rain 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 Battle’s 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 brain’s 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.