Region of injuries Flashcards
Percentage TBI deaths occur within 2 hours
50% occur within 2 hours and are untreatable
Mortality rate from severe blunt trauma TBI
30%
Percentage of all major trauma patients have a TBI
Have a TBI with other associated injury
20%
20%
Primary vs Secondary brain injury
Primary - structral and biochemical injury that occurs at time of impact
Primary vs Secondary brain injury
Primary - Structural and biochemical brain injury that occurs at time of impact
Secondary - Subsequent brain injury and neuronal cell damage/death occuring after primary injury
Causes of secondary brain injury (5+2)
Systemic
- Hypotension
- Hypoxia
- Hypercarbia/Hypocarbia
- Hypo/Hyperglycaemia
- Acidosis
Intracranial
- Raised ICP due to cerebral oedema or haematoma
- Seizures
Hyper/Hypocarbia mechanism of injury on TBI
Hyper - cerebral vasodilation and raised ICP
Hypo - Cerebral vasoconstriction and hypoperfusion
Main goal of ED in trauma patient with TBI
Prevention of secondary brain injury and expedite transfer to definitive neurosurgical or intensive care facility.
Definition of TBI
TBI is caused by external (mechanical) force that causes temporary or permanent damage to /impairment of the brain (or the skull) that may affect one or more of the following:
- Conscious state
- Brain structure/anatomy
- Brain function including motor/sensory function, cognition and physiologic regulation
- Psychosocial function
Causes of TBI (5)
Transport related
Low fall >64
Low fall <65
High fall >1m
Struck by person or object
Chnce of pre hospital death from penetrating brain injury
Chance of survival after arrival by GCS
90%
GCS 3-8 = 0-8%
GCS 9-15 = 90%
Unsurvivable features with Penetrating brain injury with fragments traversing the midline (4)
Post-resuscitative GCS of 3
Fixed and dilated pupils
Prolonged periods of hypotensoin, hypoxia or asystole
CT evidence of ‘ground glass brain’ (gross brain swelling with loss of grey/white differentiation and general hypodensity)
CT findings associated with poor outcome following a civilian gunshot wound to the head (9)
Multilobar or bihemispheric injury
Ventricular injury with haemorrhage
Diffuse fragmentation
Missile passing through the geographic centre of the brain (thalamus and basal ganglia)
Midline shift >10mm on CT
Compressed or obliterated basal cisterns
Intracerebral haemorrhage/SAH
High volume of contused brain
Posterior fossa wound with brainstem involvement
Clinical findings related to poor outcome following civilian gunshot wound to the head (5)
GCS <5 on admission
Dilated, unreactive pupils
Occipital entry wound
Hypotension on admission
High ICP
Other factors related to poor outcome gunshot to head (5)
High velocity missile
Suicide attempt (except isolated frontal injury)
Increased retrieval time
Coagulopathy or DIC
Advanced age
Complications of gunshot wound to head (6)
Brain abscess
Meningitis
Cerebrovascular injury: pseudoaneurysm, dissection, stroke (may develop 1-2 weeks after injury
Migrating metal fragments
Seizures
Chronic lead poisoning
Stages of blast injuries (4)
Primary effects - direct effects of pressure wave
Secondary effects - penetrating wounds from fragments
Tertiary effects - the blast hurls/tosses the patient or surrounding structures collapse onto patient
Quaternary - burn or inhalation of toxic fumes
Diffuse axonal injury CT findings
Initial CT can by normal in 50-80% of patients
Subsequent MRI shows axonal injury in 70% of patients
Normal CT for a comatose patient should raise suspicion for DAI
Classifications for TBI (3)
Clinical (using indices of severity such as GCS)
Pathoanatomical
Physical mechanism
Essential elements of TBI Hx (7)
Even though difficult to obtain
Mechanism - speed of vehicle/impact, protective gear, contact surface
Pre-hospital - duration of LOC, best worst GCS, duration of antegrade amnesia
Comorbidities - coagulopathy, anti-coagulant medication, pre-existing neurological conditions
Associated injuries - especially spinal injuries
Lateralising neurological symptoms - parasthesia, weakness, ataxia
Alcohol or other drug ingestion
Hx of vomiting
Signs of BOS fracture (6)
CSF leak from nose or ears Rhinorrhoea/otorrhoea
Bilateral peri-orbital haematoma ‘Racoon eyes’
Subconjunctival haemorrhage with posterior limit not visible suggests orbital fracture
Haemotympanum
Bruising over mastoid (can be delayed) ‘Battle’s sign
Fractures may be diagnosed during scalp wound assessment by careful exploration or radiographically
Intubating pre CT GCS
Traditionally taught
GCS <8
Generally all patients with GCS <9 will need intubation prior to CT due to the loss of protective airway reflexes with lower GCS’s
Caution with alcoholics - some may not require intubation
Exceptions for CT in GCS<8 (3)
Non surviveable
Pt not for active treatment
Frequent flyer with intoxication - needs senior input and risk assessment
Head injury with GCS 13 to 15 within 2 hours with definite or ‘probable’ LOC
No risk factors
CT
Many studies clearly show these patients do not need a brain CT - radiological incidence very low and injuries do not require surgical intervention
This group at increased risk of concussion
Risk factors in TBI that support need for CT (11+1)
Severe and/or persistent headache
Vomiting
Retrograde amnesia >30 minutes
Age >65
Anticoagulant drugs (excluding aspirin)
Seizure
TBI associated with dangerous mechanism
Suspected skull fracture
Sign of basal skull fracture
Drug or ETHO intoxication
Additional - communication difficulty/patient reliability
Senior clinician preference
Indications for surgery in SDH (3)
Acute SDH with thickness >10mm or midline shift greater than 5mm should have surgical evaulation regardless of GCS
All patients in coma with acute SDH (GCS<9) should undergo ICP monitoring
A comatose pt (GCS<9) with acute SDH <10mm and midline shift <5mm if:
- GCS decreases by 2 or more points
- Asymmetric or fixed and dilated pupils
- ICP >20mmHg
Lucent period head injury
Which vessels 95% cause
Extradural
Arterial (middle meningeal)
Indications for surgery EDH
GCS score
Pupil abnormality
Vague!
