Cheshire and Mersey Critical Care Network

Neuro Critical Care Work Book

Workbook Series

Number: xx1

Created by

Helen Jones RGN, MSC, Local Service Improvement Lead and Senior Sister, the Walton Centre for

Neurology & Neurosurgery NHS Trust.

Acknowledgement: Professor P Eldridge, Neurosurgical Consultant, the Walton Centre for

Neurology & Neurosurgery NHS Trust

Version 1 May 2012

Status Final

Changes H Jones

Review date 2014 May

Author Helen Jones

Owner Cheshire and Mersey Critical Care Network

CONTENTS Page

2

Introduction 4

Terminology 9

Anatomy and Physiology 10

Neurological conditions in critical care 33

Neurological assessment 43

Traumatic Brain Injury 60

Sedation scoring 80

Subarachnoid haemorrhage 89

Competencies and records of supervised practice

INTRODUCTION

3

This workbook has been produced to assist healthcare professionals in critical care in caring for

patients with intracranial injury and disease. Many of these patients require admission to critical

care and application of subsequent treatments to prevent secondary problems.

The book provides information regarding normal physiology, pathophysiology and neurological

assessment.

To determine your competence you are required to complete the following: -

Attendance at formal Trust/Unit training sessions.

Successful completion of the workbook.

Competency assessment

How to use this workbook

The workbook is divided into sections. There are questions and activities included which form an

important part of your learning and training. Please attach separate sheets if needed. It is your

evidence of learning.

You will need to obtain and read several documents to assist you in completing this workbook and you

will require access to books and other reference materials (see bibliography). When completed this

workbook will form part of your evidence of learning, professional development and competence. Please

keep this package in your portfolio as it could be used to gain further credits at university or college and

assist in meeting KSF and national competency requirements.

To help you with this work book, you need to revise the following:

Physiology of the brain and spinal cord, GCS

4

Learning Outcomes

Having completed this pack you will be able to: -

State the gross functions of the nervous system

Demonstrate a basic understanding of neurological conditions which may require critical care

Assess a patient using the Glasgow Coma Scale

Demonstrate an understanding of the pathophysiology of head injury

Demonstrate understanding of raised intracranial pressure and treatment options

Demonstrate an understanding of sedation use in critical care

Demonstrate an understanding of Subarachnoid haemorrhage and treatment

Expanded Scope of Practice (Nursing)

Nursing the head injured and neurologically compromised patient requires advanced

understanding of physiology and the mechanism of injury not covered in nurse training. Additional

training is therefore required to ensure competency in this area.

In line with the Scope of Professional Practice (NMC, 2008) the Cheshire and Mersey Critical Care

Network views practice from the following two perspectives: -

Clinical Practice

Clinical practice may be defined as an aspect of care, which may be undertaken by

Nurses/Midwives/Others who accept accountability for their actions and feel competent to

undertake a procedure. There is no formal assessment for these practices but there may be aspects

of care, which require a period of supervised, guided practice. This should form part of

preceptorship/mentorship or supervision programmes.

5

Expanded Practice

An expanded scope of practice may be defined as an aspect of care which may be undertaken by

Registered Nurses who have undergone the specified training and assessment, accept

accountability for their actions, feel competent to undertake the aspect of care, and have the

authority of the Trust to do so.

Professional implications

The publication of The Scope of Professional Practice by the NMC (2008) was an acknowledgement

that practice takes place in a context of continuing change and development. The principles on

which any development in the scope of practice must evolve are as follows:

1. The interests of the patient must predominate.

2. The practitioner must maintain their knowledge, skill, and competence.

3. The practitioner must also acknowledge the limits of their knowledge, skill, and

competence.

4. The practitioner must not jeopardise standards and must comply with the Code of Conduct.

5. The practitioner must recognise their direct and personal accountability.

6. The practitioner must avoid inappropriate delegation.

Nurses are first and foremost legally responsible for each and every nursing action undertaken or

omitted, and must practice in accordance with the standard of care of a reasonably prudent nurse

practicing under the same or similar circumstances.

The law relating to negligence principally seeks to identify conduct that does not reach an acceptable

professional standard. The registered nurse owes the patient in her care an individual and personal

duty of care. The duty of care encompasses the professional, moral, ethical, and sociological sphere

within which nursing operates. Deviation from this in any way is negligence. The individual holds

6

primary liability for his or her own actions. If the patient suffers harm from the nurse’s negligent

action or omissions, that nurse remains primarily liable, and could be sued directly.

ACTIVITY 1

Locate the following documents and familiarise yourself with their contents:

NMC - Code of Professional Conduct

NMC - The Scope of Professional Practice

For all procedures consult The Royal Marsden Manual (Dougherty et al, 2004)

Trust/Unit incident reporting policy

Medical Device/Equipment Guidelines

Trust frameworks, guidelines, protocols and documentation related to neuro critical care.

NB. To help you with this workbook, you also need to revise the physiology of the nervous system.

ACTIVITY 2

Describe why you are undertaking learning in neuro critical care

- To update / increase clinical skills and knowledge.

- Part of personal development.

7

- Function as effective member of the Critical Care team

- Participate in attempts to reduce related clinical incidents as an effective knowledgable practitioner.

