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The brain andmeninges 155
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Body of lateral ventricle
Anterior horn
Third ventricle
Fourth ventricle
Figure16.2 The ventricular system. Reproduced from Ellis H, Mahadevan V (2019) Clinical Anatomy, 14th edn. Oxford:
Wiley- Blackwell.
Interventricular foramen
Posterior horn
Aqueduct
Inferior horn
Non- communicating or
obstructive hydrocephalus
CSF cannot escape from within the brain to the basal
cisterns. This may be due to congenital narrowing of
the aqueduct of Sylvius
which is a congenital downward protrusion of the
cerebellum into the foramen magnum (with consequent occlusion of the foramina of the fourth ventricle) frequently associated with spina bifida. It may
also be acquired as a result of cerebral abscess or
tumour, either within or adjacent to a ventricle.
11
or the Chiari malformation,12
Communicating hydrocephalus
CSF can escape from within the brain, but absorption
via the villi is prevented as a result of the obliteration
of subarachnoid channels. It may be congenital, as a
result of failure of development of the arachnoid villi,
or it may be secondary to meningitis or bleeding into
the subarachnoid space (e.g. head injury, aneurysm
rupture, arteriovenous malformation).
11
Franciscus Sylvius (1614–1672), Professor of Medicine,
Leiden, e Netherlands.
12
Hans Chiari (1851–1916), Viennese Pathologist,
successively Professor at Strasbourg, France, and Prague,
Czech Republic; he also described the syndrome of hepatic
venous outow obstruction.
Clinical features
Clinically, hydrocephalus may be divided into two
important groups. The first is the acquired variety,
which presents with features of raised intracranial
pressure described at the beginning of this chapter.
The second comprises patients with congenital
hydrocephalus, who show the characteristic picture
of enlargement of the skull (comparison should be
made with the size of an infant’s skull of the same age
obtained from standard charts) over which the scalp
is stretched with dilated cutaneous veins. The fontanelles are enlarged and tense, and fail to close at the
normal times. Typical of this condition is the downward displacement of the eyes (‘sun setting’), and
there may be an associated squint and nystagmus.
Papilloedema is not present in these cases. There may
be late epilepsy, and mental impairment may be considerable when there is extensive thinning of the cerebral cortex. There may be associated congenital
deformities, especially spina bifida.
In some infants with congenital hydrocephalus,
natural arrest occurs, presumably as a result of recanalization of the subarachnoid spaces. In the remainder, there is steady progression with inevitable mental
deterioration and high mortality unless adequate
treatment is instituted.
Special investigations
• CT or MR scans confirm ventricular enlargement
and can identify causes of obstruction.
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• Cranial ultrasound through the fontanelle is
useful in children.
•
Dynamic CSF studies allow monitoring of CSF
pressures over time as well as the measurement of
the resistance to CSF outflow.
Treatment
The goal of treatment is to divert the CSF around the
blockage by means of a shunt. For noncommunicating (obstructive) hydrocephalus, direct
removal of the occluding mass lesion is desirable.
Decompression of the hydrocephalus can be
achieved by diverting the CSF into the peritoneum
(ventriculoperitoneal shunt) or right atrium via the
internal jugular vein (ventriculoatrial shunt). The
shunts comprise silicone catheters with a regulator
valve mechanism in the middle to permit CSF flow at
a certain ventricular pressure without overdrainage of
the CSF.
In non-
communicating (obstructive) hydrocephalus, an artificial outlet may be created through the
floor of the third ventricle into the basal cisterns
(endoscopic third ventriculostomy).
Normal pressure hydrocephalus
In elderly patients, there is a form of chronic hydrocephalus that is associated with normal CSF pressures but disordered CSF dynamics. This normal
pressure hydrocephalus is characterized by a triad of
gait disturbance, dementia and urinary problems. It is
important as it is a treatable cause of dementia.
