A summary of head injury and traumatic injury diagnosis and management. For any medical student or healthcare provider.

1. TRAUMATIC BRAIN
INJURY
Wanjau George kariuki
Alicen Jeruto Kiprop

2. Outline.
• Introduction
• Epidemiology.
• Aetiology
• Pathophysiology
• Classification.
• Management
• complications

3. Introduction.
• Head injury- trauma to the head
• Traumatic brain injury- An alteration in brain
function, or other evidence of brain pathology,
caused by an external force1.

4. Epidemiology.
• Is a major public health concern worldwide.
• 69 million people are estimated to sustain TBI
each year2.
• Head injury following road traffic collision is more
common in LMICs, and the proportion of TBIs
secondary to road traffic collision is likewise
greatest in these countries

5. epidemiology Of Head Injuries In
Kenya 3
• 1979-1985 (pre-ct scan era)
• Mortality 16% in adults and 1.4% in children.
• The male to female ratio was 7:1. in adults
and 1.1:1 in children.
• Most of the TBI in adults in the pre-CT scan
period were due to either road traffic
accidents (46%) or assaults (40%),
• Children falls from a height being most
frequent (50%) followed closely by road traffic
accidents (42%).

6. epidemiology Of Head Injuries In
Kenya 3
• 1999-2009 CT scan era
• The male to female ratio in patients with
severe TBI (GCS 8 and below) was 8:1 while
the overall mortality was 57%

7. Aetiology.
• Road traffic accidents – commonest- about 48-
53%
• Falls – 20-28%
• Sports and recreation activities- 3-9%
• Assault

8. Pathophysiology.
• Normal cerebral blood flow is 55mL/100 gm/min
• If this rate drops below 20 mL/100 gm/min infarction will result
• The flow rate is related to cerebral perfusion pressure (CPP)
• CPP (75–105 mmHg) = MAP (90–110 mmHg) − ICP (5–15 mmHg).
• Monro-Kellie Doctrine
• Skull is a confined rigid space contains the brain, CSF and blood
• The sum of the Intracranial volumes of blood, brain, CSF is constant,
and that an increase in any one of these must be compensated by an
equal decrease in another, otherwise pressure will rise.
• Once ICP rises, it results decreased CBF and eventually brain
herniation

9. Classification.
• According to
• Severity
• Morphology
• Mechanism of injury

10. Severity.
• Depending on GCS
• Minor- GCS15
with no LOC
• Mild-14/15 with
LOC
• Moderate-9-13
• Severe- 3-8

11. Mechanism of injury.
Missile injury
• damage is the result of
an object entering the
cranial cavity and
dissipating energy
through the brain.
• Damage is often focal
and the extent relates to
the velocity of the
missile.
• High velocity vs low
velocity
Non-missile injury
• rapid deceleration and
acceleration which causes the
brain to move within the
cranial cavity and to come into
contact with bony
protuberances within the
skull.
• This results in contusions,
lacerations, and shearing
strains within the brain
substance.
• The acceleration/deceleration
forces rather than actual
impact against the skull are
the critical factors in
producing brain injury

12. Morphology.
• Primary injury - occurs at
the time of impact
• Secondary brain injury-
occurs as a result of
events after the initial
injury.
• Causes of secondary
injury
• Hypoxia: PO2<8kPa
• Hypotension: systolic
blood pressure (SBP) < 90
mmHg
• Raised intracranial
pressure (ICP): ICP > 20
mmHgLow
• cerebral perfusion
pressure (CPP): CPP < 65
mmHg
• Pyrexia
• Seizures
• Metabolic disturbance

13. Primary brain injury.
Contusion
Diffuse axonal injury
concussion

14. Cerebral contusion.
• Occurs at the time of injury as the result of
contact between the brain and bony
protuberances of the skull base.
• Have a characteristic distribution- orbital
surface of frontal lobes, frontal poles, around
the Sylvian fissure, temporal poles, and
undersurface of temporal lobes.
• They occur on the crests of gyri but commonly
extend into subcortical white matter.

15. Cerebral contusion.
• rarely require immediate surgical treatment.
• must be admitted for observation as these lesions will tend to mature and
expand for 48–72 hours following injury.
• delayed surgical evacuation to reduce the mass effect

16. Diffuse axonal injury.
• Most common cause of coma after head injury.
• Widespread axonal injury occurs as a result of
shear and tensile strains.
• Least severe- in the parasagittal white matter
of the cerebral hemispheres.
• Moderately severe- least + focal lesions in the
corpus callosum.
• Very severe- discrete lesions are found in the
dorsolateral quadrants of the rostral
brainstem.

18. Concussion.
• Concussion is transient loss of consciousness
following non-penetrating closed head injury
without gross or microscopic brain damage.

19. Indications for CT-Scan (NICE)
• GCS <13 at any point
• GCS 13/14 at 2 hrs.
• Neurological deficits.
• Suspected skull
fracture.
• Seizures.
• More than 1 episode
of vomiting.
Urgent CT scan if
• Age>65.
• Coagulopathy.
• Dangerous
mechanism of injury.
• Anterograde
amnesia.