Cerebral contusions indications for surgery
GCS 6-8
Frontal or temporal contusions larger than 20cc in volume with midline shift >5mm
Any lesion larger than 50cc in volume
Indications for surgery in posterior fossa bleeds
Mass effect on CT
- Distortion/dislocation/obliteration of 4th ventricle
- Compression or effacement of basal cisterns
- Obstructive hydrocephalus
Neurological dysfunction or deterioration attributable to the lesion
Types of Brain Herniation (6)
Uncal (transtentorial)
Central Subfalcine (cingulate)
External (trans-calvarial)
Upward (transtentorial)
Tonsillar
Uncal herniation syndrome (3)
What does it herald
Contralateral hemiparesis - pressure on corticospinal tracts
Reduced consciousness - pressure on midbrain
Ipsilateral CN III palsy/dilated pupil/blown pupil - Pressure of nerve against tentorial notch, most peripheral fibres damaged resulting in pupil dilation
Imminent deterioration and death
(Transtentorial)
Central herniation Syndrome (3)
Subfalcine
Cause
Caused by diffuse brain welling or large supratentorial mass effect
Altered consciousness - ICP elevation, reduced perfusion
Initially small reactive pupils - loss of sympathetic output from hypothalamus, also decorticate (flexor) movements
Then pupils enlarge to midposition - midbrain failing, posturing becomes decerebrate
Cingulate lobe
Pinching anterior cerebral artery potentially leading to stroke
Cerebellar tonsillar herniation mechanism (3)
Causing
ICP rise in posterior fossa, pressure gradient increases across the foramen magnum
Cerebellar tonsils pushed into/through foramen magnum
Compresses the medulla/medullary respiratory centre
Causes apnoea, LOC (if not already), resp dysfunction and death
Compression of which structure causes CF obstruction and triples risk of raised ICP
Basal cisterns
Decorticate movement
Flexor
Decerebrate
Extensor
Indications for operative repair of depressed skull fractures (4)
Depth of the depressed fragments is equal or greater than the width of surrounding bone
Cosmetic areas such as forehead
Compound/open fractures
Significant underlying intracranial bleed that requires surgery
Cerebral perfusion pressure equation
CPP=MAP-ICP
Normal ICP range
Target in TBI
Normal 5-15mmHg
Target <20-25mmHg in TBI
Target for CPP
60mmHg (50-70mmHg)
Target MAP for TBI pt ICP of 20-25mmHg
MAP 70-85mmHg
Transient ICP reduction stretegies (6)
Sedation/analgesia/paralysis to prevent coughing/straining
Hyperosmolar therapy
Ventilation: Low-normocarbia, minimal PEEP
Normothermia
Avoid neck constriction - remove C-spine collar ETT tie above ear
Tilting bed 15-30 degrees head up
Definitive ICP reduction (2)
Draining of CSF via drain
Craniotomy/craniectomy
ICP measuring devices (2)
Codman monitor - ‘bolt’
Intraventricular catheters - can be combined with closed drainage system (external ventricular drain) which combines monitoring and ability to drain
Mannitol in TBI dose
0.25-2g/kg as 20% solution
Generally 1g/kg
Equate to 5ml/kg
Over 30 minutes
Mannitol complications (6)
Hypotension
Electrolyte imbalance - hyperkalaemia
Marked osmotic diuresis - catheter required
Rebound raised ICP
Neurological and renal complications osmol >320mOsm/L
Extravasation may cause tissue necrosis
Hypertonic saline dose
2ml/kg
3% and 5% available
End points of hypertonic saline
Na 150-155
Osmolarity <360mOsm/L
