Head Injury, Traumatic Brain Inury

1. HeadInjury
Dr Kariuki P.M.
Surgery CME
21/06/2019

2. DEFINITIONs
Head injuries include both injuries to the brain
and those to other parts of the head, such as
the scalp and skull
Trauma to the head causing neurological
manifestations.
Variable presentation
Head injury and traumatic brain injury(TBI) are
often used interchangeably
TBI encompasses broad range of pathological
injuries to the brain of varying clinical severity
that result from head trauma

4. Thefowinggroupsofpatientsareat particularrisk:
• The elderly (risk of falls, cerebralatrophy)
• Infants (large head size, compressibleskull,
risk of non‐accidentalinjury)
• Patients with a bleeding diathesis (e.g.on
warfarin)
• Chronic alcoholics (at risk of falls and assaults,
cerebral atrophy, coagulopathy due to chronic
liver disease)

5. Some soberingfacts
• Traumatic brain injury (TBI) is still the major cause
of death under 45years of age.
Chirurg.2009 Feb;80(2):153‐64 [Diagnosis and treatmentof traumaticbraininjury.]
• Patients > or =65 years who survived mild TBI have
decreased functional outcome at 6 months
compared with younger patients
JTrauma.2004 May;56(5):1042‐8 The effectof age onfunctional outcome in mild traumatic brain injury:6‐month
report of a prospectivemulticentertrial.MosenthalAC et al.
• Female sex (particularly those age > or =55 y)
is associated independently with higher
mortalityin
isolated severeTBI
Am JSurg.2009 Feb;197(2):155‐8 Severe traumatic brain injury:is there a genderdifferencein mortality? Ottochian
M et al.

6. Anatomy andPhysiology
What are the unique features of
brain anatomy and physiology,
and how do they affect patterns
of brain injury?

7. Anatomy andPhysiology
Effects
● Rigid, non-expansile skull filled with
brain, CSF, and blood
● Cerebral blood flow (CBF)
usually autoregulated
● Autoregulatory compensation
disrupted by brain injury
● Mass effect of intracranial haemorrhage

9. Layers of the Scalp
Five layers; the first three layers are bound together and move as a
unit
S-SKIN
C-Connective tissue,dense fibro-fatty ,contain scalp vessels,highly
vascularised, vessels don’t constrict its wall adherent to fibro fatty-
apply pressure
A-aponeurosis of galea
L- loose areolar layer,potential space,contain large amount of
bleed
P ericarinium

11. Pathophysiology
Head injury
Primary brain injury
direct damage that occurs at time of injury
Secondary brain injury
systemic
intracranial causes

12. Secondary brain injury
Head injury
Systemic causes
Hypoxia
Hypo- or hypercarbia
Hypovolaemia
Hypo- or hypertension
Hypo- or hyperglycaemia
These are all preventable causes

13. Secondary brain injury
Head injury
Intracranial causes
Seizures
Cerebral oedema and raised intracranial
pressure (ICP)
Intracranial haematomas
These are all treatable causes

14. SecondaryBrainInjury
• Oncetheprimarybraininjuryhasbeenrecognized,the main
objective of the management of acute traumatic brain
injury is the prevention of secondary braininjury.

15. MONRO-KELLIE DOCTRINE
• The cranium is a “rigid box” and its total volume
remains constant.
• Increase in volume of the cranial compartments
(brain, blood and/or CSF) will elevate intracranial
pressure(ICP).
• If one of these three compartments increase in
volume,it must occur at the expense of volume
of the other two elements

16. • Normal intracranial pressure~ 0-10mmHg (5-18 cmH2O)
• Monro-Kellie Doctrine - "The total volume of intracranial
contents must remain constant"
• The cranial cavity: brain 1400gm, 75mL of blood, and
75mL of CSF.
• Addition of a mass e.g. a haematoma results in the
squeezing out of an equal volume of CSF & venous blood
to maintain the ICP.
• When this compensatory mechanism is exhausted, there
is an exponential increase in ICP for even a small
additional increase in the volume of the haematoma

17. Classificationofheadinjuries
By mechanism ofinjury
•blunt andpenetrating
•Blunt trauma can be of high or low
velocity (eg, motor vehicle crashes,
falls, and bluntassault.)

