TRAUMATIC BRAIN INJURY

1. RUTAYISIRE Francois Xavier
PG Y I
TRAUMATIC BRAIN INJURY

2. TBI
 Alteration in the brain function, or other evidence
of brain pathology, caused by external force.
 Traumatically induced structural injury of the brain
or physiologic disruption of normal brain function
resulting from an external force.

3. EPIDEMIOLOGY
 Globally, the annual incidence of TBI is variably
estimated at 27 to 69 million with incidence rate of
369 per 100,000 population.
 Global TBI prevalence is estimated at 55.5 million
with prevalence rate of 759 per 100,000.
 TBI is the leading cause of death in North America for
individuals between the ages of 1 to 45 yrs
 1.74 million people sustain a traumatic brain injury (TBI) in
the US every year, and in 2016 there were prevalence of
2.35 million TBI cases in the United States
 Most, 75 to 95 percent, are mild and several cases go
unreported

4. Rwanda
 A retrospective descriptive analysis performed using
SAMU records captured on an electronic database from
December 2012 through May 2016.
 The incidence of TBIs in Kigali was 234 crashes per
100,000 people.
 The mean age was 30.5 (SD = 11.5) years and 81.5% (n =
1,615) were men.
 The most common mechanisms were road traffic incidents
(RTIs; 78.5%, n = 1,535), assault (10.7%, n=216), and falls
(7.8%, n=156).
 Most patients experienced mild TBI (Glasgow Coma Score
[GCS] ≥ 13; 83.5%, n = 1,625).
 In total, TBIs were involved in 67.0% of all mortalities seen
by SAMU.

5. MECHANISM OF INJURY
The physical mechanisms of brain injury are
classified using the following categories:
• Impact loading - Collision of the head with a solid
object at a tangible speed
• Impulsive loading - Sudden motion without
significant physical contact
• Static or quasistatic loading - Loading in which
the effect of speed of occurrence may not be
significant

6. PATHOPHYSIOLOGY
 Brain metabolism
Brain oxygen consumption (CMRO2, cerebral metabolic rate for
oxygen) is about 3.5 ml 100 g–1min–1. The brain relies on bloodborne
glucose for 90% of its energy requirements.
 Cerebral blood flow and autoregulation
Normal cerebral blood flow is approximately 55 ml 100 g–1min–1 and is
usually maintained at a constant level via mechanisms termed cerebral
autoregulation.
 This is despite variations in mean arterial pressure (MAP) of between 50
and 150 mmHg.
 In TBI, mechanisms of cerebral autoregulation become disordered.
 Cerebral blood flow then fluctuates with MAP and the brain is more
vulnerable to hypotension.

8. TBI
 PRIMARY TBI
 Occurs at the time of impact from external force on
the brain
 FOCAL: skull fractures
intracranial hematomas
lacerations
contusions
penetrating wounds
• DIFFUSE: DAI
 SECONDARY TBI
 Injuries from intracranial hematomas, edema,
hypoxia, ischemia from raised ICP

9. Causes of secondary brain
injury
■ Hypoxia: PO2 < 60 MmHg
■ Hypotension: systolic blood pressure (SBP) < 90 mmHg
■ Raised intracranial pressure (ICP): ICP > 20 mmHg
■ Low cerebral perfusion pressure (CPP): CPP < 65 mmHg
■ Pyrexia
■ Seizures
■ Metabolic disturbance

10. CLINICAL TBI CLASSIFICATION
 FOCAL BRAIN INJURIES:
 Readily visible injuries using standard imaging techniques
occurring at a specific region of the brain
 PRIMARY VASCULAR INJURIES CAUSING BLEEIDNG :
o WITHIN THE BRAIN
E.g: Intracerebral hematomas; tissue tears
o ON SURFACE OF THE BRAIN
E.g: Epidural, subdural hematoma and subarachnoid
hemorrhage
o ON CORTICAL GRAY MATTER
E. g: Cerebral contusions
 High occurrence in Severe and moderate TBI

11. CLINICAL TBI CLASSIFICATION
 DIFFUSE BRAIN INJURIES
 Injuries not localized to one area and more
distributed throughout the brain
 Can appear over time following the injury
 Predominant injury in Mild TBI
 DIFFUSE AXONAL INJURY(DAI)
 Most common diffuse TBI

12. Taking a history in head injury
■ Mechanism of injury
■ Loss of consciousness or amnesia
■ Level of consciousness at scene and on transfer
■ Evidence of seizures
■ Probable hypoxia or hypotension
■ Pre-existing medical conditions
■ Medications (especially anticoagulants)
■ Illicit drugs and alcohol

