Assessment of BTF

Assessment of
traumatic brain
injury, acute
The right clinical information, right where it's needed
Last updated: Nov 20, 2018

Table of Contents
Summary 3
Overview 7
Aetiology 7
Emergencies 10
Urgent considerations 10
Diagnosis 16
Step-by-step diagnostic approach 16
Differential diagnosis overview 23
Differential diagnosis 24
Diagnostic guidelines 33
Online resources 35
References 36
Images 46
Disclaimer 49
Summary
◊ Definitions :
Head injury is defined as any trauma to the head, with or without injury to the brain. The head injury
can be described as minimal, minor, moderate, or severe, based on symptoms after the injury.
Patients with minimal head injury are those with trauma to the head and no loss of consciousness,
a normal Glasgow Coma Scale (GCS) score, and no symptoms of head injury. Minor head injury
patients have a GCS of 13 to 15 after head injury.[1]
Traumatic brain injury (TBI) is a non-specific term describing blunt, penetrating, or blast injuries to
the brain. TBI can be classified as mild, moderate, or severe, typically based on the GCS and/or
neurobehavioural deficits after the injury.
The term 'concussion' is often used interchangeably with mild TBI and minimal or minor head injury
in the sports literature. Both the Centers for Disease Control and Prevention and the World Health
Organization agree that mild TBI is due to a blunt or mechanical force that results in some type of
transient confusion, disorientation or loss of consciousness lasting not more than 30 minutes, and
possibly associated with transient neurobehavioural deficits and a GCS no worse than 13 to 15.[2]
[CDC: heads up] However, there is ongoing debate about whether patients with a GCS of 13 should
instead be classified as having moderate TBI.
◊ Classification :
TBI can be classified in numerous ways, including type, severity, location, mechanism of injury, and
physiological response to injury. This heterogeneity is considered to be one of the most significant
barriers to establishing effective therapeutic interventions in TBI.[3] Efforts in the US and the UK to
standardise the naming, definitions, and classification of TBI subgroups have the potential to reduce
the variability in data coding and improve the quality of data gathering in TBI research.[4] [5] [6]
◊ Classification by clinical severity :

The GCS has been used extensively to classify TBI into levels of severity and prognosis.[7] [8] After
traumatic brain injury, there is an inverse relationship between the GCS score and the incidence
of positive findings on CT; in fact, the rate of intracranial injury (ICI) and need for neurosurgical
intervention doubles when the GCS drops from 15 to 14.[9] [10]
• Mild/Minor TBI: GCS 13-15; mortality 0.1%
• Moderate TBI: GCS 9-12; mortality 10%
• Severe TBI: GCS <9; mortality 40%.
Many authors recommend that patients with a GCS of 13 be classified as moderate instead of mild
or minor, due to the higher incidence of ICI and poor outcomes in these patients.[11] [12] [13] [14]
Clinical guidelines in Australia recognise the increased morbidity associated with a GCS of 13, and
limit the classification of mild TBI to those patients with a GCS of 14 or 15.[15]
The Mayo classification system for TBI classifies patients with TBI into definite, probable, and
possible, based on the patient’s clinical and CT findings.[16]
◊ Classification by broad aetiology :

• Blunt TBI: occurs when external mechanical force leads to rapid acceleration or deceleration
with brain impact. It is typically found in the setting of motor vehicle-related injury, falls, crush
injuries, or physical altercations.
• Penetrating TBI: occurs when an object pierces the skull and breaches the dura mater, seen
commonly in gunshot and stab wounds.
• Blast TBI: commonly occurs after bombings and warfare, due to a combination of contact and
inertial forces, overpressure, and acoustic waves.[17]
◊ Classification by involvement :
TBI can be classified by area involved, as in diffuse or focal, although the two types frequently
coexist.
• Diffuse brain injury includes diffuse axonal injury (DAI), hypoxic brain injury, diffuse cerebral
oedema, or diffuse vascular injury.[18]
• Focal injury includes specific lesions such as contusions, intracranial haematomas, infarctions,
axonal tears, cranial nerve evulsions, and skull fractures.[18]
◊ Classification by injury progression :

Primary injury is due to the immediate mechanical force, whether blunt, penetrating, or blast, and
may include the following:
• Skull fracture
• Contusion
• Haematoma
• Subarachnoid or focal haemorrhage
• Axonal shear or laceration.
Secondary injury refers to the evolving pathophysiological consequences of the primary injury and
encompasses a multitude of complex neurobiological cascades altered or initiated at a cellular level
following the primary injury, and may include the following:[18]
• Cerebral oedema
• Increased intracranial pressure (ICP)
• Haemorrhage
• Seizures
• Ischaemia
• Infection.
◊ Epidemiology of TBI :
TBI is a substantial cause of morbidity and mortality, leading to more than 2 million accident and
emergency department visits annually in the US,[19] and more than 1 million in the UK.[20] A 2017
review highlighted the higher burden of disability and death due to TBI in low- and middle-income
countries compared with high-income countries.[21]
Around 80% of patients with TBI have minor head injury, and are treated and released without
hospital admission or intervention other than diagnostic imaging.[22] About 20% have injuries that
require hospitalisation, 6% suffer permanent disability, and about 3% die.[23] [24]
TBI is the most common cause of death in people under the age of 25. It most frequently occurs
in very young children (age 0 to 4 years) and in adolescence and young adulthood (age 15 to 24
years), with a subsequent peak in incidence in older adults (over age 65). Older age comprises the
group with the highest rates of TBI-related hospitalisations and deaths.[25] [26]
Males are over-represented by 3:1 in all subgroups of TBI. Neurosurgical intervention (craniotomy,
elevation of skull fracture, ICP monitor, or ventriculostomy) is required in about 40% of patients with
severe TBI, about 10% of patient with moderate TBI, and about 1% of patients with minor TBI.[8] [27]
Post-concussive syndrome is the neurobehavioural sequelae of even mild TBI, which encompasses
somatic, cognitive, and affective domains, and patients commonly report headache, dizziness,
difficulty concentrating, and depression. Approximately 30% of children and adults experience
persistent post-concussive symptoms more than 30 days after injury.[28] [29]
Medical costs and losses due to either temporary or permanent gaps in productivity are estimated
to annually exceed £15 billion in the UK[30] [31] and $70 billion in the US.[32] Even in mild TBI,
persistent neurocognitive dysfunction can occur, exacting a significant emotional toll on patients and
families, and a financial toll on society. Some patients with a discharge diagnosis of mild TBI will
have symptoms at 3 months post-injury. [33]
◊ Epidemiology of specific injuries :