Additional resources
Case 30: A cerebral mass on MR imaging
Case 31: A cerebral vascular catastrophe
Case 32: A baby with a large head
Head injury
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Stephen Price
Learning objectives
✓ To know the common causes of coma.
✓ To be able to recognize the severity of a head injury and understand the
principles of management.
17
Head injury is a major cause of death in children and
young adults. Many survivors of head injury are
catastrophically disabled. Recognizing a severe head
injury and administering prompt and appropriate
care is important for all medical practitioners who, if
not receiving patients with such injuries under their
care, may nevertheless be bystanders witnessing such
an injury. If presented with a patient in ‘coma’ (see
Box17.1) other causes of unresponsiveness should be
considered.
Head injuries are generally classified as closed
(concussional) or open (penetrating).
Types ofinjury
Injuries are usefully classified according to the structures
involved (scalp, skull and underlying brain) together
with the mechanism of the injury, be it penetrating
or blunt, and whether an acceleration/deceleration
and/or a rotational brain injury occurred. In reality,
isolated injuries are uncommon, and patients more
typically experience blunt injury fracturing the skull
in which acceleration/deceleration of the brain also
occurs.
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
Scalp injuries
Most scalp injuries are simple penetrating injuries, which
are readily managed by debridement and suture. When
the skull is also penetrated, the brain may be lacerated.
However, if the injury occurred when the head was stationary, in the absence of acceleration and deceleration,
consciousness may not be lost and neither the patient nor
the doctor may appreciate the true extent of the injury.
Skull injuries
Injuries to the skull are a result of crushing or some
other severe force. The skull fractures along its weakest
plane, which varies according to the position of the
injuring force. Typically, this is a linear fracture of
the skull vault, but may extend into the skull base.
Asimple crush injury to a stationary head may leave the
scalp intact and not disturb consciousness in the absence
of acceleration and deceleration forces, although the
subsequent skull X-
fracture that are important to note (see Box17.2).
ray may show extensive fractures.
Fractures involving paranasal
air sinuses: cerebrospinal uid
rhinorrhoea
Fractures extending through any of the paranasal air
sinuses (frontal, ethmoid or sphenoid) communicate
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Box 17.1 Causes ofcoma
The emergency department doctor is often called
upon to make a diagnosis of a patient in coma. The
following are the common causes to be considered,
the first three groups accounting for the great
majority of cases.
•
Central nervous system:
–
Trauma.
–
Disease (e.g. cerebrovascular accident (most
common), epilepsy, subarachnoid haemorrhage,
cerebral tumour, abscess, meningitis).
•
Drugs/toxins:
–
Alcohol.
–
Carbon monoxide.
–
Barbiturates, aspirin, opiates, etc.
•
Diabetes:
–
Hyperglycaemia.
–
Hypoglycaemia.
•
Uraemia.
•
Hepatic encephalopathy in liver failure.
•
Hypertensive encephalopathy.
•
Profound toxaemia.
•
Hysteria.
It is usually straightforward to determine that
unconsciousness is due to trauma, but it is important
to remember that a drunk or epileptic person, for
example, may have struck their head in falling so
that the condition is complicated by a head injury.
with the outside and are, therefore, compound (open)
fractures, as the overlying dura is usually breached.
This external communication may manifest as a runny
nose (rhinorrhoea), the clear cerebrospinal fluid (CSF)
being rich in glucose and low in mucin content (and
positive for beta trace protein), compared with the
normal nasal secretion, which contains no sugar and
is rich in mucin. Such a connection may also be
indicated by intracranial air (aerocele) or fluid in one
of the sinuses on a computed tomography (CT) scan.
Anosmia may occur if the fracture crosses the cribriform plate. Such patients are at risk of meningitis.
Some CSF leaks heal spontaneously, particularly those
involving the temporal bone, but a persistent leak will
require craniotomy and dural repair or endonasal
repair. Vaccination against Pneumococcus is recommended where there is any suggestion of a CSF leak.
