This document discusses head injuries, including their epidemiology, pathophysiology, types, and management. Head injuries are a major public health problem worldwide and are mostly caused by road traffic accidents and assaults. The main types of head injuries discussed are cerebral contusions, diffuse axonal injury, cerebral edema, traumatic intracranial hematomas such as extradural, subdural, subarachnoid and intracerebral hemorrhages, and concussions. Initial management focuses on preventing secondary brain damage through measures such as neurological observation, immobilization, intubation if needed, and transport to a dedicated neurological facility for patients with more severe injuries.

1. Head Injury
KHAING ZAY AUNG
8.3.2017

2. Synopsis
1. Epidemiology
2. Pathophysiology
3. Types of head injury
4. Initial management of head
injuries
5. Management of head
injuries
6. Medical care
2

3. Epidemiology
• Major public health problem worldwide
• Causes disability in young people and makes
considerable demand of health resources
• Mostly due to RTAs and assaults
• RTAs are tenth cause of death throughout the world
• Head injuries are steadily decreasing each year in
developed countries owing to increased road traffic
safety and safety at the work place
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4. Pathophysiology of head injuries
• Most are caused by blunt trauma
• RTAs, Assaults and falls – in adults
• Falls and injuries from recreational activities in
children
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5. • The goal of head injury management
Prevention of secondary brain damage
Giving the best environment for brain recovery from primary brain
injury
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6. • Primary brain injury
• Injury caused by direct insult to the brain
• Secondary brain injury
• Secondary brain damage occurs from hypoxia, hypotension,
intracranial haematomas or brain oedema.
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7.  Brain - dependent on continuous cerebral blood flow for oxygen
and glucose delivery
 CBF - about 55 mL/minute for every 100 g of brain tissue
 Ischaemia < 20 mL/min >>> infarction unless promptly corrected
 CPP (75–105 mmHg) = MAP (90 – 110 mmHg) − ICP (5 – 15
mmHg)
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8.  Cerebral autoregulation - a constant CBF across a range of MAP
between 50 and 150 mmHg
 Neurosurgical emergencies, especially head injury, lead to brain
swelling, bleeding and hydrocephalus.
 common pathophysiology - elevated ICP and reduced CPP and
CBF
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9. Monro Kellie doctrine
• the cranium is a ‘rigid box’ containing a ‘nearly incompressible
brain’.
• initially accommodated by exclusion of fluid components - venous
blood and cerebrospinal fluid (CSF).
• Further expansion >>>> an exponential rise in intracranial pressure
• hypoperfusion and herniation
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10. 10

11. Hutchison’s pupils
•Left (Normal)
•Stage I
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Rt.(Haematoma) Left (Normal)
Stage I
Stage II
Stage III
Stage IV

12. Head injury can result in …
1. Direct trauma
2. Cerebral contusion
3. Diffuse axonal injury
4. Cerebral oedema
5. Traumatic intracranial haematomas
6. Concussion
7. Other injuries associated with brain injuries
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13. 1. Direct trauma
• In blunt trauma, the energy of impact is spread over a
large area of the skull
• Whereas penetration injuries cause most of their
damage by direct trauma
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14. 2. cerebral contusion
• Contusion of brain may occur at the site of impact
“coup injury”
• Or most severe at the opposite site of the injury –
“countercoup injury”
• Sudden acceleration and deceleration of the brain
within the skull causes the opposite poles of the brain
to collide against the inside ridges of the skull bone ,
leading to severe brain contusions
14

15. Coup and countrecoup injury
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16. 3. Diffuse axonal injury
• Caused by sheering forces from acceleration and
deceleration of the brain following blunt trauma
• Rotation forces cause petechial hemorrhages, particularly
in the upper brainstem, cerebellum and corpus callosum
• Widespread myelin degeneration a few weeks after the
injury
• CT can demonstrate multiple patechial h’ge
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18. 18

19. 4. Cerebral oedema
• Occurs as a result of vasomotor failure leading to brain
swelling around the cerebral contusions
• Or as a result of cytotoxic effects throughout the brain
• Brain oedema causing increased ICP
• Can result in herniation of the brain
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20. 5. Traumatic intracranial haematomas
• Extradural
• Subdural
• Subarachnoid and
• Intracerebral haemorrhages
20