Most patients have a combination of injuries.
Traumatic subarachnoid haemorrhage (SAH) is one of the most common CT findings in TBI,
occurring in about 30% to 40% of patients with moderate to severe TBI, and 5% of patients with
minor TBI.[8] [34] [35] SAH is frequently associated with other injuries. SAH is associated with
a poorer outcome in patients with moderate or severe TBI, although it is unclear whether the
SAH is simply a marker of severity of injury, or if the poorer outcomes are due to subsequent
vasospasm.[36]
Subdural haematomas (SDH) are the most common type of mass lesion in TBI, seen in about 20%
of patients with moderate to severe TBI, and in about 30% of fatal TBI. SDH occur in only 3% of
patients with minor TBI. SDH that lead to hospitalisations or deaths are most commonly secondary to
motor vehicle-related injury in younger adults, and to falls in older adults.[8] [27]
Epidural haematomas (EDH) are seen in about 10% of patients with moderate to severe TBI and
about 1% of patients with minor TBI. The incidence of EDH is highest among adolescents and young
adults, most commonly between 20 and 30 years of age. Most cases of EDH are caused by traffic
accidents, falls, and assaults.[8] [34]
Contusions occur in 20% to 30% of patients with moderate to severe TBI, and 6% of patients with
minor TBI.[8] [35] [37]
Intracerebral haematomas occur in 10% to 30% of patients with moderate to severe TBI, and <1% of
patients with minor TBI.[8] [18]
Diffuse axonal injury (DAI) is probably present in a majority proportion of patients with TBI to some
degree, although low grade axonal injury is usually microscopic and not detected by CT. The initial
CT is normal in 50% to 80% of patients ultimately diagnosed with DAI, but MRI shows evidence of
axonal injury in 70% of patients with moderate to severe TBI. Axonal injury is detected in <1% of
patients with minor TBI on CT, although the degree of microscopic injury is greater on MRI. Some
degree of DAI is thought to be present in all TBI-related fatalities and those resulting in a persistent
vegetative state.[8] [38]
Skull fractures occur in about 5% of patients with mild TBI and up to 50% of those with severe TBI.
Most skull fractures are due to falls, assaults, or motor vehicle-related injuries. The most common
fractures are simple linear fractures, comprising >50% of all skull fractures. Less than 1% of patients
with minor TBI have a depressed skull fracture.[8]
Penetrating injuries are classified as high- or low-velocity, and may be self-inflicted, non-intentional,
or related to an assault. A single gunshot wound to the head has 50% mortality.[39]
Blast injuries are a leading cause of TBI in active duty military personnel in war zones, accounting for
about 60% of all severe TBI.[40] [41]
Assessment of traumatic brain injury, acute Overview
Aetiology
The most common causes of TBI are the following:
OVERVIEW
• Falls - 35%
• Motor vehicle-related injury - 17%
• Non-intentionally being struck by or against an object - 16%
• Assaults - 10%.
Falls are the most common cause of TBI, primarily occurring in very young children and older adult age
groups. Falls are the second leading cause of TBI-related mortality, and occur most frequently in people over
age 65 years.[23] Age is a much stronger predictor of poor outcome, in any type of TBI, than the specific
cause of the injury.[25] [42]
Motor vehicle-related injuries are the second leading cause of TBI, and are the leading cause of TBI-related
deaths. Motor vehicle-related injuries include those due to motor vehicles, motorcycles, and bicycles, as well
as pedestrians struck by vehicles. Mortality is greatest in people ages 20 to 24.[23]
Being non-intentionally struck by or against an object is the third leading cause of TBI. It more commonly
causes mild-to-moderate TBI, and associated mortality is the lowest of the common causes of TBI. These
injuries encompass being non-intentionally struck (hit) by or crushed by a human, animal, or inanimate object
or force other than a vehicle, and therefore include injuries due to contact sports or high-risk recreational
activities.[23] More than 1 million sports-related concussive injuries occur annually in the US, and, although
rare, fatal brain injuries have been documented in almost every contact sport.[43]
Assaults are currently the fourth leading cause of TBI and the third leading cause of TBI-related deaths, with
mortality highest in the 20- to 35-year-old age group. Firearms are the most common cause of mortality due
to assault.[23]
Aetiology of specific injuries

The aetiology of TBI can be considered under the following categories: haemorrhage, brain tissue injury,
diffuse axonal injury, skull fractures, penetrating injuries, blast injuries, and mild TBI.
Haemorrhage
Traumatic subarachnoid haemorrhage (SAH) is caused by tearing of the pial vessels and, if severe,
haemorrhage can extend into the ventricles, causing intraventricular haemorrhage. Traumatic SAH is
associated with a poorer outcome in patients with moderate or severe TBI, but it is unclear whether the
SAH is simply a marker of severity of injury or if the haemorrhage itself causes poorer outcomes due to
vasospasm.[44]
Subdural haematoma (SDH) most often occurs as a result of tearing of the bridging veins coursing to the
dural venous sinuses. SDH most commonly occurs after a motor vehicle-related injury or fall, and people with
pre-existing cerebral atrophy or coagulopathies have an increased risk of SDH.
Epidural haematoma (EDH) is a collection of blood between the skull and the dura, typically caused by
a direct force to the skull from a motor vehicle injury, fall, or assault. Classically, a blow to the side of the
head causes a temporal bone fracture with associated middle meningeal artery disruption and subsequent
haematoma formation.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 20, 2018.
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Intracerebral haematomas are thought to be caused by a tear of a parenchymal vessel or the coalescence of
cerebral contusions.
Brain tissue injury

OVERVIEW
Contusions are caused by direct trauma, or due to acceleration-deceleration injury causing the brain to
impact the frontal or temporal regions of the skull, resulting in multiple punctate haemorrhages and oedema.
Diffuse axonal injury

Diffuse axonal injury (DAI) occurs due to a rapid rotational or deceleration force that causes stretching
and tearing of neurons, followed by focal areas of haemorrhage and oedema. In mild axonal injury,
damage is typically microscopic. In more severe injury, the CT may be normal or may show small petechial
haemorrhages and oedema located at the grey-white matter junction (Grade 1) as well as in the corpus
callosum (Grade 2) and in the brainstem (Grade 3); the grades correspond well with severity of injury and
ultimate outcomes. An MRI is indicated when the CT does not explain the clinical findings. Severe DAI can
result in almost instantaneous loss of consciousness and lead to a persistent vegetative state.[38]
Skull fractures
Skull fractures are caused by direct impact and may be linear or comminuted. Fractures may be located
on the cranial vault or in the basilar skull, and may have a varying degree of depression. Fractures can be
closed or open, communicating externally via wounds, facial sinuses, the auditory canal, or the oropharynx.
The location of skull fractures has implications for adjacent anatomical structures as follows:
• Fractures of the temporal bone that cross the meningeal artery are associated with epidural
haematomas; those that cross a dural sinus can cause significant subdural haemorrhage and
haematoma formation.
• The bones of the base of the skull are relatively thick; therefore, any basilar skull fracture implies a
serious mechanism of injury with high risk of intracerebral injury.
• Because the dura is tightly adhered to the base of the skull, basilar skull fractures are frequently
associated with dural tears and cerebrospinal fluid leaks.
• Fractures that involve the carotid canal can cause carotid artery dissection.
• Basilar skull fractures that extend to the petrous part of the temporal bone can damage cranial nerves
VII and VIII.
Penetrating injuries
Penetrating injuries are either high- or low-velocity. High-velocity missiles such as bullets can cause skull
fractures, parenchymal lacerations, contusions, axonal shear, and haematoma formation. Low-velocity
wounds such as a knife wound can penetrate the thinner bones of the skull, including the orbital wall and
parts of the temporal bone. Damage to the parenchyma tends to be limited to the wound tract in low-velocity
injuries, but high-velocity missiles can cause concomitant blast injury to surrounding structures.
Blast injuries
Blast injuries cause a variety of complex damage patterns. The initial blast wave is thought to cause a
concussive shearing force that leads to axonal injury, SAH, and contusions. The secondary blast effects of
flying debris can cause penetrating injuries, and the tertiary effects are the acceleration-deceleration impact
injuries seen after the blast wave passes.
8 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 20, 2018.
TBI due to blast is most commonly manifest as diffuse axonal injury, contusion, and subdural
haemorrhage.[45] Patients with moderate to severe TBI due to blasts or explosions tend to be self-evident
due to their decreased Glasgow Coma Scale (GCS) score, but may be undiagnosed in the presence of
a normal GCS. Studies have shown that there is a significant overlap in the diagnosis of post-concussive
OVERVIEW
syndrome and post-traumatic stress disorder after mild TBI in the setting of blast injury.[46]
Mild TBI
Mild TBI accounts for about 75% of all TBI, and a growing body of literature suggests that microscopic injury
at the level of the neuronal membrane initiates a cascade of neurohormonal and neuroexcitatory processes
that result in the cognitive, somatic, and affective symptoms patients experience after mild TBI. These
injuries are undetected by standard CT, but white matter changes can be visualised using diffusion tensor
imaging (an advanced MRI technique).[47]
9
Assessment of traumatic brain injury, acute Emergencies
Urgent considerations
(See Differential diagnosis for more details)
Management of patients with TBI requires rapid and thorough assessment, and frequently requires initiation
of treatment prior to definitive diagnosis. All patients with suspected TBI should be treated in a manner
that carefully achieves and maintains physiological parameters, with the goal of averting damage due to
secondary injury. Polytrauma is frequently the rule, and the approach to patients with TBI must be systematic
to ensure that occult injuries are identified. Neurosurgical intervention can be expected in about 40% of
patients with severe TBI and about 10% of patients with moderate TBI.[27] [32]
Initial approach: airway, breathing, circulation, disability

