Page 317 - Medicine and Surgery

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Chapter 7: Disorders of conciousness and memory 313

Penetrating trauma: Penetration of the skull by an ex- swelling of the brain. Petechial haemorrhage may

ternal object such as a bullet. occur in the corpus callosum and brain stem.
Axonal damage appears as swollen torn ends of the

axon.
Pathophysiology
The pathology of head injury can be divided into two
groups: Complications
Primary brain damage: Short term: Vascular, e.g. meningeal artery tear, caus-

i Cerebral contusions occur as the brain moves ing extradural haematoma, or dural vein tear causing a
within the skull, causing bruising of the brain, par- subdural haematoma. Subarachnoid and intracerebral
ticularly on the side of the trauma (coup lesion) and haemorrhage may also occur. Headache, dizziness and
ontheoppositesideofthebrain(contrecoup).Con- depression are common after a head injury.
tusions heal by gliosis stained with haemosiderin. Long term:
ii Diffuse axonal injury due to shearing forces caus- Posttraumatic epilepsy.
ing damage to cortical white matter tracts. Patients Chronic traumatic encephalopathy (the punch drunk
who survive such injury may have severe brain syndrome seen in professional boxers).
damage. Benign positional vertigo.
Secondary brain damage occurs after the initial Hydrocephalus.

trauma, and is the result of problems in maintain-
ing blood and oxygen supply to the brain due to hy-
Management
poxia (e.g. airway obstruction, respiratory failure) or
Resuscitation including intubation and ventilation as
masseffectfromhaematoma.Thedegreeofsecondary
required.Ifneckinjuryissuspected,thepatientshould
brain damage can be influenced by medical or surgi-
be immobilised until a spinal cord injury or unstable
cal treatment, whereas primary brain damage occurs
cervical spine has been excluded.
at the time of injury and therefore can only be in-
Assessment of the severity of coma by the Glasgow
fluenced by other factors such as car design to reduce
Coma Scale, and full neurological and general exami-
pedestrianinjury.Followingtrauma,thebrainismuch
nation. The decision to admit for observation is based
more susceptible to hypoxia and hypotension due to
on the history and assessment at presentation. In these
disruption of autoregulation and impaired vascular
cases, it is important to continue at least hourly neu-
supply.
rological observations (vital signs, GCS and pupillary
sizes/responses). Osmotic diuretics such as mannitol
Clinical features
may also be used to reduce brain oedema.
Ina mild injury the patient is stunned or dazed for a few Investigations including routine investigations (FBC,
seconds or minutes. Loss of consciousness is transient
U&Es and clotting) and a CT brain where indicated.
and following this the patient remains alert with no In severe cases initial management may include ad-
amnesia. In more severe injuries, there is persistent post-
mission to intensive care for intracerebral pressure
traumatic amnesia. Neurological signs including papil-
monitoring and management, e.g. with mannitol and
loedema (although rare) and any evidence of penetrat-
diuretics.
ing injury or skull fracture should be looked for. Patients
All patients require close monitoring to check for devel-
may have other injuries depending on the nature of the
opment of complications that require urgent treatment.
accident or trauma. The Glasgow Coma Scale is used to
CT brain is urgently indicated if
assess the level of consciousness (see Table 7.10). level of consciousness depressed (A GCS score of <8
following resuscitation).
Macroscopy/microscopy the GCS score falls despite initial management.
Early contusions appear as petechial haemorrhages. presence of skull fractures.

Over a period of several hours there is oozing of the patient is difficult to assess, e.g. due to alcohol or
blood and the contusions become haemorrhagic with drug intoxication.