21. Extradural haematoma
• Blood clot between skull bone and dura mata
• Classic history – initial brief loss of consciousness
followed by a lucid interval that can last minutes to
hours
• Followed by sudden deterioration in the level of
consciousness
• 85% of pts – middle meningeal artery is the source of
bleeding
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22. • In < 30 yrs – 40% - associated with skull #
• In > 30 yrs – almost all pt is associated with skull #
• Associated with SDH in 20%
• Mortality – 20-55%
• With early treatment – can be reduced up to 5-10%
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23. • On CT - high density collection beneath the skull bone,
• Shape of bilenticular lens
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24. Subdural hematomas
• Collection of blood in the subdural space
• Used to classified according to the age of hematoma
• Acute – within 72 hrs
• Subacute – within 3 days to 3 wks
• Chronic - if >3 wks
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25. • Hyperdense SDH or acute SDH
• Clot is higher density than the brain on CT
• Takes the shape of the brain
• >1 cm thick-
• Volume > 80 ml removal requires
craniotomy
(thickness x height x length)/2
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26. • Also depend on midline shift and GCS
• If removed within 4 hrs, survival can be expected up to
70%
• If delayed >4 hrs – only 10%
• Monitoring of ICP is recommended after surgery
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27. • Mixed density SDH
• Treated in the same fashion as hyperdense lesions
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28. • Isodense SDH
• Density of clot become the same as density of the brain
• Challenging diagnosis
• Indirect signs – midline shift, effacement of the lateral
ventricle of effacement of the ipsilateral sulci
• Can be evacuated thr’ burr holes
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29. • Hypodense SDH
• Lower density than the brain
• Can be drained via burr holes
• Can leave subdural drain in situ – to prevent tension
pneumocephalus
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30. 6.Traumatic intra-cerebral hematomas
• Difference between cerebral contusion and traumatic
intracerebral haematoma is arbitrary
• Both are characterized by hyperdense parenchymal
lesions on CT
• Contusions often reach cerebral cortex and they appear
bigger than the actual masses
• Traumatic ICH – more distinct and their size and mass
effect appear proportionate to midline shift
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31. Traumatic SAH
• Blood in the subarachnoid space following trauma
• Worse outcome
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32. 7. Hydrocephalus
• Uncommon cause of raised ICP in head injuries in the
acute stage
• Can happen when a bld clot obstructs the fourth
ventricle or the cerebral aqueduct
• My also follow traumatic SAH
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33. 8. Concussion
• Concussion is transient loss of consciousness following
non-penetrating closed head injury without gross or
microscopic brain damage
33

34. 9.Other injuries associated with brain
injuries
• Scalp lacerations
• Scalp haematomas
• Skull #
• Dural fistulas and CSF leakes
• Cranial nerve injuries and
• Other injuries
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35. Skull #
• Simple linear # of the skull vault
• Depressed skull fracture if bone fragments were
depressed deeper than the inner table of the skull
• Compound skull fracture when the skin or the mucosa
overlying the skull fracture is deficient
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36. CSF leaks
• CSF rhinorrhea or otorrhoea indicates that there has
been a breach of the dura
• Often occurs in association with skull base fractures
• To confirm – beta 2 transferrin
• Reason to treat – recurrent meningitis in these pt
• Often due to streptococcus pneumonia
• Diagnosis – fine slice CT or MRI
• Persistant CSF leaks or those complicated by
meningitis require dural repair
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37. Cranial nerve injuries
• Anterior fossa # - can be injuired to olfactory or optic
cranial nerves
• The sixth nerve is also susceptible to injury because of
its long intracranial course
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38. Initial management of head injuries
• According to ATLS
• Followed by a primary survey looking for life-
threatening conditions – pneumothorax,
hemoperitoneum, cardiac tamponade, tension
pneumothorax
38