The initial approach to a patient with TBI includes the rapid assessment of airway, breathing, circulation,
and disability, with appropriate interventions as indicated. The pre-hospital environment should be secured
to minimise risk to bystanders and emergency personnel. The UK National Institute for Health and Care
Excellence guidelines, Advanced Trauma Life Support protocols and the European Trauma Course are
EMERGENCIES
useful guides in the initial assessment and management of patients with TBI.[20] [48] [49] Polytrauma is
common and systemic injuries confer a significantly greater threat to life than does isolated TBI.[48] About
40% to 50% of patients with severe TBI have other co-existing serious traumatic injuries, and up to 10%
have co-existing spinal cord injury.[50] [51] Cervical collars and spinal boards should be instituted until spinal
injury has been ruled out.
The airway and breathing

The initial assessment of airway and breathing must coincide with assessment of need for cervical spine
immobilisation, due to the increased risk of cervical spine injury in patients with TBI.[20] [48] Hypoxia and
hypercapnia are both known to worsen outcomes in TBI. Studies have shown that even one episode of
hypoxia is significantly associated with a worse outcome, and periods of hyper- or hypocapnia are both
associated with poorer outcomes.[52] In the pre-hospital setting, airway adjuncts should be initiated if the
patient with TBI is not spontaneously breathing, not able to maintain an open airway or not able to maintain
>90% oxygen saturation with supplementary oxygen.[53] Upon arrival in the emergency department,
guidelines from the US and the UK suggest placement of a definitive airway in the patient with TBI and
a Glasgow Coma Scale (GCS) score of <9.[20] [48] Although neuromuscular blockade does not affect
pupillary response, it is important to document the baseline neurological examination, and to use short-acting
paralytics that allow for frequent re-assessment of the neurological status.[54]
Oxygenation and ventilation parameters should be monitored using continuous pulse oximetry.[32] Ventilation
should be monitored using continuous capnography with an end-tidal CO₂ target of 35 to 40 mmHg.[53] [55]
[56]
Routine hyperventilation should not be performed and is only indicated as a temporising measure when a
patient with TBI has clinical evidence of cerebral herniation, such as asymmetric pupils, dilated and non-
reactive pupils, extension motor posturing, progressive neurological deterioration, or flaccidity.[53]
Circulation
Even one episode of pre-hospital or in-hospital hypotension negatively impacts outcome after brain injury.[26]
[57] [58] [59] [60] In most cases hypotension is caused by extracranial bleeding, although autonomic
dysfunction due to the TBI can contribute to hypotension. Past studies have shown that a systolic BP of less
than 90 mmHg is associated with poor outcomes in TBI.[57] [58] Other studies suggest that a target of 90
mmHg underestimates hypotension-related secondary brain injury and may worsen outcomes.[61] [62] In
2012, a study suggested that patient outcomes improved when systolic BP was maintained at ≥100 mmHg
for patients 50 to 69 years old, or at ≥110 mmHg for patients 15 to 49 years old, or over 70 years old.[62]
The Brain Trauma Foundation has adopted these higher, age-based systolic BP targets as a Level 3
recommendation in its 2016 guideline update.[7]
The concern that fluid resuscitation may worsen cerebral oedema and/or bleeding is theoretical, and studies
have repeatedly demonstrated that patients who remain normotensive have improved outcomes. Isotonic
saline remains the resuscitative fluid of choice for patients with isolated TBI,[63] with blood products used as
appropriate in the polytrauma patient. Saline should be given in 2-litre boluses in the adult patient and 20 mL/
kg boluses in the paediatric patient.[53]
Disability: initial neurological examination

A brief, focused neurological examination should be performed with attention to the Glasgow Coma
Scale (GCS), pupillary examination, and motor function. The GCS is widely used to assess the level of
EMERGENCIES
consciousness in patients with TBI, and provides fairly good prognostic information (when score is very low
or very high) that allows the physician to plan for expected diagnostic and monitoring requirements.[64] A
score of 13 to 15 is associated with good outcomes, although it cannot be used to rule out intracranial injury.
A score of less than 9 is associated with clinical deterioration and poor outcomes. Serial GCS monitoring
provides clinical warnings of deterioration. The Simplified Motor Score (obeys commands = 2, localises
pain = 1, and withdraws to pain or worse = 0) has been shown to have predictive power similar to the
GCS.[65] Similarly, use of a binary assessment of the GCS-motor (GCS-m) score to determine if the patients
obeys commands or not (i.e., GCS-m score <6 if patient does not obey commands; GCS-m score=6 if patient
obeys commands) has been proposed as a triage tool for out-of-hospital care. A retrospective analysis found
a GCS-m score of <6 predicts serious injury as well as the total GCS score.[66] The FOUR scale, which
adds brainstem reflexes and respiratory patterns to motor and eye findings, has also been shown to have
similar predictive power to the GCS.[67] [68]
11
EMERGENCIES Assessment of traumatic brain injury, acute Emergencies
The adult and paediatric GCS

Used with kind permission from Dr Micelle J. Haydel
Pupillary reflexes function as an indication of both underlying pathology and severity of injury, and should
be monitored serially. The pupillary examination can be assessed in an unconscious patient or in a patient
receiving neuromuscular blocking agents or sedation.[18] [69]
• Pupil size:
• The normal diameter of the pupil is between 2 and 5 mm, and although both pupils should be
equal in size, a 1-mm difference is considered a normal variant.
• Abnormal size is noted by anisocoria: >1 mm difference between pupils.
• Pupil symmetry:
• Normal pupils are round, but can be irregular due to ophthalmological surgeries.
• Abnormal symmetry may result from compression of CNIII can cause a pupil to initially become
oval before becoming dilated and fixed.
• Direct light reflex:
• Normal pupils constrict briskly in response to light, but may be poorly responsive due to
ophthalmological medications.
• Abnormal light reflex may be seen in sluggish pupillary responses are associated with increased
intracranial pressure (ICP). A non-reactive, fixed pupil has <1 mm response to bright light and is
associated with severely increased ICP.
Sedation and analgesia

Patients with moderate TBI often have considerable agitation, and patients with multi-trauma often have
other painful injuries. Pain and agitation are thought to amplify the metabolic demands due to associated
increases in heart rate, blood pressure, temperature, and ICP.[48] Pain and agitation can also lead to
difficulties in obtaining imaging studies and evaluating physiological responses to resuscitative measures.
The disadvantages to using analgesics or sedatives include the potential for depression in cardiorespiratory
function and compromised assessment of neurological status. Analgesic and anxiolytic medications should
be given after a full neurological examination has been performed, and then in consideration of the overall
haemodynamic status of the patient. Short-acting agents are preferable until the patient has been stabilised
EMERGENCIES
and has a definitive diagnosis.
Approach to elevated ICP

