Care of patients with brain injury in the

critical care environment

1 June, 2002

Richard Hughes, RN.

Senior Staff Nurse, Intensive Care Unit, St Thomas Hospital, Guys and St Thomas Hospital NHS
Trust, London
It is estimated that between 750 000 and one million individuals with head injuries attend
accident and emergency (A&E) departments in the UK every year. Approximately 150 000 to 200
000 are admitted to hospital and, of these, 5% require admission to a neurosurgical unit (Flint,
1997).

It is estimated that between 750 000 and one million individuals with head injuries attend accident
and emergency (A&E) departments in the UK every year. Approximately 150 000 to 200 000 are
admitted to hospital and, of these, 5% require admission to a neurosurgical unit (Flint, 1997).
Males are twice as likely to be victims of traumatic brain injury, with the incidence highest between the
ages of 15 and 35 years (Hughes, 2000). It is estimated that a quarter of head-injured patients seen
in A&E have recently consumed alcohol (Withington, 1997).
However, while these statistics may sound excessive, it is important to point out that the mortality of
coma-inducing traumatic brain injury has fallen from 50% to 25% over the past 20 years. This is
largely due to legislative measures such as compulsory seat belts in cars, anti-drink-drive campaigns
and increased bicycle helmet use (Hughes, 2000)
This paper describes types of brain injury and discusses the nursing care of brain-injured patients in
the critical care setting, focusing on the management of raised intracranial pressure.
Brain injury
There are two broad categories of brain injury, primary and secondary.
Primary brain injury This is sustained at the time of the insult or accident (Flint, 1999). Primary
brain injuries include lacerations or contusions of the brain substance and direct disruption of brain
tissue by shearing of axons and disruption of blood vessels (Wong, 2000).
Secondary brain injury This is attributable to a decrease in cerebral oxygen delivery as a result of
hypertension, hypoxia, cerebral oedema, intracranial hypertension or abnormalities in cerebral blood
flow. Although the severity of primary brain injury cannot be reduced, secondary brain injury can be
minimised if appropriate therapies are implemented in time (Wong, 2000).
Types of primary brain injury
Subdural haematoma This is a form of focal (localised) brain injury and is usually venous in origin.
It may not necessarily be associated with a skull fracture and can be acute or chronic in formation.
Patients with acute subdural haematomas will display symptoms within 48 hours after injury. The
deterioration can be due to swelling of the temporal lobe (Hughes, 2000). Such injuries tend to carry a

poor prognosis (Withington, 1997). Those with a chronic subdural haematoma may not display
symptoms until two weeks after the injury has been sustained.
Extradural haematoma Another form of focal injury, this type of haematoma may occur with a
relatively minor blow to the head, commonly around the temple where the bone is thin, resulting in
damage to the middle meningeal artery. Within a matter of hours a significant space-occupying blood
clot may compress the brain. The clot can cause a rapid rise in intracranial pressure (ICP) and can
lead to secondary brain injury. Death is likely to ensue unless the collection of blood is evacuated
promptly (Flint, 1999).
Midline shift Unilateral lesions such as haematomas may cause a lateral distortion of the brain, often
referred to as a midline shift (Hinds and Watson, 1996). Hughes (2000) states that when midline
structures are pushed laterally, cerebrospinal fluid (CSF) drainage is obstructed, causing the ventrical
to dilate, further increasing the ICP. During this phase there may be changes in the respiratory rate
and pattern, an increase in the systolic blood pressure due to brain ischaemia and a fall in pulse rate,
as the heart attempts to pump blood into vessels with increased resistance as a result of the raised
ICP. This response is known as the Cushing reflex (Metheny, 1996).
Focal contusions These injuries are often seen after falls and blows to the head when brain tissue is
bruised. Patients often display symptoms of a severe concussion. Brain oedema from significant
contusions may lead to clinical deterioration due to swelling and brain shift (Hughes, 2000).
Axonal injury Axonal injury ranges from mild concussion, where no structural lesion is found and
complete recovery ensues, to diffuse axonal injury where prolonged coma and death may result
(Withington, 1997).
The term diffuse implies the brain injuries are associated with more widespread damage than focal
injuries, which tend to be localised (Hudak, 1998). This occurs where angular acceleration has been
much greater, leading to the shearing of axonal tracts (Hughes, 2000).
Skull fractures
There are several types of skull fracture, the presence of which greatly increases the risk of
complications in head-injured patients (Withington 1997):
- Linear. A non-displaced fracture to the cranium. This may be associated within secondary intracranial
bleeding if it crosses an area with underlying vessels
- Depressed. This fracture can cause compression of the brain tissue and there is the potential for
bony fragments to enter the cranial cavity. These fractures may be compound in nature
- Basilar. This is where one or more of the five bones at the base of the skull have sustained a
fracture. Symptoms may include CSF leakage, otorrhoea, rhinorrhoea, positive Battles sign (bruising
around the mastoid region behind the ears), and racoon eyes (subconjunctival haemorrhage)
(Withington, 1997).
Intracranial pressure
The brain occupies about 80% of the space within the cranial vault, with CSF and blood occupying