Box 17.2 Physical signs ofskull fractures
Anterior fossa
•
Nasal bleeding.
•
Orbital haematoma (see text).
•
Cerebrospinal fluid rhinorrhoea.
•
Cranial nerve injuries, nerves I–VI.
Middle fossa
•
Orbital haematoma.
•
Bleeding from the ear.
•
Cerebrospinal fluid otorrhoea (rare).
•
Cranial nerve injuries, nerves VII and VIII.
Posterior fossa
•
Bruising over the suboccipital region, which
develops after a day or two (Battle’s sign
•
Cranial nerve injuries– nerves IX, X and XI (rare).
1
).
Fractures ofthe petrous temporal
bone: CSF otorrhoea or rhinorrhoea
Fractures through the petrous temporal bone may
result in CSF otorrhoea, as CSF passes through into
the external auditory meatus either directly or via the
mastoid air cells or middle ear in the presence of a
ruptured tympanic membrane. If the tympanic membrane is intact, CSF rhinorrhoea occurs via the
Eustachian tube. Involvement of the inner ear will
result in deafness and is frequently associated with a
lower motor neuron facial nerve palsy. Spontaneous
resolution of the leak is usual.
Fractures through thetemporal
bone: middle meningeal vessels
A fracture through the temporal bone may disrupt the
middle meningeal artery and/or vein as they traverse the
bone, and result in an extradural haemorrhage, which
may not manifest immediately (see later in this chapter).
Depressed fractures
A localized blow drives a fragment of bone below the
level of the surrounding skull vault. Such fractures
are often compound, as the overlying scalp is torn.
1
William Henry Battle (1855–1936), Surgeon, St omas’s
Hospital, London, UK.
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The depressed bone may be left if it is not deeply
depressed (less than the skull thickness) and not otherwise troublesome. Indications for elevation include
the debridement of a contaminated wound, depression greater than the bone thickness, associated
intracranial haematoma or epileptic focus.
Orbital haematoma
Fractures of the anterior and middle cranial fossae are
very frequently associated with orbital haematoma;
blood tracks forward into the orbital tissues, into the
eyelids and behind the conjunctiva. It may be difficult
to differentiate this from a ‘black eye’, which is a
superficial haematoma of the eyelid and surrounding
soft tissues produced by direct injury.
An orbital haematoma is suggested by the follow-
ing features:
•
Subconjunctival haemorrhage, the posterior limit
of which cannot be seen.
•
Absence of grazing of the surrounding skin.
Confined to the margin of the orbit (owing to its
•
fascial attachments), whereas a black eye frequently
extends onto the surrounding cheek.
•
Mild exophthalmos and a degree of ophthalmoplegia.
• Bilateral haematoma.
There may also be some confusion in making a diagnosis between a subconjunctival and conjunctival
haemorrhage. The subconjunctival haemorrhage
extends from the orbit, forwards and deep to the
conjunctiva; there is, therefore, no posterior limit to the
haemorrhage. A conjunctival haemorrhage results
from a direct blow on the eye and produces a small haematoma clearly delimited on the conjunctiva itself.
(ischaemia), intracranial haemorrhage or meningitis.
These are the main causes of inafter head injury.
hospital mortality
Diffuse brain injury
Diffuse neuronal injury occurs as a result of shearing
movements, the worst being rotational shearing, as occurs
when a blow is delivered off centre. The result is axon damage and rupture of the small vessels, particularly serious in
the brain stem. A severe rotational shearing force may be
transmitted down along the axis of the brain, and such
forces shearing through the brain stem are usually fatal.
Localized brain injury
Local brain damage occurs as the brain impacts
against the skull.
