Head injuries Flashcards
Brain metabolism
20% total body oxygen
25% total body glucose
uses almost all aerobic metabolism due to damaging effects of lactate
doesn’t store oxygen/glucose - tightly coupled to cerebral blood flow
CBF
cerebral blood flow
controlled by local concentration of CO2
Active brain area produces CO2: cerebral capillaries/arterioles vasodilate
–> active area gets more blood flow
Cerebral perfusion pressure
CPP = Mean arterial pressure - ICP
Cerebral autoregulation
keeps cerebral blood flow constant despite a wide range (50-130 mmHg) of cerebral perfusion pressures
brain not bombarded by minor fluctuations in systemic blood pressure
Autoregulation lost following trauma
ICP
Normally ~10 mmHg
>20 abnormal
>40 potentially lethal
Monroe-Kelly doctrine
Skull is a rigid structure that cannot expand
Initially CSF/blood inside large veins are shunted outside
eventually compensation exhausted, pressure rises dramatically
Primary brain injury
occurs at time of trauma
permanent
no therapy
Secondary brain injury
delayed
preventable
include:
hypoxia, hypotension, infection, seizure, electrolyte abnoramlities and raised ICP (herniations/local hypoperfusion)
GCS eyes
spotaneous 4
to voice 3
to pain 2
none 1
GCS best verbal response
oriented, converses 5 disoriented, converses 4 inappropriate words 3 incomprehensible sounds 2 none 1
GCS best motor response
obeys 6 localizes to pain (eg cross midline) 5 withdraws 4 flexion 3 extension 2 none 1
GCS severity
3-7 severe brain injury
8-12 moderate
13-15 mild
intubate
Uncal herniation
also: trans-tentorial
temporal lobe swells and presses medially onto CN III (dilated pupil), cerebral peduncle (contralateral plegia), reticular activation centre of brainstem (coma)
Tonsillar herniation
whole brain squeezed downwards into foramen magnum
compresses tonsils of cerebellum against medullar
–> respiratory arrest, death
Cushing’s response/triad
cardiovascular response to elevated ICP
increased body BP –> reflexive bradycardia
–>respiratory iregularities due to medullary hypofusion
head injury - airway management
intube if:
- airway needs protection (unconscious, airway damage/facial smash)
- ventilation is inadequate
head injury - breathing management
ventilate if:
- low PaO2
- high PaCO2 (could vasodilate and cause increased ICP –> secondary injury)
Head injury deficit assessment
mini-neuro exam
LOC - GCS
lateralizing findings: pupils; if bilateral blown pupils –> death
motor
Head injury diagnostics
most useful - CT scan
Epidural bleed
lens-shaped
initially no primary injury
if treated, no secondary injury
Subdural bleed
torn vein, big potential space
crescentic hematomas
chronic subdural –> kind of looks like water
–> happens to the elderly (brain smaller so not as noticeable clinically_
Intracerebral bleed
diffuse axonal injury
high speed MVA
Brain injury treatment
Craniotomy (remove blood clots)
External ventricular drain (drain CSF)
osmotic diuretic/Mannitol (reduce brain vol)
Hyperventilation (reduce blood volume by v/c, too much can be dangerous)
Barbiturate coma/cooling (reduce metabolic demand)
Acceleration/deceleration injuries
contusions
subdural hematoma
axon/vessel shearing
mesencephalic hematoma
Coup
damage at site of blow
contrecoup
damage at opposite site of below
Coup-contrecoup
acute decompression causes cavitation followed by a wave of acute compression
Mild brain injury outcomes
GCS13015
Post-concussive symptoms: headache, fatigue, dizziness, nausea, blurred vision, diplopia, memory impairment, tinnitus, irritability, low concentration
50% at 6 weeks, 14% at 1 year
Moderately traumatic brain injury outcomes
GCS 9-12
Proportional to age and CT findings
60% good recovery, 26% moderately disabled, 7% severely disabled, 7% vegetative/dead
Late complications of head/brain injury
Seizures
- 5% of head injury patients
- increased with local brain damage/intracranial hemorrhage
Meningitis - CSF leak
Hydrocephalus - acute or delayed
