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Neurological care 

Neurological care
Chapter:
Neurological care
Author(s):

Heather Baid

, Fiona Creed

, and Jessica Hargreaves

DOI:
10.1093/med/9780198701071.003.0008
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date: 25 September 2020

Neurological assessment

If an actual or potential neurological abnormality has been identified during a general ABCDE assessment (see Neurological care p. [link]) or while monitoring the patient, a more detailed and focused neurological assessment can provide further information to guide clinical management.

Focused health history

Subjective information about the neurovascular history can be taken from the patient if they are awake, or from other sources (e.g. family, caregivers, or patient notes).

Neurological symptom enquiry

  • Headaches.

  • Dizziness.

  • Vertigo.

  • Fainting.

  • Seizures.

  • Numbness and tingling.

  • Weakness.

  • Visual disturbance.

  • Hearing loss.

  • Tinnitus.

  • Balance problems.

  • Memory change.

  • Loss of sense of smell and/or taste.

Focused physical assessment

  • Table 8.1 provides a summary of a neurologically focused assessment, although a full assessment is not relevant for sedated patients, in whom the findings could be potentially misleading.

  • Table 8.2 lists the tests that relate to the cranial nerves.

  • Only assess sedation level and pupil responses for sedated patients.

Table 8.1 Neurologically focused assessment

Higher functions

Cranial nerves

Motor–sensory

  • Mentation

  • Speech

  • Gait

  • Coordination

  • Testing of cranial nerves I–XII

  • (see Table 8.2)

  • Movement

  • Sensation

  • Reflexes

Table 8.2 Cranial nerve examination

Cranial nerve

Nerve name

Normal function

Tests

I

Olfactory

Smell

Ask if there are problems with smell or taste

II

Optic

  • Visual acuity

  • Visual fields

  • Near and distant vision

  • Confrontation test

  • II

  • III

  • Optic

  • Oculomotor

  • Pupils: sense

  • Pupils: react

Pupils—equal, round reactive to light (direct and consensual)

  • III

  • IV

  • VI

  • Oculomotor

  • Trochlear

  • Abducens

Eye movements

  • Follow finger—H shape

  • Check for nystagmus and ptosis

V

Trigeminal

  • Motor: jaw

  • Sensory: face

  • Jaw movements

  • Sensation in three facial divisions

VII

Facial

Face movements

Raise eyebrows, close eyes tight, puff cheeks, whistle, smile

VIII

Vestibulocochlear

  • Hearing

  • Balance

  • Whisper test (ability to hear whispering)

  • Romberg’s test (stand with eyes closed)

  • IX

  • X

  • Glossopharyngeal

  • Vagus

Pharynx

  • Swallowing ability

  • Check uvula is in midline

XI

Spinal accessory

  • Trapezium

  • Sternocleido-mastoid

Raise shoulders and turn head against resistance

XII

Hypoglossal

Tongue movement

  • Stick out tongue

  • Move tongue from side to side

Mentation

  • Assess consciousness:

    • alertness

    • awareness of self and surroundings

    • responsiveness.

  • Assess cognition:

    • sensory input

    • orientation to person, place, and time

    • information storage (short- and long-term memory)

    • information processing (judgement, reasoning).

  • Use tools and scoring systems such as the GCS (see Neurological care p. [link]), AVPU, and CAM-ICU (see Neurological care p. [link]) as appropriate to the clinical context.

  • If the patient has long-term mentation dysfunction, consider whether there is further mental and functional decline due to a new and acute neurological abnormality.

Speech

  • Clarity.

  • Volume.

  • Content.

  • Ability to express thoughts.

Gait

  • Posture—symmetry, ability to stay upright.

  • Weight-bearing.

  • Gait pattern—normal, limping, shuffling, uncoordinated.

  • Head-to-toe gait.

Coordination

  • Ask the patient to touch your finger and then to touch their nose.

  • Opposition test—thumb tip touches each fingertip individually.

  • Rapid alternating movements—flipping hand back and forth on opposite palm.

  • Rub heel up and down opposite shin.

Motor–sensory

  • Tone:

    • Assess the tonicity of arms and legs through passive movements.

    • Hypotonicity—flaccid muscles.

    • Hypertonicity—rigidity, contractures, spasticity, stiff muscles.

  • Power:

    • Arm drift—ability to keep the arms stretched out with palms up and eyes closed.

    • Assess strength against resistance of arms and legs.

  • Sensation:

    • Assess the ability to feel light touch without paraesthesia throughout the arms and legs.

    • Assess the ability to identify painful stimuli.

  • Reflexes:

    • Assess for the presence of deep tendon reflexes using a tendon hammer—biceps, triceps, supinator, knee, and ankle.

    • Plantar reflex—rub an object from the heel of the foot up the outer edge and across to the big toe (the normal response in adults is downward flexion of the toes).

Causes of key abnormalities

  • Change in level of consciousness and/or cognition.

  • Pupil abnormalities.

  • Sensation abnormalities.

Laboratory investigations

The following blood and laboratory tests may be useful:

  • FBC

  • U&E

  • LFTs

  • clotting

  • arterial blood gas analysis, including lactate

  • glucose.

Glasgow Coma Scale (GCS)

Appropriate clinical assessment of neurological status provides the nurse with the most sensitive measure of neurological deterioration. The Glasgow Coma Scale (GCS) is the tool generally used by nurses in the UK to assess neurological function.

Unfortunately this tool becomes less reliable when the patient is artificially sedated with medication. However, it is essential that every critical care nurse has an adequate understanding of the GCS and its potential limitations in critical illness. It consists of three assessment areas—eye opening, verbal response, and motor function. Tables 8.3, 8.4, and 8.5 summarize the responses and their associated scores. The maximum possible score is 15 and the minimum possible score is 3.