Coup and contre- coup (Figure17.1)
The direct impact of the brain on the skull at the site of
injury and the contreagainst the opposite wall of the skull result in oedema
and bruising at the sites of impact. Common sites of
impaction are the frontal lobes in the anterior fossa
and temporal lobes within the middle fossa, with
contre- coup to the occipital lobes.
coup injury as it rebounds
Laceration within theskull
The brain may impinge on sharp bony edges within the
skull, such as the sphenoid ridge, and sustain a laceration.
Brain injuries
Brain injury can be divided into primary and secondary injuries.
trauma, and may have several components which,
apart from direct penetrating injuries, are the result
of the brain being relatively mobile within the skull
and it being violently forced into sudden acceleration and deceleration. These result in both diffuse
and local effects.
and are the result of hypoxia, hypercapnia, hypotension
Cerebral perfusion
Understanding the mechanisms underlying the
regulation of cerebral perfusion, and how these may
be affected in trauma, is important in the management
of patients with a head injury. The main regulatory
factors are described below.
Systemic arterial pressure
Cerebral perfusion is normally autoregulated by the
vasoactive cerebral arterioles to maintain constant
cerebral blood flow over a wide range of systemic blood
pressures. If systemic arterial pressure falls, cerebral
vasodilation occurs to compensate; a further fall may
160 Head injury
Cerebral perfusion pressure MAP ICP
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Blow
Direct 'coup' injury
'Contre-coup'
injury from brain
hitting opposite
part of skull
Figure17.1 Coup and contre- coup injuries– mechanism.
exceed the arterioles’ ability to compensate, and cerebral ischaemia occurs. The arterioles are also sensitive
to the presence of vasoactive mediators, the most
important being pH, and its proxy, Pco
arterial Pco
tion, and in the presence of oedema may further raise
intracranial pressure and result in exacerbation of the
brain injury, one of the causative factors in secondary
brain injury. Intensive care management aims to avoid
hypercapnia. Reduction of the Pco
constriction and hence more ischaemia. As a result,
hyperventilation, once employed to reduce Pco
now rarely used and only with suitable monitoring.
(hypercapnia) causes cerebral vasodila-
2
. An increase in
2
can lead to vaso-
2
, is
2
Intracranial pressure
Since the skull is a closed compartment, a rise in
intracranial pressure (ICP) will reduce the cerebral
perfusion pressure.
where MAP is the mean arterial blood pressure. Initial
increases in ICP (i.e. due to an expanding haematoma)
are compensated by reduction of CSF volumes within
the cranial cavity. Once the compensatory mechanisms are overcome then small changes in volume
will lead to very large increases in ICP. A rise in ICP
coupled with hypotension in trauma victims with
head injuries reduces cerebral blood flow, and the
resultant ischaemia increases ICP further as well as
affecting the cardiorespiratory centres in the floor of
the fourth ventricle, leading to reflex increase in systemic pressure and bradycardia– the Cushing reflex.
Hence, hypotension in head injury victims is seldom
due to the head injury.
Management ofthe
patient witha head
injury
The management of a patient with a head injury can
be divided into the following:
• Initial assessment.
• Immediate management.
• Delayed management.
2
Harvey Cushing (1869–1939), Professor of Surgery, Harvard
Medical School, Boston, MA, USA. He was one of the
founders of neurosurgery.
2
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In practice, the initial assessment and immediate
management frequently overlap according to clinical
priorities.
Initial assessment
The initial assessment is an active process and not
just a period of history taking. However, the history is
most important, in particular the account of a witness,
as most victims of major head injuries are unable to
give an accurate history.
History
Important points to note in the history are as follows.
The mechanism of the injury. This may enable
•
some prediction as to the likely injuries, both
visible and within the cranium. The nature of
the injurious force and its direction relative to
the recipient are important.
• The immediate condition of the injured person.
What was the patient like immediately after the
injury? In particular, note the level of consciousness in terms of an accepted scale such
as the Glasgow Coma Scale (see Box 17.3), as
well as other vital signs (pulse, respiration,
blood pressure), the size and reaction of the
pupils and recorded limb movements (was the
patient moving their arms and legs after the
accident?).
