Neurosurgery- Head injury / Traumatic brain injury

1. Dr. Dhaval Gohil
Neurosurgery Resident
NIMHANS, Bangalore

2. 1. Introduction
2. Sequelae of TBI (Pathophysiology)
3. Classification
4. Initial management of TBI
5. Individual pathology and its management

3. 1. Understanding of How brain reacts to
trauma
2. Basic Neurological assessment of TBI, and
alarming signs
3. Indication of Neuro-specific investigation
4. Normal and abnormal CT scan
5. Basic Emergency Neuro management

4. TBI is defined as “brain damage resulting from
external forces, as a consequence of direct impact,
rapid acceleration or deceleration, a penetrating
object or blast waves from an explosion.”
The term head injury is often substituted for TBI, but it
is broader because it may include injuries to the face
and scalp, such as lacerations and abrasions, which
may occur without underlying brain trauma.

5. • More than 10 million people worldwide suffer TBI serious
enough to result in death or hospitalization each year 1
• The World Health Organization (WHO) forecasts that by
2030, TBI be a leading cause of disability and death
worldwide 1
• It has been estimated that TBI accounts for 9% of deaths
around the world and is a threat to health in every country1

6. • incidence of 120 per 100,0003
• Road traffic injuries are the leading cause (60%) of TBIs
followed by falls (20%-25%) and violence (10%). 2
• 7th leading cause of mortality in India and (78% of these
deaths are due to RTA alone 3
• Alcohol involvement is known to be present among 15%-
20% of TBIs at the time of injury2

7. • TBI often referred as ‘silent epidemic’. Silent insofar as
society don’t take it as a health problem until it happens and
also unaware of chronicity of it’s sequelae.
• TBI is ‘heterogeneous’ disease as its demographic factors,
manifestations varies widely
• An understanding of the sequelae after Traumatic brain injury
is paramount for its management.

10. Primary insult results in tissue deformation that causes damage
to neurons, glia, axons, and blood vessels that manifests as
primary injury

11. Primary

12.  Primary injury followed by a more delayed phase of injury,
which is mediated by intracellular and extracellular biologic
pathways and can be present for minutes, hours, days, and even
weeks after the primary insult called as secondary injury.
 Example of secondary injury – Synaptic dysfunction, axonal
degeneration, neuronal death
Mechanisms – calcium overload, excitotoxicity, mitochondrial
Dysfunction, inflammation

13. • During time lapse between primary and secondary injury
many patients experience superimposed secondary
insults.
• Five secondary insults consistently correlated with poor
outcome: arterial hypotension, reduced cerebral
perfusion pressure (CPP), elevated ICP, hypoxemia, and
pyrexia.4
• Preventing/treating secondary insult and hence
secondary injury remains a focus of TBI Management

14. The blood-brain barrier compartmentalizes the brain from the
circulation so that only lipid-soluble molecules, or molecules that
can use specialized transport systems, can enter the brain.
The structural basis of the blood-brain barrier is the endothelial
cell with its tight junctions lining the cerebral vessels.
Water can enter the brain uncontrollably if the barrier is disrupted
or if osmotic forces across the barrier are sufficient to drive water
into the cerebral tissues

16. type of cerebral
edema
BBB status mechanism Othes
Cytotoxic Intact -In ability of neurons to
maintain osmotic
homeostasis (i.e. cell
damage)
- systemic water overload
MC type of edema in
trauma
Vasogenic Damaged BBB Malfunction leading to
uncontrolled entry of water
in tissue
- MC type of edema
overall, seen in
neoplasm, abscess,
hemorrhages etc
- Excellent response to
steriods except in
trauma
Interstitial Intact Overproduction of CSF or
failure of egress of CSF
- Water flux across BBB
has no role
-Choroid plexus
papilloma
-SAH

17. The single most important and unique aspect of the brain: It lives
in a closed “box.”
Monroe-Kelly doctrine : total volume of intracranial content is
constant
Intra cranial volume = Volume CNS ++ Volume CSF + Volume blood + Volume lesion
(1400) (1100) (150) (150)
The normal mean ICP is less than 15 mm Hg or 200 mm H2O for
a patient in the lateral decubitus position.

18. Physiologic compensation:
Depending of expansion of lesion:
reduction in CSF volume (the ventricles and sulci are effaced) 
blood volume  brain itself as “herniation”.
The intracranial compartment is subdivided by dural boundaries;
the tentorium cerebelli - supra and infratentorial compartments,
and
the falx - divides the supratentorial compartment into two equal
right and left compartments.
Depending on the location of the space-occupying lesion, the
brain may be forced out of one compartment into another. Such
shifts are brain herniations.