13. Examination in head injury
■ Glasgow Coma Score
■ Pupil size and response
■ Lateralising signs
■ Signs of base of skull fracture
Bilateral periorbital oedaema (raccoon eyes)
Battle’s sign (bruising over mastoid)
Cerebrospinal fluid rhinorrhoea or otorrhoea
Haemotympanum or bleeding from ear
■ Full neurological examination: tone, power, sensation,
reflexes

14. MANAGEMENT OF MILD HEAD
INJURY
(GCS 14–15)
 The majority are discharged from the emergency department after
history, examination and a period of observation.
 GCS of 15/15 with no focal neurological deficit;
 Be accompanied by a responsible adult and should not be under the
influence of alcohol or other drugs;
 verbal and written head injury advice must be given to the patient and
their accompanying adult.
 Written head injury advice describes to patients the symptoms that
should prompt them to obtain further medical advice, which usually
involves a return to the emergency department. These include
persistent or worsening headache despite analgesia, persistent
vomiting, drowsiness, visual disturbance such as double or blurred
vision, and development of weakness or numbness in the limbs.
 Some patients with mild head injury are at significant risk of intracranial
haematoma and require a computerised tomography (CT) scan.

15. NICE guidelines for computerized
tomography (CT) in head injury
■ Glasgow Coma Score (GCS) < 13 at any point
■ GCS 13 or 14 at 2 hours
■ Focal neurological deficit
■ Suspected open, depressed or basal skull fracture
■ Seizure
■ Vomiting > one episode
Urgent CT head scan if none of the above but:
■ Age > 65
■ Coagulopathy (e.g. on warfarin)
■ Dangerous mechanism of injury (CT within 8 hours)
■ Antegrade amnesia > 30 min (CT within 8 hours)

16. Medical management of raised intracranial pressure
■ Position head up 30º
■ Avoid obstruction of venous drainage from head
■ Sedation +/– muscle relaxant
■ Normocapnia 4.5–5.0 kPa
■ Diuretics: furosemide, mannitol
■ Seizure control
■ Normothermia
■ Sodium balance
■ Barbiturates

17. CONCUSSION
 Often viewed as Mild TBIs with no gross
structural damage secondary to an non
penetrating TBI
 Usually follow direct blows to the head with
subsequent acceleration/deceleration forces
 Varying levels of transient altered mental status;
from confusion to LOC for a few minutes;
common in players.

18. IMAGING PARAMETERS

19. IMAGING PARAMETERS

20. CONTUSION
 Bruise of the brain when the force from trauma
causes breakdown of small vessels and
perivascular hemorrhage into the brain
 The brain sustains injury as it collides with the
rough, bony surfaces (coup injury) and rarely
causes significant mass effect.
 May occur in brain tissue opposite to the site of
impact (contre-coup injury) from deceleration
against the skull.
 May enlarge or progress to frank hematomas esp
during the first 24 hrs.
 Contused areas appear bright on CT scan.

23. DIFFUSE AXONAL INJURY
(DAI)
 Caused by damage to axons throughout the brain
(white matter tracts in the brain) from rotational
acceleration and then deceleration
 Extensive ,generalized damage to the white matter
of the brain
 Could occur as a result of ischemia
 Can be a result of primary blast exposure
 Axonal disruption or complete rupture with small
hemorrhages
 Hemorrhage is classically seen in corpus
callosum and dorsolateral midbrain (MRI)

24. DIFFUSE AXONAL INJURY
THE ADAMS DAI CLASSIFICATION
 GRADE 1:
 Mild DAI with microscopic white matter changes in the
cerebral cortex, corpus callosum and brainstem
 GRADE 2:
 Moderate DAI with gross focal lesions in the corpus
callosum
 GRADE 3:
 Severe DAI with finding as grade 2 and additional focal
lesion in the brainstem

25. PENETRATING INJURY
 Complex and must be evaluated individually
 2 subtypes:
 Missiles : from bullets or fragmentation devices
 Nonmissiles: from knives, spears or ice picks
 Management:
 SXR and CT scans to assess the nature of injury
 Cerebral angiography if object near major artery or
venous sinus
 Operative exploration
 Object extending out of the cranium
 Debridement, irrigation, hemostasis and definitive closure
 Antibiotics

26. TRAUMATIC INTRACRANIAL
HEMATOMAS
 Contribute to death and disability secondary to
head injury
 Mechanisms:
 can expand rapidly
 Cause brain shift
 Cause subsequent herniation

27. EPIDURAL HEMATOMA
 Accumulation of blood between the skull and the
dura mater
 Usually results from arterial disruption, especially
middle meningeal artery.
 Classic three-stage clinical presentation in 20-
50% of cases
 Initially unconscious from concussion
 Lucid interval
 Herniation
 CT Scan: bright, biconvex (LENTIFORM) blood
clot respecting cranial suture lines