18. Classificationofheadinjuries
By morphology
Diffuse injuries
These range from simple concussion with an excellent prognosisto
diffuse axonal injury with associated grimprognosis
Focal injuries
• Basal skull fractures have an associated risk of CSF leak.
• Clinical symptoms (eg, raccoon eyes, Battle’s sign, otorrhea,
and rhinorrhea) should increase the index of suspicion in
identifying basal skullfractures.
• Extradural
• Subdural
• Intracerebral
• Traumatic SAH
By clinical impact: GCSlevel

19. Head injuryclassificationin the
emergency department
A commonpresentation
• 80% Mild Head Injury = GCS 14 – 15
• 10% Moderate Head Injury = GCS 9 – 13
• 10% Severe Head Injury GCS = 3 – 8

20. GCS
 GCS is used both for the initial assessment and
classification of closed head injuries and for
serial assessment of closed head injuries.
 Initial GCS on admission to hospital is used to
classify head injuries into the broad prognostic
groups of mild (GCS 14-15), moderate (GCS 9-
13) and severe (GCS 3-8).
 There is good quality evidence to relate initial
GCS score to outcome.

21. Glasgow Comma Scale

22. Glasgow Comma Scale…

25. Extradural haemorrhage (aka
epidural hemorrhage)
Uncommon.
—Lenticular shaped opacity onCT
—Most commonly (80%) due to tearing of
middle meningeal artery due to a temporal
fracture
—Classically (i.e.<50%) have lucid period
after injury before subsequentlydeteriorating
(“talk and die”).

26. Concussions
Patients with mild head injuries typically
have concussions.
A concussion: physiologic injury to the brain
without any evidence of structural alteration.
postconcussive syndrome (PCS) (30%). PCS
consists of a persistence of any combination
of the following after a head injury:
headache, nausea, emesis, memory loss,
dizziness, diplopia, blurred vision, emotional
lability, or sleep disturbances
 Concussions are graded on a scale of I-V.

27. Concussions: Grading
A grade I concussion: a person is confused temporarily but
does not display any memory changes.
In a grade II concussion, brief disorientation and
anterograde amnesia of less than 5 minutes' duration are
present.
 In a grade III concussion, retrograde amnesia and loss of
consciousness for less than 5 minutes are present, in
addition to the 2 criteria for a grade II concussion.
 Grade IV and grade V concussions are similar to a grade III,
except that in a grade IV concussion, the duration of loss of
consciousness is 5-10 minutes, and in a grade V
concussion, the loss of consciousness is longer than 10
minutes.

28. ExtraduralHaematoma

30. Subdural haemorrhage
More common
—especially in the presence ofcerebral
atrophy (e.g. elderly and alcoholics)
— Concave shaped on CT
—Dueto tearing of bridging veins draining
cerebral cortex.
— Maypresent as acute or chronic

31. Subdural
haematoma

33. Intracerebral hemorrhage
— Ranging from contusions tohaematoma.
— Can evolve overtime.

34. Intracerebral Haematoma / Contusion
Large Frontal Contusion with
Shift

36. Diffuse BrainInjury
Normal
CT
Diffuse
Injury

37. Minor Head Injury‐Assessment
• Do the ABCDE’sinitially
• Initial period of clinical observation: at least 4hours
• Assess for riskfactors
• CT‐scan if GCS <15 at 2 hrs. post injury or any other RF detected
• (Consider) Admissionin present of any RF
• In case of doubt or deterioration consult neurosurgical service regarding
further management anddisposition
• D/Cwith head injury device at 4 hrs post injury if clinical improving with
either normal CT‐scan or noRF’s

38. RiskFactors
• Persistent GCS <15at 2hrs. postinjury
• Prolonged loss of consciousness (>5mins)
• Prolonged anterograde or retrograde amnesia (>30mins)
•
•
•
Post traumatic seizure
Focal neurological deficit
Clinical suspicion of skullFx
• Repeated vomiting (>2occasions)
• Persistent severeheadache
• Age > 65years
• Known coagulopathy
• Deterioration inGCS
• Multi systemtrauma
• Dangerous mechanism
• Intoxication
• Known neurological/neurosurgicalimpairment
• Delayed presentation
• Failure of clinicalimprovement

39. Minor HeadInjury
GCS 14 -15
High Risk
= any RF present
Low Risk
= no RF, normal CT-scan

40. Indications forCT‐scan
• Mild head injury with at least 1 risk factor
present
• Any moderate headinjury
(9‐13)
• Any severe headinjury
(8 or less)