Table 8.3 GCS: eye opening

Descriptor

Score

How to assess

Spontaneous

4

  • Eyes open spontaneously when beginning assessment

  • No need to talk or touch the patient to stimulate eye opening

To speech

3

  • Patient opens their eyes to normal voice

  • No need to raise voice or shout

To pain

2

Patient opens their eyes to painful stimuli. This should be either trapezius squeeze or supraorbital pressure (if the patient has no facial fractures)

None

1

No response

Table 8.4 GCS: verbal response

Descriptor

Score

How to assess

Orientated

5

Patient is orientated to time, place, and person and can therefore specify:

  • the month and year

  • where they are

  • who they are

Confused

4

Patient is unable to specify the above coherently, but can talk in sentences. Content may be inaccurate

Inappropriate words

3

Patient utters only occasional words, no sentences noted in speech, may use expletives

Incomprehensible sounds

2

No word formation is noted. Patient may moan, groan, or cry out

None

1

No verbal response; include tracheostomy and endotracheal patients in this category

Table 8.5 GCS: motor response

Descriptor

Score

How to assess

Obeys commands

6

Patient is able to obey a simple commend such as ‘Squeeze my hand and let go’ or ‘Move your fingers.’ Best response only is scored. No need to differentiate between left and right

Localizes to pain

5

When painful stimuli are applied to the trapezius muscle, patient moves their hand to above the area to localize the pain source

Flexion to pain

4

Similar to localization, but patient does not move hand above painful stimuli, but there is a movement towards stimuli

Abnormal flexion to pain

3

Patient flexes arm at elbow and rotates wrist simultaneously. Indicative of nerve damage

Extension

2

Represents severe damage at brainstem level. Patient extends or straightens limbs. Arms may be rotated inwards

None

1

No response. May indicate paralysis, deep coma, or drug-induced coma

Teasdale and Jennet1 designed the GCS to be used alongside other neurological assessments. These include:

  • pupil response

  • comparative motor assessment

  • physiological indicators.

It is important to note that once the patient is sedated the critical care nurse is more reliant on pupil changes and physiological status.

Pupil responses

Pupil changes are attributable to pressure on the third cranial nerve (oculomotor nerve), and normally indicate pressure that may be a result of the early stages of tentorial herniation. Initial changes occur ipsilaterally (on the same side as injury), but later changes are contralateral (on the opposite side to injury). Pupil changes tend to present progressively. Initial and later changes are as follows:

  • Pupil shape becomes ovoid.

  • Pupil begins to dilate ipsilaterally, but still reacts to light.

  • Pupil fixes ipsilaterally.

  • Contralateral changes occur.

Physiological changes

There is a pattern of physiological changes as intracranial pressure increases. This pattern is referred to as Cushing’s triad, and represents the body’s attempt to compensate for rising intracranial pressure and the effects of increasing pressure on the brainstem. Changes include:

  • hypertension with a widening pulse pressure

  • bradycardia caused by midbrain compression

  • alterations to respiratory rate (may not be apparent in ventilated patients).

Comparative motor assessment

Motor assessment is part of the GCS, but during GCS assessment ‘best motor function’ is tested. Comparative motor function testing is observing for differentiation in sides; therefore this test is looking for signs of contralateral weakness or hemiparesis. Contralateral changes occur because the nerve fibres cross over at the decussation of pyramids in the medulla oblongata. Subjective assessment of limb power may be unreliable, so it is normally preferable to use an objective assessment. Details of an objective assessment are shown in Table 8.6.

Table 8.6 Objective limb assessment tests

Neurological classification

Criteria

Normal power

Patient can match resistance; therefore they are able to hold limb up despite moderate attempts to push limb down

Mild weakness

Patient can hold limb up against mild resistance, but this may be overcome if resistance is increased

Severe weakness

Patient is able to move limb, but not against resistance

Flexion, extension, no power

Tested as in GCS using painful stimuli

Other signs of rising intracranial pressure

It is important that the critical care nurse also monitors the patient for other signs that may indicate a rising ICP, including fluid and temperature regulation problems.

Diabetes insipidus

Diabetes insipidus may occur as the intracranial pressure rises. As tentorial herniation begins, pressure increases around the area of the hypothalamus and pituitary gland. Pressure on the posterior part of the pituitary gland inhibits the production of antidiuretic hormone, and massive diuresis occurs. Therefore it is important to observe for any increases in urine output that are not attributable to increased fluid intake (e.g. from volume resuscitation). Synthetic antidiuretic hormone may be administered to prevent hypovolaemia, which would worsen cerebral blood flow and potentially further increase ICP.

Pyrexia

Temperature increases may also reflect increasing pressure on the hypothalamus. However, they may also indicate the presence of infection, so should be viewed alongside the patient’s white cell count and other markers of infection.

Reference

1 Teasdale G and Jennett B. Assessment of coma and impaired consciousness: a practical scale. Lancet 1974; 2: 81–4.Find this resource:

Monitoring

Alongside assessment of neurological status using the GCS and associated tools, some critically ill patients may require more advanced neurological monitoring. This is especially important once the patient is sedated, as traditional forms of assessment then become less reliable. A number of monitoring tools are available for this. They include:

  • intracranial pressure monitoring

  • cerebral (brain) oxygen monitoring

  • transcranial Doppler monitoring

  • electroencephalogram (EEG)

  • sedation monitoring.

Intracranial monitoring

Intracranial pressure is the pressure exerted within the cranium by the brain, the blood, and the cerebrospinal fluid. Therefore if one of these three components changes, the pressure within the cranium (i.e. the ICP) will alter. Although the Monro–Kellie hypothesis describes the ability for some compensation to occur, this is relatively limited, so it is important to have an accurate reflection of ICP in some critically ill patients.

Normal ICP

  • Normal ICP is generally considered to be < 10 mmHg.

  • ICP of > 20 mmHg is normally treated in critical care.

  • Prolonged increases in ICP are associated with increased neurological damage and increased mortality rates.

Cerebral perfusion pressure

Although ICP may be useful in the management of the critically ill patient, cerebral perfusion pressure (CPP) may provide a better guide to brain perfusion. CPP is calculated by the monitor if ICP measurement is in situ. The calculation generally used is CPP = MAP – ICP. Normal CPP is 70–90 mmHg.

ICP and CPP measurements are normally utilized to:

  • diagnose cerebral pressure and perfusion problems

  • monitor the effects of medical and nursing interventions on ICP

  • enable calculation of CPP

  • guide treatment plans.

ICP monitoring

Several types of monitoring tools are available. The gold standard is considered to be ventricular monitoring, where the ICP probe is inserted into the lateral ventricles. The benefit of intraventricular systems is that CSF drainage may be facilitated to reduce an increased ICP.

Other types of ICP monitoring include subdural monitoring and parenchymal monitoring.

Risks associated with ICP measurement include:

  • infection

  • haemorrhage

  • poor positioning

  • malfunction

  • obstruction.

Brain tissue oxygenation monitoring

The need to monitor brain oxygen levels directly has led to the development of tools that can measure (among other parameters) brain tissue oxygen levels.

These tools provide values for the partial pressure of brain oxygen (PbtO2). This gives more accurate information about oxygen delivery and demand, and may be used to measure local areas of oxygenation within the brain. This may then be utilized to guide therapy.

  • Normal PbtO2: 25–50 mmHg.

