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Neurosurgical Training > Neurotrauma and intensive care > Flashcards

Neurotrauma and intensive care Flashcards

1
Q

Def: WHO TBI

A

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

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2
Q

Menon Def: TBI

A

Alteration in brain function or other evidence of brain pathology caused by an external force

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3
Q

Most common cause of TBI in lower and middle-income countries?

A

Motor vehicles

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4
Q

Most common cause of TBI in Europe?

A

Falls

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5
Q

Incidence rate of TBI related hospital admissions?

A

262 per 100,000

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6
Q

Main causes of TBI

A

RTA

Falls

Violence

Work and sports

Others

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7
Q

What is the reduction in life-expectancy after receiving in patient rehab for TBI?

A

9 year reduction

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8
Q

Mortality incidence of TBI in Europe?

A

11.2/100,000

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9
Q

Classification of TBI:

Mechanism

A

Closed

Penetrating

Crush

Blast

Combined

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10
Q

Clinical severity grading of TBI?

A

Mild, Moderate, Severe

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11
Q

TBI clinical grading:

Mild severity

A

14-15

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12
Q

TBI clinical grading:

Moderate severity

A

9-13

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13
Q

TBI clinical grading:

Severe

A

GCS 3-8

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14
Q

Injury burden grading of TBI

AIS

A

Using Abbreviation Injury Score

Severity scoring for 6 body regions

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15
Q

ISS

A

Aims to summarise the total burden of injury by adding the quadratic scores of the three body regions with the highest score

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16
Q

What are two models that can be used to prognosticate TBI?

A

IMPACT

CRASH

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17
Q

Features of IMPACT

A

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)

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18
Q

Additional factors impacting on Px in head injury

A

MRI burden of injury

Comorbidities

ISS

Time to craniotomy >4h

Autoregulatory indices

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19
Q

Which biomarkers have been suggested as tools for prognostication in TBI?

A

S100 beta protein

ApoE4

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20
Q

S100 beta protein

A

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

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21
Q

ApoE4

A

ApoE4 allele might be associated with poor prognosis in patients with severe TBI

May also be used as a biomarker

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22
Q

Features of GOS

A

Initially described as a global assessment of function following TBI

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23
Q

GOS

Number of categories

A

5

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24
Q

GOS 1

A

Dead

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25
Q

GOS 2

A

PVS

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26
Q

GOS 3

A

Severe disability (conscious but dependent)

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27
Q

GOS 4

A

Moderate disability (independent but disabled)

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28
Q

GOS 5

A

Good recovery

(Can resume normal activities)

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29
Q

GOS E

Number of categories

A

8

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30
Q

GOSE 1

A

Dead

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31
Q

GOSE 2

A

PVS

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32
Q

GOSE 3

A

Lower severe disability

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33
Q

GOSE 4

A

Upper severe disability

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34
Q

GOSE 5

A

Lower moderate disability

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35
Q

GOSE 6

A

Upper moderate disability

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36
Q

GOSE 7

A

Lower good recovery

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37
Q

GOSE 8

A

Upper good recvoery

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38
Q

Neuropsychological sequelae of TBI

A

Mood disturbance

Cognitive impairment

Personality changes

Social

Family effects

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39
Q

Mortality in patients with severe TBI

A

36%

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40
Q

Rate of good recovery in patients with severe TBI?

A

5%

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41
Q

Mortality in patients with moderate TBI?

A

7%

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42
Q

Rate of good recovery in patients with moderate TBI

A

60%

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43
Q

Def: Primary brain injury

A

Mechanical load that translates into deformation of cerebral tissue which then initiate cellular responses that lead to disturbances in autoregulation and metabolism

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44
Q

Consequences of impact loading

A

Skull #

EDH

Contusions (coup or contrecoup)

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45
Q

Pathology of contrecoup lesions

A

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.

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46
Q

Contusion after early trauma

A

More severe at the crest of gyrus than at the sulcus

Associated with swelling that subsides with time

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47
Q

Consequences of impulse loading

A

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.

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48
Q

Mobility of brain parenchyma

A

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.

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49
Q

What structures are vulnerable to DAI?

A

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.

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50
Q

What movements are necessary to generate SDH?

A

General translational and angular motion of the head.

Rotational insults induce shear straing.

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51
Q

With what injury mechanism are SDH most prealent?

A

When a single inertial load combineswith a minor trauma impact load

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52
Q

Static or quasi-static loading

A

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.

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53
Q

Morphological classification of TBI

A

Focal or diffuse

Anatomical

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54
Q

Epidemiology of EDH

A

2% of all brain injuries

More common in patients <50

Particularly in paediatric patients primarily due to meningeal and diploic bein haemorrhage

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55
Q

Pathology of EDH

A

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

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56
Q

What causes the occasional delayed presentation in children?

