1. Classification of Head Injuries Scalp Injuries Scalp Injuries Skull Injuries Skull Injuries Intra-cranial Injuries (Brain 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. I. Primary Brain Injury: at the time of the impact (e.g. contusions and lacerations) and is irreversible. II. Secondary Brain Injury:occurs at some time after the moment of impact and is often preventable. II. Secondary Brain Injury:occurs at some time after the moment of impact and is often preventable. The management of head injury is aimed at preventing secondary injury. The management of head injury is aimed at preventing secondary injury.

4. The causes of secondary brain injuries Hypoxia. Hypoxia. Hypotension: systolic blood pressure (SBP) <90 mmHg Hypotension: systolic blood pressure (SBP) <90 mmHg Raised intracranial pressure (ICP): ICP>20 mmHg Raised intracranial pressure (ICP): ICP>20 mmHg Low cerebral perfusion pressure (CPP): CPP<65 mmHg Low cerebral perfusion pressure (CPP): CPP<65 mmHg Pyrexia Pyrexia Seizures Seizures Metabolic disturbances Metabolic disturbances

5. I. Primary Brain Injury 1. Diffuse Axonal Injury. 2. Cerebral Concussion. 3. Brainstem and hemispheric (Cerebral ) Contusion. 4. Cortical Lacerations.

6. 1. Diffuse Axonal 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. 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. 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. Severity can range from mild damage with confusion to coma and even death.

7. 1. Diffuse Axonal Injury

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

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

18. 2. Cerebral Concussion

19. 3. Brainstem and hemispheric (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. These are areas of bruising and swellings with intact pia arachnoid, localized or generalized oedema and haemorrhage due to tearing of blood vessels.

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

21. 3. Cerebral Contusion

26. Resolution of Contusion

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

28. 4. Cerebral Laceration

29. II. Secondary Brain Injury 1. Brain Oedema (Cerebral Swelling). 2. Intracranial Haemorrhages. 3. Infection. 4. Seizures. 5. Hydrocephalus. 6. Vascular Changes (Cerebral ischemia). 7. Cerebral Herniation. 8. CSF Rhinorrhoea.

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

31. 1. Brain Oedema (Cerebral Swelling)

33. 2. Intracranial Haemorrhages a. Extradural Haematoma a. Extradural Haematoma b. Subdural Haematoma: acute or chronic b. Subdural Haematoma: acute or chronic c. Intracerebral Haematoma c. Intracerebral Haematoma d. Subarachnoid Haemorrhage d. Subarachnoid Haemorrhage

34. 2. Intracranial Haemorrhages

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

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

37. a. Extradural Haematoma CT scan will show biconvex or lens configuration. CT scan will show biconvex or lens configuration. They are more likely to occur in the younger age group. They are more likely to occur in the younger age group. An extradural haematoma is a neurosurgical emergency. An extradural haematoma is a neurosurgical emergency. Surgical treatment by evacuation of haematoma via CRANIOTOMY. Surgical treatment by evacuation of haematoma via CRANIOTOMY. Care must be taken in assessing patients with linear fractures crossing the middle meningeal territory. Care must be taken in assessing patients with linear fractures crossing the middle meningeal territory.

38. a. Extradural Haematoma

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

44. b. Subdural Haematoma

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

49. 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. 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. 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 via craniotomy is mandatory. Acute Subdural Haematoma are rapidly evolving lesions and early evacuation via craniotomy is mandatory.

50. Acute Subdural Haematoma

51. Subacute Subdural Haematoma

52. 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. 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. 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 patients present with progressive neurological deficits more than 3 weeks after the trauma. The initial head injury is often completely forgotten. The initial head injury is often completely forgotten.

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

54. Chronic Subdural Haematoma

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

56. c. Intracerebral Haematoma CT scan: appear as hyperdence lesions with associated mass effect and midline shift. 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. 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. Small inracerebral haematomas may not require removal, but be aware that they can expand.

57. c. Intracerebral Haematoma

60. d. Subarachnoid Haemorrhage Trauma is the commonest cause of SAH although aneurysms are the most common cause of spontaneous SAH. Trauma is the commonest cause of SAH although aneurysms are the most common cause of spontaneous SAH. Traumatic SAH is managed conservatively. Traumatic SAH is managed conservatively.

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

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

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

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

65. Intraventricular blood can lead to Hydrocephalus

66. 6. Vascular changes (cerebral ischemia) This occurs after sever head trauma and is caused by hypoxia, impaired cerebral perfusion or both. 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. 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. Toxic chemicals accumulation like glutamate and free radicals will lead to neuronal damage.

67. 7. Cerebral Herniation a. Subfalcine Herniation a. Subfalcine Herniation b. Uncal Herniation b. Uncal Herniation c. Tentorial Herniation c. Tentorial Herniation d. Tonsillar Herniation d. Tonsillar Herniation

68. 7. Cerebral Herniation

70. a. Transtentorial Herniation a. Transtentorial Herniation

71. a. Transtentorial Herniation

72. b. Foramen magnum herniation b. Foramen magnum herniation

73. b. Foramen magnum herniation

74. c. Subfalcine Herniation c. Subfalcine Herniation

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

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

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