Patients with TBI and elevated ICP may exhibit vomiting, altered mental status, occulomotor defects,
and pupillary deficits. Late signs of elevated ICP and herniation include bilateral fixed and dilated pupils,
Kussmaul respirations, and Cushing’s Triad (increased systolic BP, bradycardia, and increased pulse-
pressure). Treatment of increased ICP must focus on volume reduction of one of the following: brain
parenchyma, cerebrospinal fluid, intravascular blood volume, or an intracranial mass lesion.
Primary interventions include the following:
• Raising the head of the bed to 30°. This is thought to improve venous outflow and cerbral perfusion
pressure,[70] although a Cochrane review found insufficient evidence to either support or refute this
practice.[71]
• Analgesics and sedation to ease pain and agitation are thought to reduce metabolic demands.
• Hyperventilation has been used as a temporising measure to reduce ICP by causing vasoconstriction,
by reducing the pCO₂ to 30-35 mmHg. When used, hyperventilation should be limited to brief periods
of up to 30 minutes to treat acute cerebral herniation, and it should be closely monitored using
advanced brain-tissue oxygen monitoring.[70] Hyperventilation should not be used for long-term
prophylaxis, and it should be avoided during the first 24 hours after injury.[7]
Secondary interventions include the following:
• Diuresis: mannitol or hypertonic saline are used in the setting of severe TBI in an attempt to lower
intractably elevated ICP. To date there is not sufficient clinical evidence to recommend one osmotic
agent over another.[7] Mannitol is a volume expander that reduces blood viscosity, and a powerful
diuretic that dramatically reduces the intracerebral volume. Hypertonic saline mobilises free water
across the blood-brain membrane by osmosis, reducing intracerebral volume.
• High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum
standard treatment.[7] High-dose barbiturate therapy commonly lowers systemic blood pressure
13
and may require volume replacement or vasoactive agents to prevent or ameliorate systemic
hypotension.[72]
• Traditionally, ICP monitoring is indicated in TBI patients with a GCS <9 and evidence of an injury on
CT. ICP monitoring may also be indicated in the setting of a normal CT in TBI patients with motor
posturing and a systolic BP 90 mmHg or less.[73] One study challenges the idea that care guided
by ICP monitoring is superior to that guided by CT and clinical examination, while another study
introduces the concept of predicting sustained rises in ICP using dynamic monitoring of MAP and
ICP.[74] [75]
• Decompressive hemicraniectomy: indications vary. Medical management should be optimised first. In
general, craniectomy may be indicated in the following settings:[73] [76]
• Epidural haematoma: any size EDH with focal neurological deficits and a GCS<9; EDH >30cm³
in size
• Subdural haematoma: SDH >10 mm thick; SDH with a midline shift >5 mm; any SDH with a
GCS <9, if ICP >20 mmHg
• Contusions or intraparenchymal haemorrhage: lesions 20 cm³ or greater in volume with midline
EMERGENCIES
shift 5 mm or more; Any lesion 50 cm³ or greater in size

• Posterior fossa haemorrhage or haematoma: lesions that compress the fourth ventricle or basal
cisterns, or the presence of obstructive hydrocephalus.
• Hypothermia and corticosteroids have no role in the treatment of TBI.[35] [77] [78]
Coagulopathy: pre-existing
Patients with pre-existing coagulopathy have a poorer outcome than the general population. Reversal agents
are prothrombotic and many patients have a poor outcome despite rapid reversal.[79]
• All antiplatelet or anticoagulant agents should be stopped and/or reversed in the setting of traumatic
intracranial haemorrhage.
• Serial PT, PTT, INR, and platelet and fibrinogen levels should be followed in patients with severe TBI.
Correction of coagulopathy can be achieved using vitamin K (useful in patients with warfarin-related
prolongation of INR), FFP, platelets (goal platelet count is >100,000/microlitre), cryoprecipitate (used in
patients with low fibrinogen levels), protamine (used for patients on heparin), activated factor VIIa, and
prothrombin complex concentrate.[79] [80]
Coagulopathy: TBI-induced
TBI has a strong association with abnormalities throughout the coagulation cascade, and prolongation
of PT has been shown to be an independent risk factor of poor outcome after TBI.[81] While FFP has
been a standard part of the treatment in trauma-induced coagulopathy, more recent use of prothrombin
complex concentrate has been advocated due to its more concentrated volume.[82] Recombinant activated
VIIa has been shown to decrease need for transfusion of packed red cells and plasma in patients with
coagulopathy secondary to TBI, but has not been shown to translate into consistent improved outcomes.[80]
[83] The CRASH-2 trial has shown promise in the use of tranexamic acid (TXA) in patients with traumatic
haemorrhage, but has not been shown to improve outcomes in patients with TBI.[84] [85]
Triage to appropriate hospital

If the patient is being evaluated in the pre-hospital or community setting without neurosurgical services,
the providers should be aware of the indications for transport to a facility with neurosurgical capacity. In the
UK, the NICE Guidelines recommend transport to an Emergency Department at an Acute Care Hospital if
a patient has any of a number of signs or symptoms after head injury.[20] [NICE: head injury overview] In
the US, guidelines from the Brain Trauma Foundation recommend that all regions have an organised trauma
care system with protocols to direct EMS regarding destination decisions for patients with severe TBI.[53]
Post-injury monitoring
Post-trauma monitoring will vary depending on the clinical findings and the results of the diagnostic workup.
Patients with moderate or severe TBI should be admitted to a hospital with neurosurgical consultants, and an
ICU able to provide monitoring to identify and limit secondary brain injury. Most patients with polytrauma and/
or those that do not attain a normal neurological examination while in the emergency department will benefit
from a similar hospitalisation, and may require re-imaging as the clinical picture changes. A systematic
review found that patients with minor/mild TBI and an initially abnormal CT did not benefit from routine repeat
EMERGENCIES
CT, but should be re-imaged based on neurological deterioration.[86]
Patients with a normal neurological examination and negative CT scan (or where scanning was not
indicated), may be discharged home after 2 hours of observation under the care of a responsible
individual.[87] [88] [89] [90] Patients should be provided with written information regarding signs and
symptoms that should prompt a return to the emergency department, including focal weakness, persistent or
worsening headache or vomiting, decrease in consciousness, rhinorrhoea, otorrhoea, or agitation.
15
Assessment of traumatic brain injury, acute Diagnosis
Step-by-step diagnostic approach

Initial presentation
In most patients with TBI the presentation is obvious, although some patients present with an altered mental
status and little or no physical evidence of trauma. Without a reliable witness, it is not uncommon for a
patient initially thought to have an altered mental status due to stroke, seizure, psychosis, or intoxication to
ultimately be found to have an occult TBI.
History
After initial resuscitation and management of ABCDs, a focused history should be performed on every
patient with a TBI or unknown cause of altered mental status. A detailed description of the traumatic event
should be solicited from the patient, family members, emergency medical services, first responders, or
police. Witnesses or individuals who know the patient may be helpful in ascertaining the details of the
traumatic event and environment, as well as the patient’s normal level of functioning. It is important to keep
the differential diagnoses broad to avoid making an error of premature closure. The history should include
the following:
• Mechanism of injury and detailed description of the injury
• Loss of consciousness, amnesia, lucid periods