•
Any change in the condition of the injured person.
As well as establishing the patient’s condition
when first seen after the injury, it is also important
to establish whether the condition has changed at
all. For example, if the patient was talking and
moving all limbs and is now comatose, it suggests
that an intracranial mass lesion such as an intracranial haemorrhage is developing.
The prior condition of the injured person. As
•
much history as possible about the injured
person should be obtained from relatives and
friends. Was the patient drunk at the time? Is the
patient diabetic and so could the coma be hypoglycaemic? Does the patient have a glass eye
or is he or she on treatment for chronic glaucoma to account for the absence of pupillary
responses?
• What other injuries has the person sustained?
Patients who are unstable due to severe chest or
abdominal trauma need these managing first to
prevent secondary brain injury.
Examination
Your examination should reassess the patient’s
conscious level to decide whether the condition has
worsened or improved, and look for associated
injuries, in particular major occult injuries such as a
tension pneumothorax or fractured spine. In patients
with major injuries, the priorities for examination are
usually quoted in terms of the ABC of resuscitation, to
which may be added an additional C.
•
Airway. Is the airway clear without obstruction
such as vomitus or blood? If the patient is not
maintaining the airway, intubation with an
endotracheal tube should be performed.
Occasionally, this may not be possible and a
tracheostomy may be required.
• Breathing. Is the patient breathing spontaneously
or should ventilation be instituted? Avoiding
hypercapnia is desirable to reduce ICP (see
Chapter16). An arterial blood sample for estimation of oxygen carriage should be taken as soon as
convenient, and the patient should be monitored
by pulse oximeter to ensure adequate haemoglobin oxygen saturation.
• Circulation. The patient’s pulse and blood pressure should be taken and monitored. Raised
ICP results in bradycardia and hypertension
(Cushing reflex; see earlier in this chapter).
Hypotension is rarely due to head injury and an
alternative cause should be sought (a ruptured
spleen, a haemothorax or a fractured pelvis, for
example). Occasionally, extensive scalp bleeding may result in hypotension, as may a head
injury in a child.
Cervical spine. Every patient who sustains a head
•
injury should be considered to have a cervical
spine injury as well until proved otherwise by
good-
quality radiography or CT scan. The neck
should, therefore, be immobilized in a hard
collar.
Following the initial ABC, a full central nervous
system (CNS) examination should be performed as
well as complete examination of the chest, abdomen and limbs. Particular attention should be paid
to the parts that are usually forgotten, including
examining the back for evidence of trauma and
integrity of the spine, and a rectal examination with
particular attention to anal tone (or its absence in
spinal injury) and the position of the prostate in the
male (a ruptured urethra results in a displaced
prostate).
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Box 17.3 The Glasgow Coma Scale (GCS)
Eye opening
4 Spontaneously.
3 To speech/command.
2 To pain.
1 None.
Best verbal response
5 Orientated– knows who and where they are.
4 Confused conversation– disorientated; gives
confused answers to questions.
3 Inappropriate words– random words; no
conversation.
2 Incomprehensible sounds.
1 None.
Decorticate Decerebrate
Arms adducted,
flexed and
internally
rotated to lie
across chest
Best motor response
6 Obeys commands.
5 Localizes pain.
4 Flexes to pain– flexion withdrawal of limb to painful
stimulus.
3 Abnormal (decorticate) flexion– upper limb
adducts, flexes and internally rotates so that it lies
across chest; lower limbs extend (Figure17.2).
2 Extends to pain (decerebrate)– painful stimulus
causes extension of all limbs.
1 None.
When assessing the GCS, it is very important that an
adequate stimulus is applied.
Arms extended
and internally
rotated
Legs extended
Ankles plantar
flexed
Figure17.2 Decerebrate and decorticate postures.
