ASUHAN KEPERAWATAN

CEDERA KEPALA
LEARNING OBJECTIVES
By the end of this chapter the reader will be able to:
❏ Identify the anatomical areas where traumatic head injuries
occur
❏ Identify common head and brain injuries
❏ Defi ne primary and secondary brain injury
❏ Understand factors that affect intracranial pressure and
cerebral perfusion pressure
❏ Describe assessment and management priorities in relation
to ABCDE.
ANATOMY
The head is divided up into four areas – frontal, temporal,
parietal and occipital (Figure 3.1). Head injuries may involve
one or a number of structures within these areas, including
the scalp, bone, brain tissue and blood vessels.

Scalp
The scalp is made up of fi ve layers and may be remembered
using the mnemonic SCALP:
• Skin
• subCutaneous tissue
• galea Aponeurosis (a fi brous muscle layer)
• Loose areola tissue (beneath the galea where emissary veins
are situated. These connecting veins drain blood from the
sinuses in the dura to the central circulation)
• Periosteum.
Bone
Once the fontanelles have fused, the skull or cranium is a
‘fi xed box’, which protects the brain. The facial bones provide
a structure for the face. Fractures of the skull are described
according to shape, site and displacement, and whether they
are depressed or not.

Linear fractures
Linear fractures are usually caused by blunt trauma and
consist of a line or crack in the bone. In the temporal region
the bone is thin and closely associated with the middle meningeal
artery.3 A fracture in this region can tear the artery,
which is a common cause of an extradural haematoma (discussed
later).
Linear fractures may not necessarily need any treatment,
however there is a risk of underlying brain injury. For this
reason any patient in whom there is clinical suspicion of a
skull fracture should have a CT scan
Depressed or compound fractures
Injury to the skull when bone is displaced inwards is known
as a depressed skull fracture. The bone can be broken into a
number of pieces (described as comminuted) and if there is
an associated scalp wound present then the fracture is classifi
ed as being open or compound. Depressed fragments of
bone can damage the underlying brain tissue, therefore an
early neurosurgical referral should be made.2 Compound
skull fractures pose a risk of infection, therefore tetanus prophylaxis
and antibiotics are required.
Base of skull fractures
The base of the skull is composed of fi ve areas:
• Base of the orbit
• Sphenoid (part of the ethmoid bone)
• Temporal bone
• Occiput
• Cribriform plate.
Some clinical signs may indicate that a base of skull fracture is
present.2,3
Frontal base of skull fractures may present with:
• Subconjunctival haemorrhage – the border of the clot on the
sclera extends to back of the eyeball.
• Periorbital bruising or racoon eyes – this may indicate a base
of skull fracture or it may indicate haemorrhage collected
beneath the galea aponeurosis.
• Rhinorrhea – cerebrospinal fl uid (CSF) leak from the nose
(indicating a tear in the dura mater).
Mid base of skull fractures may present with:
• Otorrhea – CSF leak from the ear (indicating a tear in the
dura mater).
• Haemotypanum – blood behind the tympanic membrane.
• Mastoid process bruising or Battle’s sign (NB this will only
develop after 4–6 hours in a supine patient)
Facial fractures
Fractures of the facial bones and underlying tissue injury are
not generally life threatening unless they compromise the
airway or cause severe haemorrhage.4 However, facial fractures
associated with head injuries are often caused by severe force,
such as a head hitting the windscreen in a road traffi c accident
or assault to the head and face with a blunt object. Patients
may present with obvious bleeding, facial swelling and facial
deformity. Fractures of the middle third of the face can be
broadly placed into one of three categories (Figure 3.2):
• Le Fort I – involving the maxilla
• Le Fort II – involving the maxilla and the nasal bones
• Le Fort III – involving the maxilla, the nasal bones and the
zygomatic bones
Le Fort III injuries are the most serious as they may result in
airway compromise. Injuries which cause severe nasal bleeding
may be managed by using nasal compression balloons
(Epistats) or nasal packing.
Meninges
The meninges are situated between the inside of the skull and
the brain (Figure 3.3).
The meninges consist of three layers:
• The dura mater – the outer fi brous membrane that lies close
to the skull.
• The arachnoid layer – the soft cobweb-like structure beneath
which cerebrospinal fl uid (CSF) circulates.
• The pia mater – the soft membrane that is attached to the
outer surface of the brain.
Brain
The brain is composed of the cerebrum (divided into two
cerebral hemispheres), the cerebellum and the brainstem.
Within the brainstem there is:
• The midbrain (containing the reticular activating system
responsible for the awake state)
The pons and the medulla (which contains the cardiorespiratory
control centres).
The tentorium is a fold of the dura mater that separates
the cerebral hemispheres from the cerebellum and the
brainstem.
PHYSIOLOGY
Primary and secondary brain injuries
Injuries to the brain can be described as primary or
secondary.2,5
Primary injury occurs at the time of the incident and is
irreversible. These injuries can be focal, affecting one area of
the brain. These include:
• Contusions
• Haematomas
• Lacerations
Injuries can be diffuse affecting the whole brain, including
concussion and shearing injuries.
Secondary damage, which may be preventable or reversible,
occurs at a later stage due to:
• Brain tissue hypoxia
• Oedematous brain tissue
• Systemic hypotension, causing the brain to be
underperfused.
concussion and shearing injuries.
Secondary damage, which may be preventable or reversible,
occurs at a later stage due to:
• Brain tissue hypoxia
• Oedematous brain tissue
• Systemic hypotension, causing the brain to be
underperfused.

