Neurotrauma and intensive care Flashcards
Def: WHO TBI
Acute injury to the brain resulting from mechanical energy to the head from external physical force excluding injuries relating to illicit drug, alcohol or substance, medication or caused by other treatment or injuries
Menon Def: TBI
Alteration in brain function or other evidence of brain pathology caused by an external force
Most common cause of TBI in lower and middle-income countries?
Motor vehicles
Most common cause of TBI in Europe?
Falls
Incidence rate of TBI related hospital admissions?
262 per 100,000
Main causes of TBI
RTA
Falls
Violence
Work and sports
Others
What is the reduction in life-expectancy after receiving in patient rehab for TBI?
9 year reduction
Mortality incidence of TBI in Europe?
11.2/100,000
Classification of TBI:
Mechanism
Closed
Penetrating
Crush
Blast
Combined
Clinical severity grading of TBI?
Mild, Moderate, Severe
TBI clinical grading:
Mild severity
14-15
TBI clinical grading:
Moderate severity
9-13
TBI clinical grading:
Severe
GCS 3-8
Injury burden grading of TBI
AIS
Using Abbreviation Injury Score
Severity scoring for 6 body regions
ISS
Aims to summarise the total burden of injury by adding the quadratic scores of the three body regions with the highest score
What are two models that can be used to prognosticate TBI?
IMPACT
CRASH
Features of IMPACT
Developed on patients with moderate to severe brain injury
Looked at factors such as structural imaging (CT)
Secondary insults (hypoxia, hypovolaemia)
Laboratory data (glucose, Hb)
Additional factors impacting on Px in head injury
MRI burden of injury
Comorbidities
ISS
Time to craniotomy >4h
Autoregulatory indices
Which biomarkers have been suggested as tools for prognostication in TBI?
S100 beta protein
ApoE4
S100 beta protein
Biomedical marker for diagnosis, monitoring and prognosis of TBI severity.
Preoperative estimation of serum S100beta can be used as a prognostic inidicator for post-operative survival and neurological outcome
ApoE4
ApoE4 allele might be associated with poor prognosis in patients with severe TBI
May also be used as a biomarker
Features of GOS
Initially described as a global assessment of function following TBI
GOS
Number of categories
5
GOS 1
Dead
GOS 2
PVS
GOS 3
Severe disability (conscious but dependent)
GOS 4
Moderate disability (independent but disabled)
GOS 5
Good recovery
(Can resume normal activities)
GOS E
Number of categories
8
GOSE 1
Dead
GOSE 2
PVS
GOSE 3
Lower severe disability
GOSE 4
Upper severe disability
GOSE 5
Lower moderate disability
GOSE 6
Upper moderate disability
GOSE 7
Lower good recovery
GOSE 8
Upper good recvoery
Neuropsychological sequelae of TBI
Mood disturbance
Cognitive impairment
Personality changes
Social
Family effects
Mortality in patients with severe TBI
36%
Rate of good recovery in patients with severe TBI?
5%
Mortality in patients with moderate TBI?
7%
Rate of good recovery in patients with moderate TBI
60%
Def: Primary brain injury
Mechanical load that translates into deformation of cerebral tissue which then initiate cellular responses that lead to disturbances in autoregulation and metabolism
Consequences of impact loading
Skull #
EDH
Contusions (coup or contrecoup)
Pathology of contrecoup lesions
High positive pressure at coup site and transmission of force vector through the brain parenchyma, generating a slapping effect to the contrecoup site.
At the cellular level, high negative pressure at the contrecoup site, the development of cavitation bubbles known as contrecavitations and the brain parenchyma bouncing against the inner posterior skull are associated with contrecoup lesions.
Contusion after early trauma
More severe at the crest of gyrus than at the sulcus
Associated with swelling that subsides with time
Consequences of impulse loading
Occurs due to inertial forces during translational or rotational motion.
CSF significantly increases convolutional gliding and shear strain
Brain displacement lags behind skull and dura and occurs in different regions of the brain parenchyma itself causing WM damage.
Mobility of brain parenchyma
More mobile relative to the region of the skull base
White matter is stiffer than grey matter and thus more strain is distributed at the interface.
What structures are vulnerable to DAI?
Vascular, neural and dural elements (e.g. distal ICA, optic and oculomotor nerves, olfactory nerves and pituitary stalk) that tether the brain to the skull are most susceptible.