A

Dura is tightly adherent to skull

Lower venous pressure

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57
Q

Radiographic categorisation of EDH

A

Type 1- acute

Type 2- subacute

Type 3- chronic

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58
Q

Radiographic progression of EDH

A

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.

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59
Q

What proportion of patients experience the lucid interval classic for EDH?

A

15-20%

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60
Q

Features of neurological deterioration after EDH

A

Contralateral hemiparesis

Ipsilateral oculomotor nerve paresis

Decerebrate rigidity

Arterial hypertension

Cardiac arrhythmias

Respiratory disturbanecs if uncorrected leading to apnoea and death.

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61
Q

Pathophysiology of SDh

A

Tearing of dural bridging veins

Tearing of superficial pial arteries

62
Q

Acute SDH

A

Crescent-shaped, hyperdense collection

63
Q
A

ASDH

64
Q

Subacute SDH

A

Isodense

Symptomatic improvement

7-21/7

65
Q
A

Subacute SDH

66
Q

Chronic SDH

A

>21/7

Hypodense

May not present symptomatically until there is significant mass effect

67
Q
A

Chronic SDH

68
Q

Clinical features of ASDH

A

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

69
Q

Post-op complications for SDH evacuation

A

Reaccumulation

Infection (e.g. osteomyelitis, meningitis, ventriculitis)

70
Q

Mortality rates in acute traumatic SDH

A

22-66%

71
Q

Mortality rate for ASDH decompression within 4h

A

30%

72
Q

The mortality rate for acute SDH evacuated after 4h

A

90%

73
Q

Predictors for prognosis in SDH

A

Time to evacuation

Age

Extent of neurological deficit

Sex

Post-op ICP

74
Q

Mannitol dose?

A

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

75
Q

DECRA trial

Question?

A

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

76
Q

DECRA trial

Bottom line

A

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

77
Q

RESCUE ICP

Question?

A

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)?

78
Q

RESCUE ICP

Bottom line

A

. 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.

79
Q

Polar TBI

Question?

A

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

80
Q

POLAR TBI

Outcome?

A

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

81
Q

Pathophysiology of CSDH

A

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

82
Q

Clinical features of CSDH

A

Headache

Hemiparesis

Speech disturbance

Behavioural disturbance

Coma if large and untreated

83
Q

Treatment of bilateral CSDH

A

More likely to progress to coma rapidly and are consequently treated at a lower absolute volume.

84
Q

Locations of CSDH

A

Most commonly over the cerebral convexity but can be interhemispheric or over the tentorium and more rarely in the posterior fossa.

85
Q

Treatment of CSDH

A

One or two burrholes

Mini-craniotomy

Closed drainage systems

86
Q

Risks of treatment for CSDH

A

Infection

Seizures

Recurrence

87
Q

Santarius et al 2009

A

The recurrence rate of subdurals can be reduced by subdural drain for 48h with no significant increase in morbidity.

88
Q

Features of SAH in TBI

A

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

89
Q

Secondary insults associated with traumatic SAH

A

May contribute to cerebral swelling

Haemodynamically significant vasospasm (can be observed as early as 2 days post-injury)

Disturbance of cerebral autoregulation

90
Q

Associations of traumatic SAH

A

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.

91
Q

Epidemiology of IVH in TBI

A

1.5-3% of all head trauma

Predominantly severe.

92
Q

Pathophysiology of traumatic IVH

A

Damage to septum pellucidum, choroid plexus and subependymal forniceal veins are seen at post-mortem exams in patiets with primary IVH

93
Q

Px in TBI with iVH

A

22% regain independence

94
Q

Types of cerebral contusions

A

Focal or mutlifocal

Cortical or subcortical regions

Herniating contusions

Intermediary contusions

95
Q
A

Cerebral contusion

96
Q

Herniating contusions

A

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.

97
Q

Intermediary contusions

A

Subcortical lesions affecting the corpus callosum, basal ganglia, hypothalamus and brainstem.

98
Q

When does cerebral oedema peak following TBI?

A

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.

99
Q

DAI pathophysiology

A

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.

100
Q

DAI Grading system

A

Adams

1-3

Based on MR

101
Q

Adams Grade 1

A

Grey-white matter interface (commonly parasagittal white matter of frontal lobes and periventricular temporal lobes)

102
Q

In which patients are cerebral contusions more severe?