  • Ischaemic PbtO2: < 15 mmHg

  • Brain cell death PbtO2: < 5 mmHg.

These monitors are usually ‘multimodal’, and have the facility to measure local brain temperature and ICP.

When using systems that measure brain oxygenation it is important to remember that this information must be considered alongside other variables to provide a holistic picture of the patient’s condition.

Transcranial Doppler

The transcranial Doppler is a non-invasive tool that utilizes ultrasound technology to measure blood velocity in the cerebral arteries (usually the middle cerebral artery, but it can also assess the anterior and posterior cerebral arteries, the ophthalmic artery, and the internal carotid artery).

The Doppler works by emitting a signal from a probe which generates a wavelength signal as it is reflected by the red blood cells. This in turn is converted to a waveform which provides important information about the blood flow in that vessel. The Doppler machine is able to provide information about systolic, diastolic, and mean blood flow velocity. It may be used in several different groups of patients to provide information to guide treatment. Uses include:

  • assessment of vasospasm and hyper-perfusion states in patients with subarachnoid haemorrhage and traumatic brain injury

  • estimation of cerebral perfusion pressure when invasive monitoring is not or cannot be used

  • determination of the adequacy of collateral blood flow during carotid artery surgery

  • assessment of embolisms in patients with stroke or transient ischaemic attack (TIA).

Electroencephalograms

The electroencephalogram (EEG) may be a useful tool for highlighting some problems in neurological patients. However, it is important to note that it does require skilled interpretation to determine changes to the patient. Put simply, the EEG measures voltage fluctuations within the brain. This activity is recorded by using surface or needle electrodes and is then converted to a trace on the EEG monitor. Within critical care areas it may be used:

  • to monitor cerebral activity

  • to monitor patients with epilepsy, especially when muscle relaxants are being used, as these may prevent outward signs of seizure activity

  • to confirm the diagnosis of epilepsy

  • to help to predict the outcome for a patient in a coma

  • as an adjunct in determining brainstem death (not part of the formal process for determining brainstem death in the UK; see Chapter 19)

  • to monitor cerebral activity when using barbiturates (thiopental, phenobarbitone, phenobarbital) in head injury patients.

Sedation monitoring

Sedation monitoring may be utilized within critical care to assess the patient’s level of sedation. One of the most commonly used tools for sedation monitoring is the Bispectral Index (BIS).

In some neurological patients it may be desirable to keep the patient heavily sedated (especially during the acute phase when ICP management is a significant issue). However, increasingly it is becoming more desirable to keep sedation levels to a minimum to prevent complications associated with over-sedation. Over-sedation within critical care is associated with:

  • an increased incidence of ventilator-associated pneumonia

  • longer patient stays

  • the development of acute delirium.

Traditionally, EEGs have been used in specialist areas to determine brain function, identify burst suppression, and provide an indication of levels of sedation. However, these require specialist interpretation and are time consuming to analyse correctly.

Sedation monitoring was originally used in operating theatres, to ensure that effective levels of sedation were maintained throughout surgical procedures. However, many critical care units now utilize this technology to asses sedation levels in critically ill patients.

Sedation monitoring provides a non-invasive method of assessing objective criteria for the effectiveness of sedation based on the EEG trace.

  • For the purpose of simplification, three elements of the EEG trace (amplitude, frequency, and phase) are converted into a numerical value from 0 to 100 (see Box 8.1).

  • This removes the need for specialist interpretation, and makes interpretation of the EEG data much easier.

  • The numerical value (from 0 to 100) provides an indication of the level of sedation achieved by means of medication.

Measurement of sedation levels by sedation monitoring may therefore be useful for a number of purposes, including:

  • avoidance of over-sedation

  • monitoring burst suppression in patients with epilepsy

  • monitoring burst suppression in patients on barbiturate infusions

  • ongoing research into its value as an early prognostic tool for traumatic brain injury.

However, it is suggested that although sedation monitoring remains a useful indicator, there are a number of factors that may make the readings unreliable.2 These include:

  • interference from other medical devices

  • changes induced by some medications

  • some neurological pathologies.

Although sedation monitoring does provide some useful data which may enable decisions to be made about sedation levels in critically ill patients, Bigham and colleagues2 suggest that figures derived from monitoring should not be used in isolation, and that other indicators should also be taken into account.

Reference

2 Bigham C, Bigham S and Jones C. Does the bispectral index monitor have a role in intensive care? Journal of the Intensive Care Society 2012; 13: 314–19.Find this resource:

Traumatic brain injury

Definition

Traumatic brain injury occurs when there is damage to the brain as a result of trauma. Trauma may be caused by:

  • acceleration injuries, in which a moving object strikes the head

  • acceleration and deceleration injuries, in which the head strikes a stationary object

  • coup and contrecoup mechanisms of injury, in which the brain moves backward and forward within the cranial cavity

  • rotational injuries, in which neurons within the brain are rotated and stretched

  • penetration injuries, in which a sharp object penetrates the brain.

Head injuries are classified in several ways. A key classification is into primary and secondary injuries.

  • Primary injury occurs at the time of trauma. The effects of primary injury may be irreversible.

  • Secondary injury occurs after the initial event and worsens the initial damage. Secondary injury may be caused by hypoxia, hyercapnia, hypotension, infection, ischaemia, cerebral oedema, seizures, or hyperglycaemia. Much of the management of the head-injured patient is geared toward prevention of secondary damage.

Alongside the classification into primary and secondary injuries, head injuries may also be categorized according to the area affected.

  • Extradural haematoma—a collection of blood between the skull and the outside of the dura, often as a result of middle cerebral artery laceration. Patients often present with a brief period of lucidity followed by rapid neurological deterioration. The arterial bleed may quickly compromise the patient and cause herniation. Therefore prompt treatment is required.

  • Subdural haematoma—a collection of blood between the dura and the arachnoid layer, often caused by tearing of the bridging veins. It may present as an acute, subacute, or chronic injury. It has a worse prognosis than extradural haematoma.

  • Contusions—caused by laceration of vessels in the microvasculature, which results in bleeding or bruising into the brain tissue. Cerebral contusions may develop into an intracerebral haematoma.

  • Intracerebral or intraparenchymal haematoma—a collection of blood within the parenchyma. It may be caused by trauma or hypertension (stroke), and it can result in delayed neurological deterioration.

  • Subarachnoid haemorrhage—a collection of blood within the subarachnoid space. It may be caused by an aneurysm or by tearing of the microvessels in the arachnoid layer as a result of trauma. The patient may require cerebral angiography to exclude an aneurysmal bleed.