20. Site of Herniation Structures involved Clinical Symptoms
Subfalcine (Cingulate) Cingulate gyrus Confusion and drowsiness
Pericallosal artery C/L lower limb weakness
Urinary incontinence
Lateral (Uncal) I/L Occulomotor nerve I/L mydriasis, ptosis
I/L cerebral peduncle C/L hemiparesis,
drowsiness
Any side Posterior cerebral
artery
C/L homonymous
hemianopia
C/L cerebral peduncle Kernohan’s notch
phenomena
Central (axial) Basilar artery branches,
brainstem, reticular
formation
Impaired consciousness,
impaired eye movements,
“Cushing triad” –
hypertension, brady,
respiratory irregularity
Duret hemorrhage
Tonsillar Medulla Apnea
Fungus cerebri parenchymal protrusion Variable

24. 1. Clinical
2. Radiological
3. Anatomical

25. Glasgow Coma Scale
First described in 1974 by Graham Teasdale and Byan Jennete
Limitations
- Sedation and neuromuscular blockade
- Alcohol intoxication
- Intubation
- Eye and Oral injury

27. Pediatric Glasgow Coma Scale: (less than 5 years of child) (inappropriate to use “obeys to command” and “oriented”
1 2 3 4 5 6
Eyes Does not open eyes
Opens eyes in
response to painful
stimuli
Opens eyes in
response to speech
Opens eyes
spontaneously
N/A N/A
Verbal No verbal response Inconsolable, agitated
Inconsistently
inconsolable, moaning
Cries but consolable,
inappropriate
interactions
Smiles, orients to
sounds, follows
objects, interacts
N/A
Motor No motor response
Extension to pain (
decerebrate response)
Abnormal flexion to
pain for an infant (
decorticate response)
Infant withdraws from
pain
Infant withdraws from
touch
Infant moves
spontaneously or
purposefully

28. brain injury is classified as:
Severe, with GCS < 8–9
Moderate, GCS 8 or 9–12 (controversial)
Minor, GCS ≥ 13.
*Patients who are intubated receive a verbal score of “T” and the
scale is adjusted to 3T-11T.

29. 1.Marshall score
2.Rotterdam score (recent, more accurate)
basal cisterns midline shift epidural mass
lesion
Traumatic IVH or
SAH
0: normal
1: compressed
2: absent
0: no shift or <= 5
mm
1: shift > 5 mm
0: absent
1: present
0 : absent
1: present
Add +1 to total score
mortality at six months increases with the score: 5
score 1: 0%
score 2: 7%
score 3: 16%
score 4: 26%
score 5: 53%
score 6: 61%

30. Rotterdam score = 2
Hence predicted mortality at 6 months = 7%

31. 1. Scalp-
(Contusion, laceration )
2. Skull-
fractures (linear, depressed, comminuated, diastatical)
3. Meninges
(subdural, epidural, subarachnoid)
4. Brain parenchyma and ventricles
(contusions, intraparenchymal hematoma, concussion,
TAI, blunt cerebrovascular injury, intraventricular
hemorrhage)

32. ABCDEs of Trauma Care –
A: Airway and c-spine protection
B: Breathing and ventilation
C: Circulation with hemorrhage control
D: Disability/Neurologic status
E: Exposure/Environmental control

33. Ask patient a question and assess, If patient is unresponsive
then observe chest movements, snoring or gurgling sounds,
auscultation and gag reflex.
- Lateral position is patient mouth is filled with vomits or blood
 suction  remove foreign bodies including dentures
-Jaw thrust (to open airway)  oro/naso tracheal airway 
intubation
Cervical spine stabilization during airway management :
Hard cervical collar or manual stabilization
Avoid hyper extension of neck

34. Jaw thrust
Manual cervical spine stabilization

35. Single episode of hypoxia after TBI increases mortality by 60-
80% 6
-Monitor by auscultation, pulse oximetry
-Oxygen at 6-10 L/min nonrebreathing face mask
-Ventilation if patient is unable to breath
-Appropriate management of specific conditions like tension
pneumothorax (16 G needle decompression), open pneumothorax (3
side bandage), massive hemothorax (chest tube), flail chest (analgesia,
Oxygenation, PPV etc)

