Brain injury

For both treatment and medicolegal purposes, it is important to have an understanding of the mechanisms as to how brain injuries evolve. Abrupt deceleration of a moving head is characterised by a relatively minor injury at the site of impact (coup injury) and an extensive contusion of the brain opposite the point of impact [contre-coup injury] (French-‘counter-blow’)]. Contusions are most likely along the undersurface of the frontal lobes, the tips of the temporal lobes and along the falx.

Abrupt acceleration of an unsupported head occurs when the head is struck by a moving object. The skull accelerates against the brain causing an extensive coup injury of the brain. The remainder of the brain may remain unchanged. When a well-supported head is struck by a moving object, there is little movement of the skull and brain. Most of the force is absorbed by the skull, which will fracture. Damage to the underlying brain results from direct perforation or laceration by skull fragments.

It is thus easy to understand why most cerebral contusions occur without skull fracture and why patients with spectac­ular fractures are often awake with only minor neurological dysfunction.

Primary brain injury is caused at the time of impact and is irreversible (Fig. 35.14). Secondary brain injury develops subsequent to the impact damage (Table 35.1). The manage­ment of head injuries focuses on reducing secondary injuries.

Primary brain injury

Cerebral concussion

This is a clinical diagnosis and is manifested by temporary dysfunction that is most severe immediately after injury and resolves after a variable period. It may be accompanied by autonomic abnormalities including bradycardia, hypotension and sweating. Loss of consciousness often, but not invariably, accompanies concussion. Amnesia for the event is common and varying degrees of temporary lethargy, irritability and memory dysfunction are hallmarks.

Postconcussion syndrome can accompany head trauma and consists of headaches, irritability, depression, lassitude and vertigo. It is more frequent after minor head trauma due to people trying to return to work too quickly.

Cerebral contusion and laceration

This can be demonstrated by CT as small areas of haemorrhage in the cerebral parenchyma. They usually produce neurological deficits that persist for longer than 24 hours. Contusions may resolve together with the accompanying deficit or they may persist. Blood—brain barrier defects and cerebral oedema are common and these lesions enlarge or coalesce with time.

Even without a skull fracture, if sufficient force is delivered to the skull the brain might become lacerated as a result of rapid movement and shearing of brain tissue. The pia and arachnoid may be torn and intracerebral haemorrhage may accompany this lesion. Focal deficits are the rule.

Diffuse axonal head injury

This type of brain damage occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons, especially at the grey/white matter interface. Severity can vary from mild confusion to coma and even death. Macroscopically, punctate haemorrhages are visible, especially in the corpus callosum and superior cerebellar peduncle. Microscopically, retraction balls reflecting axonal damage and microglial clusters (hypertrophied microglia) are found diffusely in the white matter.

Secondary brain damage

Intracranial haematomas

Intracerebral haematoma. These appear as hyperdense lesions on CT with associated mass effect and midline shift. They are due to areas of contusion coalescing into a contusional haematoma. They may appear to have a mixed density.

Extradural haematoma occurs usually as a result of squa­mous temporal bone fractures with laceration of the middle meningeal artery. They can also arise from fractured bone edges or rarely from the dural venous sinuses. The potential space between the dura and bone is developed by the expand­ing haematoma allowing it to take on the familiar convex configuration due to the adherence of the dura to the inside of the calvarium (Fig. 35.15). The degree of trauma might not be severe and there is typically a lucid interval following the trauma. Frequently, patients present in coma and require urgent evacuation via a burr hole prior to formal craniotomy (Fig. 35.16). Patients do well if delay is minimised.

Subdural haematomas. They are the most common intracranial mass lesions resulting from head injury. Most result from torn bridging veins draining blood from the cortex to the dura. They can also arise from cortical lacerations or bleeding from the dural venous sinuses. They are usually associated with more severe, high-velocity trauma with a poorer outcome, usually in older patients. The blood follows the subdural space over the convexity of the brain and appears as a concave hyperdense lesion. Acute subdural haematomas are more rapidly evolving lesions and early evacuation is mandatory (Fig. 35.17).

