Neurosurgery

 
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Fifth stage 

Neuro-Surgery

Lec-5 

د. عبدالرحمن 

2/5/2016 

Intracranial Injuries (Brain Injuries)

Classification of Head Injuries: 

  Scalp Injuries 
  Skull Injuries 
  Intra-cranial Injuries (Brain Injuries) 

C. Intracranial Injuries (Brain Injuries) 

Types of Brain Injuries: 

  Primary Brain Injury: at the time of the impact (e.g. contusions and lacerations) and is 

irreversible. 

  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 causes of secondary brain injuries: 

  Hypoxia. 
  Hypotension: systolic blood pressure (SBP) <90 mmHg 
  Raised intracranial pressure (ICP): ICP>20 mmHg 
  Low cerebral perfusion pressure (CPP): CPP<65 mmHg 
  Pyrexia 
  Seizures 
  Metabolic disturbances 

I. Primary Brain Injury: 

  Diffuse Axonal Injury. 
  Cerebral Concussion. 
  Brainstem and hemispheric (Cerebral ) Contusion. 
  Cortical Lacerations. 

 
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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. 
  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. 

2. Cerebral Concussion 

  There is slight brain distortion.  
  This is a clinical diagnosis, and is manifested by temporary cerebral dysfunction. 
  Latin (concutere) means shake. 
  The clinical presentations includes: 

o  Autonomic abnormalities including bradycardia, hypotension and sweating 
o  Loss of consciousness often but invariably accompanies concussion. 
o  Amnesia of events is common. 
o  Temporary lethargy. 
o  Irritability. 
o  Cognitive dysfunction. 

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. 

  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. 

4. Cortical Lacerations 

  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. 

 
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II. Secondary Brain Injury 

  Brain Oedema (Cerebral Swelling). 
  Intracranial Haemorrhages. 
  Infection. 
  Seizures. 
  Hydrocephalus. 
  Vascular Changes (Cerebral ischemia). 
  Cerebral Herniation. 
  CSF Rhinorrhoea. 

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. 

2.  Intracranial Haemorrhages 

  Extradural Haematoma 
  Subdural Haematoma: acute or chronic 
  Intracerebral Haematoma 
  Subarachnoid Haemorrhage 

a. Extradural Haematoma 

  Usually due to TRIVIAL trauma. 
  Source of bleeding(Haematoma): 

o  Linear squamous temporal skull fractures with laceration of a branch of the 

underlying middle meningeal artery. 

o  Fractured bone edges. 
o  Laceration of the dural sinuses. 

  Clinical Picture; includes: 

o  Stage of concussion. 
o  Stage of lucid interval 
o  Stage of compression: shown clinically as: 

  Gradual progressive deterioration in the level of consciousness. 
  Contralateral hemiparesis due to cortical compression. 

 
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  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). 
 

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

meningeal territory.  

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. 

Acute Subdural Haematoma 

  Usually due to MORE SEVER high velocity trauma and thus associated with a poorer 

outcome. 

  Source of bleeding (haematoma): include: 

o  Most result from torn bridging veins or focal tears of a cortical artery. 
o  Cortical lacerations or contusions. 
o  Bleeding from tears in the dural venous sinuses. 

  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 via 

craniotomy is mandatory. 

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. 

 
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  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. 
  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 are evacuated by drilling burrholes over the collection and washing it out with 

warmed saline. 

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.  
  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. 

d. Subarachnoid Haemorrhage 

  Trauma is the commonest cause of SAH although aneurysms are the most common 

cause of spontaneous SAH. 

  Traumatic SAH is managed conservatively. 

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. 
  Presentations: either: 

1. Meningitis. 
2. Brain abscess. 
3. Subdural empyemas. 

  These can all exacerbate situation of raised intracranial pressure. 

 
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4. Seizures 

  They can increase both brain metabolism and blood flow, therefore increasing 

intracranial pressure. 

5. Hydrocephalus 

  Acutely due to obstruction of CSF outflow due to intraventricular blood. 
  Delayed post-traumatic communicating hydrocephalus due to impaired CSF 

reabsorption following traumatic subarachnoid haemorrhage  

  Intraventricular blood can lead to  Hydrocephalus 

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. 

7. Cerebral Herniation 

  Subfalcine Herniation 
  Uncal Herniation 
  Tentorial Herniation 
  Tonsillar Herniation 

a. Transtentorial Herniation 

b. Foramen magnum herniation 

c. Subfalcine Herniation

8. CSF rhinorrhea 

  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. 
  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.