1. Classification of Head Injuries
Scalp Injuries
Skull Injuries
Intra-cranial Injuries (Brain Injuries)

2. C. Intracranial Injuries (Brain Injuries)

3. Types of Brain Injuries
I. Primary Brain Injury: at the time of the impact (e.g. contusions and lacerations) and is irreversible.
II. Secondary Brain Injury: progressive brain damage arising from events developing as a result of the primary brain injury.
The management of head injury is aimed at preventing secondary injury.

4. I. Primary Brain Injury Diffuse Axonal Head Injury.
Cerebral Concussion.
Cerebral Contusion.
Cerebral Laceration.

5. 1. Diffuse Axonal Head Injury
Prolonged post-traumatic state in which there is loss of consciousness from the time of injury that continues beyond 6 hours.
Occurs as a result of mechanical shearing at the grey-white matter interface.
This causes disruption and tearing of axons, myelin sheaths and blood capillaries.
Severity can range from mild damage with confusion to coma and even death.

6. 1. Diffuse Axonal Head Injury

7. 1. Diffuse Axonal Head Injury

8. 1. Diffuse Axonal Head Injury

9. 1. Diffuse Axonal Head Injury

10. 1. Diffuse Axonal Head Injury

11. 1. Diffuse Axonal Head Injury

12. 1. Diffuse Axonal Head Injury

13. 1. Diffuse Axonal Head Injury

14. 1. Diffuse Axonal Head Injury

15. 2. Cerebral Concussion There is slight brain distortion.
This is a clinical diagnosis, and is manifested by temporary cerebral dysfunction.
Latin (concutere) means shake.

16. 2. Cerebral Concussion The clinical presentations includes:
1. Autonomic abnormalities including bradycardia, hypotension and sweating
2. Loss of consciousness often but invariably accompanies concussion.
3. Amnesia of events is common.
4. Temporary lethargy.
5. Irritability.
6. Cognitive dysfunction.

17. 2. Cerebral Concussion

18. 3. Cerebral Contusion
These are areas of bruising and swellings with intact pia arachnoid, localized or generalized oedema and haemorrhage due to tearing of blood vessels.

19. 3. Cerebral Contusion Clinical presentations:
1. Prolonged periods of unconsciousness.
2. Focal neurological deficits that persist for longer than 24 hours.
CT scans demonstrates contusions as small areas of haemorrhage in the cerebral parenchyma.
Contusions may resolve with the accompanying deficits or they may persist.

20. 3. Cerebral Contusion

21. 3. Cerebral Contusion

22. 3. Cerebral Contusion

23. 3. Cerebral Contusion

24. 3. Cerebral Contusion

25. Resolution of Contusion

26. 4. Cerebral Laceration
It is due to rapid movement and shearing of brain tissue.
The pia arachnoid is torn, with bloody effusion in the CSF.
Intracerebral haemorrhage may accompany this lesion.
Focal deficits are the rule.

27. 4. Cerebral Laceration

28. II. Secondary Brain Injury
Brain Oedema (Cerebral Swelling).
Intracranial Haematomas.
Infection.
Seizures.
Hydrocephalus.
Vascular Changes (Cerebral ischemia).
Cerebral Herniation.
CSF Rhinorrhoea.

29. 1. Brain Oedema (Cerebral Swelling)
Can be local (around a haematoma) or diffuse.
It is due to intracellular or extracellular accumulation of fluid.
It leads to raised intracranial pressure, which itself causes problems.
It is more common and more dangerous in children.

30. 1. Brain Oedema (Cerebral Swelling)

31. 1. Brain Oedema (Cerebral Swelling)

32. 2. Intracranial Haematomas
a. Extradural Haematoma
b. Subdural Haematoma: acute or chronic
c. Intracerebral Haematoma

33. 2. Intracranial Haematomas

34. a. Extradural Haematoma
Usually due to TRIVIAL trauma.
Source of bleeding(Haematoma):
1. Linear squamous temporal skull fractures with laceration of a branch of the underlying middle meningeal artery.
2. Fractured bone edges.
3. Laceration of the dural sinuses.

35. a. Extradural Haematoma
Clinical Picture; includes:
Stage of concussion.
Stage of lucid interval
Stage of compression: shown clinically as:
Gradual progressive deterioration in the level of consciousness.
Contralateral hemiparesis due to cortical compression.
Tentorial herniation, with compression of oculomotor nerve, with dilatation of ipsilateral pupil.
As the coma deepens the blood pressure rises and the pulse and respiration slow down (i.e. features of increased intracranial pressure).

36. a. Extradural Haematoma
CT scan will show convex lens configuration.
They are more likely to occur in the younger age group.
An extradural haematoma is a surgical emergency.
Care must be taken in assessing patients with linear fractures crossing the middle meningeal territory.