10% each respectively. These volumes are relatively consistent and result in a normal ICP. To enable
the ICP to remain within the normal limits of 0-15mmHg (Beitel, 1998), any alteration in the volume
of one of the above components must be offset by a reciprocal change in the other two: this is known
as the Monro-Kellie hypothesis (Chambers, 1999). However, due to the limitations caused by a rigid
structure such as the skull, when this mechanism is exhausted, displacements or herniation of the
brain may occur. Coning (or tentorial herniation, to give it its correct name), during which the
brainstem descends down through the foramen magnum, is an example of this (Chitnavis and Polkey,
1998). Increases in the ICP can also lead to a reduction in the level of blood flowing through the brain,
which in turn can lead to a reduced level of cerebral perfusion.
The brain has various mechanisms that regulate ICP, which are listed on the summary page, 597. The
anatomy and physiology of the brain is also summarised on page 597.
Autoregulation and cerebral perfusion pressure
Autoregulation ensures an adequate supply of oxygen and nutrients to the brain. In the event of
cerebral trauma or neurological disease, however, the autoregulatory mechanisms that control ICP
may be disrupted, causing a subsequent and sustained increase in ICP to 15mmHg or higher (Hickey,
1997).
Cerebral perfusion pressure (CPP) is a measure of the force by which blood is driven through the
cerebral circulation (Chitnavis and Polkey, 1998) and is defined on page 597. Autoregulation is said to
fail when the CPP is below 60mmHg or greater than 100mmHg (Johnson, 1999). CPP is a good
reflection of the adequacy of blood perfusion to the brain.
Beitel (1998) points out the evidence to date supports the active maintenance of CPP at a minimum of
70mmHg in an effort to avoid cerebral vasodilatation, increasing cerebral blood volume and
consequently, ICP. Mortality and morbidity are known to be associated with CPP below 70mmHg
(Beitel, 1998).
The drug of choice to maintain required CPP tends to be noradrenaline, whose main action is on the
alpha receptors in the peripheral arterioles, causing vasoconstriction and a rise in mean arterial blood
pressure (MAP) (Opie, 1991), and therefore in CPP and cerebral blood flow (Hall, 1997).
Nursing management in critical care
The critical-care nurse needs to be alert to the potential problems that may be encountered by the
brain-injured patient, who may be at risk of sudden deterioration at any time. This involves taking an
holistic view of the patient.
Respiratory care Hypoxia after head injury is common for a number of reasons: inadequate airway
clearance leading to poor tidal volumes, associated chest trauma and aspiration and hypermetabolic
state post-injury, which will increase tissue oxygen requirements (Arbour, 1998). It is important that
arterial oxygen levels be kept above 10kPa (Hall, 1997; Arbour, 1998), with arterial oxygen saturation
over 90% at all times (Wong, 2000).
Problems with oxygenation can be improved with the addition of positive end expiratory pressure
(PEEP) in intubated and ventilated patients, although this should be used judiciously as it can cause
ICP to rise due to the increase in physiological dead space caused by overdistension of normally
compliant lungs (Hickey, 1997).