The conscious level: theGlasgow
Coma Scale
Vague terms such as comatose, semi- comatose,
unconscious, stuporose and so on should be avoided.
Instead, the conscious level is charted according to
the patient’s motor, verbal and eye- opening responses
Legs extended
Ankles plantar
flexed as in
decorticate
to stimuli; these are very much the reactions of a
patient recovering from deep anaesthesia. The most
commonly used scale is the Glasgow Coma Scale
(GCS) (see Box17.3), in which the responses within
each group are allotted a score, the normal being 15.
A mild head injury may score 13–15, a severe injury
8or less.
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Pupil size andresponses
If a cerebral hemisphere is pressed upon by an enlarging
blood clot, the third cranial nerve on that side
becomes compressed by descent of the uncus over
the edge of the tentorium cerebelli. Paralysis of the
third nerve (which transmits parasympathetic
pupilloconstrictor fibres) results in dilation of the
corresponding pupil (owing to the intact unopposed
sympathetic supply) and failure of the pupil to
respond to light. An important sign of cerebral compression is, therefore, dilation and loss of light reaction of the pupil on the affected side although,
occasionally, pupillary dilation will be a false localizing sign and will be on the side opposite the mass
lesion. Because the optic nerve pathway is intact, a
light shone into this unreacting pupil produces constriction in the opposite pupil (consensual reaction to
light). As compression continues, the contralateral
third nerve becomes compressed, and the opposite
pupil in turn dilates and becomes fixed to light.
Bilateral fixed dilated pupils in a patient with head
injury indicate very great cerebral compression from
which the patient rarely recovers. Occasionally, local
trauma to the nerves from extensive skull-
base
fractures may produce the same findings.
Pulse, respiration andblood
pressure
With increasing ICP, the pulse slows and the blood
pressure rises (Cushing reflex; see earlier in this chapter),
the respirations become stertorious and eventually
Cheyne–Stokes
3
in nature.
Special investigations
With respect to head injury, there are three immediate investigations that may be indicated.
1
Skull X- ray used to be the initial investigation but
has been replaced owing to the ready availability of
CT. It may have a role in children as part of a skeletal
survey in suspected non- accidental injury.
2 CT scan should be performed on all patients with
significant head injuries (see Box17.4) as indicated
by impaired conscious level (GCS <15), history of
penetrating injury or suspected fracture, signs of a
basal skull fracture (e.g. CSF rhinorrhoea or otor-
3
John Cheyne (1777–1836), an Edinburgh- trained Physician
who migrated to Ireland. William Stokes (1804–1878),
Physician, Meath Hospital, Dublin, Ireland.
Box 17.4 Indications forCT scan
•
Impaired conscious level, GCS <13 on initial
assessment or GCS <15 at 2 hours after the
injury.
•
Suspected open or depressed skull fracture or
suspected penetrating injury.
•
Basal fracture of skull (possibly indicated by
cerebrospinal fluid rhinorrhoea or otorrhoea,
periorbital haematoma– Battle’s sign).
•
Focal neurological signs, fits or any other
neurological symptoms.
•
Deteriorating conscious level.
•
More than one episode of vomiting.
•
Amnesia for 30min before impact.
•
Coagulopathy/anticoagulation in patients with a
history of significant trauma or impaired
consciousness.
rhoea, bilateral orbital haematoma [Battle’s sign]),
post- traumatic seizure, focal neurological deficit or
recurrent (>1) vomiting or amnesia for more than
30min prior to impact. Other indications include a
history of loss of consciousness or amnesia and a
history of significant trauma, coagulopathy (e.g.
patient on anticoagulation), or age over 65 years.
The resulting images may then be viewed locally or
transmitted to a regional neurosurgical centre for
specialist opinion.
3 Cervical spine X- ray is necessary in all unconscious
patients following head injury, unless included in
the CT scan. Other indications include neck pain
and/or tenderness with a history of possible neck
trauma, or where exclusion of neck trauma is necessary prior to intubation for other surgery.