28. EPIDURAL HEMATOMA
 OPEN CRANIECTOMY:
 For evacuation of congealed clot and hemostasis
 Clot volume > 30 cm3
 Clot volume > 20 cm3 in basitemporal and posterior
fossa
 CONSERVATIVE MANAGEMENT
 Clot volume <30 cm3, maximum thickness<1.5 cm,
midline shift <5mm,GCS Score >8 with no deficits.
 PROGNOSIS
 Good outcome in 85 to 90% of patients with rapid
CT scan and intervention and if no associated
intracranial injuries.

29. EDH

30. SUBDURAL HEMATOMA
 Most lethal of all head injuries with mortality rate
of 30-90%
 MAY BE :
 ACUTE: < 3 days
 SUBACUTE: 4 – 20 days
 CHRONIC: > 21 days
 Chronic SDH may completely organize and
resolve or may calcify

31. SUBDURAL HEMATOMA
 ACUTE SUBDURAL HEMATOMA
 Incidence: 12 to 20 % of severe TBIs
 Accumulation of blood between the arachnoid
membrane and the dura
 Usually results from slow venous bleeding,
typically from tearing of BRIDGING VEIN running
from the cerebral cortex to the dura sinuses
 Elderly ad alcoholic patients are at higher risk of
acute SDH due to brain atrophy
 CT Scan: bright crescent-shaped (LUNATE) clot

32. SUBDURAL HEMATOMA
 OPEN CRANIOTOMY
 Any GSC with clot thickness > 10 mm, midline shift
> 5 mm, or GCS drop by two or more from the time
of injury.
 CONSERVATIVE MANAGEMENT
 Clot thickness < 10 mm, midline shift < 5 mm
 With GCS<9 or deteriorated by 2 GCS with pupillary
asymmetry
 Requires frequent neurologic exams until the clot
stabilizes based on serial head CT Scans

34. SUBDURAL HEMATOMA
 CHRONIC SUBDURAL HEMATOMA
 Collection of blood breakdown products that is at
least 2 to 3 weeks old
 Acute-on-chronic SDH
 Phenomenon where small, recurrent hemorrhages expand
the collection enough to make it symptomatic
 Risk factors:
 Hx of head injury or no clear hx of head trauma
 Alcoholics, Elderly and patients on anticoagulation
 Signs:
 Headache(80%), seizures, confusion (33%), contralateral
hemiparesis (60%) or coma (28-100%), papilledema (25%)

35. CHRONIC SDH
 Intravenous administration of contrast to look for
enhancement of the inner membrane particularly
for isodense CSDH

36. ACUTE-ON-CHRONIC SDH
Elderly patient with headache, progressive left
hemiplegia and lethargy with hx of a fall 4 weeks
before presentation.

37. CHRONIC SDH
 SURGICAL DRAINAGE
 If chronic SDH > 10mm
 Any symptomatic SDH
 BURR HOLE: successful in 86 to 95%
 TWIST DRILL CRANIOSTOMY
 OPEN CRANIOTOMY
 If hematoma is too congealed for irrigation drainage,
membranes prevent effective drainage or persistent
hemorrhage
 PREVENTION OF REACCUMULATION
 Subdural shunt for 1 to 2 days
 Mild hydration and bed rest with head of the bed flat
 Follow up head CT Scan

38. TRAUMATIC SUBARACHNOID
HEMORRHAGE
 Caused by trauma
 Small capillaries tear and ultimately spill blood
transiently into the subarachnoid space.
 Not as severe as spontaneous aneurysmal
subarachnoid hemorrhage because blood is
projecting into the subarachnoid space under
arterial pressure.
 May complicate into hydrocephalus within 3
months

39. INTRAPARENCHYMAL
HEMORRHAGE
 Bleeding may occur in a contused area of the
brain.
 MASS EFFECT from developing hematomas may
present as a delayed neurologic deficit.
 DELAYED TRAUMATIC INTRACEREBRAL
HEMORRAGE: (DTICH)
 Most likely to occur in the first 24 hrs ( but from 6 to 30
days) in 1 to 7 % of cases
 Craniotomy if:
o Clot volume > 50 cm3
o Any clot volume > 20 cm3 with neurologic deterioration
(GCS 6-8) and associated midline shift(MLS) > 5 mm
or basal cistern compression

40. SKULL FRACTURES
 From transmission of significant amount of force
to the head
 CLOSED versus OPEN FRACTURES
 Fractures lines may be:
 Linear
 Stellate
 Comminuted
 Depressed
 OPEN FRACTURES
 Surgical repair of the scalp and operative debridment

