shock
- Distributive shock caused by cervical or high thoracic SCI resulting in impaired descending sympathetic pathway.
- PNS causes bradycardia and hypotension
- Over vigorous fluid resuscitation is dangerous due to compromised CO
- Max. 500mL fluid bolus.
Neurogenic shock pathophysiology
- Occurs from a severe cervical or high thoracic (above T6) spinal injury causing interruption of autonomic pathways, leading to decreased systemic vascular resistance (vasodilation) and sometimes altered vagal tone (causing bradycardia).
- Loss of sympathetic tone occurs below the level of injury, causing unopposed PNS stimulation and vasodilation leading to hypotension.
- The lack of SNS tone results in the inability to redirect blood from the peripheries to the core circulation, also leading to excessive heat loss and hypothermia (flushed appearance below level of injury and pale above where SNS is still intact).
- Relative hypovolaemia as blood volume has not changed, rather the size of blood vessels has increased, resulting in severe reduction of oxygen delivery to cells > reduced O2 delivery leads to tissue hypo perfusion = distributive shock
- The higher the SCI, the more severe the symptoms
- Injury above T1 has potential to disrupt entire SNS = severe
- Neurogenic shock can occur from complete or incomplete SCI.
Describe why a patient appears flushed below level of injury and pale above?
- The lack of SNS tone results in the inability to redirect blood from the peripheries to the core circulation, also leading to excessive heat loss and hypothermia (flushed appearance below level of injury and pale above where SNS is still intact)
Spinal Shock
Temporary flaccid paralysis and loss of reflexes below the level of spinal cord lesion for 24-48 hours.
Spinal cord injury assessment
- Major trauma criteria = spinal precautions
- Pt who do not meet major trauma criteria require clearance.
- Any one of criteria indicate spinal precautions:
○ >60 YO
○ Hx bone disease (OA, OP, RA)
○ Drugs or alcohol
○ Significant distracting injury
○ Neurological or motor deficits
○ Spinal column pain or bondy tenderness
Pt cannot rotate and turn head 45 degrees left and right
NEXUS Criteria for C-Spine immobilisation
If any present:
* Neurological deficit present
* Midline spinal tenderness
* Altered level of consciousness (GCS <15)
* Intoxication distracting injury
- Distracting injury
Where is the phrenic nerve located?
C3-5
What are four types of skull fractures?
- Linear: single fracture that goes through the entire thickness of the skull
- Depressed
- Basilar: linear fractures through base of skull
- Left (maxillary) fractures
What are the three types of LeFort fractures
LeFort I: Palate fracture
LeFort II: Nose and palate fracture
LeFort III: entire face fracture
