The document discusses head injury and traumatic brain injury (TBI). Some key points: - Head injury is a common cause of emergency department visits, accounting for 3.4% of presentations. TBIs are a leading cause of death and disability, especially in young adults aged 15-24. - Head injury ranges from mild concussion to severe brain injury resulting in death. Common causes are motor vehicle accidents, falls, firearms, and assaults. - Primary brain injury occurs at impact, while secondary brain injury develops after from factors like hypoxia, hypotension, increased intracranial pressure, fever, seizures, and metabolic disturbances. - Glasgow Coma Scale is used to assess head injury severity

1. By : Dr.
Grkreddy
Dept of
Neurosurgery
HEAD INJURY AND TRUMATIC BRAIN
INJURY

2.  Head injury is a frequent cause of emergency
department attendance, accounting for approx 3.4% of
all presentations.
 Traumatic brain injuries (TBIs) are a leading cause of
morbidity, mortality, disability, socioeconomic losses and
poor quality of life among survivors.
 It is the most common cause of death in young adults
(age 15–24 years)
 More common in males than females

3.  Head injury’ is defined as any trauma to the
head, other than superficial injuries to the face.
 It includes injury to the scalp, skull &/or brain.
 There is a wide spectrum of head injury from mild
concussion to severe brain injury resulting in
death.

4. The top causes of TBI are:
Commonest causes:
 MVA
 Firearms or explosions
 falls
 fighting

5. Pathophysiology of head injury:
 Cranial volume : fixed
 80% : Cerebrum, cerebellum & brainstem
 12% : Blood vessels & blood
 8% : CSF
 Monroe-Kelli Doctrine
 Defines the relationship between the volumes of the three
compartments
 The expansion of one compartment MUST be accompanied by
a compensatory reduction in the volumes of the other
compartments to maintain a stable intracranial pressure (ICP)

7. Compensatory Mechanisms After Head Injury

8.  The management of the patient following a head injury
requires the identification of the pathological processes
that have occurred.
 The pathological processes involved in a head injury are:
 Direct trauma
 Cerebral contusion
 Intracerebral shearing
 Cerebral swelling (oedema)
 Intracranial haemorrhage
 Hydrocephalus.

9. Primary vs secondary brain injury:
 Primary brain injury occurs at the time of impact and includes injuries
such as brainstem and hemispheric contusions, diffuse axonal injuries and
cortical lacerations.
 Secondary brain injury occurs at some time after the moment of impact
and is often preventable.
The principle causes of secondary brain injury are:
 Hypoxia
 Hypotension(SBP<90mm hg)
 Raised ICT(>20mm Hg)
 Low cerebral perfusion pressure
 Pyrexia
 Seizures
 Metabolic disturbances

11. b. Diffuse

12. TBI
CLOSED HEAD
INJURY
OPEN HEAD
INJURY
No obvious external signs,
resulting from –motor vehicle
crashes, falls, child abuse, or
domestic violence, child
violence..
Obvious external wound
For example a gunshot wound
or object penetrating the skull.

13.  Glasgow Coma Scale:
 Developed by Teasdale and Jennett in 1974
 Originally designed for measure 6 hours after injury to
provide long term prognostic information about
mortality and disability
 Now, standardized to measure 30 min after injury and
repetitive measurements throughout patient’s stay
 Should be performed after adequate resuscitation as it
is sensitive to hypotension, hypoxia, intoxication and
pharmacologic intervention.
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course

14. Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course
Glasgow Coma Scale (GCS)
Eye Opening Opens spontaneously 4
Responds to verbal command 3
Responds to pain 2
No eye opening 1
Verbal Oriented 5
Disoriented 4
Inappropriate words 3
Incomprehensible speech 2
No verbal response 1
Motor Obeys commands 6
Localizes to pain 5
Withdraws to pain 4
Flexion to pain (Decorticate posturing) 3
Extension to pain (Decerebrate posturing) 2
No motor response 1
Ghana Emergency Medicine Collaborative
Advanced Emergency Trauma Course

15. Pupillary Size & Reactivity
 Fixed Dilated Pupil : Ipsilateral Intracranial Hematoma
resulting in uncal herniation
 Bilateral Fixed + Dilated : Poor Brain Perfusion, bilateral
uncal herniation or severe hypoxia
 Indicative of very poor neurological outcome
Neurological Posturing
 Decorticate Posturing
 Upper extremity flexion with lower extremity extension
 Cortical Injury above the midbrain
 Decerebrate Posturing
 Arm extension and internal rotation with wrist flexion
 Indicative of brainstem injury
 Very Poor predictor of outcome

16. Based on Glassgow coma scale:
 Minor head injury
(GCS 15 with no loss of consciousness)
 Mild head injury
(GCS 14 or 15 with loss of consciousness)
 Moderate head injury
(GCS 9 -13)
 Severe head injury
(GCS 3 -8)

17. Mild head injury:
 The majority of patients presenting to the emergency
room with head injuries fall under this category.
 These patients are awake but may be amnesic for events
surrounding the injury.
 May be a history of a brief loss of consciousness often
further confounded by alcohol or other intoxicants.