• Seizures, confusion, deterioration in mental status
• Vomiting or headache
• Drug or alcohol use
• Current intoxication: shown to have an increased association with intracranial injury detected on
CT[91]
• Chronic: associated with cerebral atrophy, thought to increase risk of shearing of bridging veins
• Past medical history, including any central nervous system surgery, past head trauma, haemophilia, or
DIAGNOSIS
seizures
• Current medications, including anticoagulants
• Age: TBI in older age has a poorer outcome in all subgroups.
Physical examination
A thorough physical examination must be performed after the initial ABCDs have been addressed. In addition
to vigilance for occult injuries, the physician should perform the physical examination with careful attention to
the following:
• Serial Glasgow Coma Scale (GCS) and pupillary examinations should be performed every 15 minutes
until the patient is stable, to immediately identify deterioration in neurological function.
• Head and neck
• Inspection for cranial nerve deficits, periorbital or postauricular ecchymoses, cerebrospinal fluid
rhinorrhoea or otorrhoea, haemotympanum (signs of base of skull fracture)
[Fig-2]
[Fig-3]
• Fundoscopic examination for retinal haemorrhage (sign of abuse)[92] and papilloedema (sign of
increased intracranial pressure [ICP])
• Palpation of the scalp for haematoma, crepitance, laceration, and bony deformity (markers of
skull fractures)
• Auscultation for carotid bruits (sign of carotid dissection)
• Evaluation for cervical spine tenderness, paraesthesias, incontinence, extremity weakness,
priapism (signs of spinal cord injury)
• Obvious foreign bodies or impaled objects should not be removed until the dura is opened in the
operating room and the procedure can be performed under direct visualisation.
• Cardiovascular status requires continuous cardiac and serial blood pressure monitoring. Any episodes
of hypotension must be addressed immediately.[58] [59]
• Respiratory status requires continuous pulse oximetry and, in intubated patients, continuous end-tidal
CO₂ capnography. Any episodes of hypoxia must be addressed immediately.[58] [59]
• Extremities should receive motor and sensory examination (for signs of spinal cord injury).
GCS and pupillary examinations

The GCS is widely used to assess the level of consciousness in patients with TBI, and provides fairly good
prognostic information (when score is very low or very high) that allows the physician to plan for expected
diagnostic and monitoring requirements.[64] A score of 13 to 15 is associated with good outcomes, although
it cannot be used to rule out intracranial injury. A score <9 is associated with clinical deterioration and poor
outcomes. Serial GCS monitoring provides clinical warnings of deterioration.
GCS has 3 components: best eye response (E), best verbal response (V), and best motor response (M).
Scoring for each component should be documented separately (e.g., GCS 10 = E3 V4 M3). Deficits of the
motor component have the strongest correlation with poor outcome in patients with TBI.[93] [94] Patients
with oral/ocular trauma or those who are intubated, medicated, or very young can be challenging to assess,
although recent studies have shown that alcohol intoxication has little effect on the GCS, unless the blood
alcohol level is much >200 mg/dL.[95] [96]
DIAGNOSIS
17
The adult and paediatric GCS

DIAGNOSIS
The following scoring system is applied:[45]
• GCS of 13-15 is associated with mild brain injury

• GCS of 9-12 is associated with moderate brain injury
• GCS of <8 is associated with severe brain injury.
Although a GCS of 13 is classically considered as mild, many experts believe that it should be considered
within the moderate category. It is worthwhile noting that the scale severity is inversely correlated to
numerical magnitude. GCS can be serially performed by different members of the healthcare team in order
to monitor neurological status; inter-rater reliability is generally considered to be good, although this has been
questioned.[97] [98] [99] [100] [101]
Pupillary reflexes function as an indication of both underlying pathology and severity of injury, and should be
monitored serially.[69] The pupillary examination can be assessed in an unconscious patient or in a patient
receiving neuromuscular blocking agents or sedation.[18] Pupils should be examined for size, symmetry,
direct/consensual light reflexes, and duration of dilation/fixation. Abnormal pupillary reflexes can suggest
herniation or brainstem injury. Orbital trauma, pharmacological agents, or direct cranial nerve III trauma may
result in pupillary changes in the absence of increased ICP, brainstem pathology, or herniation.
• Pupil size:
• The normal diameter of the pupil is between 2-5 mm, and although both pupils should be equal
in size, a 1-mm difference is considered a normal variant.
• Abnormal size is noted by anisocoria defined as >1 mm difference between pupils.
• Pupil symmetry:
• Normal pupils are round, but can be irregular due to ophthalmological surgeries.
• Abnormal symmetry may result from compression of CNIII can cause a pupil to initially become
oval before becoming dilated and fixed.
• Direct light reflex:
• Normal pupils constrict briskly in response to light, but may be poorly responsive due to
ophthalmological medications.
• Abnormal light reflex may be seen in sluggish pupillary responses associated with increased
ICP. A non-reactive, fixed pupil has <1 mm response to bright light and is associated with
severely increased ICP.
GCS and pupillary assessment are most reliable in haemodynamically stable patients without hypoxia or
hypotension as these may alter the patient's clinical examination.
Laboratory investigations
Baseline laboratory investigations should include:
• FBC including platelets

• Serum electrolytes and urea
•
DIAGNOSIS
Serum glucose
• Coagulation status: PT, INR, activated PTT
• Blood alcohol level and toxicology screening if indicated
• Urine analysis.
[VIDEO: Venepuncture and phlebotomy animated demonstration ]
Arterial blood gas is not typically indicated in TBI, as the decision to secure a definitive airway is based
on clinical findings and expected course of hospitalisation. A patient with a GCS of <8, or any patient with
TBI who is not spontaneously breathing, not able to maintain an open airway, or not able to maintain >90%
oxygen saturation with supplementary oxygen, requires a definitive airway.
In the past 10 years, researchers have evaluated several potential biomarkers for identifying patients with
significant intracranial injury on CT. S-100beta and glial fibrillary acidic protein have both shown promise, but,
to date, their specificity and sensitivity are not superior to the validated clinical decision guidelines.[102] [103]
[104] [105]
19
Imaging in patients with TBI and suspected intracranial injury

Non-contrast computed tomography (CT) is the imaging modality of choice for patients with TBI and
suspected intracranial injury; it is able to detect the vast majority of clinically important injuries and can guide
in the medical and surgical management of TBI.[106] [107] [108]
Consensus recommendations from the American College of Radiology continue to support CT use as a first-
line imaging modality in patients with TBI.[109] The following CT findings are associated with a poor outcome
in TBI: midline shift, subarachnoid haemorrhage into, or compression/obliteration of, the basal cisterns.[73]
MRI is indicated when the clinical picture remains unclear after a CT, in order to identify more subtle lesions,
such as those found in diffuse axonal injury (DAI). An immediate CT is indicated in all patients with TBI with
penetrating injuries; suspected basilar, depressed, or open fracture; GCS <13; or focal neurological deficits.
MRI is contraindicated if there is any suspicion that a metal object has penetrated the skull.
Mild/minor TBI (concussion)

The diagnosis of mild TBI (mTBI) is dependent on careful history taking and examination. The patient’s
history and collateral interviews are important in generating a diagnosis.[110] As per the definitions of TBI,
careful assessment of loss of consciousness, retrograde amnesia, post-traumatic amnesia, confusion and
disorientation, and focal neurological deficit should be performed.[110] In addition, signs and symptoms
may be influenced by alcohol, drugs, or medications.[110] To date, the diagnosis of mTBI is primarily
based on clinical history and examination. CT is typically normal following mild TBI, although a significant
number of patients are left with neurocognitive deficits and may benefit from follow-up with a neurologist and
consideration of diffusion tensor imaging.[111] [112]
Imaging in patients with mild/minor TBI

The use of CT in patients with isolated minor head injury or mild TBI is controversial. To date, over 20 clinical
decision rules have been published,[22] but the New Orleans Criteria and the Canadian CT Head Rule stand
out for their high sensitivity (99% to 100%) in repeated external validations in patients with and without loss of
consciousness, as well as in patients with a GCS of 13-15.[88] [113] [114] [115] [116] Both guidelines include
the following variables: some form of vomiting, advanced age, altered mental status, and signs of head
DIAGNOSIS
trauma on physical examination. In the UK, the National Institute for Health and Care Excellence guidelines
for the approach to patients with minor TBI include the variables from the Canadian CT Head Rule. [NICE:
head injury overview] In the US, the Centers for Disease Control and Prevention has adapted the variables
from the New Orleans Criteria in the approach to adult patients with mild TBI. [CDC: mild TBI pocket guide]
New Orleans criteria