The main goal of treating head injuries is to recognise the

primary injury and reduce or prevent the secondary brain
injury.
In order to do this it is essential that intracranial pressure
and cerebral perfusion pressure are understood.
Intracranial pressure
Three components are responsible for regulating intracranial
pressure (ICP):6
Volume of the brain + volume of CSF +
volume of cerebral blood = ICP
If one of the three components increases, such as the volume
of the brain due to a haemorrhage, then there is a compensatory
decrease in the other two components, allowing more
space for the swollen brain:
• Vasoconstriction occurs reducing the volume of cerebral
blood fl ow
• CSF production decreases and CSF gets displaced into the
spinal subarachnoid space.
This process is called autoregulation, which helps to maintain the
ICP within the normal range of 0–15 mmHg.
Autoregulation can only occur up to a point and once the ICP rises above 20
mmHg the compensatory mechanisms
described above fail. Sustained ICP of >20 mmHg
is associated with poor outcome for the head injured
patient
In the severely head injured patient with a raised ICP, alteration
of the cerebral blood vessels occurs. The cerebral vascular
resistance increases causing the blood pressure to rise, to try
to overcome the raised ICP. This hypertension associated with
severe head injuries is known as Cushing’s response2 and is a
late sign.
Cerebral perfusion pressure
The cerebral blood fl ow in the brain is approximately
700 ml/min.7 This is maintained at a relatively constant rate
by the constriction and dilation of the cerebral vessels. In
order to ensure that the brain tissue is well oxygenated and
perfused it is essential that cerebral perfusion pressure (CPP)
is maintained within normal limits, 60–70 mmHg.
CPP is calculated thus:
Mean arterial pressure (MAP) + ICP = CPP
MAP is calculated by taking one-third of the difference
between the systolic and diastolic blood pressure and adding
it to the diastolic. See Box 3.1 for an example.
In an adult, the CPP should be maintained >70 mmHg and
in young children >50 mmHg. A CPP of <50 mmHg is associated
with ischaemic brain injury.
In a normotensive patient with no brain injury and a
presumed normal ICP the CPP will be within normal limits.
See Box 3.2 for an example.
However, in a traumatically injured patient who is hypovolaemic,
hypotensive and has sustained a severe head injury
SPECIFIC BRAIN INJURIES

Concussion
Concussion is defi ned as a temporary loss of consciousness or cerebral
disturbance with no long term neurological deficit following a head injury.5
Some patients may complain of a headache, amnesia, and nausea or vomiting.
Whilst there is no defi nitive treatment for concussion, a CT scan is warranted
to rule out cerebral contusion. The patient can normally be discharged home
following a normal CT with head injury instructions