Pre-oxygenation before suctioning should be mandatory (Hall, 1997), and each pass of the catheter
limited to 10 seconds, with appropriate sedation to limit the (inevitable) transient rise in ICP (Johnson,
1999).
Current trends aim to normalise carbon dioxide levels at 4.5kPa, while maintaining a pH of between
7.35 and 7.45 (Hall, 1997).
Care should be taken to ensure endotracheal tube tapes are not causing venous compression around
the neck, and that the head and neck are kept in neutral alignment to optimise venous drainage and
return (Hall, 1997).
Haemodynamic/fluid management The minimum monitoring required for a critically head-injured
patient should include continuous arterial blood pressure monitoring (rather than non-invasive
methods in order to enable measurement of CPP), core body temperature, respiration rate and pattern
and continuous ECG. These patients may develop arrhythmias due to induced hypothermia and/or
electrolyte imbalances (Arbour, 1998). ICP monitoring should be employed in head-injured patients
who are ventilated and paralysed where neurological deterioration cannot be readily observed clinically
(Chitnavis and Polkey, 1998).
It is important to avoid dehydration because in pyrexial, hypermetabolic patients fluid losses can be
significant (Arbour, 1998). Generally, 5% dextrose, which acts as free water is avoided, as these
patients are at risk of cerebral oedema, and a lowered serum sodium predisposes to this condition
(Metheny, 1996). Therefore serum electrolytes and osmolality must be regularly monitored, with the
nurse being particularly alert to the development of sodium imbalances. Very accurate fluid balance
documentation, urinary catheterisation and blood electrolyte and clotting monitoring are required.
In certain instances, mannitol, an osmotic diuretic, may be used to decrease ICP and increase CPP by
creating an osmotic gradient, drawing water out of the brain tissue and producing an osmotic diuresis
(Hall, 1997). Under such circumstances, it is vital to measure serum osmolality, which should not be
allowed to exceed 310mOsm/kg (Wong, 2000), as the diuresis from mannitol administration may
exacerbate hypovolaemia and hypotension (Metheny, 1996).
Temperature control In head-injured patients with hypoxia and ensuing ischaemia, the oxygen
demand of brain tissue escalates (Chambers, 1999). The brains metabolic rate increases by
approximately 7% for each degree centigrade increase in temperature (Johnson, 1999). This elevated
metabolism increases cerebral blood volume, thereby increasing ICP (Hickey, 1997). There may also
be damage to the temperature-regulating centre in the hypothalamus, which may cause body
temperature to fluctuate (Wong, 2000).
ECG monitoring and regular electrolyte observation is essential in these treatments, as hypothermia
stimulates cellular uptake of potassium which is then reversed in re-warming and can cause overshoot
hyperkalaemia (Chambers, 1999).
There appears very little evidence to support the use of induced hypothermia (Chambers, 1999), and
a recent study by Clifton et al (2001) concluded that a body temperature decreased to 338C within
eight hours of injury was not effective in improving outcomes in patients with severe brain injury.

Blood glucose control Hyperglycaemia is known to exacerbate cerebral lactic acidosis (Wong, 2000)
and consequently aggravates cerebral ischaemia in head injury. Therefore glucose solutions should be
avoided, and initially hourly blood sugar monitoring/insulin infusion implemented to keep blood
glucose below 11mmol/L (Hughes, 2000).
Positioning Positions that restrict venous drainage from the brain through the internal jugular vein
may cause a significant rise in ICP (Johnson, 1999). In a comprehensive review of the literature, Beitel
(1998) found that elevation of the head from 15 to 30 degrees was associated with a mean decrease
in ICP in all patients. There was no statistically significant impact on CPP between 15 or 30 degrees,
but elevation of the head to 60 degrees produced a significant reduction in CPP. This may be
associated with the extreme hip flexion which occurs in this position as this is known to increase ICP
(Hall, 1997).
Beitel (1998), underlining that evidence-based practice can only occur if research evidence exists,
concludes that the only position that research has consistently shown to be acceptable is a head
elevation of 30 degrees. This is supported by Winkelman (2000).
Nutritional support Severe head injury is associated with a hypermetabolic state with, in some
cases, the metabolic rate increasing by as much as 40 to 100% (Hinds and Watson, 1996). It is
therefore important to begin feeding as early as possible, preferably enterally. The feeding tube should
always be passed via the orogastric route in head-injured patients, unless a basal skull fracture has
been definitively ruled out (Withington, 1997).
General nursing care
Although research on the effects of environmental stimuli on ICP is limited, it is recommended that the
presence of unpleasant stimuli is reduced as much as possible (Johnson, 1999).
The sedative agent propofol is often used in head-injured patients, as it reduces cerebral metabolic
rate and cerebral blood flow (BMA/RPSGB, 2001). Its popularity is in part due to its short half-life and
effectiveness before unpleasant procedures such as pulmonary suctioning, change of position and
mouth care.
Gentle touch and massage may also be beneficial (Arbour, 1998), with family participation thought to
be highly effective (Hall, 1997).
Conclusion
Nursing care of the head-injured patient can present many challenges for the critical care nurse and,
as a consequence, a thorough knowledge of the dynamics of ICP and the factors associated with its
increase is required (Johnson, 1999).
There is much debate surrounding many treatments in these patients, such as the level of
hyperventilation (if any) required and the use of induced hypothermia. However, much of the research
available on the adverse effects of nursing activities (such as mouth care, positional changes) on ICP
is dated. In these times of evidence-based practice there is clearly a need for further research to be
undertaken in many areas in the care of the head-injured patient.