  • Diffuse axonal injury—caused by tearing of the neuronal axons. It is normally associated with rotational and acceleration–deceleration injury. It usually worsens during the first 12–24 hours. The patient may present in a deep coma with little alteration to the initial CT scan. Later scans may show severe cerebral oedema.

Assessment findings

Patients will present with:

  • changes to neurological function noted from in-depth neurological assessment

  • deteriorating levels of consciousness (those with a GCS score of < 8 normally require intubation)

  • changes on the CT scan

  • possible haemodynamic changes (hypertension, bradycardia).

Treatment

Treatment aims to prevent secondary injury and should follow an ABCDE approach.

  • The patient’s ability to maintain their airway should be assessed.

  • The patient should be intubated if the GCS score is < 8.3

  • Intubation may also be necessary if the patient requires scanning and cannot cooperate due to decreasing levels of consciousness. Intubation might also be deemed necessary for inter-hospital transfer to a specialist centre.

  • Adequate respiratory assessment is vital in all patients. This group of patients may be susceptible to aspiration pneumonia, especially if consciousness was lost prior to hospitalization.

  • Care should be taken to maintain oxygen saturations above 95%. This may require supplemental oxygen.

  • Consideration must be given to other significant injuries that might have an impact on respiratory function.

  • If the patient is intubated, mechanical ventilation will be required.

  • Arterial blood gases may be manipulated using ventilation. High levels of CO2 will increase ICP. Low levels will reduce cerebral blood pressure. Normal parameters are usually as follows:

    • PaO2: 13 kPa

    • PaCO2: 4.5–5 kPa.

  • Ventilated patients should have optimum levels of sedation and analgesia to prevent increases in ICP.

  • Chest physiotherapy and regular turning are required to reduce the likelihood of chest infection and associated hypoxia. Sedation may be required prior to the commencement of chest physiotherapy. Pre-oxygenation may be required prior to suctioning.

  • Patients should be nursed at 30° to avoid VAP.

  • Care should be taken with positioning if the patient has a suspected spinal injury.

  • Cardiovascular and fluid assessment is required for all patients.

  • Continuous cardiac monitoring should be commenced for all patients.

  • Fluid replacement may be given to initially increase blood pressure. This should be isotonic in nature, and 5% glucose should be avoided (as it will increase blood glucose levels and potentially cause fluid shifts and/or the development of cerebral oedema).

  • Fluid output should be monitored carefully. A sudden increase in output may be suggestive of diabetes insipidus.

  • In patients with severe head injury, blood pressure is normally artificially elevated with inotropes to maintain cerebral perfusion pressure. In patients in whom CPP is not recordable (i.e. those without ICP monitoring) it may be desirable to aim for a higher mean blood pressure using inotropic support.

  • Temperature should be monitored carefully. Pyrexia will increase oxygen demand and potentially worsen cerebral oedema.

  • Manipulation of temperature using therapeutic hypothermia may be required in an attempt to reduce cerebral oedema.

  • Blood electrolytes should be closely monitored for signs of abnormalities.

  • VTE assessment and prophylaxis will be required.

  • Regular neurological assessment using the GCS, pupil size, limb assessment, and cardiovascular changes should be conducted at least hourly for patients with a GCS score of > 9.

  • Changes in neurological assessment findings should be escalated immediately.

  • In patients who are sedated, neurological assessment will be dependent upon pupil assessment, cardiovascular changes, and potential changes in fluid output. Pupil assessment should be performed at least hourly, or more often if the patient’s condition deteriorates.

  • Patients should receive appropriate levels of sedation and analgesia. Boluses may be required prior to care delivery, but care should be taken to avoid sudden drug-related hypotension.

  • When ICP monitoring is being used, care should be taken to maintain ICP and CPP within set parameters. If the ICP rises, a stepwise approach should be taken to determine the cause of the increase, and appropriate treatment to reduce the ICP should be initiated. Table 8.7 describes a stepwise approach to ICP reduction.

  • Medical intervention should be sought if ICP remains elevated despite attempts to reduce it.

  • Quick and timely intervention should be provided if ICP remains high. Table 8.8 describes the emergency management of raised ICP.

  • Care should be taken to ensure that consideration is given to other injuries that may have resulted from trauma. An advanced trauma life support (ATLS) survey (see Neurological care p. [link]) should have been conducted in the Emergency Department, and other specialists involved as required.

  • Patients will require early establishment of nutritional support. This is likely to be enteral, and care should be taken to avoid nasogastric tube insertion in patients with skull fractures.

  • Medication may cause a tendency to constipation, so early assessment of elimination needs and appropriate medication is essential.

  • Psychological care and communication should be provided for the patient and their family.

  • Pressure area assessment and appropriate interventions will be required.

Table 8.7 Stepwise approach to reducing ICP

Intervention

Rationale

Has pupil assessment changed?

May indicate worsening neurological status. Inform medical team. Consider emergency treatment such as mannitol/hypertonic saline

Has patient position changed?

Patients need to be nursed in neutral alignment to promote venous return from the cerebral circulation. Patient should be nursed at 30° head-up angle (unless contraindicated)

Are the endotracheal tapes too tight? Is the neck collar too tight?

This will restrict venous return and increase ICP

Is the patient showing signs of distress? Is the patient adequately sedated?

Consider increasing sedation to reduce ICP. Take care not to reduce blood pressure as a result of increasing sedatives

Is blood glucose level elevated?

Hyperglycaemia may increase cerebral oedema and should be avoided

Are arterial blood gases within set parameters?

Consider whether recent changes in ventilation have altered CO2 levels. Liaise with anaesthetists to maintain within set parameters

Table 8.8 Emergency management of raised ICP following consultation with medical staff

Potential intervention

Rationale

Consider drainage of CSF if patient has appropriate ICP-monitoring system

Removal of CSF may reduce ICP. Lumbar puncture is not appropriate, as this may cause tentorial herniation

Manipulate arterial blood gases to reduce CO2 levels

A reduced CO2 level may reduce ICP. However, prolonged reduction will have a detrimental effect on cerebral blood and should be avoided

Administer osmotic diuretic

This may provide a short-term solution to cerebral oedema, but care should be taken to avoid hypotension due to fluid depletion. Serum osmolality should be monitored, as this intervention is unlikely to be effective if osmolality is high

Consider therapeutic hypothermia

Lowering the body temperature will reduce cerebral oxygen requirements

Consider barbiturate coma therapy

This may lower ICP, as it reduces cerebral oxygen requirements and may be neuroprotective. It is a longer-term solution, as barbiturate infusions have a long half-life