Splenium of the corpus callosum
Dorsolateral brainstem can also experience DAI due to a similar trajectory to that of the skull base.
What movements are necessary to generate SDH?
General translational and angular motion of the head.
Rotational insults induce shear straing.
With what injury mechanism are SDH most prealent?
When a single inertial load combineswith a minor trauma impact load
Static or quasi-static loading
Occurs with gradual compression (e.g. closing elevator door)
Steady load results in skull fractures and cerebral injuries that are deeper than cortical contusions from an impact load.
In contrast to blunt impact trauma, energy from crushing trauma tends to be transmitted to the foramina and hiatus of the middle cranial fossa, causing damage to associated cranial nerves, SNS and intima of blood vessels.
Morphological classification of TBI
Focal or diffuse
Anatomical
Epidemiology of EDH
2% of all brain injuries
More common in patients <50
Particularly in paediatric patients primarily due to meningeal and diploic bein haemorrhage
Pathology of EDH
Either due to fracture of the squamous part of temporal bone causing MMA laceration
Venous sinus injury
Fracture haematoma
EDH constrained by periosteum which passes through the cranial sutures so EDH do not cross suture line
What causes the occasional delayed presentation in children?
Dura is tightly adherent to skull
Lower venous pressure
Radiographic categorisation of EDH
Type 1- acute
Type 2- subacute
Type 3- chronic
Radiographic progression of EDH
A hyperdense lesion with swirl sign indication of bleeding, rise in pressure eventually produces a tamponade of the bleeding site and progresses to type II, a homogenous hyperdense and organised clot. Type II is characterised by a low-density collection to blood resorption by perivascular tissue along with a contrast-enhanced membrane consisting of neovascularity and granulation tissue.
What proportion of patients experience the lucid interval classic for EDH?
15-20%
Features of neurological deterioration after EDH
Contralateral hemiparesis
Ipsilateral oculomotor nerve paresis
Decerebrate rigidity
Arterial hypertension
Cardiac arrhythmias
Respiratory disturbanecs if uncorrected leading to apnoea and death.
Pathophysiology of SDh
Tearing of dural bridging veins
Tearing of superficial pial arteries
Acute SDH
Crescent-shaped, hyperdense collection
ASDH
Subacute SDH
Isodense
Symptomatic improvement
7-21/7
Subacute SDH
Chronic SDH
>21/7
Hypodense
May not present symptomatically until there is significant mass effect
Chronic SDH
Clinical features of ASDH
Stereotypic motor disorders
Impaired oculomotor reflexes and following uncal herniation, unilaterally fixed and dilated pupils.
Arterial bleeds are associated with larger clots near the Sylvian fissure
Post-op complications for SDH evacuation
Reaccumulation
Infection (e.g. osteomyelitis, meningitis, ventriculitis)
Mortality rates in acute traumatic SDH
22-66%
Mortality rate for ASDH decompression within 4h
30%
The mortality rate for acute SDH evacuated after 4h
90%
Predictors for prognosis in SDH
Time to evacuation
Age
Extent of neurological deficit
Sex
Post-op ICP
Mannitol dose?
0.25-1g/kg body weight
Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial causes
DECRA trial
Question?
Looked at the use of bifrontotemporoparietal decompressive craniectomy in adults under the age of 60y with refractory intracranial hypertension and diffuse brain injury
Within 72h of injury
Australia, NZ and Saudi Arabia
DECRA trial
Bottom line
DECRA trial showed that patients undergoing craniectomy had worse ratings on the GOS-E at 6 months than those receiving standard care (P = 0.03), although the rates of death were similar at 6 months (19% and 18%, respectively).
Reduced ICP
RESCUE ICP
Question?
NEJM
Hutch 2016
In patients with traumatic brain injury (TBI) and intracranial hypertension refractory to medical management, does decompressive craniectomy as a last-tier intervention improve outcomes as measured by the Extended Glasgow Outcome Scale (GOS-E)?
RESCUE ICP
Bottom line
. This trial showed that craniectomy increased the number of favorable outcomes compared to continued medical management and that for every 100 patients managed surgically vs medically there were 22 more survivors. Of these 22, 27% were in a vegetative state, 36% had lower severe disability (dependent on others for care) and 36% had upper severe disability (independent at home) or better. This informs the debate around historical concerns that decompressive craniectomy simply increases the number of patients who survive in a vegetative state. While surgical intervention did result in more vegetative patients than medical management, it also resulted in higher rates of upper severe disability, which is considered a favorable outcome. The rates of moderate disability and good recovery were similar to those who received medical management.