41. CTscan?
These patients should not routinely have CT
scanning if they have all of the following features:
All of...
On initial assessment:
•GCS 15 at two hours post injury
•No focal neurological deficit
•No clinical suspicion of skull fracture
•No vomiting
•No known coagulopathy or bleeding disorder
•Age <65 years
•No post traumatic seizure
•Nil or brief loss of consciousness (<5min)
•Nil or brief post traumatic amnesia (<30min)
•No severe headache
•No large scalp haematoma
•Isolated head injury
•No dangerous mechanism
•No known neurosurgery / neurological impairment
•No delayed presentation or representation.
After a period of observation (until at least four hours
post time of injury):
•GCS 15/15
•No post traumatic amnesia (A-WPTAS 18/18)
•Normal mental status including alertness, behaviour and
cognition.
•No clinical deterioration during observation.
•Clinically returning to normal
These patients should have early CT scanning if
available, if they have any of the following features:
Any of...
On initial assessment:
•GCS<15 at two hours post injury**
•Focal neurological deficit
•Clinical suspicion of skull fracture
•Vomiting
•Known coagulopathy or bleeding disorder
•Age >65
•Witnessed seizure
•Prolonged loss of consciousness (>5min)
•Prolonged post traumatic amnesia (>30min)
On serial assessment:
•Decrease in GCS
•Persistent GCS<15 at two hours post injury
•Persistent abnormal alertness/behaviour/cognition
•Persistent post traumatic amnesia (A-WPTAS<18/18)
•Persistent vomiting (≥2 occasions)
•Persistent severe headache
•Post traumatic seizure
Clinical judgement required if:
•Initial GCS 14 within two hours of injury**
•Large scalp haematoma or laceration
•Associated multi-system injuries
•Dangerous mechanism
•Known neurosurgery/neurological impairment
•Delayed presentation or representation
** NOTE: Includes patients with abnormal GCS due to
drug or alcohol ingestion.

42. Canadian CT Head Rule
• Rule
• Head CT not required if NONE of the following are present
• Age ≥ 65 years
• Vomiting > 2 time
• Suspected open or depressed Skull Fracture
• Signs suggesting basal skull fracture:
– Hemotympanum
– Racoon eyes
– CSF otorrhea or rhinorrhea
– Battle's sign (bruising around mastoid process)
• GCS < 15 at 2 hours post injury
• Retrograde Amnesia > 30min
• Dangerous mechanism
– Pedestrian struck by vehicle
– Ejection from motor vehicle
– Fall from elevation >3 feet or 5 stairs

43. Nice Guidelines
• • GCS less than 13 on initial assessment in the emergency department.
• • GCS equal to 13 or 14 at 2 hours after the injury on assessment in the emergency
department.
• • Suspected open or depressed skull fracture.
• • Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid
otorrhoea, Battle’s sign).
• • Post-traumatic seizure.
• • Focal neurological deficit. •
• More than one episode of vomiting.
• • Amnesia for greater than 30 minutes of events before impact
• CT with any of the following risk factors, provided they have experienced some loss of
consciousness or amnesia since the injury:
• • Age greater than or equal to 65 years.
• • Coagulopathy (history of bleeding, clotting disorder, current treatment with warfarin).
• • Dangerous mechanism of injury (a pedestrian struck by a motor vehicle, an occupant
ejected from a motor vehicle or a fall from a height of greater than 1 metre or five
stairs

44. • Plain X-rays of the skull have no role in the
diagnosis of significant brain injury. However,
they are useful as part of the skeletal survey
• Perform cervical spine radiographs if gcs is 8
or less
• Skull X-rays in conjunction with high-quality
in-patient observation also have a role
where CT scanning resources are
unavailable.

45. Standard carefor severe
HI
• Initial systematic assessment and resuscitation of ABCDEs.
• Early intubation.
• Supportive care of ABCDEs with appropriate attention to positioning (30°
head up), basic nursing care and avoidance of hyperventilation.
• Prevention of secondary brain injury by avoiding hypoxaemia (O2 saturation
<90%) and hypotension (systolic BP<90).
• Early CT scan to identify acute neurosurgical lesions.
• Early neurosurgical consult
• Early retrieval consult if transfer required
• Consider use of anticonvulsants to prevent early post traumatic seizures
• Consider ICP monitoring to guide management of cerebral perfusion
pressure.
• Low threshold to repeat CT scan if patient condition changes
• ICU admission
• Routine repeat CT scan at 24 hours
• Brain injury rehabilitation consult
• Minimum supportive care aims:
PaO2 > 60, SaO2 > 90, PaCO2 35 – 40, Systolic BP > 90, Head up 30°