Contusion
Contusion is bruising of the brain tissue, often with associated swelling. This may
be caused by the brain being shaken around in the skull (rapid acceleration –
deceleration) or if the brain has been bruised by a bony prominence or skull
fracture. Contusions are usually diagnosed on CT scan; however suspicion
may be raised if the patient exhibits signs of prolonged loss of consciousness or
reduced level of consciousness following the injury. Patients should be admitted
to hospital to ensure that the contusion is not evolving into an intracerebral
haematoma. This is especially important for high risk patient groups such as
those taking anti coagulants or with clotting disorders.
Traumatic axonal injury
Traumatic axonal injury usually results from a rapid acceleration–deceleration
force, such as a high-speed road traffi c accident. Stretching and shearing occurs
causing swelling and injury to the axons within the brain tissue. This can lead to
permanent disability and is associated with high morbidity and mortality.

Extradural haematoma
An extradural haematoma is a bleed that occurs outside the dura mater beneath
the skull. Classically it occurs due to an injury in the temporal region where
branches of the middle meningeal artery are situated. Arterial injury causes
bleeding, resulting in the dura being separated away from the skull. The
expanding haematoma compresses the brain beneath it. Usually the bleed is rapid
and the patient will quickly lose consciousness at the time of the injury occurring.

However, a proportion of patients will have a lucid period following the injury
and then deteriorate swiftly into unconsciousness as the bleeding progresses.
Following CT scan, patients with an extradural haematoma need emergency
neurosurgery to evacuate the haematoma
Subdural haematoma
This is the most common intracranial bleed associated with severe head injury
and is associated with a worse outcome than for an extradural haematoma. A
haematoma forms beneath the dura mater as a result of injury to bridging veins

A subdural haematoma can be acute or chronic. Acute injury usually manifests

itself within the fi rst few hours and can quickly evolve in size leading to reduced
level of consciousness and coma. A CT scan will reveal the location of the
haematoma and an urgent neurosurgical referral should be made for further
management.

Chronic subdural haematomas may appear days, weeks or months after the
injury and they are common in small children and older patients. Venous in
origin, bleeding is slow and there may be more space for the haematoma to build
up due to a smaller or atrophied brain. This means that the signs and symptoms
may be subtle and the patient deteriorates slowly. In the older patient, symptoms
may be dismissed as confusion, dementia or falls. Once a chronic subdural
haematoma has been confi rmed on CT scan the patient should be referred to a
neurosurgeon.
Intracerebral haematoma
An intracerebral haematoma is where bleeding has occurred deep within the brain
tissue. These bleeds are often caused by severe force and may be associated with
subdural haematoma. Following diagnosis on CT scan, an urgent neurosurgical
referral is necessary. Patients with large intracerebral haematomas may need
surgery, however smaller clots may be treated conservatively, with the patient
closely observed for deterioration indicating an ongoing bleed or increasing
intracranial pressure.

Penetrating injuries to the brain

Gunshot wounds to the brain are associated with very high mortality rates.3 Other
penetrating injuries can be sustained by objects such as knives or scissors being
pushed through the skull with a great deal of force. If a patient presents with a
penetrating object in situ, it must not be removed until the patient has had a CT
scan and a senior surgeon is present.
PRIMARY SURVEY ASSESSMENT AND RESUSCITATION

As part of the assessment process a number of important

points from the history should be established which may give
an indication of whether there has been an injury to the brain.
These include:
• Mechanism of injury
• Whether or not there was a loss of consciousness or amnesia.

The conscious patient should be questioned about:

• The presence of a headache
• Nausea/vomiting
• Visual disturbances.
Airway with cervical spine control

As for all trauma patients, assessment of the airway with simultaneous cervical
spine control is the fi rst priority for the head injured patient. Any patient with a
head or facial injury must be expected to have a cervical spine injury until proven
otherwise by a senior clinician. There is a 5% association of cervical spine injury
with severe head injury.

Patients with a suspected base of skull fracture should not have a nasopharyngeal
airway inserted because of the risk of passing the airway into brain tissue.
Early tracheal intubation is indicated for the head injured patient with a GCS < 9.2
Patients with severe facial injuries that cannot maintain a patent airway due to
bleeding, swelling or deformity, should be intubated early. Severe damage to
the face and upper airway may mean that a surgical airway (as described in
Chapter 2) is the most expedient method of securing a patent airway.