37. a. Extradural Haematoma

38. a. Extradural Haematoma

39. a. Extradural Haematoma

40. a. Extradural Haematoma

41. a. Extradural Haematoma

42. b. Subdural Haematoma
They are the most common intracranial mass lesions resulting from head trauma.
They are classified depending on how long they take to present clinically following the injury into:
Acute Subdural Haematoma: less than 3 days
Subacute Subdural Haematoma: 4-21 days
Chronic Subdural Haematoma more than 21 days.

43. b. Subdural Haematoma

44. b. Subdural Haematoma

45. b. Subdural Haematoma

46. b. Subdural Haematoma

47. Acute Subdural Haematoma
Usually due to MORE SEVER high velocity trauma and thus associated with a poorer outcome.
Source of bleeding (haematoma): include:
Most result from torn bridging veins or focal tears of a cortical artery.
Cortical lacerations or contusions.
Bleeding from tears in the dural venous sinuses.

48. Acute Subdural Haematoma
Clinical Picture: patient will present with a picture similar to that of an extradural haematoma, but there is persistent loss of consciousness with no lucid interval.
Ct scan will show a concave hyperdence collection because blood follows the subdural space over the convexity of the brain.
Acute Subdural Haematoma are rapidly evolving lesions and early evacuation is mandatory.

49. Acute Subdural Haematoma

50. Subacute Subdural Haematoma

51. Chronic Subdural Haematoma
Most common in infants and in adults over 60 years of age secondary to SLIGHT blow to the head which may pass unnoticed.
Source of bleeding (haematoma): usually from bridging veins as they pass to the venous sinuses.
The patients present with progressive neurological deficits more than 3 weeks after the trauma.
The initial head injury is often completely forgotten.

52. Chronic Subdural Haematoma
CT scan: the acute clotted blood is initially appears white (hyperdence), but as it liquefies, it slowly becomes black (hupodense).
They should be drained if they continue to enlarge.
They are evacuated by drilling burrholes over the collection and washing it out with warmed saline.

53. Chronic Subdural Haematoma

54. c. Intracerebral Haematoma
This is the least common of traumatic haematoma.
They are due to areas of traumatic contusion coalescing into a contusional haematoma.
Disrupted cerebral tissue release thromboplastins that potentiate haemorrhage.

55. c. Intracerebral Haematoma
CT scan: appear as hyperdence lesions with associated mass effect and midline shift.
Large intracerebral haematomas should be evacuated unless the patient’s neurological state is improving.
Small inracerebral haematomas may not require removal, but be aware that they can expand.

56. c. Intracerebral Haematoma

57. c. Intracerebral Haematoma

58. c. Intracerebral Haematoma

59. 3. CNS Infection Causes: includes: 1. Penetrating skull trauma.
2. Depressed skull fractures.
3. Base of skull fractures.
All these will provide portal for CNS infection.

60. 3. Infection Presentations: either: 1. Meningitis. 2. Brain abscess.
3. Subdural empyemas.
These can all exacerbate situation of raised intracranial pressure.

61. 4. Seizures
They can increase both brain metabolism and blood flow, therefore increasing intracranial pressure.

62. 5. Hydrocephalus
a. Acutely due to obstruction of CSF outflow due to intraventricular blood.
b. Delayed post-traumatic communicating hydrocephalus due to impaired CSF reabsorption following traumatic subarachnoid haemorrhage

63. Intraventricular blood can lead to Hydrocephalus

64. 6. Vascular changes (cerebral ischemia)
This occurs after sever head trauma and is caused by hypoxia, impaired cerebral perfusion or both.
The injured brain loses its ability to autoregulate, and so be unable to maintain cerebral blood flow with a decreased blood pressure.
Toxic chemicals accumulation like glutamate and free radicals will lead to neuronal damage.

65. 7. Cerebral Herniation b. Foramen magnum c. Subfalcine
a. Transtentorial.
b. Foramen magnum
c. Subfalcine

66. 7. Cerebral Herniation

67. 7. Cerebral Herniation

68. a. Transtentorial Herniation

69. a. Transtentorial Herniation

70. b. Foramen magnum herniation

71. b. Foramen magnum herniation

72. c. Subfalcine Herniation

73. c. Subfalcine Herniation

74. 8. CSF rhinorrhoea
Occurs secondary to a fracture involving the paranasal sinuses (frontal, ethmoidal or sphenoid) associated with dural tear.
A piece of brain tissue is forced into the dural tear and prevents its healing.
This complication is liable to be followed by meningitis.

75. 8. CSF rhinorrhoea The patient is treated early with antibiotics.
Indications for surgery (repair of tear) includes:
a. Persistence of rhinorrhoea more than 10 days
b. Presence of a fracture involving the frontal or ethmoidal sinus.
c. Occurrence of meningitis.

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