41. DEPRESSED SKULL
FRACTURES
 Results from a focal injury of significant force with
incidence of 6 %
 Significantly depressed if the outer table of the
one or more of the fractured segment lies below
the inner table of the surrounding skull.
 Signs: amnesia, seizures, focal neurological
signs, CSF leakage
 WHEN SURGERY:
 Elevation of the fragment , repair of dural disruption with
hematoma, if compound (or open) fracture, epileptic
focus……Elevation with debridment, Duraplasty and
antibiotics

42. DEPRESSED SKULL
FRACTURES

43. HOW TO MANAGE?

44. ASSESSMENT OF THE
PATIENT
 GENERAL PHYSICAL CONDITION
 INSPECTION
 Evidence of basal skull fracture:
 Racoon’s eyes
 Battle’s sign
 CSF rhinorrhea/ othorrhea
 Hemotympanum or laceration of external auditory canal
 Check for facial fractures
 Evidence of seizures
 NEUROLOGIC EXAM
 Cranial nerve exam
 Optic nerve function: vision, pupillary reflex, fundoscopic
exam
 CN VII: Check of facial asymetry
 CN VI: palsy in case of increased ICP

45. ASSESSMENT OF THE
PATIENT
 LEVEL OF CONSCIOUSNESS
 GCS
 MOTOR EXAM
 SENSORY EXAM
 REFLEXES

47. CLASSIFICATION
 GCS: to establish the level of consciousness
defines the severity of a TBI within48 hrs of
injury
 Spontaneous or simulated verbal response
 Motor response
 Eye opening response
 Length of unconsciousness dictates the severity
of brain injury
 Mild TBI: GCS :13-15
 Moderate TBI : 9-12
 Severe TBI : 3-8

48. CRITERIA FOR DISCHARGE IN
MINOR TBI

50. MANAGEMENT
 INITIAL RESUSCITATION
 AIRWAYS
 BREATHING
 CIRCULATION
 Monitor BP and avoid hypotension(s BP<90 mmHg)
 Avoid hypoxia (PaO2<60 mmHg or O2 saturation <90%)
 Look for another cause of shock
 DISABILITY
 LOC, pupil size and reactivity, mvts of extremities and
Reflexes
 EXPOSURE

51. INTUBATION AND
HYPERVENTILATION
 INTUBATION:
 Depressed LOC(GCS<8) patient cannot protect
airways
 Severe maxillofacial trauma where patency of
airways is at risk
 HYPERVENTILATION:
 Prophylactic hyperentilation (PaCo2 <25 mmHg) is not
recommended
 Maintain Pa Co2 between 30-35 mm Hg
 HPV should only be used brief as TEMPORIZING
MEASURE when CT or clinical signs of IC-HTN are
present.

52. MANNITOL
 INDICATIONS:
 Evidence of raised ICP, mass effect with sudden
deterioration
 To assess salvageability in patients with no evidence of
brainstem function
 CONTRAINDICATIONS:
 No prophylactic administration is recommended
 Hypotension and hypovelemia
o Fluid resuscitate the patient before mannitol.
o Use hypoventilation if hypovolemia until mannitol can
be used

54. RAISED INTRACRANIAL
PRESSURE
 INTRACRANIAL COMPARTMENT is comprised
of 3 separate contents
 Brain parenchyma (83%), CSF (11%), Blood (6%)
 NORMAL HOMEOSTASIS
 Edematous brain initially causes extrusion of CSF to the
spinal compartment
 Blood, especially that of venous origin is extruded away
from the brain
 If failure of compensatory mechanisms, pathological brain
compression and ensuing death

55. RAISED INTRACRANIAL
PRESSURE
 CPP= MAP- ICP
 Normal CPP is > 50 mmHg, and if < 40 mmHg,
there is impairment in CBF.
 Normal ICP: 10- 15 mmHg, raised ICP:>20
mmHg
 CUSHING’S TRIAD: Hypertension, bradycardia
and respiratory irregularity(in 33%)

57. REFERENCES
 Greenbeerg Handbook of Neurosurgery
 Traumatic brain injury incidence clinical overview
and Policies in the US Military Health Systems
since 2000
 TBI: current treatment strategies and future
endeavors
 Rosenberg, A., Mukeshimana, L., Uwamahoro,
A., Dworkin, M., Nsengimana, V., Kankindi, E., . .
. Jayaraman, S. (2020). The Initial Prehospital
Management of Traumatic Brain Injuries in Kigali,
Rwanda. Prehospital and Disaster Medicine,
35(5), 533-537.
doi:10.1017/S1049023X20000813