ACTIVITY 1
Look at a diagram of the brain, for example that provided by Tortora and Grabowski (2001) or in a
textbook in your local health-care library.
- Identify the 12 cranial nerves, their location and their function
- Review the neurological transmitter system, including synaptic activity and neuropeptides and their
function
- Explain the formation and circulation of cerebrospinal fluid
- Identify arterial and venous blood flow through the brain
ACTIVITY 2
Arrange a visit to the accident and emergency department or radiology/imaging department at your
place of work, or local to your practice. Ask for a member of the senior nursing staff (for example an
emergency nurse practitioner) or medical/technical staff to discuss head CT scans and skull X-rays
with you. Most A&E departments will have a teaching pack available on this area for training and
education and should be able to show you some good examples of a fractured skull, haematoma,
cerebral haemorrhage and mid-line shift.
ACTIVITY 3
A male patient is admitted to your ward following a road traffic accident and has sustained a head
injury. The CT scan shows a small localised haematoma and the patient is awaiting a bed in a regional
neurology unit for surgical treatment. The patient can be roused but is not fully conscious; he is
thirsty but has a high blood sugar; he is anxious and wants to walk around; and he has a fever.
What are your care priorities for:
- Neurological assessment and management
- Haemodynamic and temperature assessment and management
- Fluid and electrolyte assessment and management
ACTIVITY 4
Review the following drugs which may be used in patients with neurological conditions with a
colleague and pharmacist and identify the indications for use, mode of action, side-effects and
therapeutic monitoring. How would the affects of ageing affect both neurological function and the use
of these drugs?
- Mannitol for cerebral oedema
- Propofol for sedation

- Levodopa (used in parkinsonism)

- Aspirin (anti-platelet agents and heparin)
- Diazepam (used in status epilepticus)
- Phenytoin (anti-epileptic medication)
- Carbamazepine (for trigeminal neuralgia)

Arbour, R. (1998) Aggressive management in intracranial dynamics. Critical Care Nurse 18: 3, 30-40.
Beitel, J. (1998) Positioning and intracranial hypertension: implications of the new critical pathway for nursing
practice. Canadian Association of Critical Care Nurses 9: 4, 12-16.
British Medical Association/Royal Pharmaceutical Society of Great Britain. (2001) British National Formulary
(No 41). London: BMA/RPSGB.
Chambers, S. (1999) Induced hypothermia for head injury. Nursing in Critical Care 4: 3, 112-116.
Chitnavis, B., Polkey, C. (1998) Intracranial pressure monitoring. Care of the Critically Ill 14: 3, 80-84.
Clifton, G., Miller, E., Choi, S. et al. (2001) Lack of effect of induction of hypothermia after acute brain injury. New
England Journal of Medicine 344: 8, 556-563.
Flint, G. (1999) Head injuries. British Journal of Theatre Nursing 9: 1, 15-21.
Hall, C. (1997) Patient management in head injury care: a nursing perspective. Intensive and Critical Care Nursing
13: 329-337.
Hickey, J. (1997) The Clinical Practice of Neurological and Neurosurgical Nursing. Philadelphia, Pa: Lippincott.
Hinds, C., Watson, D. (1996) Intensive Care: A concise textbook (2nd edn). London: Saunders.
Hudak, C. (1998) Critical Care Nursing: A holistic approach (7th edn). Philadelphia, Pa: Lippincott.
Hughes, R. (2000) Neurological Emergencies (3rd edn). London: BMJ Publishing.
Johnson, L. (1999) Factors known to raise intracranial pressure and the associated implications for nursing
management. Nursing in Critical Care 4: 3, 117-120.
Metheney, N. (1996) Fluid and Electrolyte Balance (3rd edn). Philadelphia, Pa: Lippincott.
Moore, P., Knowles, M. (1999) Jugular venous bulb oxygen saturation monitoring in neuro critical care. Care of
the Critically Ill 15: 5, 163-165,

Opie, L. (1991) Drugs for the Heart (3rd edn). Philadelphia, Pa: Lippincott.
Tortora, G.J., Grabowski, S.R. (2001) Principles of Human Anatomy (9th edn). Chichester: John Wiley & Sons.
Withington, S. (1997) Textbook of Intensive Care. London: Chapman and Hall.
Winkelman, C. (2000) Effects of backrest position on intracranial and cerebral perfusion pressures in traumatic
brain-injured adults. American Journal of Critical Care 9: 6, 373-380.
Wong, F. (2000) Prevention of secondary brain injury. Critical Care Nurse 20: 5, 18-27.
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