Chapter 23. Head injuries
The central nervous system has no stores of oxygen or glucose; if the blood supply is interrupted, depriving the brain of oxygen, consciousness is lost within 15–20 seconds. The brain cells will then die within 3–4 minutes.
Because the skull is a rigid box, tissue swelling or bleeding within it will lead to an increase in pressure. As the pressure rises, the brain is pushed down, impacting on rigid structures such as the tentorium and the foramen magnum. This leads to reduced consciousness and eventually causes death by coning, the compression of cardiorespiratory centres within the brainstem.
Any head injury should raise the suspicion of associated c-spine injury.
Risk factors for head injury include:
• Alcohol abuse
• Drug abuse
• Anticoagulants
• Blood clotting disorders
• Other drugs including tranquillisers
• The elderly especially with dementia.
The key to the optimal management of head-injured patients is the prevention of secondary brain damage by appropriate attention to the airway, breathing and circulation.
Primary and secondary brain injury
Definitions: The brain injury sustained at the time of the accident is known as the primary injury and cannot be reduced once it has occurred
Secondary brain injury is a combination of factors that lead to additional brain injury and cell death following the primary injury
Any episode of hypoxia or hypotension will significantly worsen the patient’s outcome from head injury. As hypoxia affects the brain as a whole there is generalised swelling – cerebral oedema – which results in raised intracranial pressure (ICP). When the intracranial pressure approaches the arterial pressure, blood cannot flow through the brain and so cells will die.
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| Figure 23.1. |
| Primary and secondary brain injury. |
The important blood pressure for the brain is not the mean arterial pressure (MAP) alone, but the perfusion pressure (PP). The cerebral perfusion pressure is the mean arterial pressure minus the mean intracranial pressure (MICP): PP = MAP − MICP.
Both a fall in mean arterial pressure and a rise in intracranial pressure may therefore reduce cerebral perfusion pressure and produce secondary brain injury.
Treatment should aim to maintain the cerebral perfusion pressure and keep the patient’s arterial pressure near normal limits and above 100 mmHg in the adult. Raised central venous pressure also leads to increased ICP. Anything that increases central venous pressure, for example a tension pneumothorax, must also be treated.
Signs of raised intracranial pressure:
• Decreasing level of consciousness
• Increasing blood pressure (late)
• Falling pulse rate (late)
• Decreasing respiratory rate (late)
• Pupillary dilation (late).
Generalised brain injury
Generalised or diffuse injuries represent a spectrum of injury from mild concussion with rapid and complete recovery to diffuse axonal injury (DAI) which is the principal cause of long-standing coma following head injury. Coma may last days or weeks or may be permanent.
Focal brain injuries
Localised or focal brain injuries consist of:
• Cerebral contusion
• Intracranial haemorrhages
• Lacerations and penetrating injuries.
Intracranial haemorrhage
Intracranial haemorrhage may be:
• Extradural bleeding: <1% of injuries, may be fatal but complete recovery is possible if treated within 2 hours
• Subdural bleeding: 30% of injuries, good recovery if treated within 2 hours but some residual disability is common
• Intracerebral bleeding: this is within the brain tissue itself
• Subarachnoid bleeding: within the subarachnoid space, produces headache and decreasing consciousness.
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| Figure 23.2. |
| Anatomy of intracranial bleeding. |
Extradural haematoma – a history of rising intracranial pressure
An extradural haematoma is bleeding within the skull. Although the initial injury to the brain is liable to have caused concussion, the patient often recovers temporarily (a lucid interval) before deteriorating. As the size of the haematoma increases, intracranial pressure increases and the conscious level deteriorates.
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