36. •Resuscitate with 2 large-bore (14- to 16-gauge) intravenous
catheters, using warmed fluids and packed RBCs if necessary
•Healthy adult: 2 L (or 20 mL/kg in pediatric patients) immediately.
Older patients with co morbidities smaller boluses (250-500 mL) to
prevent fluid overload.
•Control hemorrhage.
•Treat cardiac tamponade, cardiac arrest, and massive
hemothorax, consider immediate resuscitative thoracotomy:
abdominal bleeding; pelvis/long bone fracture

37. • Neurological assessment
- GCS
- Pupils
- Limb Movements
- Role of mannitol (only if Signs of herniation is present and BP
normal or high)
Bolus: 0.25 to 1g/Kg (starts effect 1-5min peak 20-60min)
Long term ICP reduction: 0.25 to 0.5 g/Kg repeated 2 to 6hrly
100 ml of 20% mannitol contains 20g of mannitol
side effects- hypovolemia, renal failure (S. Osm <320 mOsm)

38. - Role of prophylactic hypothermia- no evidence of benefit
- Role of steroids- no evidence of benefits
- Analgesics- PCM preferred over NSAIDs
Role of Hyperventilation- should be avoided in first 24 hour of
trauma when CBF is critical. Can be used only as a temporary
measure to reduce ICP in emergency situation.
Role of Prophylactic Antiepileptic medications:
10-20 mg/Kg iv loading over 20mins f/b 5mg/Kg divided in 3
doses for 7-14 days

39. - Undress the patient to inspect hidden injuries, if any
- Environment should be controlled
(eg to prevent hypothermia) blankets

40. • Window – bone, parenchymal
• Density
• Symmetry
• Areas- Sulci-Gyri, Ventricles and
subarachnoid spaces (importance of SAH)
• Structures

47. • Window – bone, parenchymal
• Density
• Symmetry
• Areas- Sulci-Gyri, Ventricles and
subarachnoid spaces (importance of SAH)
• Structures

48. 1. Adult- Canadian CT head rule 16
2. Children- Pediatric Emergency Care Applied Research
Network (PECARN) 17

51. - Vascularized, and when lacerated, bleeds copiously
- Scalp is highly resilient, and only the most severe avulsing
injuries lead to permanent damage (eg avulsion injuries usually
result from entanglement of hair in machinery or in vehicular
accidents in which the head is dragged on the pavement)
TREATMENT:
- control bleeding by direct pressure
-wash wound with clean water/normal saline. Primary suturing f/b
sterile dressing If there is no underlying skull fracture

53. Linear skull # Depressed skull # Comminuted skull #

54. Medical management: In most cases
-Wound care
-Analgesic
-Antibiotics if wound is infected
Surgical management : Elevation of depressed fracture
Indications: 7
1.Depressed more than thickness of adjacent bone
2.Evidence of dural penetration/parenchymal injury
3.Presence of hematoma / pneumocephalus
4.Wound infection
5.Gross cosmetic deformity
6.Frontal sinus involvement

55. Definition: transient alteration of consciousness following a non-
penetrating blow to the head.
Mildest form of diffuse injury, commonly occurs in athletes
Manifestation: transient LOC less than 1 min , mild headache,
immidiate post traumatic anterograde amnesia / confusion
Mechanism: transient torsion with malfunction of the reticular
activating system.

56. Imaging:
no structural abnormalities or minimal swelling. CT is done to r/o
other serious injuries.
PET scan s/o global reduction in cerebral glucose metabolism
Management:
Reassurance, for persistent headache acetaminophen preferred
over NSAIDs. Amitryptaline can be useful for headache and
anxiety
Complication: there is substantial concern that repetitive minor
head trauma may initiate a chronic neurodegenerative process
called chronic traumatic encephalopathy (CTE).

57. Corsellis and colleagues, in 1973, showed that boxer's brains with
dementia pugilistica showed neuronal loss and neurofibrillary
tangles, and coined the term chronic traumatic encephalopathy
(CTE), has subsequently been seen in non-boxers experiencing
varying degrees of repetitive head injury.
Manifest as gradually progressive memory dysfunction, behavioral
disturbances, chronic headaches.
finding being the deposition of tau in neurons.
CTE can be established only at autopsy

58. severely impaired in the absence of gross lacerations or hematomas.
They have sustained widespread microscopic axonal injury evidenced by the
presence of ruptured axons that retract to form spheroids. Ie retraction balls
(swollen proximal ends of severed axons)
When the axonal injury occurs in the context of trauma, the process is
designated as TAI rather than diffuse axonal injury, because the process may
be focal, multifocal, or diffuse.

