Care of patients with brain injury in the critical care environment | nursing times

Richard Hughes, RN. Senior Staff Nurse, Intensive Care Unit, St Thomas’ Hospital, Guy’s 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). 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 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._ 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._