46. Management of icp
• 1. Elevation of head 20-30 degrees
• To promote venous drainage from the head.
• 2.Ventilation o2 by mask
• Prevention of hypoxia and hypercapnia which increase ICP
• 3. Mannitol.
• i. Effective doses range from 0.25-1 gram/kg, given by intermittent bolus infusion
every 4-6 hrs.
• ii. Euvolemia must be maintained.
• iii. Monitor osmolality. Do not exceed 320mOsm/kg
• 4. Hyperventilation
• To blow out the co2 and reduce hypercapnia and maintain pCO2 of 30-35 mmHg
• 5. Hypertonic Saline
• 6. Anticonvulsant therapy
• Phenytoin is used to prevent or control seizure activity that increases cerebral
blood flow and subsequently intracranial pressure. Anticonvulsant medications
should be used for 1 wk

47. Management of icp…
• 7. Nimodipine
• The calcium channel blocker reduces death and severe disability
when instituted acutely in patients with head injuries.
• 8. Relieve and prevent pyrexia which increases intracranial
pressure. eg NSAIDS Provision of .analgesia has similar effects
• 9.Sedatives
• High dose diazepam may be considered for hemodynamically
stable, salvageable, severe head injury patients with intracranial
hypertension refractory to maximal medical and surgical therapy.
Other narcotics may depress respiration
• 10. Steroids Dexamethasone use is controversial in head injury
• 11. decompressive craniectomy

48. Blood Pressure Management in
Traumatic Brain Injury
• high systemic blood pressure after TBI center around a catecholamine
excess state, elevation in intracranial pressure (ICP)
• may be protective to a point, by maintaining CPP
• may also cause secondary brain damage by aggravation of vasogenic
edema and intracranial hypertension, potentially as a result of
increased hydrostatic capillary pressure in the brain
• Early hypotension has been linked with poor outcomes following
severe TBI, and guidelines suggest early and aggressive management
of hypotension after TBI.
• Despite these recommendations, no guidelines exist for the
management of hypertension after severe TBI,
• Focus of care after traumatic brain injury is maintenance of CPP
• Treatment of acute hypertension in TBI is not recommended
• However, ideal CPP(60-70, ICP<20, MAP 80>90

49. The Depressed Skull Fracture

50. The Depressed Skull Fracture
 Simple depressed fractures in neurologically intact infants are treated
expectantly. These depressed fractures heal well and smooth out with time,
without elevation.
 Open fractures, if contaminated, may require antibiotics in addition to tetanus
toxoid.
 Surgical elevation If:
• evidence of dural penetration,
• significant intracranial hematoma,
• depression >50%,
• depression greater than 1 cm
• frontal sinus involvement,
• gross cosmetic deformity,
• wound infection or gross wound contamination
• pneumocephalus,.

51. Complications of head injury.
• CN palsies and Focal neurological signs
• Hydrocephalus
• Convulsive disorder/epilepsy
• Psychiatric disorders
• Cerebrospinal fluid fistulae, either in the form of
rhinorrhea or otorrhea
• Posttraumatic movement disorders Tremor,
dystonia, parkinsonism, myoclonus
• Vascular injuries
• Speech disorders

52. Controversies/ RCT Findings
 There are currently no convincing data to support infection prophylaxis in
patients with TBI, especially in light of data suggesting that prophylaxis
might predispose patients to more severe infections when infections would
arise
 Currently available evidence from RCTs does not support prophylactic
antibiotic use in patients with basilar skull fractures, whether there is
evidence of CSF leakage or not. Antibiotics have not been shown to
decrease the risk of meningitis in patients with base of skull fractures with
or without CSF leaks
 current literature guidelines indicates that the incidence of early PTS
appears to be reduced with the addition of prophylactic antiseizure
medications. However, there is currently no evidence to indicate that
prophylactic antiseizure medications alter mortality or incidence of late
PTS, and it is still unknown whether or not this course of therapeutic
prophylaxis is currently benefitting patients
 Based on the results of the CRASH trial, steroids should not be used
routinely in the treatment of acute traumatic head injury, as they appear to
increase mortality.

53. To Read:
’
 Cushing s response – bradycardia , irreggular
respiration and hypertension
CEREBRAL HERNIATION SYNDROMES
KERNOHAN’S NOTCH
Benefit and harm of treating high blood
pressure in TBI patients
external ventricular drainage (EVD)
systems