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
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.