CT is required for patients with minor head trauma (minor head injury defined as loss of consciousness in
patients with normal findings on a brief neurological examination and a GCS score of 15, as determined by a
physician upon arrival at the emergency department) with any one of the following:[116]
High risk (for neurosurgical intervention)
• Headache
• Vomiting
• Aged over 60 years
• Drug or alcohol intoxication
• Persistent anterograde amnesia (deficits in short-term memory)
• Evidence of traumatic soft-tissue or bone injury above clavicles
• Seizure (suspected or witnessed).
Where possible, a history of coagulopathy should be obtained and considered with respect to CT scanning.
Canadian CT head rule

CT is required for patients with minor head injuries (minor head injury defined as witnessed loss of
consciousness, definite amnesia, or witnessed disorientation in patients with a GCS score of 13-15) with any
one of the following:[8]
[VIDEO: Canadian Head CT Rule for Minor Head Injury ]
• High risk (for neurological intervention):
• GCS <15 at 2 hours after injury

• Suspected open or depressed skull fracture
• Any sign of basal skull fracture (haemotympanum, raccoon eyes [periorbital ecchymosis],
cerebrospinal fluid otorrhoea/rhinorrhoea, Battle's sign [ecchymosis of the mastoids])
• Two or more episodes of vomiting
• Age ≥65 years
• Medium risk (for brain injury on CT):
• Amnesia more than 30 minutes before impact (retrograde amnesia)

• Dangerous mechanism (pedestrian struck by motor vehicle, occupant ejected from motor
vehicle, fall from height >1 metre [3 feet] or >5 stairs).
Assessing infants and children with mild/minor TBI

Routine use of imaging to diagnose mild TBI in children in the acute setting is not recommended.[117]
Validated clinical decision rules, such as the Pediatric Emergency Care Applied Research Network
DIAGNOSIS
(PECARN) decision rule, effectively identify children at low risk for intracranial injury (and those at increased
risk, for whom head CT may be indicated).[117]
PECARN clinical decision rule
Clinical decision rules to identify children who benefit from CT after head injury have been derived from three
large prospective studies (PECARN, CATCH, and CHALICE).[118] [119] [120] In 2017, a prospective study of
over 20,000 children demonstrated that, of the three rules, the PECARN clinical decision rule has the highest
sensitivity for identifying children with clinically important TBI.[121] Based on the PECARN guidelines, CT
is indicated for all children with a GCS score <15, altered mental status (agitation, somnolence, repetitive
questioning, slow to verbal response), palpable skull fracture, or suspected basilar skull fracture.[118] Further
indications for CT differ based on patient age.
Additional PECARN indications for CT in children <age of 2 years:[118]
• Loss of consciousness >3 seconds

• Non-frontal scalp haematoma
• Not acting normal (per parent)
21
• Severe mechanism of injury: motor vehicle accident with ejection, death of passenger, rollover, struck
by vehicle, fall >3 feet (0.9m), head struck by high impact object.
Observation for 6 hours is an option for patients >3 months (and <2 years) if no more than one of the four
criteria is present. CT is indicated for new, worsening, or unresolved symptoms by 6 hours.
Additional PECARN indications for CT in children >age of 2 years:[118]
• Loss of consciousness
• Severe headache
• Vomiting
• Severe mechanism of injury: motor vehicle accident with ejection, death of passenger, rollover, struck
by vehicle, fall >3 feet (0.9m), head struck by high impact object.
Observation for 6 hours is an option for patients >2 years if no more than one of the four criteria is present.
CT is indicated for new, worsening, or unresolved symptoms by 6 hours.
Symptom scales and cognitive testing in children
Validated, age-appropriate symptom rating scales (e.g., Post-Concussion Symptom Scale, Health
and Behaviour Inventory, Post-Concussion Symptom Inventory, or Acute Concussion Evaluation) and
computerised cognitive testing should form part of the diagnostic evaluation.[117] [122] These tools can be
used to record neurocognitive insults, and to guide activity restrictions and appropriate follow-up. Resources
to help implement the recommendations made by the US Centers for Disease Control and Prevention
(CDC) in their guideline on the diagnosis and management of mild TBI in children are available via the CDC
website. [CDC: pediatric mTBI guideline]
DIAGNOSIS
Differential diagnosis overview
Common
Skull fracture (excl. base of skull)
Base of skull fracture
Cerebral contusion
Intracerebral haemorrhage
Subdural haematoma
Epidural haematoma
Intraventricular haemorrhage
Traumatic subarachnoid haemorrhage
Mild traumatic brain injury
DIAGNOSIS
23
Differential diagnosis
Common
Skull fracture (excl. base of skull)
History Exam 1st Test Other tests
history of a high- evidence of scalp »head CT (non- »skull x-ray: skull

velocity, direct impact to haematoma, contrast): will detect fracture
skull, a fall from height, crepitance, laceration most skull fractures Plain radiographs of
or motor vehicle-related or bony deformity; using the bone the skull may identify
injury Glasgow Coma windows, and most
Scale (GCS) score underlying injury using skull fractures but are
and focal deficits the brain windows; of very limited value
vary depending on compared with a in the diagnosis of
underlying intracranial suture, a fracture intracerebral injury.
injury tends to be wider at
the centre and more
narrowed at the ends,
more than 3 mm in
width, and runs in
straight lines with
angulated turns; a
fracture can be linear or
comminuted, and may
be depressed through
the inner table
The presence of skull
fracture is indicative
of high-force impact
with potentially
DIAGNOSIS
underlying brain
pathology and warrants
a neurosurgical consult.
In addition to
visualisation of the
fracture, CT will
diagnose underlying
brain pathology, if
any.[123]
Depressed fractures
increase the risk
of parenchymal
pathology.[124]
Common
history of high-velocity post-auricular or »head CT (non- »test for

impact to the back of periorbital ecchymosis, contrast): will detect cerebrospinal
the head; may report cerebrospinal most skull fractures fluid leak on
clear fluid or blood fluid otorrhoea using the bone bloody discharge,
draining from nose or or rhinorrhoea, windows, and most tau-transferrin
ears; may report facial haemotympanum, underlying injury using measurement: tau-
numbness, vertigo, or cranial nerve VII and the brain windows transferrin positive
hearing deficits VIII deficits[124] A basilar fracture This test is the most
is often difficult to sensitive and specific;
see on CT. Thin however, analysis
section images with is complex and
dedicated temporal timely, making it less
bone cuts may aid applicable when results
visualisation.[124] are required urgently.
Basilar skull fractures »test for

can be linear or cerebrospinal fluid
leak on bloody
comminuted. Fluid discharge, glucose
(blood) in the measurement:
mastoid air cells or glucose positive
pneumocephaly in Mucus has no glucose
the temporal region and should test
suggest a fracture negative. However,
through the petrous test is not reliable
part of the temporal or specific for
DIAGNOSIS
bone. cerebrospinal fluid.
The presence of False positive if

a skull fracture contaminated with
warrants immediate blood, false negative
neurosurgical if cerebrospinal fluid
consultation. CTA or glucose low.
angiogram indicated
»test for
if fracture line near cerebrospinal fluid
carotid foramen or dural leak, application of
sinuses. bloody discharge to
tissue paper: positive
halo/double ring sign
(a drop of the bloody
discharge is applied
to tissue paper; a
clear halo that extends
beyond the central spot
of blood suggests a
cerebrospinal fluid leak)
25
Common