Polar TBI
Question?
In patients with severe blunt traumatic brain injury (TBI) does early and sustained cooling compared with standard care improve neurological outcomes at 6 months?
JAMA 2018
POLAR TBI
Outcome?
aAm for normothermia in my patients with TBI
Significantly: hypothermia did not improve 6 month outcome, but increased pneumonia, ventilation days, bradycardia and noradrenaline use
Hypothermia did not reduce ICP
Pathophysiology of CSDH
Minor head injury that leads to a small haematoma from tearing of the stretched bridging veins that span the subdural space and are thus unsupported in those with cerebral atrophy.
The initial insult is often forgotten.
In a subset of patients an inflammatory neomembrane forms and potentiates ongoing haemorrhage and swelling of the enclosed haematoma by the breakdown of blood products and the development of an osmotic gradient across the neomembrane.
The clinical presentation can thus be several weeks after the initial insult
Clinical features of CSDH
Headache
Hemiparesis
Speech disturbance
Behavioural disturbance
Coma if large and untreated
Treatment of bilateral CSDH
More likely to progress to coma rapidly and are consequently treated at a lower absolute volume.
Locations of CSDH
Most commonly over the cerebral convexity but can be interhemispheric or over the tentorium and more rarely in the posterior fossa.
Treatment of CSDH
One or two burrholes
Mini-craniotomy
Closed drainage systems
Risks of treatment for CSDH
Infection
Seizures
Recurrence
Santarius et al 2009
The recurrence rate of subdurals can be reduced by subdural drain for 48h with no significant increase in morbidity.
Features of SAH in TBI
Frequent finding in closed head injuries due to direct damage to cortical vessels.
Correlates with poorer outcome and more severe injury,
Appears to be a reflection of a greater degree of violence at injury rather than secondary injury
Secondary insults associated with traumatic SAH
May contribute to cerebral swelling
Haemodynamically significant vasospasm (can be observed as early as 2 days post-injury)
Disturbance of cerebral autoregulation
Associations of traumatic SAH
Associated with the progression of associated cerebral contusions
More time spent on ICU
Less likely to be discharged home
1.5x more likely to due during acute hospitalisation
In penetrating TBI there is a significant association between SAH and poor outcome.
Epidemiology of IVH in TBI
1.5-3% of all head trauma
Predominantly severe.
Pathophysiology of traumatic IVH
Damage to septum pellucidum, choroid plexus and subependymal forniceal veins are seen at post-mortem exams in patiets with primary IVH
Px in TBI with iVH
22% regain independence
Types of cerebral contusions
Focal or mutlifocal
Cortical or subcortical regions
Herniating contusions
Intermediary contusions
Cerebral contusion
Herniating contusions
Occur when one tissue is displaced from one cranial compartment to another, typically along the margin of the falx, the tentorium or the foramen magnum, leading to compression of the herniating tissue.
Intermediary contusions
Subcortical lesions affecting the corpus callosum, basal ganglia, hypothalamus and brainstem.
When does cerebral oedema peak following TBI?
24h
Associated with marked reduction of CBF to the contused cortex which normalises 7/7 after injury during which focal areas of hyperaemia can appear.
Can be delayed as long as 10/7.
DAI pathophysiology
Caused by angular acceleration leading to damage of axonal integrity.
Diffuse brain injury is seen in up to 50% of TBIs
Defined as diffuse damage in the cerebellar hemispheres, corpus callosum, brainstem and cerebellum. Long tract structures (axons and blood vessels) are, particularly at risk.
DAI Grading system
Adams
1-3
Based on MR
Adams Grade 1
Grey-white matter interface (commonly parasagittal white matter of frontal lobes and periventricular temporal lobes)
In which patients are cerebral contusions more severe?
Frontal and temporal lobes
Those without lucid intervals
Adams Grade II
Focal lesions in the corpus callosum (commonly posterior body and splenium)
Adams Grade III
Brainstem (commonly dorsolateral and rostral midbrain, cerebellar peduncles, medial lemnisci and corticospinal tracts)
Px in DAI based on Adams garde
Grade I and II typically show marked improvement in GCS within 2/52
Grade III requires 2 months for recovery
Definitive diagnosis of DAI
Established by immunostaining for B-APP and autopsy and identifying axonal retraction balls in deep white matter.