A

Frontal and temporal lobes

Those without lucid intervals

103
Q

Adams Grade II

A

Focal lesions in the corpus callosum (commonly posterior body and splenium)

104
Q

Adams Grade III

A

Brainstem (commonly dorsolateral and rostral midbrain, cerebellar peduncles, medial lemnisci and corticospinal tracts)

105
Q

Px in DAI based on Adams garde

A

Grade I and II typically show marked improvement in GCS within 2/52

Grade III requires 2 months for recovery

106
Q

Definitive diagnosis of DAI

A

Established by immunostaining for B-APP and autopsy and identifying axonal retraction balls in deep white matter.

107
Q

Def: mild TBI/concussion

A

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.

108
Q

What proportion of TBI patients categorised as “mild”

A

75%

109
Q

Def: Penetrating brain injury

A

Non-blunt projectile breaching cranium and dura mater.

Associated with worse Px

110
Q

Def: Perforating brain injury

A

When a projectile also causes an exit wound

111
Q

Features of high-velocity penetrating brain injury

A

Generates wave of compression and re-expansion (cavitation wave) and inflicts focal shearing damage, parenchymal contusions and haematomas

112
Q

What Ix should be performed in addition to plain CTH for penetrating brain injury?

A

CTA

113
Q

High-risk factors in penetrating brain injury

A

Track crossing ventricle

Involving both hemispheres

Crossing the geographical centre of the brain

Associated vascular injury

114
Q

Rate of seizures in PBI?

A

35-50%

115
Q

What proportion of CO goes to the brain?

A

20%

116
Q

What proportion of resting O2 is consumed by the brain?

A

20%

117
Q

What is the CMRO2 of the brain

A

3.5ml O2/ 100g/ min

118
Q

What happens to glucose metabolism following TBI?

A

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.

119
Q

What happens to CMRO2 in TBI

A

Reduces in comatose patients with TBI

120
Q

What is the Hagen-Poiseuille law?

A

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.

121
Q

Autoregulation maintains perfusion at what CPP?

A

60-160

122
Q

What happens to autoregulation in severe TBI?

A

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)

123
Q

Impact of blood viscosity on CBF

A

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

124
Q

What is CO2 reactivity?

A

The Process by which the PaCO2 affects CBF and the cerebral vasculature

Hypercarbia results in vasodilation

Hypocarbia in vasoconstriction

125
Q

How is PaCO2 reactivity mediated?

A

Changes in perivascular pH via carbonic anhydrase

126
Q

What is the acetazolamide challenge?

A

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.

127
Q

Blood gas changes in TBI

A

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.

128
Q

Implications of CO2 reactivity?

A

Causes both changes in CBF and AVDO2

129
Q

IMPACT trial and secondary brain injury

A

Identified hypoxia (20%) and hypotension (18%) of TBI patients.

130
Q

What are the 5 clinical variables that have repeatedly correlated with poor outcome in TBI?

A

Arterial hypotension

Hypoxaemia

Reduced CPP

Raised ICP

Pyrexia

131
Q

Glutamate mediated excitotoxicity in TBI

A

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.

132
Q

Lactate/pyruvate ratio

A

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

133
Q

Lactate/pyruvate ratio in severe TBI

A

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.

134
Q

What is PRx

A

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.

135
Q

Monroe Kelly doctrine

A

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.

136
Q

Types of cerebral oedema

A

Vasogenic

Cytotoxic

Interstitial

Osmotic

137
Q

Vasogenic oedema

A

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.

138
Q

Cytotoxic oedema

A

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.

139
Q

Osmotic oedema

A

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.

140
Q

Interstitial oedema

A

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.

141
Q

Changes in oedema after TBI

A

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.

142
Q

Evidence for mannitol

A

Can initiate more tan 10% reduction in ICP among 86% of patients with autoregulation but only 35% of patients with impaired autoregulation.

143
Q

Mannitol MOA

A

Osmotic diuretic

Free radical scavenger

Improving microvascular flow by dehydrating endothelial cells

Reducing HCt as well as the osmotic load.

144
Q

What is the 1o cause of all TBI deaths?

A

Intractable ICP (46%)

145
Q

Mannitol dose

A

1g/kg IV

Should be given once patient adequately volume resuscitated as can add to hypovolaemia

146
Q

ISS rate goes from ?

A

0-75

147
Q

Categorisation of secondary brain insults following TBI?

A

Systemic

Intracranial

148
Q

Systemic insults following TBI

A

Hypoxia

Hypotension

Hypocapnia

Hypercapnia

Hypothermia

Hyperthermia

Hypoglycaemia

Hyperglycaemia

Hyponatraemia

Hypernatraemia

Hyperosmolality

Infection

149
Q

Intracranial secondary insults following TBI

A

Seizure

Delayed haenatona

SAH

Vasospasm

HCP

Neuroinfection

150
Q
A

Neurosurgical Training (7 decks)

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