20. Intracranial hematomas.

21. Extradural hematoma
• Aka epidural hematoma.
• Is a neurosurgical
emergency
• Common in young people
• In < 30 yrs. – 40% -
associated with skull #
• In > 30 yrs. – almost all
associated with skull #
• 20% associated with
subdural hematoma

22. Extradural hematoma
• Temporal region most affected as the pterion
is thin and it overlies a large vessel.1
• Classical presentation(1
3 of patients)
• Injury›››› lucid interval(headache but
otherwise normal) ››››rapid deterioration as a
result of brain compression
• There may be no primary brain injury with an
EDH.
• Mortality – 20-55% With early treatment –5-
10%

23. Extradural hematoma
• CT scan shows lentiform
(lens shaped or biconvex)
hyperdense lesion
between the skull and
brain.
• There may be an
associated mass effect on
the underlying brain,
with or without a midline
shift.
• Areas of mixed density
may be seen in a lesion
that is actively bleeding.

24. Extradural hematoma.
• Surgical management
is evacuation via a
craniotomy

25. Acute subdural hematoma.
• Accumulates
between dura and
arachnoid mata
• Due to disruption of
cortical vessels or
brain laceration
• Almost always
associated with
primary brain injury

26. Acute subdural hematoma.
• Pts. present with
impaired level of
consciousness from
the time of injury
which may
deteriorate as the
hematoma expands.
• Mortality with
treatment is as high
as 40%

27. Acute subdural hematoma.
• The CT appearance
of an ASDH is
hyperdense (acute
blood) but the
haematoma spreads
across the surface of
the brain(concave)

28. Acute subdural hematoma.
• The treatment of an ASDH is usually
evacuation via a craniotomy.
• Small haematomas with little mass effect may
be managed conservatively in.
• It may be inappropriateto perform surgery on
cases with a very poor prognosis: factors
• best GCS
• pupillary reactivity
• Age
• presence of anticoagulants

29. Chronic subdural hematoma.
• Common in elderly
esp those on
antiplatelet/anticoag
ulant therapy.
• Hx of minor head
trauma
days,weeks,months
• Clinical features of
CSDH include
• headache,
• cognitive decline
• focal neurological
deficits
• seizures.
• exclude hypoxic,
metabolic and
endocrine disorders

30. Chronic subdural hematoma.
• Treatment of a CSDH and most acute-on-
chronic subdural haematomas is evacuation via
burr hole(s) rather than craniotomy.
• This is an important distinction as burr holes
can be easily performed under local anesthetic
in an elderly patient with extensive
comorbidity

31. Ct findings- subdural hematoma

33. Intra-cerebral haemorrhage
• Haemorrrhage within the brain tissue
• Two main types
• Intraparennchymal
• Intraventricular
• causes
• Hypertensive vasculopathy (70-80%)
• Ruptured AVM
• Blood dyscrasias.

34. Management.

35. Supportive Measures.
• Endotracheal intubation for patients with GCS<8
and poor airway protection.
• Cautiously lower blood pressure to a MAP less than
130 mm Hg, but avoid excessive hypotension.
• Rapidly stabilize vital signs, and simultaneously
acquire emergent CT scan.
• Maintain euvolemia, using normotonic rather than
hypotonic fluids, to maintain brain perfusion
without exacerbating brain edema
• Avoid hyperthermia.
• Facilitate transfer to the operating room or ICU.

36. Decrease cerebral edema.
• Modest passive hyperventilation to reduce
PaCO2
• Mannitol, 0.5-1.0 gm/kg slow iv push
• Furosemide 5-20 mg iv
• Elevate head 20-30 degrees, avoid any neck
vein compression
• Sedate and paralyze if necessary (struggling,
coughing etc will elevate intracranial
pressure)

37. Surgery.
• Surgical Evacuation of hematoma:
• No surgical intervention if collection <10ml unless;
• The GCS score decreases by 2 or more points
between the time of injury and hospital evaluation
• The patient presents with fixed and dilated pupils
• The intracranial pressure (ICP) exceeds 20 mm
• Surgical decompression
• hematoma >10mm
• or >5mm midline shift
• Hematoma>30mls

38. Types of surgery.
• Burr-hole
• Craniotomy-bone flap is temporarily removed
from the skull to access the brain
• Craniectomy–in which the skull flap is not
immediately replaced, allowing the brain to
swell, thus reducing intracranial pressure
• Cranioplasty-surgical repair of a defect or
deformity of a skull.

39. Mild head injury
• Discharge after history, physical examination and a
period of observation. (hours)
• Must met the following criteria before discharge
• GCS 15/15 with no neurological deficits
• In the company of an adult.
• Not under influence of drugs/ alcohol.
• Verbal and written advice on head injury given
(symptoms that should prompt a revisit)
• CT-scan done***

40. Complications.
• Neurological deficits
or death
• Seizures
• Obstructive
Hydrocephalus
• Spasticity
• Urinary
complications
• Cushing’s ulcer
• Neuropathic pain
• Deep venous
thrombosis
• Pulmonary emboli
• Cerebral herniation
• Aspiration
pneumonia

41. Glasgow outcome score

42. References.
• Oxford Textbook of
Surgery
• Merck Manuals-
Professional Version
• Bailey and Love
• Uon online
repository.

43. The end