Consider decompressive craniectomy

Surgical intervention to reduce ICP has been shown to be effective. It is only available in specialist neurosurgical centres

Reference

3 National Institute for Health and Care Excellence (NICE). Head Injury: triage, assessment, investigation and early management of head injury in children, young people and adults. CG176. NICE: London, 2014. Neurological care www.nice.org.uk/guidance/cg176Find this resource:

Subarachnoid haemorrhage

Definition

A subarachnoid haemorrhage is a collection of blood in the subarachnoid space. It may be caused by trauma (see Neurological care p. [link]) or be due to bleeding into the subarachnoid space. Bleeding is usually caused by rupture of a cerebral artery aneurysm, but may also be caused by arteriovenous malformation, hypertension, and tumours. At the time of the bleed, blood is forced into the subarachnoid space. Mortality and morbidity remain issues in the management of subarachnoid haemorrhage, and complications include:

  • aneurysmal rebleeding

  • cerebral vasospasm

  • sodium imbalance (syndrome of inappropriate antidiuretic hormone or cerebral salt wasting)

  • communicating hydrocephalus.

Assessment

Patients with subarachnoid haemorrhage may present with:

  • a violent, sudden ‘thunderclap’ headache

  • signs of cranial nerve dysfunction

  • nausea and vomiting

  • signs of meningeal irritation (neck stiffness, photophobia, pain in the back and neck, nausea and vomiting)

  • neurological dysfunction. This may include:

    • hemiparesis or hemiplegia

    • cognitive deficits

    • speech disturbances

    • deteriorating GCS score

    • Cushing’s triad related to cerebral oedema development.

Generally patients will be admitted to critical care if they:

  • are at high risk of deterioration

  • have a poor-grade aneurysm according to the World Federation of Neurosurgeons Scale (WFNS)4

  • are presenting with deteriorating neurological function

  • are unable to protect their own airway.

The WFNS (alongside other scoring systems)4 is used to determine the severity of the bleed and to guide treatment and predict morbidity and mortality.

Additional assessments may include:

  • CT scan

  • CT angiography (CTA)

  • MRI scan

  • cerebral angiogram

  • lumbar puncture (unless there is raised ICP).

Treatment

Definitive treatment is to secure the aneurysm to prevent rebleeding, as the mortality and morbidity rates are high. Statistical data suggest that as many as 30% of patients will rebleed.5 Treatment may be endovascular or surgical, and includes:

  • Guglielmi detachable coils (GDC)

  • balloon remodelling

  • surgical clipping of the aneurysm.

Following successful intervention to secure the aneurysm, care should be based on an ABCDE approach.

  • The patient’s ability to maintain an airway should be assessed.

  • Generally, if the GCS score is < 8, intubation may be desirable.

  • Adequate respiratory assessment is vital in all patients. Breathing may be compromised by the use of analgesia for pain control of the severe headache.

  • Care should be taken to maintain oxygen saturations above 95%. This may require supplemental oxygen.

  • If the patient is intubated, mechanical ventilation will be required.

  • The patient may be at risk of developing neurogenic pulmonary oedema, so careful assessment and chest auscultation are essential.

  • Arterial blood gases may be manipulated by the use of ventilation. A usual target gas would be PaO2 13kPa and normal CO2 value.

  • Sedation and analgesia should be administered to reduce pain and promote patient comfort. Care should be taken not to decrease the blood pressure, as this may reduce cerebral perfusion pressures and increase the likelihood of complications.

  • Once the aneurysm has been secured, the patient should be nursed at 30° to increase venous return and avoid VAP.

  • Cardiovascular and fluid assessment is required in all patients. Patients are particularly at risk of sodium imbalances, especially hyponatraemia. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is dilutional hyponatraemia due to water retention. Cerebral salt wasting (CSW) is hyponatraemia caused by fluid and sodium depletion. Correct diagnosis and treatment of SIADH and CSW are essential, and their symptoms and management are described in Table 8.9.

  • Continuous cardiac monitoring should be commenced on all patients.

  • Dehydration should be avoided. Fluid replacement should be given to maintain normal blood volume prior to intervention. Usual fluid intake following an aneurysmal bleed would be 3–4 L. This should be isotonic in nature, and 5% glucose should be avoided.

  • ECGs may show ST-segment depression. The exact mechanism is not known, but care should be taken to initially eliminate a cardiac cause of ST depression.

  • Regular neurological assessment using the GCS, pupil size, limb assessment, and cardiovascular changes should be conducted at least hourly. Early changes may be subtle but require medical attention (e.g. pronator drift).

  • Changes in neurological assessment findings should be escalated immediately.

  • In patients who are sedated, neurological assessment will be dependent upon pupil assessment, cardiovascular changes, and potential fluid output alterations. Pupil assessment should be performed at least hourly, or more often if the patient’s condition deteriorates.

  • ICP may be monitored in some critically ill patients. Quick and timely intervention should be provided if ICP remains high.

  • Oral nimodipine should be administered to prevent the development of vasospasm.

  • Patients should be carefully monitored for signs of vasospasm. There are several potential treatments for vasospasm, including:

    • induced hypertension (caution is needed with cardiac patients)

    • balloon angioplasty

    • intra-arterial vasodilator therapy

    • studies utilizing medication such as clazosentan, IV magnesium, and statins are ongoing.

  • Patients should be monitored for signs of the development of communicating hydrocephalus.

  • Regular pain assessment and management with appropriate analgesia are paramount.

  • VTE assessment and prophylaxis will be required. However, low-molecular-weight heparin is not advisable until the aneurysm has been secured.

Table 8.9 Symptoms and management of SIADH and CSW

SIADH symptoms

CSW symptoms

  • High CVP

  • Low serum sodium levels

  • Low urine output

  • Normal specific gravity

  • Low serum osmolarity

  • Normal urinary sodium levels

  • Absence of peripheral oedema

  • Low CVP

  • High urine output

  • Normal specific gravity

  • High or normal serum osmolarity

  • Variable urine osmolarity

  • High urinary sodium levels

SIADH management

CSW management

Fluid restriction flowing correct diagnosis of SIADH

Hypertonic saline

  • Care should be taken to increase the sodium levels slowly to avoid complications of fast correction, such as central pontine myelinolysis.

  • During treatment the patient should be monitored closely for signs of cerebral vasospasm or neurological deterioration.