Def: mild TBI/concussion
Transient neurological disturbance caused by rapid linear and/or rotational acceleration and deceleration forces resulting in a disruption in cerebral structure of vascular phsyiology.
Can be clinically based on LOC, loss of memory, alteration in mental state, focal neurological deficit.
What proportion of TBI patients categorised as “mild”
75%
Def: Penetrating brain injury
Non-blunt projectile breaching cranium and dura mater.
Associated with worse Px
Def: Perforating brain injury
When a projectile also causes an exit wound
Features of high-velocity penetrating brain injury
Generates wave of compression and re-expansion (cavitation wave) and inflicts focal shearing damage, parenchymal contusions and haematomas
What Ix should be performed in addition to plain CTH for penetrating brain injury?
CTA
High-risk factors in penetrating brain injury
Track crossing ventricle
Involving both hemispheres
Crossing the geographical centre of the brain
Associated vascular injury
Rate of seizures in PBI?
35-50%
What proportion of CO goes to the brain?
20%
What proportion of resting O2 is consumed by the brain?
20%
What is the CMRO2 of the brain
3.5ml O2/ 100g/ min
What happens to glucose metabolism following TBI?
Aerobic metabolism is the primary method of energy production.
Disturbed after TBI with a significant increase in anaerobic glycolytic turnover and elevated extracellular lactate.
Hyperglycolysis contributes to prolonged elevated lactate: glucose, CSF lactic acidosis and impaired mitochondrial function
Duration and extent of hyperglycolysis may correlate with the severity of the injury.
What happens to CMRO2 in TBI
Reduces in comatose patients with TBI
What is the Hagen-Poiseuille law?
Law of laminar flow in a cylindrical tube.
Can be used to describe CBF after TBI
CBF = k[CPP x d(4)]/ 8xlxv
Where K is a constant
d is the vessel diameter
l is artery length
v is blood viscosity.
Autoregulation maintains perfusion at what CPP?
60-160
What happens to autoregulation in severe TBI?
Autoregulation is impaired or absent in the majority of severe TBI patients at some point in their clinical course
When autoregulation is lost, the brain becomes vulnerable to systemic pressure disturbances leading to secondary insults (e.g. ischaemia from reduced CBF or oedema from excessive CBF)
Impact of blood viscosity on CBF
Hct and serum fibrinogen affect CBF and induce an autoregulatory response under normal physiological circumstances.
Increase in viscosity causes an increase in arterial dilatation as it reduces metabolic supply.
Following acute cerebral infarction, HCt and fibrinogen are associated with reduced CBF
What is CO2 reactivity?
The Process by which the PaCO2 affects CBF and the cerebral vasculature
Hypercarbia results in vasodilation
Hypocarbia in vasoconstriction
How is PaCO2 reactivity mediated?
Changes in perivascular pH via carbonic anhydrase
What is the acetazolamide challenge?
The normal response to acetazolamide administration is vasodilation and augmentation of CBF to 30-60% over 10-15 minutes
A failure to vasodilate in response to acetazolamide implies maximal vasodilation.
Blood gas changes in TBI
Hyperaemia and metabolic acidosis in CSF are associated with the acute phase of TBI (first 24h)
Persistent loss of CO2 reactivity risks severe neurological compromise.
Implications of CO2 reactivity?
Causes both changes in CBF and AVDO2
IMPACT trial and secondary brain injury
Identified hypoxia (20%) and hypotension (18%) of TBI patients.
What are the 5 clinical variables that have repeatedly correlated with poor outcome in TBI?
Arterial hypotension
Hypoxaemia
Reduced CPP
Raised ICP
Pyrexia
Glutamate mediated excitotoxicity in TBI
Glutamate activates NMDAR triggering neuronal depolarisation with unchecked Ca influx into mitochondria due to impaired ATP synthesis.
Mitochondrial dysfunction leads to damaged tissue energy failure.
These intracellular changes lead to cerebral oedema, raised ICP, vascular compression and herniation.
Lactate/pyruvate ratio
Measured with microdialysis
Marker of anaerobic respiration and correlates with outcome after TBI.
The raised ratio can be due to cerebral ischaemia or mitochondrial dysfunction.
Lactate is metabolised to pyruvate in the mitochondria of axons and astrocytes
Lactate/pyruvate ratio in severe TBI
Studies of patients with GCS <^ report a 25% incidence of reduced oxidative metabolism and metabolic crisis (LPR >40) despite absence of systemic ischaemia which suggest LPR is an indicator of widespread mitochondrial dysfunction causing metabolic depression following TBI.