Immediate management
Admission to hospital (see Box 17.5), CT scanning
(see Box17.4) and neurosurgical referral should all
be considered. Consultation with a neurosurgeon is
indicated for persistent coma (GCS ≤8), persistent
unexplained confusion lasting more than 4 hours,
deterioration in GCS and progressive focal neurological signs as well as those in whom neurosurgery
is indicated (see later in this chapter). Transfer
should only occur after initial resuscitation and stabilization of the patient.
The immediate management of complicated cases
will include correcting any problems identified in the
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Box 17.5 Indications foradmission following
ahead injury
•
Persisting confusion or impaired conscious level
(GCS <15), in spite of favourable imaging.
•
Skull fracture or other significant abnormality on
imaging.
•
Neurological symptoms or signs, including
headache and fits and cerebrospinal fluid leaks.
•
Difficulty in assessing the patient, particularly
children, those under the influence of alcohol
or recreational drugs, those with other injuries
or in shock, and those with pre-
neurological conditions, for example
Parkinson’s disease.
•
Complicating medical condition other than head
injury, such as anticoagulant therapy.
•
Lack of responsible adult to supervise the patient,
or other adverse social conditions.
Notes
•
Patients who are discharged home should be
given written instructions about the possible
complications and what action should be
taken.
•
Post- traumatic amnesia with full recovery is not
considered an indication for admission.
•
No patient presenting with a head injury should be
allowed home until their GCS is normal (15).
existing
Delayed management
Management ofminor head injuries
With respect to the head injury, there follows a period
of observation, with attention paid to the following:
•
Conscious level– according to the GCS.
•
Vital signs– pulse, blood pressure, temperature,
oxygen saturation.
Pupil size and responses– dilation of a pupil, loss
•
of response to light or asymmetry are late signs of
increasing ICP; ICP monitoring – done with a
catheter placed within the ventricles, which will
help direct treatment and facilitate drainage of
intracranial fluid to lower pressure.
Management ofsevere head injuries
With severe head injuries the aim of management is
to prevent secondary injury. This is done by:
•
Maintaining blood pressure – patients need accu-
rate fluid balance and may need inotropic support.
Maintaining adequate oxygenation and avoidance
•
of hypercapnia.
Avoidance of hyperthermia.
•
•
Monitoring ICP.
Managing high intracranial
pressure
initial assessment, such as draining a pneumothorax,
instituting ventilation if the patient is unable to
maintain the airway or to breathe, and performing a
laparotomy and/or orthopaedic procedures when
appropriate.
Following the initial brain injury, further deteriorati on
may be due to the following factors:
•
Increasing cerebral oedema as the brain swells
consequent upon the damage it sustained.
• Intracranial haemorrhage– extradural, subdural
or intracerebral.
• Hypoxia, due to impaired ventilation or
ischaemia.
• Infection, secondary to compound fractures
including fractures involving the paranasal sinuses
or petrous temporal bone.
• Hydrocephalus, either communicating or
noncommunicating.
In an unconscious, ventilated patient, it is important
to monitor ICP.
Intraparenchymal probes are commonly used for
this. A high ICP can be treated as follows.
Paralyse and sedate the patient: this prevents the
•
patient ‘fighting’ with the ventilator and having
increases in intrathoracic pressure. Most sedatives
used (e.g. propofol) reduce cerebral metabolic
activity, thus reducing the demand for blood to the
brain. In extreme cases with uncontrolled ICP,
attempts to cause ‘electrical silence’ of the brain
with barbiturates can be considered.
• Reduce venous congestion: this is done by nursing
in a slight head- up position and ensuring ties for
endotracheal tubes do not compress the neck.
• Ensuring adequate blood pressure: falls in blood
pressure lead to vasodilation in areas of the brain
that are autoregulating. Reversing even slight falls
in blood pressure can have a profound improvement in ICP.
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