References

4 Drake CG et al. Report of World Federation of Neurological Surgeons Committee on a universal subarachnoid hemorrhage grading scale. Journal of Neurosurgery 1988; 68: 985–6.Find this resource:

5 Hickey J. The Clinical Practice of Neurological and Neurosurgical Nursing, 6th edn. Wolters Kluwer Health/Lippincott Williams & Wilkins: Philadelphia, PA, 2009.Find this resource:

Seizures (status epilepticus)

Definition

Status epilepticus is a clinical term that refers to:

  • continuous seizures lasting at least 5 min

  • two or more seizures without a period of consciousness between them.

The most common type of status epilepticus is generalized or tonic–clonic seizures. However, it is important to note that other seizure types may fit into this category.

Causes

There are many factors that may cause the patient to develop status epilepticus. These include:

  • pre-existing epilepsy

  • non-compliance with anticonvulsant therapy

  • traumatic brain injury

  • subarachnoid haemorrhage or stroke

  • CNS infection

  • cerebral tumours

  • cerebral hypoxia

  • metabolic abnormalities

  • drug toxicity

  • chronic alcoholism.

Assessment

The patient will present with signs of generalized seizures that either:

  • are longer than 5 min in duration or

  • involve no recovery of consciousness between seizures.

Treatment

Management should follow an ABC approach.

  • The patient should be positioned lying on their side to maintain their airway.

  • An artificial airway may be inserted, but only if it is possible to do so without injuring the patient. This will not be possible during the tonic phase of the seizure.

  • Patients with refractory status epilepticus may require intubation.

  • Suctioning may be required to maintain airway patency.

  • High-flow oxygen should be administered.

  • Respiration should be assessed, and if no respiration is apparent, appropriate respiratory resuscitation should be commenced.

  • Patients who are intubated will require mechanical ventilation.

  • Cardiovascular status should be evaluated with an appropriate CVS assessment.

  • Intravenous access should be secured.

  • IV fluids may be required.

  • A neurological assessment should be conducted and the cause of the seizure identified where possible.

  • Anti-epileptic drugs should be administered (see Table 8.10).

  • It may be necessary to commence:

    • EEG therapy

    • vasopressors to increase ICP

    • ICP monitoring.

  • Acidosis should be corrected if present.

  • Appropriate critical care support should be provided until the patient is stable.

Table 8.10 Anti-epileptic drugs for status epilepticus, adapted from NICE guidelines6

Stage

Anti-epileptic drug

Early

  • Lorazepam IV (this may be repeated after 10–20 min)

  • If patient normally takes regular anti-epileptic medication this should be administered

Established

  • The following drugs may be administered:

  • Phenytoin

  • Fosphenytoin

  • Phenobarbital bolus

Refractory

  • General anaesthesia maintained with midazolam or propofol

  • Thiopental infusion (up to 3 days)

  • EEG monitoring

  • Medication should be continued until 12 h after the last seizure noted on EEG

Reference

6 National Institute for Health and Care Excellence (NICE). The Epilepsies: the diagnosis and management of the epilepsies in adults and children in primary and secondary care. CG137. NICE: London, 2012. Neurological care www.nice.org.uk/guidance/cg137/resources/guidance-the-epilepsies-the-diagnosis-and-management-of-the-epilepsies-in-adults-and-children-in-primary-and-secondary-care-pdf

Guillain–Barré syndrome

Definition

Guillain–Barré syndrome (GBS) is an acute inflammatory neuropathy. There are several subtypes of GBS, including:

  • acute inflammatory demyelinating polyneuropathy

  • acute motor axonal neuropathy

  • acute motor and sensory axonal neuropathy

  • Miller Fisher syndrome.

The neuropathy is caused by an acute demyelination process triggered by an autoimmune response. GBS has three phases:

  • acute

  • plateau

  • recovery.

Causes

It is thought that a number of different factors may be responsible for triggering an autoimmune response. These include:

  • acute viral illness

  • Campylobacter jejuni infection

  • post vaccination (rare).

Assessment findings

GBS is generally characterized by:

  • bilateral motor weakness

  • bilateral flaccid paralysis

  • areflexia.

Patients may also present with:

  • respiratory failure

  • dysphagia

  • pain

  • autonomic dysfunction (arrhythmias, paroxysmal hypertension, urinary retention).

GBS has no effect on:

  • levels of consciousness

  • cognitive function

  • pupillary signs.

Treatment

Treatment is largely supportive in nature, but patients may receive high-dose intravenous immunoglobulin or plasmapheresis in an attempt to shorten the duration of the illness. Intravenous immunoglobulin (IVIG) is usually the treatment of choice as it is easier to administer. Plasmapheresis may be undertaken in specialist centres. Supportive treatment will follow an ABCDE approach.

  • Respiratory assessment is vital to detect early signs of respiratory failure.

  • Tracheal intubation may be indicated if:

    • bulbar function is compromised

    • forced vital capacity is deteriorating

    • the patient is showing signs of respiratory failure or tiring.

  • Early insertion of a tracheostomy is normally indicated to promote patient comfort and reduce the use of sedatives. Later the tracheostomy will be useful for facilitating weaning.

  • Respiratory assessment is needed to monitor for complications of intubation, such as VAP.

  • Careful CVS assessment should be undertaken to monitor for signs of autonomic dysfunction.

  • Treatment for paroxysmal hypertension is not normally required.

  • Fluid may be required to treat any hypotensive episodes.

  • The patient may be prone to postural hypotension.

  • Monitor for signs of arrhythmias (bradycardia or tachycardia).

  • Careful fluid balance should be maintained.

  • Excessive fluid loss from diaphoresis may require replacement.

  • Neurological assessment is needed to determine signs of deteriorating or improving neurological function.

  • Careful pain assessment is required, as the patient may experience severe pain. Often this may be neurogenic in nature and require appropriate neurogenic medication such as nortriptyline, amitriptyline, or pregabalin. Other analgesics such as paracetamol and non-steroidal anti-inflammatory drugs may be useful, although sometimes pain is refractory to these and stronger analgesia may be required.

  • Perform careful assessment of the limbs to prevent secondary complications. Regular physiotherapy is essential. The patient may require limb splints or supports to promote normal posture and prevent complications.

  • Sleep patterns should be monitored. Sleep deprivation may be caused by alterations to sleep pattern resulting from autonomic changes.

  • Psychological support is essential, as the patient will be ventilated yet cognitively intact. As a result they often appear to be extremely anxious and agitated. The nurse’s visible presence and positive reinforcement about the potential for recovery are essential.

  • The patient should be referred to a speech and language therapist for support with communication.

  • VTE assessment and appropriate prophylaxis are required.

  • All necessary supportive care should be provided (see Chapter 3).

The patient should be monitored carefully for complications, which may include:

    • urinary retention

    • constipation

    • paralytic ileus

    • postural hypotension

    • autonomic disturbances.