59. Symptoms: Generally comatose or variable degree of
unconsciousness from the instant of injury, and subsequently
have only limited recovery.
Grading:
Grade 2 and 3 can be seen on imaging.
The principal mechanical loading: rotational acceleration
Grade of TAI Description
Grade I Diffuse axonal damage in corpus callosum, white matter of cerebral
hemisphere, brain stem and cerebellum
Grade II Grade I plus Focal lesion (punctate hemorrhage) in corpus callosum
Grade III Grade II plus focal lesion in brain stem

60. IMAGING:
Hemorrhagic TAI (<20%) – T2 weighted gradiant ECHO and SWI – based on
paramagnetic effect of blood products like Hb, appear as area of signal void (hypo
intens) (punctate or strich hemorrhages)
Non hemorrhagic TAI – DWI and DTI , assesses the microscopic motion of water
molecules in brain tissue, DTI is 3D imaging of diffusion, Within normal white
matter tracts with their parallel fiber bundles, water diffuses more freely along the
direction of the white matter fibers than transverse to the fibers.

61. • No definitive management
• ICP management if edema present
• Supportive and general nursing care

62. - Accumulations of blood in “potential space” between the
inner table of the skull and the outer surface of the dura
mater (periosteal layer)
- 2% of all types of head injury and in up to 15% of lethal
head injuries 8
- Temporoparietal > anterior cranial fossa > posterior fossa
> parasagittal regions. Usually occur skull fracture involving
the groove of the middle meningeal artery, lucid in the early
phases, timely surgical evacuation.

63. - Age: less common in infants, very young children and elderly
- Symptoms: hemiparesis (C/L or I/L), decreased level of
consciousness, and dilation of the I/L pupil. Lucid interval-
named by Jacobson in 1886: initial LOC  transient complete
recovery rapid progression of neurological deterioration
present in 14%-21%9
concurrent brain injuries such as acute subdural hematoma,
contusions, and lacerations in approximately 30% of cases of
EDH, unconscious from the time of injury.
- Excellent prognosis if treated timely whereas intradural lesions
Experience good outcomes only in 44%10

64. Venous EDH:
-10-40% of all EDH
- Occurs in children
- frequently occurs at anterior temporal pole (sphenoparietal sinus)
- Usually benign due to low pressure bleed
IMAGING
CT: biconvex hyper dense.
Presence of low-density areas within an EDH, or evidence of
contrast extravasations into the hematoma on a post contrast
head CT are indications of hyper acute or active bleeding into the
hematoma, and may portend rapid expansion of the hematoma
and could be associated with worse prognosis.

65. -EDH generally does not cross suture lines, can cross dural fold
Swirl sign

66. Features Management
>30 mL volume, regardless of
GCS score
Surgical evacuation
<30 mL volume, and
<15 mm thickness, and
<5 mm midline shift, and
GCS score >8 without focal
neurological deficit
Conservative management with
intensive monitoring and serial
imaging
9729: Youman’s textbook 7th
edition

68. Collection of blood occurring between the inner aspect of the
dura mater and the arachnoid
bilateral in 15% of cases
Classification: Seen on imaging as crescent-shaped extra-axial
collection overlying a cerebral convexity
Type Days Consistency Appearance on
CT
Acute 0-2 Clotted blood Hyperdense
Sub acute 2-14 Clotted and fluid blood Isodense
Chronic >14 fluid blood Hypodense

70. In Indian setting MC cause of ASDH is RTA f/b falls and assault ,
Order is reverse in Western world.
The mortality rate of traumatic ASDH varies from 30% to 90%,
Mechanism of Acute SDH
1. Contact load- ASDH with coexisting contusions and lacerations, with
intracerebral hemorrhage, burst lobe with the temporal or frontal lobes are most
frequently involved. Usually unconscious from the time of injury.
2. Inertial load - ASDH can sometimes result from rupture of bridging veins or
superficial cortical arteries. there may be little or no concomitant contusion or
laceration. may experience a lucid interval. MC mechanism in RTA

72. Features Management
>10 mm thick or >5 mm midline
shift
Surgical evacuation
<10 mm thick and <5 mm
midline shift, and
GCS score <9 with ≥2 point
decrease, and/or
pupillary dysfunction, and/or
ICP >20 mm Hg
Surgical evacuation
<10 mm thick and <5 mm
midline shift, GCS >=9, normal
pupil, ICP < 20 mmHg
Antiedema measures and serial
imaging