18. CRITERIA FOR ADMISSION:
 Significant posttraumatic amnesia (over 1 hr)
 History of loss of consciousness (over 15 mins)
 Deteriorating level of consciousness
 Moderate to severe headache
 Intoxication with alcohol or drugs
 Skull fracture
 CSF leak - otorrhea or rhinorrhea
 Significant associated injuries
 No reliable companion at home
 Abnormal CT scan

19. Moderate head injury:
 These patients are able to follow simple commands, they
can deteriorate rapidly
 Therefore, they should be treated similar to the severely
head-injured patient

20. Severe head injury:
 Patients are unable to follow simple commands even after
cardiopulmonary stabilization.
 These pts are at maximal risk of suffering significant
morbidity & mortality.
 The management of a patient following a severe head
injury depends on the patient’s neurological state and the
intracranial pathology resulting from the trauma.
 If the CT scan shows an intracranial haematoma
causing shift of the underlying brain structures then this
should be evacuated immediately.

21.  If there is no surgical lesion, or following the operation, the
management consists of:
(a) Careful observation using a chart with the Glasgow coma
scale.
(b) Measures to decrease brain swelling
(i) careful management of the airway to ensure adequate
oxygenation and ventilation. Hypercapnia will cause cerebral
vasodilatation and so exacerbate brain swelling
(ii) elevation of the head of the bed 20°
(iii) fluid and electrolyte balance.

22.  Maintenance of isotonic fluid requirements, avoiding
dextrose solutions until the patient is able to commence
naso gastric feeding.
 Blood loss from other injuries should be replaced with colloid
or blood and not with crystalloid solutions.
 Care should be taken to avoid over hydration, as this will
increase cerebral edema.

25. Scalp injuries:
 Scalp injuries are usually the result of
direct impact.
 They may manifest as
 abrasion, bruising, laceration
 subcutaneous hemorrhage (caput
succedaneum)
 subgaleal hemorrhage
 subperiosteal
hemorrhage(cephalhematoma)

26. • Highly vascular, bleeds briskly
 Hemostasis : direct pressure
 Treatment :
 Exploration & Thorough debridement
 The closure should be performed in two layers if
possible, with apposition of the galea prior to closing the
skin.

28. Fractures of the skull:

29. Types of fractures:
 Linear :
 low-energy blunt trauma over a wide surface area of the
skull.
 It runs through the entire thickness of the bone
 May run through a vascular channel, venous sinus
groove, or a suture leading to epidural hematoma, venous
sinus thrombosis and occlusion, and sutural diastasis
 May be simple / comminuted
 Most patients with linear skull fractures are asymptomatic
and present without loss of consciousness.

30.  Depressed :
 High-energy direct blow to a small surface area of the
skull with a blunt object.
 Comminution of fragments starts from the point of
maximum impact and spreads centrifugally
 Open / closed
 May be associated with
 Dural tears
 Hemorrhage
 Pressure on cerebral cortex/ dural sinuses.

31. Criteria to elevate depressed skull
fractures in an adult
 > 8-10 mm depression or thickness of skull
 deficit related to underlying brain
 CSF leak (i.e. dural laceration)
 open (compound) depressed fracture
 Conservative treatment is recommended for
fractures overlying a major dural venous
sinus

32. Clinical diagnosis:
 CSF otorrhea or rhinorrhea
 Hemotympanum Or laceration of
external auditory canal
 Postauricular ecchymoses
(Battle‘s sign)
 Periorbital ecchymoses
(raccoon's eye) in the absence
of direct orbital trauma

33.  Cranial nerve injury:
 VII and/or VIII: usually associated with temporal bone
fracture
 Olfactory nerve (I) injury: often occurs with anterior fossa
BSF and results in anosmia, this fracture may extend to the
optic canal and cause injury to the optic nerve (lI)
 VI injury: can occur with fractures through the clivus
Severe basilar skull fractures may produce shearing injuries to
the pituitary gland

34. Basilar fractures:
 Most basilar skull fractures are extensions of fractures through
the cranial vault
 Ant cranial fossa: may open into the frontal, sphenoid or
ethmoid sinuses, often running across the cribriform plate.
 Middle cranial fossa: may involve the petrous temporal bone
 Posterior cranial fossa
Basal skull fractures are harder to document on plain x-rays and
usually require CT scanning

35. Epidural haematoma:
EDH occurs in the potential
space between the dura and the
cranium
EDH results from interruption of
dural vessels, including branches of
the middle meningeal arteries(most
common), veins, dural venous
sinuses, and skull vessels..

36. As many as 10-20% of all patients with head
injuries are estimated to have EDH
Approximately 17% of previously
conscious patients and have EDH,
deteriorate into coma .

37. The most commonly region involved with EDH
is the temporal region (70-80%) because the
temporal bone is relatively thin and the middle
meningeal artery is close to the inner table of the
skull.
The incidence of EDH in the temporal region is
lower in pediatric patients because the middle
meningeal artery has not yet formed.