Myasthenia gravis

Definition

Myasthenia gravis is a chronic disease of the neuromuscular junction caused by an autoimmune response that destroys and therefore reduces the number of acetylcholine receptor sites at the postsynaptic membrane.

The severity of the myasthenia depends upon the number of sites destroyed. A decrease in the number of receptor sites will affect muscle contraction. This may result in some degree of muscle weakness, severe muscle weakness, or muscle fatigue.

The course of the illness is extremely variable, and in some patients muscle weakness may develop over a period of time, whereas others may present with rapid deterioration of muscle function.

When the intercostal muscles are affected, the patient develops dyspnoea and may require ventilation.

Diagnosis

Diagnosis is dependent upon:

  • patient history and physical examination

  • positive edrophonium test

  • antibody titre for acetylcholine receptor

  • repetitive muscle stimulation

  • electromyography (EMG)

  • MRI and/or CT scan of the thymus gland.

Causes

The exact cause of myasthenia gravis is uncertain. It is known to be caused by an autoimmune reaction, but it is not clear what triggers the autoimmune response. Studies have shown that a high proportion of patients with myasthenia gravis have an enlarged thymus gland or a thymus tumour.

Assessment findings

The patient will present with muscle weakness and fatigue. In myasthenia gravis, patients may develop gradual onset, the severity of which is classified from type 0 to 5. Patients are normally admitted to critical care units if they have any of the following:

  • a myasthenic crisis (a sudden relapse of myasthenic symptoms)

  • a cholinergic crisis (an event precipitated by the toxic effects of cholinergic inhibitor drugs used for the treatment of myasthenia)

  • thymectomy for post-operative observation.

Patients with a myasthenic crisis will present with symptoms of:

  • decreased bulbar functioning

  • decreased function of the muscles of ventilation (intercostal and diaphragm)

  • decreased muscle use in all muscles.

Therefore patients will have symptoms that include:

  • increasing general weakness

  • severe fatigue

  • dysphagia

  • neck muscle weakness

  • respiratory muscle weakness

  • decreased vital capacity

  • respiratory failure.

Patients with a cholinergic crisis will typically present with:

  • initial gastronintestinal problems such as cramping and diarrhoea (muscarinic effects)

  • later signs (nicotinic effects) that are rapid in nature, and include:

    • severe muscle weakness

    • increased pulmonary secretions

    • acute respiratory failure.

A edrophonium test may be used to distinguish between myasthenic and cholinergic crises. However, if the patient is unable to cooperate it may not be appropriate. The edrophonium test should only be performed by a skilled healthcare professional, and atropine (antidote to edrophonium) must be available.

Treatment

Treatment is largely supportive in nature, but medical treatments may be given to reduce the time required in critical care.

Treatments for myasthenic crisis include the following:

  • Immunosuppression—steroids and other immunosuppressant drugs may be given. Prednisolone is normally the drug of choice. It is normally given until the patient starts to show signs of improvement, and then gradually weaned to a maintenance dose. Azathioprine is usually given if prednisolone is contraindicated.

  • Plasmapheresis or IVIG may be given. Plasmapheresis is usually only undertaken in specialist centres. IVIG is generally the treatment of choice as it is easier to administer.

Supportive care will utilize an ABCDE approach:

  • In severely ill patients, priority is given to airway and respiratory assessment to determine the need for intubation and ventilation.

  • An in-depth respiratory assessment including forced vital capacity should be undertaken.

  • The quality of the patient’s voice may also indicate the degree of deterioration.

  • Intubation may be required if the patient has worsening bulbar function.

  • Assessment for signs of aspiration pneumonia is important, especially in patients with decreased bulbar function.

  • Cardiovascular assessment is necessary to determine the effect of the deterioration on CVS function.

  • Fluid should be given to ensure that the patient remains hydrated.

  • Accurate fluid balance should be noted.

  • Neurological assessment is needed to determine the effects of the crisis on normal functioning. This may include:

    • assessment of motor function and strength in limbs

    • extra-ocular muscle assessment

    • head and neck strength

    • quality of voice (if extubated).

  • Medication should be reviewed. Anticholinergic drugs should be given in the event of a myasthenic crisis, but withheld and gradually reintroduced in the event of a cholinergic crisis.

  • VTE assessment and appropriate prophylaxis are required.

  • All supportive care should be provided (see Chapter 3).

Meningitis

Definition

Meningitis is acute inflammation of the meninges caused by an infectious agent. It involves the pia and arachnoid layers of the meninges, the subarachnoid space, and the CSF within the subarachnoid space. Causative bacterial organisms include:

  • Streptococcus pneumoniae

  • Neisseria meningitidis

  • Haemophilus influenzae

  • Listeria monocytogenes.

Patients may also develop viral meningitis, but this is often a mild form and very rarely requires admission to critical care. Most patients who are admitted to critical care will present with bacterial meningitis. The mortality rate for bacterial meningitis remains high, and many patients who survive are left with significant morbidities, including hydrocephalus, deafness, blindness, cognitive deficits, and epilepsy.

Causes

Meningitis occurs when bacteria gain access to the meninges. This may result from contamination through:

  • blood-borne routes

  • spread of nearby infection (e.g. ear or sinus infection)

  • CSF contamination during medical or surgical procedures (e.g. lumbar puncture, ICP monitoring).

Assessment findings

The initial signs of meningitis are associated with meningeal irritation, and include:

  • severe headache

  • stiff neck

  • signs of meningeal irritation

  • altered level of consciousness

  • photophobia

  • nausea and vomiting

  • hypersensitivity

  • seizures

  • changes in electrolyte levels (especially sodium).

Later signs of meningitis are linked to increasing ICP and the development of sepsis. Signs of increasing ICP include:

  • hypertension

  • bradycardia

  • changes to respiration.

Signs of sepsis include:

  • raised body temperature (> 38°C)

  • increased white cell count

  • increased C-reactive protein levels

  • increased serum lactate levels

  • blood pressure changes, which may initially be masked by rising ICP.

Different types of meningitis may have noteworthy signs and symptoms.

Meningococcal meningitis

  • Rapid deterioration of neurological status.

  • Petechial rash.

  • Areas of ecchymosis or skin discolouration.

Diagnosis

This may include:

  • patient history

  • lumbar puncture (contraindicated if ICP is rising)

  • CT scan

  • markers of infection and inflammation

  • blood culture.

Treatment

Bacterial meningitis is a medical emergency and prompt intervention is needed. Patients require immediate treatment with intravenous antibiotics, and local protocols will dictate which antibiotics are used. Administration of antibiotic therapy should not be delayed until the results of CSF and blood cultures are known. The suspected causative organism should be treated with appropriate antibiotics until definitive results are available.