Chronic subdural haematomas. These haematomas are most common in infants and in adults over 60 years of age. They present with progressive neurological deficits more than 2 weeks after the trauma. Often the initial head injury has been completely forgotten and the pathology has been attributed to either dementia or a brain tumour until patients are scanned (Fig. 35.18). The initial haemorrhage may be relatively small or may occur in elderly patients with large ventricles or a dilated subarachnoid space. Membranes deriving from the dura and arachnoid mater encapsulate the haematoma which remains clotted for 2—3 weeks then liquefies. The acute clotted blood initially appears white on a CT scan. As it liquefies it slowly becomes black. There is therefore a point in time where it appears isodense with brain and all that can be seen is apparent inexplicable midline shift on an otherwise normal CT. These collections can be removed by drilling burr holes and washing them out with warmed saline.

Cerebral swelling

This results from vascular engorgement, probably due to a loss of autoregulation and an increase in extracellular and intracellular fluid. The exact causative mechanisms are unclear.

Cerebral ischaemia

This is common after severe head trauma and is caused by a combination of either hypoxia or impaired cerebral perfusion. The brain is unable to autoregulate its blood supply with a decrease in blood pressure. Glutamate excess and free radical accumulation lead to neuronal damage.

Infection

Compound depressed fractures or base of skull fractures can lead to either meningitis or cerebral abscess.

Epilepsy

Seizures can increase brain metabolism and blood flow, there­by increasing ICR Prophylactic anticonvulsants given acutely for the first 2 weeks are said to be of benefit. No benefit from long-term treatment has been demonstrated.

Management

Initial assessment of head injuries must follow Advanced Trauma and Life Support (AILS®) guidelines with an initial primary survey, then resuscitation, followed by a secondary survey then definitive management or, more simply: airway, breathing, circulation, disability and exposure. Securing an adequate airway preventing obstructive breathing or hypoventilation is critical in unconscious head-injured patients, as is maintaining a decent blood pressure. Care must be taken to secure the neck and spine. When an intracranial haematoma is suspected, an early CT scan is essential.

In the assessment of a head injury points to determine from the history are:

period of loss of consciousness;

period of post-traumatic amnesia;

cause and circumstances of the injury;

presence of headache and vomiting.

The patient should be examined for evidence of injury (e.g. lacerations and grazes) and the findings clearly documented. Base of skull fracturing should be excluded and the conscious level determined on the Glasgow Coma Scale and monitored (Table 35.2). The pupillary response should be elicited to determine whether there is incipient transtentorial herniation with oculomotor palsy, limb movements and responses recorded.

Once any intracranial haematoma has been evacuated patients should then be admitted to an intensive care unit and ventilated to a PCO2 of 4—4.5 kPa. A central line, arterial line and a urinary catheter should be inserted. The head of the bed should be positioned 40~ up and the patient given analgesia (fentanyl), sedated using propofol or midazolam and paralysed (atracurium). Intravenous fluids administered should be isotonic until nasogastric feeding can be commenced. An ICP monitor (Codman or Camino) should be inserted intraparenchymally and the ICP and CPP monitored. Ideally the ICP should be maintained below 25 mmHg and the CPP above 70 mmHg. If necessary, ionotropes can be used to support the blood pressure and CPP.

Dexamethasone has no benefit. Diuretics such as mannitol and frusemide can be used to lower ICP further but the former must be used with caution in patients with large areas of blood—brain barrier breakdown for fear of potentiating the mass effect. If ICP cannot be controlled by these means alone then steps such as introducing EEG burst suppression therapy with a barbiturate (thiopentone), ventricular or lumbar CSF drainage or polar lobectomies have to be considered.

Repeat CT scan should be considered if there is a delayed deterioration in the mental state, a maintained rise in intracranial pressure or a failure to improve over 24 hours.