Not reliable.
Cerebral contusion
history of direct impact scalp trauma may be »head CT (non- »head MRI:
or acceleration/ present; depending on contrast): single or haemorrhagic
deceleration typically severity; GCS may be multiple parenchymal contusions are
due to fall or motor normal or decreased; lesions, contusions hyperdense on T1-
vehicle-related injury; if severe may have commonly found on the weighted imaging and
may have history of focal deficits, seizures, frontal and temporal hypodense on T2-
loss of consciousness or signs of increased poles; approximately weighted imaging; non-
intracranial pressure half are haemorrhagic: haemorrhagic lesions
(ICP) a focus of hyperdensity, are hypodense on T1-
surrounded by a weighted imaging and
hypodense area hyperdense on T2
representative imaging
of oedema; non- Gradient echo pulse
haemorrhagic lesions sequence can aid
may be difficult to see
on initial CT[124] in the detection of
The presence haemorrhage.[124]
of contusion
Although MRI is
warrants immediate
more accurate
neurosurgical
for demonstrating
DIAGNOSIS
consultation.
contusion, CT remains
Contusions the initial scan of choice
may progress to in trauma patients
haemorrhage; due to the speed and
therefore, any availability of this test.
deterioration in mental In addition it allows the
status warrants a rapid exclusion of other
repeat CT. important pathologies.
Midline shift,
subarachnoid
haemorrhage into
or compression/
obliteration of the
basal cisterns is
associated with a poor
outcome.[73]
Common
Intracerebral haemorrhage
history of direct impact evidence of scalp »head CT (non- »head MRI: acute
or rapid acceleration/ trauma is common; contrast): hyperdense haemorrhage is
deceleration typically seizures or focal area of haemorrhage, hyperdense on T1-
due to fall or motor neurological deficits surrounded by a weighted imaging and
vehicle-related injury; related to area of hypodense area of hypodense on T2-
witnesses may report haemorrhage may oedema weighted imaging
lucid period, followed be present; evidence Intracerebral MRI may be useful at
by progressive altered of raised ICP and haemorrhage further characterising
mental status herniation: altered
mental status, warrants immediate subacute or small
pupillary irregularity, neurosurgical lesions.
extension to pain, consultation.
respiratory irregularity,
papilloedema, fundal It is not uncommon
haemorrhage
for patients to present
with a small contusion
which then develops
into an intracranial
haematoma, typically
occurring within 48
hours of the injury.
Midline shift,
subarachnoid
haemorrhage into
or compression/
DIAGNOSIS
obliteration of the
basal cisterns is
outcome.[73]
Subdural haematoma
history of direct impact scalp trauma may »head CT (non- »head MRI: T1-
or rapid acceleration/ be present; focal contrast): weighted MRI will
deceleration due to fall neurological deficits characteristically appear as hypointense
or motor vehicle-related may develop, altered crescent-shaped; or iso-intense acutely;
injury; increased risk in mental status blood does not cross T2-weighted imaging
patients with bleeding depending on size the midline;[124] will display SDH as
diathesis, anticoagulant of lesion; may have in the setting of hyperintense within
medications, alcohol signs of increased ICP acute bleeding, the first few hours,
abuse; history of a fall as haematoma size areas of hypodense progressing to a
is more common in increases and hyperdense
27
Common
Subdural haematoma

patients with significant haematoma produce a hypointensity over the
cerebral atrophy swirling appearance ensuing week
The presence MRI can detect very
of subdural small SDH and tentorial
haematoma (SDH) and inter-hemispheric
warrants immediate SDH.[106]
neurosurgical
consultation.
Midline shift or
compression/
obliteration of the
basal cisterns is
outcome.[73]
SDH at the falx

cerebri appear as
linear hyperdensities
between the cerebral
hemispheres. SDH
at the tentorium
cerebelli may be
difficult to see on axial
DIAGNOSIS
CT, appearing as a
hyperdense tentorium.
Coronal CT may aid
in their detection.[124]
Subacute SDH may
appear isodense with
grey matter.
Epidural haematoma
history of direct impact, commonly scalp trauma »head CT (non- »MRI head: can aid
patient may have over the temporal bone; contrast): a in the visualisation
had a lucid interval focal neurological hyperdense extra-axial of small EDH; signal
and then progressive deficits and progressive lesion with smooth intensity as similar to
deterioration of GCS altered mental status margins on CT; a that seen with SDH
lentiform appearance,
forming a biconvex
Common
Epidural haematoma

shape as blood pushes
on the brain surface;
blood does not cross
suture lines; swirling
areas of varying
density indicates active
bleeding[124]
Epidural haematoma
(EDH) is a
neurosurgical
emergency and
warrants immediate
neurosurgical
consultation.
Mass effect may

be seen depending
on the extent of the
haematoma. Midline
shift, or compression/
obliteration of the
basal cisterns is
outcome.[73]
DIAGNOSIS
The origin of the
bleeding is usually
from the meningeal
vessels, with tearing of
the middle meningeal
artery occurring
in about 50% of
cases.[125] This vessel
is particularly at risk
following fracture of the
squamous region of the
temporal bone, which is
comparatively thin and
easily damaged.
29
Common
Epidural haematoma

Epidural haematoma:
CT brain scan
showing lenticular-
shaped hyperdensity
between the dura
mater and skull. (A–
C) Same patient on
different levels of
the skull, (A) being
the most caudal and
(C) the most cranial
van Dijk GW.
Practical Neurology.
2011;11(1):50-55
Intraventricular haemorrhage
history of direct impact signs are due to »head CT (non-

or rapid acceleration/ secondary obstructive contrast): blood in the
deceleration due hydrocephalus ventricles will appear as
to fall or motor and raised ICP: hyperdense, commonly
vehicle-related injury; papilloedema, seen in the lateral
DIAGNOSIS
depending on degree fundal haemorrhage, ventricles; often other

of hydrocephaly, the decreased associated pathology;
patient may present consciousness; hydrocephalus may be
with headache, signs of herniation seen
vomiting, and ataxia or include pupillary Intraventricular
have progressed to an dilation, bilateral ptosis, haemorrhage is
altered mental status impaired upgaze,
extension to pain, and indicative of severe
respiratory irregularity injury and warrants
a neurosurgical
consultation.
Midline shift, or
compression/
obliteration of the
basal cisterns is
outcome.[73]
Common
Traumatic subarachnoid haemorrhage
history of direct impact can be mild with »head CT (non- »CT angiography
or rapid acceleration/ minimal signs, or contrast): SAH on (CTA): may be
deceleration, can occur severe with signs CT can be subtle; performed if aetiology
due to a fall, but must of increased ICP: the basilar cisterns of SAH as traumatic is
rule out aneurysmal papilloedema, (suprasellar and uncertain; visualises
subarachnoid fundal haemorrhage, quadrigeminal potential vascular
haemorrhage (SAH); altered mental cisterns) should be abnormalities or active
aneurysmal SAH status, decreased inspected carefully bleeding sites
more likely if history consciousness; signs for the presence of »head MRI: SAH
of sudden onset of of herniation: pupillary SAH, which appears present
severe headache, dilation, bilateral ptosis, hyperdense compared
Rarely used to
meningeal symptoms, impaired upgaze, with cerebrospinal fluid
nausea; an be mild with extension to pain, SAH warrants diagnose SAH, but may
minimal symptoms, or respiratory irregularity urgent neurosurgical be useful when CT/
severe with symptoms CTA is negative and
of increased ICP: consultation.
vascular abnormalities
altered mental
status, decreased SAH into the basal are suspected.
consciousness cisterns is associated
»ECG: non-specific;
with a poor outcome in
ischaemic ECG
TBI.[73] changes in SAH
include ST elevation or
depression, abnormal
T-wave morphology,
prolonged QTc interval
and U-waves.[126]
DIAGNOSIS
history of high-velocity should visualise and »head CT (non- »CT angiography