73. separation of dura at points of contact with bridging veins that normally connect
venous sinuses and the cortical surface.
These veins traverse a longer, more tightly tethered course as the brain
undergoes atrophy with aging or substance abuse (high-risk Populations)
2 to 3 weeks or longer after the initiating injury.
Inciting TBI is often mild and is not recalled in up to 50% of cases.
inner and outer membranes encase a core of degenerating blood that is gradually
encroached upon by the expanding membranes. Because these membranes
possess numerous delicate blood vessels, recurrent hemorrhage occurs often
leading to gradual expansion of the lesion (CSDH is a dynamic living structure).
Surgical drainage of the hematoma and removal of the membranes is necessary
for definitive treatment.

74. Procedure Indication and Rationale
Twist drill evacuation -Patient who cant tolerate surgery (co
morbidity etc)
- emergency stabilization if OT is not
available
- high recurrence
Burr hole evacuation -Procedure of choice
-Short surgery time
-Less recurrence
Craniotomy and
evacuation
- For long standing chronic SDH with
thick membranes seen on CT
-Long surgery time, less recurrence

76. Feature EDH SDH
Crossing suture line No Yes
Crossing dural fold Yes No
Association with fracture More than 90% Less consistent
Biomechanical load Only contact load Contact or inertial

78. an area of hemorrhagic necrosis usually occurring on the crests of gyri.
Occur in 22 – 30 % of TBI1
Location: MC in sub frontal and anterior temporal area due to irregular contour of
ACF and MCF bones
Head immobile when stuck = coup injury, and mobile when stuck = contrecoup injury

79. Natural history of contusion:
Gradual resorption of damaged tissue and reactive gliosis 
sunken brown cystic spaces aka plaques jaunes. Small
contusion 2-3 weeks, larger require more time.
Blossoming of contusion: cascade : recurrent hemorrhage 
Vasogenic edema  inflammation  ischemic necrosis

80. IMAGING:
MRI T1W most sensitive (98%) (methHb), CT (56%). CT used
more often as small contusion are generally clinically not
significant 13
Acute appearing as mottled areas of intermixed high and low
CT density lesions within a superficial portion of the brain.

81. collection of confluent, relatively homogeneous blood within the
brain parenchyma exceeding 5 mm in size.
Less surrounding edema than with contusions.
Intracerebral hemorrhages are also located deeper in the brain
than contusions are.
Hematoma border well defined than contusion, can evolve with
time.
20-30% of all traumatic hematoma14

84. Features Management
Progressive neurological deterioration
referable to lesion, medically
refractory intracranial hypertension, or
mass effect on CT
Surgical evacuation
Any lesion >50 mL Surgical evacuation
Frontal or temporal contusions >20 mL,
and
GCS score = 6-8, and
≥5 mm midline shift, and/or
cisternal compression on CT
Surgical evacuation
No evidence of neurological compromise,
and
controlled ICP, and
no significant signs of mass effect on CT
Conservative management with intensive
monitoring and serial imaging

85. - Hemorrhage in the subarachnoid space between the arachnoid
and pia mater, later is adherent to brain.
- 33-60% of all severe tbi 11
- disruption of small pial vessels along the brain surface.
- IMAGING: appear as Hyperdense outline of cortical gyri
CT/MRI T2 FLAIR (most sensitive)
Complications:
1.communitcating HCP (arachnoid granulation block) non communicating HCP
(aqueduct block by large IVH or chronic ependymal proliferation i.e.
ependimitis) 2. Post traumatic Vasospasm

86. IVH has been reported in 1% to 5% of closed head injury
patients15
Sources of bleed:
Primary IVH (no parenchymal bleed) tearing of tiny
subependymal vessels choroid plexus on sagital impact causing
negative pressure due to ventricular dilation and hence traction on
vessels
Secondary IVH: intraventricular extension of hemorrhage from an
intraparenchymal hematoma, or from retrograde reflux of SAH via
the foramina of Luschka and Magendie.

87. Traumatic SAH Traumatic IVH Aneurysmal SAH

88. • Usually they resolve on their own over
weeks to months
• Analgesic and other supportive measures
• EVD placement if patient develops
hydrocephalus
• Mannitol usually has no role until massive
edema and herniation signs present

89. TBI is a heterogeneous condition with spectrum
of pathologies, Prevention is always better than
any intervention. Individual pathologies has to be
managed with good clinical judgment as time
factor is of paramount importance in TBI

90. References
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