39. Neurological assessment
• Level of consciousness
• Speech and language
• Memory
• Cranial nerve examination
• Motor and sensory examination and
• Coordination
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40. Neurological observation
• 15 minly – 4 times
• If stable – ½ hrly for 4 times
• Hourly – 4 times
• 2 hrly for 4 times
• 4 hrly for the rest of the hospital stay
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41. Assessment of the level of
consciousness
• By GCS
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42. Categorization of head injury
Low risk head injury
• Asymptomatic
• Fully conscious and oriented and no clinical or
radiological evidence of skull #
• Risk of significant intracranial pathology in this group
is <9/10,000
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43. Moderate risk of head injury
• History of ILOC
• progressive headache
• vomiting
• post traumatic seizures
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44. • post traumatic amnesia
• an unreliable history
• Signs of basilar fracture
• penetrating facial injury
• Can be discharged home if – normal CT, initial GCS
>13 and discharge GCS 15
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45. High risk head injury
• Reduced level of consciousness,
• neurological deterioration,
• focal neurological deficit,
• penetrating head injury or
• depressed skull fracture
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46. Management of head injuries
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47. Pt with GCS >13 should be admitted to hospital with the
following instructions:
1. Activity level – bed rest with head elevated by 30-45
2. Neurological observation every 2 hr
3. Feeding – nil by mouth until fully alert; advance as
tolerated
4. Analgesia – simple analgesics such as tramadol or
codeine
5. Antiemetics – as required
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48. Pt with GCS score of 9-13 should be admitted to hospital
with the following instructions:
1. Activity level – bed rest with head elevated by 30-45
2. Neurological observation every hr and consider HDU
3. Feeding – nil by mouth until fully alert; advance as
tolerated
4. Analgesia – simple analgesics such as tramadol or
codeine
5. Antiemetics – as required
6. Fluids – IV 100 ml/hr NS with 20 mm0l/l KCL
7. If not awake by 12 hrs, repeat the CT brain scan
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49. • Pt with GCS score <9 should be transferred to a
dedicated neurological facility. Prior to transfer,
consider the following problems:
• If there is any concern about hypoxia or airway
protection during interhospital transfer, intubate and
artificially ventilate the patient
• If the pt has had any seizures administer
anticonvulsants
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50. • Immobilize the spine – if any concerns about neck
injuries
• Any conerens about raised ICP, administer mannitol
2g/kg of 20% and keep PaCO2 between 3.5 and 4 kPa
during transfer
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51. Indications for intubation and artificial
ventilation
• If GCS <8 or if there is maxillofacial injuries
• If evidence of raised ICP eg: pupillary dilatation,
asymmetric pupillary reaction, progressive neurological
deterioration
• To carryout safe interhospital transfer
• To properly assess a combative or agitated pt by CT
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52. Indication for referral to ED using
emergency ambulance service
1. Pt with altered level of consciousness
2. Had seizure since the head injury
3. Evidence of basal skull fracture, s/a CSF leak from
ear or nose, panda eyes, haemotympanum or battle’s
sign
4. Focal neurological deficit
5. Deteriorating level of consciousness
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53. 6. Associated chest or abdominal trauma, limb or pelvis
trauma or significant vascular injury
7. Amnesia for the incident or subsequent events
8. Dangerous mechanism of injury
9. Medical comorbidity
10. Adverse social factors
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54. Can be sent home after injury
• Clinical history and examination indicate a low risk of
brain injury and
• the hospital admission criteria were not met
• Has appropriate support structures and competent
supervision at home
• Verbal and written head injury advice
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55. Indication for skull X ray
• Fully conscious and the mechanism of injury has not been
trivial
• Consciousness has been lost
• Amnesia
• Vomitting
• Scalp has a full thickness laceration or a boggy haematoma
• History is inadequate
• Impaired level of consciousness
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56. Indication for CT head
• Impaired consciousness
• A deteriorating level of consciousness or progressive
focal neurological deficit
• Confusion or drowsiness followed by failure to improve
within at most 4 hrs of clinical observation
• Radiological or clinical evidence of a fracture, whatever
the level of consciousness
• New focal neurological signs that are not getting worse
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57. • Full consciousnesss with no fracture but had other
features
–Severe and persistant headache
–Nausea and vomiting
–Irritability or altered behavior
–Development of a seizure
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58. Indication for cervical spine x ray
• Fully conscious pt if clinical symptoms or signs or
mechanism of injury indicate the possibility of injury to
the spine
• Persisting impaired consciousness
• Unconscious pt, not localizing pain
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59. Consultation to neurosurgeon
• CT scan in general hospital showed a recent
intracranial lesion
• The criteria for CT are fulfilled but CT cannot be done
within an appropriate time frame locally
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60. • Irrespective of the result of any CT, the pt fulfils any of
the following criteria
– Persisting coma after initial resuscitation
– Persisting confusion for more than 4 hrs
– Deterioration in the level of consciousness after admission
– Progressive focal neurological signs
– Seizure without full recovery
– Compound depressed skull fracture
– Definite or suspected penetrating injury
– CSF leak or other sign of basal skull fracture
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61. Raised ICP and ICP monitoring
• Caused by cerebral oedema or mass lesions
• Treatment of raised ICP is the treatment of the
underlying cause
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62. Indications for ICP monitoring
1. Severe head injury (GCS <8)
2. Following evacuation of a mass lesion
3. Ventilated patients with an abnormal CT
4. Multiple injuries
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63. • Contraindications of ICP monitoring
– awake pt and
– coagulopathy
• Complications of ICP monitoring
– Infection (1-2%)
– Bleeding (2-8%)
– Malfunction (6-40%)
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64. • Can be performed by inserting a transducer in the
subdural space, ventricle or brain parenchyma
• Eg: Camino bolt, Codman transducer or Spielberg
transducer
• Any ICP >25 have to treat to maintain the CPP of
>70 mmHg
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65. • Causes of raised ICP
– Reduced venous return – severe neck flexion or head down
position
– Venous thrombosis
– Sustained seizures or intracranial pathology
– Mass lesions
– Cerebral oedema
– Diffuse axonal injury or
– Ischaemia
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66. Treatment of increased ICP
• Simple measures
– Adjusting the head and neck posture
– Checking the ventilator settings and
– Control of any seizures or pyrexia
• Second-tier manoeuvres
– Increasing MAP
– Reducing the body temperature to 32-35 C – reduce the
cerebral metabolism and reduce ICP
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67. • Hyperventilation and reducing PaCO2 to 3 kPa in the
short term – reduce ICP
• Surgical decompression of the skull
• Induced barbiturate coma reduced cerebral metabolism
and also ICP
• Mannitol 2g/kg of 20% i.v over 20 mins
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68. Medical care
• Acute care
• May alter coagulation parameters (coagulopathy )
• Steroids have no benefit in acute setting
• Phenytoin – efficacy in controlling early post traumatic seizures
• Neuroprotective agents – nimodipine
• Rosuvastatin – significantly reduce amnesia
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69. Medical care
• Long term care
• For spasticity or dystonia – dantrolene, diazepam,
• Botulinum toxin
• Intrathecal baclofen
• Iv mannitol
• Non medical therapy
• Physiotherapy and supportive care
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