impact or missile palpate for scalp defect, contrast): the initial (CTA): may be required
injuries; symptoms crepitance, obvious test of choice and to evaluate further
depend on nature of skull deformity or can demonstrate vascular injuries
injury and brain regions protruding foreign body; the nature of the »MRI:
affected may have localising intracranial pathology contraindicated if there
neurological deficits or and presence or is any suspicion that
seizures absence of fractures a metal object has
and foreign bodies penetrated the skull
Penetrating injury
warrants immediate
neurosurgical
consultation.
31
Common
history of direct impact patients with severe »head CT (non- »MRI: indicated when
or rapid acceleration/ diffuse axonal injury contrast): initially CT does not explain
deceleration of (DAI) present with normal in more than patient’s symptoms;
head; depending altered mental status half of patients with more sensitive for
on severity, may or coma; classically DAI; should look for micro-haemorrhage
complain of headache have physical oedema and petechial and oedema
or vomiting, or have examination findings haemorrhage, at the
had a rapid progressive disproportionate to CT grey/white junction,
deterioration of GCS findings within the corpus
and coma callosum, and the
brainstem
DAI often coexists
with other types of
TBI and warrants a
neurosurgical consult.
◊ Mild traumatic brain injury
history of blunt trauma GCS score of 13 to »head CT (non- »head MRI: usually
or acceleration/ 15 after 30 minutes contrast): usually normal
deceleration forces; post injury or later normal MRI is indicated in
can result in confusion, upon presentation Frequently used to rule patients with continued
disorientation, for health care; other out more severe TBI.
or impaired transient neurological neurocognitive deficits.
DIAGNOSIS
consciousness, abnormalities such as These patients should

dysfunction of memory focal signs, seizure, be referred to a
around the time of and intracranial lesion neurologist.
the injury, loss of not requiring surgery
consciousness lasting may be present
30 minutes or less,
post-traumatic amnesia
for less than 24 hours;
can cause observed
signs of neurological
or neuropsychological
dysfunction such
as seizures acutely
following injury;[127]
[128] symptoms include
headache, dizziness,
fatigue, irritability, and
poor concentration
(typically referred to
as 'postconcussion
symptoms')
Diagnostic guidelines
Europe
Head injury: assessment and early management
Published by: National Institute for Health and Care Excellence

Last published: 2019
Early management of patients with a head injury
Published by: Scottish Intercollegiate Guidelines Network

Treatment of minor and severe traumatic brain injury: national reference

guidelines
Published by: Italian Ministry of Health

North America
Centers for Disease Control and Prevention guideline on the diagnosis and
management of mild traumatic brain injury among children
Published by: Centers for Disease Control and Prevention

DIAGNOSIS
Guidelines for the management of severe traumatic brain injury: 4th edition
Published by: Brain Trauma Foundation

ACS TQIP best practices in the management of traumatic brain injury
Published by: American College of Surgeons

ACR appropriateness criteria: head trauma
Published by: American College of Radiology

33
North America
Summary of evidence-based guideline update: evaluation and management

of concussion in sports
Published by: American Academy of Neurology

Guidelines for the acute medical management of severe traumatic brain

injury in infants, children, and adolescents, 2nd ed

Clinical policy: neuroimaging and decisionmaking in adult mild traumatic

brain injury in the acute set ting
Published by: American College of Emergency Physicians

Guidelines for the prehospital management of severe traumatic brain injury,

2nd ed

DIAGNOSIS
Assessment of traumatic brain injury, acute Online resources
Online resources
1. CDC: heads up (external link)
2. NICE: head injury overview (external link)
3. CDC: mild TBI pocket guide (external link)
4. CDC: pediatric mTBI guideline (external link)
ONLINE RESOURCES
35
Assessment of traumatic brain injury, acute References
Key articles
• Carney N, Totten AM, O'Reilly C, et al. Guidelines for the management of severe traumatic brain injury,
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2008 Aug;7(8):728-41. Abstract
• Pandor A, Goodacre S, Harnan S, et al. Diagnostic management strategies for adults and children
with minor head injury: a systematic review and an economic evaluation. Health Technol Assess. 2011
Aug;15(27):1-202. Full text Abstract
• Badjatia N, Carney N, Crocco TJ, et al; Brain Trauma Foundation; BTF Center for Guidelines
Management. Guidelines for prehospital management of traumatic brain injury 2nd edition. Prehosp
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45
Assessment of traumatic brain injury, acute Images
Images
IMAGES
Figure 1: The adult and paediatric GCS

Assessment of traumatic brain injury, acute Images
IMAGES
Figure 2: Haemotympanum: blood in the tympanic cavity of the middle ear (arrow)
van Dijk GW. Practical Neurology. 2011;11(1):50-55
47
IMAGES Assessment of traumatic brain injury, acute Images
Figure 3: Battle's sign: superficial ecchymosis over the mastoid process

Figure 4: Epidural haematoma: CT brain scan showing lenticular-shaped hyperdensity between the dura
mater and skull. (A–C) Same patient on different levels of the skull, (A) being the most caudal and (C) the
most cranial
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49
Contributors:
// Authors:
Micelle J. Haydel, MD
Albert J. Lauro Professor of Medicine/Emergency Medicine
Clinical Professor Medicine/Emergency Medicine, Section of Emergency Medicine, Louisiana State
University Health Science Center, New Orleans, LA
DISCLOSURES: MJH is an author of a reference cited in this topic.
// Acknowledgements:
Dr Micelle J. Haydel would like to gratefully acknowledge Dr Victoria E. Johnson, Dr Marek Ma, Dr Nathan
Ranalli, and Dr Douglas H. Smith, previous contributors to this topic. VEJ, MM, NR, and DHS declare that
they have no competing interests.
// Peer Reviewers:
David W. Wright, MD
Director of Research
Department of Emergency Medicine, Emory University, Atlanta, GA
DISCLOSURES: DWW declares that he has no competing interests.
David Sharp, MBBS, BA, MRCP, PhD

Senior Lecturer In Neurology
Imperial College, London, UK
DISCLOSURES: DS declares that he has no competing interests.

Assessment of BTF

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Assessment of BTF

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Assessment of

Last updated: Nov 20, 2018

◊ Classification by clinical severity :

◊ Classification by broad aetiology :

◊ Classification by injury progression :

◊ Epidemiology of specific injuries :

Aetiology of specific injuries

Brain tissue injury

Diffuse axonal injury

Initial approach: airway, breathing, circulation, disability

The airway and breathing

Disability: initial neurological examination

The adult and paediatric GCS

Sedation and analgesia

Approach to elevated ICP

Primary interventions include the following:

shift 5 mm or more; Any lesion 50 cm³ or greater in size

Triage to appropriate hospital

Step-by-step diagnostic approach

• Mechanism of injury and detailed description of the injury

• Loss of consciousness, amnesia, lucid periods

GCS and pupillary examinations

The adult and paediatric GCS

Used with kind permission from Dr Micelle J. Haydel

The following scoring system is applied:[45]

• GCS of 13-15 is associated with mild brain injury

• FBC including platelets

[VIDEO: Venepuncture and phlebotomy animated demonstration ]

Imaging in patients with TBI and suspected intracranial injury

Mild/minor TBI (concussion)

Imaging in patients with mild/minor TBI

New Orleans criteria

High risk (for neurosurgical intervention)

Canadian CT head rule

[VIDEO: Canadian Head CT Rule for Minor Head Injury ]

• High risk (for neurological intervention):

• GCS <15 at 2 hours after injury

• Amnesia more than 30 minutes before impact (retrograde amnesia)

Assessing infants and children with mild/minor TBI

PECARN clinical decision rule

Additional PECARN indications for CT in children <age of 2 years:[118]

• Loss of consciousness >3 seconds

Additional PECARN indications for CT in children >age of 2 years:[118]

Symptom scales and cognitive testing in children

Differential diagnosis overview

Skull fracture (excl. base of skull)

Base of skull fracture

Traumatic subarachnoid haemorrhage

Diffuse axonal injury

Mild traumatic brain injury

Skull fracture (excl. base of skull)

History Exam 1st Test Other tests

history of a high- evidence of scalp »head CT (non- »skull x-ray: skull

Base of skull fracture

History Exam 1st Test Other tests

history of high-velocity post-auricular or »head CT (non- »test for

Basilar skull fractures »test for

The presence of False positive if

Base of skull fracture

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests

History Exam 1st Test Other tests