What is PRx
Looks at the pressure reactivity index- response of ICP to CBV.
Between -1 and 1
-1 suggests good vasoreactivity.
Frequently compromised on the first day after TBI, and the loss of autoregulation in the first 48h has a strong indication for additional secondary injury.
Can allow real time CPPopt to maximise autoregulation.
Monroe Kelly doctrine
Under normal conditions, the total volume of the intracranial cavity remains constant.
Contains three components- blood, CSF and parenchyma
An increase in one leads to a compensatory reduction in another to try and maintain a constant ICP.
When compensatory mechanisms are exhausted, an exponential increase in ICP occurs.
Types of cerebral oedema
Vasogenic
Cytotoxic
Interstitial
Osmotic
Vasogenic oedema
Vasogenic edema occurs due to a breakdown of the tight endothelial junctions that make up the blood–brain barrier. This allows intravascular proteins and fluid to penetrate into the parenchymal extracellular space. Once plasma constituents cross the barrier, the edema spreads; this may be quite rapid and extensive. As water enters white matter, it moves extracellularly along fiber tracts and can also affect the gray matter. This type of edema may result from trauma, tumors, focal inflammation, late stages of cerebral ischemia and hypertensive encephalopathy.
Cytotoxic oedema
In cytotoxic edema, the blood–brain barrier remains intact but a disruption in cellular metabolism impairs functioning of the sodium and potassium pump in the glial cell membrane, leading to cellular retention of sodium and water. Swollen astrocytes occur in gray and white matter. Cytotoxic edema is seen with various toxins, including dinitrophenol, triethyltin, hexachlorophene, and isoniazid. It can occur in Reye’s syndrome, severe hypothermia, early ischemia, encephalopathy, early stroke or hypoxia, cardiac arrest, and pseudotumor cerebri.
Osmotic oedema
Normally, the osmolality of cerebral-spinal fluid (CSF) and extracellular fluid (ECF) in the brain is slightly lower than that of plasma. Plasma can be diluted by several mechanisms, including excessive water intake (or hyponatremia), syndrome of inappropriate antidiuretic hormone secretion (SIADH), hemodialysis, or rapid reduction of blood glucose in hyperosmolar hyperglycemic state (HHS), formerly known as hyperosmolar non-ketotic acidosis (HONK). Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared to the serum. This creates an abnormal pressure gradient and movement of water into the brain, which can cause progressive cerebral edema, resulting in a spectrum of signs and symptoms from headache and ataxia to seizures and coma.
Interstitial oedema
Interstitial edema occurs in obstructive hydrocephalus due to a rupture of the CSF–brain barrier. This results in trans-ependymal flow of CSF, causing CSF to penetrate the brain and spread to the extracellular spaces and the white matter. Interstitial cerebral edema differs from vasogenic edema as CSF contains almost no protein.
Changes in oedema after TBI
Three distinct mechanisms
Vasogenic- structural damage to BBB causes intravascular flow of protein-rich exudate into the interstitium, increasing extracellular volume without cell swelling.
Cytotoxic- ion influxes and increased membrane permeability causes cytotoxic oedema and cellular swelling
Osmotic- necrotic tissue is hyperosmolar, causing osmotic-gradient driven fluid accumulation in the cell.
Evidence for mannitol
Can initiate more tan 10% reduction in ICP among 86% of patients with autoregulation but only 35% of patients with impaired autoregulation.
Mannitol MOA
Osmotic diuretic
Free radical scavenger
Improving microvascular flow by dehydrating endothelial cells
Reducing HCt as well as the osmotic load.
What is the 1o cause of all TBI deaths?
Intractable ICP (46%)
Mannitol dose
1g/kg IV
Should be given once patient adequately volume resuscitated as can add to hypovolaemia
ISS rate goes from ?
0-75
Categorisation of secondary brain insults following TBI?
Systemic
Intracranial
Systemic insults following TBI
Hypoxia
Hypotension
Hypocapnia
Hypercapnia
Hypothermia
Hyperthermia
Hypoglycaemia
Hyperglycaemia
Hyponatraemia
Hypernatraemia
Hyperosmolality
Infection
Intracranial secondary insults following TBI
Seizure
Delayed haenatona
SAH
Vasospasm
HCP
Neuroinfection