It may be necessary to isolate the patient to prevent the spread of the disease. Close family members and recent contacts may require prophylactic antibiotics. Hospital infection control policies should be followed in relation to isolation procedure, and appropriate advice provided to family members and recent contacts.

The management of patients with severe meningitis is complex, and requires collaborative assessment and management. Care planning should take into account the possible complications of:

  • increased ICP

  • rapidly deteriorating neurological status

  • onset of severe sepsis

  • respiratory failure

  • seizures

  • electrolyte imbalance

  • hydrocephalus

  • possible adrenal insufficiency (meningococcal infections).

Supportive care should adopt an ABCDE approach (see also Neurological care p. [link] if the patient is presenting with signs of sepsis).

  • The patient’s ability to maintain their airway should be assessed.

  • It is likely that the patient will require intubation and ventilation.

  • Ventilation management should follow sepsis protocols (see Neurological care p. [link]).

  • Manipulation of ventilation may be required to control ICP (see Neurological care p. [link]).

  • The patient should be nursed with their head elevated to 30° to minimize the risk of VAP and reduce ICP.

  • Regular respiratory assessment is needed to determine the impact of sepsis on the respiratory system.

  • Regular chest physiotherapy is required to prevent complications associated with intubation.

  • Cardiovascular and fluid assessment is required in all patients.

  • Continuous cardiac monitoring should be commenced in all patients.

  • Blood pressure should be carefully maintained within prescribed parameters with initial fluid resuscitation and/or vasopressors.

  • Fluid balance should be closely monitored, and fluid resuscitation should follow sepsis guidelines if there is evidence of development of sepsis (see Neurological care p. [link]).

  • If the patient is pyrexial, antipyretic medication should be given (once blood cultures have been taken) to reduce the body temperature and cerebral oxygen requirements.

  • Assessment for disseminated intravascular coagulation (DIC) and other clotting abnormalities may be required.

  • Regular neurological assessment using the GCS and limb assessment should be undertaken if appropriate. If the patient is sedated, ventilated pupil changes and other physiological signs of rising ICP should be noted.

  • Changes in neurological assessment findings should be escalated immediately.

  • In patients who are sedated, neurological assessment will be dependent upon pupil assessment, cardiovascular changes, and potential changes in fluid output. Pupil assessment should be performed at least hourly, or more often if the patient’s condition deteriorates.

  • Patients should receive appropriate levels of sedation and analgesia.

  • Where ICP monitoring is being utilized, care should be taken to maintain ICP and CPP within set parameters. If ICP rises, a stepwise approach should be taken to determine the cause of the increase, and appropriate treatment to reduce ICP should be initiated.

  • Medical intervention should be sought if ICP remains elevated despite attempts to reduce it.

  • The patient should be assessed for signs of pain, and appropriate analgesia provided.

  • Reduced lighting may be required if the patient has severe photophobia.

  • All necessary supportive care should be provided (see Chapter 3).

Delirium

Definition

Delirium may be defined as an acute fluctuating disturbance of consciousness and cognition. Delirium generally develops over a short period of time and fluctuates over time. It is thought to occur in up to 80% of critically ill patients.

There are two main subtypes of delirium:

  • hypoactive—characterized by withdrawal, lack of response, and apathy

  • hyperactive—characterized by restlessness, agitation, and labile emotions.

Delirium may also exhibit mixed presentation—that is, both hypo- and hyperactive. This type is more difficult to identify in practice.7

Causes

A number of theories have been proposed to explain the pathophysiological development of delirium, including:

  • neurotransmitter imbalance

  • inflammatory processes

  • cerebral oxygenation or metabolism

  • amino acid concentration.

However, the exact pathophysiological cause is not yet known.

Risk factors have been identified, and these may be divided into host factors and illness factors (see Table 8.11).

Table 8.11 Risk factors for the development of delirium

Host factors

Illness factors

  • Age > 70 years

  • Substance misuse

  • Cognitive impairment

  • Depression

  • Hypertension

  • Smoking

  • Visual impairment

  • Hearing impairment

  • Alcohol abuse

  • Recreational drug abuse

  • Acidosis

  • Anaemia

  • Fever, infection, sepsis

  • Hypotension

  • Metabolic dysfunction

  • Respiratory disease

  • High degree of severity of illness

  • Immobility

  • Medications

  • Sleep deprivation

  • Post-operative

  • Increased bilirubin levels

  • Increased urea levels

  • Use of physical restraints

Assessment findings

Patients with delirium may present with:

  • impaired concentration

  • slow responses

  • confusion

  • visual and/or auditory hallucinations

  • restlessness

  • agitation

  • sleep disturbances

  • lack of cooperation

  • withdrawal

  • mood disturbances

  • altered communication.

Most clinical areas will use an assessment tool such as the Confusion Assessment Method (CAM) (see Neurological care p. [link]). In critical care areas it is more helpful to use the CAM-ICU to help to confirm the diagnosis.

Treatment

Initial treatment should focus on trying to establish the cause of delirium. It is helpful to rule out obvious causes of delirium, such as:

  • acute infection

  • neurological causes (e.g. cerebral oedema)

  • electrolyte disturbances

  • metabolic abnormalities

  • renal impairment

  • medication side effects

  • alcohol withdrawal.

Management will then focus on preventing harm to the patient and developing effective communication strategies.

Prevention of harm may require:

  • verbal de-escalation processes

  • non-verbal de-escalation processes

  • management of psychosis.

Communication and reorientation strategies may include:

  • regular reorientation to time, place, and person

  • contact with familiar people (family and friends), photos, and other significant objects

  • minimizing confusing stimuli

  • reducing isolation

  • correcting visual and hearing impairments

  • use of clearly visible clocks

  • early mobilization

  • attempts to maintain circadian rhythm

  • avoiding the use of physical restraints.

It may be necessary to medicate patients who are at risk of harm if other strategies fail. NICE7 recommends the short-term use of medications such as haloperidol or olanzapine. They advise that medication, if required, is started at the lowest clinically appropriate dose and titrated cautiously according to symptoms.

Reference

7 National Institute for Health and Care Excellence (NICE). Delirium: diagnosis, prevention and management. CG103. NICE: London, 2010. Neurological carewww.nice.org.uk/guidance/cg103Find this resource:

Further reading

Brummel NE and Girard TD. Preventing delirium in the intensive care unit. Critical Care Clinics 2013; 29: 51–65.Find this resource:

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