38. Commonly unilateral and associated with
skull fracture .
CT sign include a biconvex hyperdense elliptical
collection with sharply defined edge ( mixed
density suggests active bleeding)
The haematoma dose not cross suture lines
except at falx which may separate it.

41.  The typical clinical picture of an acute epidural hematoma is
 History of head injury with loss of consciousness—and
recovery.
 Headache
 Progressive hemiparesis contralateral to the side of the
lesion
 Dilated pupil ipsilateral to the lesion.
 They typically lie low in the middle cranial fossa,
occasionally in the frontal fossa and even in the posterior
fossa.

42. Treatment :
 Epidural hematomas can grow rapidly & the blood is clotted in
most cases, a craniectomy or craniotomy is required for
evacuation.
 Once the hematoma has been evacuated, the bleeding points
are controlled by coagulating the middle meningeal artery and
any penetrating vessels which may be bleeding from the outer
surface of the dura.
 Stay sutures are used to tack the dura to the surrounding bone
edges or the overlying periosteum.
 The temporalis muscle and scalp are closed in layers.

44. Subdural haematoma:
Occurs in the subdural space
(potential space b/w dura and
arachnoid membranes)
85% is unilateral
Caused mainly by traumatic
tearing of bridging veins in the
subdural space
The skull fracture +/-

45. Acute SDH present within 24 hours of injury
with decreased level of consciousness or decline
mental status
On CT a crescent fluid collection b/w the brain and
inner skull.
Crosses the suture lines but not dural
reflections

46. The appearance of SDHs on CT varies with clot age and
organization.
Hyper-acute(first hour): appear relatively iso- dense to the
adjacent cortex.
Acute: appear as homogenous hyper-dense (HU more 50-
60 ).
Sub-acute (3-21 days) the density droping to (30 HU) ; iso-
dense.
Chronic ( more than 4 wks ): becomes hypo- dense and
reach to (0 HU)

51. Subarachnoid hemorrhage:
SAH refers to extravasation of blood into the space
b/w the pia and arachniod membranes.
Rapidly progresses to coma.
Its complications include hydrocephalus,cerbral
vasospasm leading to infarction and transtentorial
herniation secondary to raised ICP.

52. Non contrast CT is sensitive
within 4-5 hrs , appears as
high density haemorrhage in
the cortical sulci ,basal
cisterns, sylvian fissures
superior cerebrallar cisterns
and in the vintricles.

54. Brain contusion:
Brain Contusions are
formed in 2 ways :
 Direct trauma.
 Acceleration/deceleration
injury.

55. Non-contrast CT usefull in the early post traumatic
period but the MR is best modality for demonstrating
of edema and contusion distribution.

57. Diffuse axonal injury
 High speed injury with streching or shearing of brain
tissue.
 Associated with LOC 50%, and persistent
vegetative state.
 Mortatility 30-40% , good outcome 20-30%

59. DAI typically consists of several focal white-grey
matter interface lesions measuring 1-15mm ,as
well as in the corpus callosum and brainstem is
characteristic finding in the acute setting.

60. 50-80% demonstrate a normal CT scan upon
presentation, and delayed CT may be helpful in
demonstrating edema or spots of hemorrhages.
MRI is better to demonstrating the small
petechial haemorrhage where not observed
through CT scan.

63. Cerebral Herniation
Transverse & vertical
 Subfalcine
 Transtentorial.
 Foramen magnum

66. CT scan:
 Computed tomography (CT) is almost routine for
patients who have had a head injury severe
enough to alter consciousness.
 The overall time required for the procedure can
be reduced to 5 or 10 min.
 It can be performed on patients requiring
respiratory assistance or circulatory support.

67. GCS<13 at any point
GCS 13-14 at 20
Focal deficit
? Open/depressed/Basal #
Post-traumatic seizure
> 1 vomiting episode
LoC or ante grade amnesia
No imaging now
CT within 1hr
+ Get help!
-
When to do CT- Scan
Coagulopathy/warfarin
+
Age  65
+
Dangerous Mex:
pedestrian rta, ejection,
fall > 1m / 5stairs.
Retrograde
amnesia>30mins
-
-
-
CT within 8hrs
+

68. FEATURES OF RAISED ICP
 Intense headache, worse when lying flat and/or with
physical exertion
 Unequal or dilated pupils
 Vomiting
 Weakness on one side of the body
 Noisy irregular breathing
 Irritable or aggressive behaviour

70. FEATURES OF RAISED ICP:
 Sedate and intubate
 Nurse patient at 30 degree
angle-aids venous drainage
Mild hyperventilation- keep
pCO2 approx 4.5kPa- if
allowed to fall lower this leads
to vasoconstriction and
subsequent ischaemia
 Mild hypothermia
 Burr
holes Evacuation
of mass lesion +/-
craniectomy
 Decom
pressive
craniectomy

71. If MARRIED; DIVORCE SPEED

72. It is good to reach LATE ,
Instead of
prefixing LATE to ur name

73. Thank
You…