ACTIVITY 3

How will you demonstrate your knowledge and competence following this training?

- Completion and assessment of the workbook

- Attend related training sessions, courses and conferences

- Self-assessment and review of personal practice

- Professional Development and peer reviews

- Incident free and safe clinical practice

TERMINOLOGY

TBI Traumatic Brain Injury

GCS Glasgow Coma Scale

EVD Extra Ventricular Drain

ICP Intracranial pressure

CPP Cerebral perfusion pressure

8

CSF cerebrospinal fluid

MAP mean arterial pressure

CNS central nervous system

PNS peripheral nervous system

SAH Subarachnoid haemorrhage

Normal A&P of the nervous system – a brief overview

It is essential to have background knowledge of anatomy and physiology in order to effectively

deliver care. This knowledge will enable you to recognise the abnormal and ensure timely

interventions are initiated. In the following section there will be an overview of this complex system.

Further reading is suggested to consolidate learning.

Section objectives:

9

1. Identify the structures within the nervous system

2. Understand how impulses are transmitted

3. Identify functions of the nervous system

Introduction:

The nervous system is the mechanism by which the body responds to environmental and

physiological changes, and creates the basis for all voluntary activity. The mechanism is principally

electrochemical and virtually all the energy consumption of the nervous system is devoted to

maintaining this system. A reflection of this is that the brain uses 20% of the oxygen consumed by

the body, 15% of the cardiac output although being less than 1% of the total mass of the individual.

It is increasingly being realised that the brain is also a highly plastic system; much more so than

previously appreciated. Put very simply, the nervous system gathers information, acts on it and has

the ability to store it. It is divided into parts:

Peripheral – Cranial and spinal nerves that connect the body to the brain and spinal cord

Central – The brain and spinal cord

Autonomic – Part of the peripheral nervous system that controls automatic functions which have no conscious control, anatomically located within both the central and peripheral parts of the nervous system

fig 1 (mstrust.org.uk)

10

Nerve cells are called neurones and they are supported by neuroglia. Glial cells are located within

the central nervous system and provide a supportive medium, provide nutrients in particular for

synaptic function and have a role in repair after injury. They actually make up around 70% of brain

cells therefore it should come as no surprise that many brain tumours arise from glial cells. Glial cells

can be sub divided into types such as astrocytes and oligodendrocytes.

Myelinated cells conduct impulses more rapidly than others because they jump between junctional

stations called nodes of ranvier. Peripheral nerves and the 12 cranial nerves have this insulating

myelin sheath along the fibre, created by Schwann cells. For the central nervous system the myelin is

created by oligodendrocytes.

There are three types of neurones which ensure communication exists between the environment

and our body.

Motor neurone

Sensory neurone

Interneurone

Interaction between these neurones is critical for control.

The motor neurones act upon organs and muscles. Because they carry instructions from the brain

and they are efferent neurones. The impulse travels from the cell body, down the axon and

eventually to the organ or muscle it supplies.

The sensory neurone receives information from the environment such as heat, cold, pain, touch and

therefore is an afferent neurone.

Efferent = output Afferent = input

An example of this you can see literally with your own eyes is the consensual light reflex. If you

shine a pen torch in one pupil it will constrict. Look over to the other pupil and you will see that this

also has constricted at the same time. This is because the afferent message from the stimulated

retina has travelled to the brain and the efferent pathway via the oculomotor nerve III has sent a

message to the other pupil to respond in the same way. This is why it is important to look at both

eyes to compare responses when assessing reaction to light. Try it in the mirror! This is an example

of how the system of neurones modulates constantly according to stimulus.

11

Modulation can be described as ‘gating’. Another example is the gate theory relating to pain

perception. A nociceptor is a sensory receptor that sends signals that cause the perception of pain in

response to potentially damaging stimulus.

Fig 2

(http://faculty.washington.edu/chudler/pain.html)

The inhibitory neurone (I) will block or ‘gate keep’ and not allow signals to pass to the projection

neurone and on to the brain.

When the stimulus is simply non painful touch then the large fibres activate and the inhibitory neurone blocks the signal and there is no perception of pain.

When there is pain the signal is sent through the small nerve fibres to the projection neurone but this time the small nerve fibres block the inhibitory neurone and pain is perceived

Blocking pain or closing the pain gate is central to pain management. In chronic pain states this modulation may behave abnormally, sometimes becoming hypersensitive so that the pain persists long after the cause of the pain has been removed.

The interneurone transfers impulses, via synapses, between the sensory and motor neurones. At a simple level this creates reflex activity; when passed though the spinal cord to the brain via many “interneurons” it forms that basis of complex voluntary activity.

How is a nervous impulse transmitted?

12

Fig 3

Sodium and Potassium are charged ions. The inside of the cell is positively charged and the outside

of the cell is negatively charged. When sodium and potassium swap between the cell membrane and

the exterior of the cell this causes the electrical impulse to travel.

Once at the end of the cell the impulse must be carried across the gap (synapse) to the next cell.

Chemical transmitters are required to do this job. The electrical energy of the impulses releases the

transmitter into the narrow synaptic gap where the chemical binds to a specific receptor which

depolarises the nerve starting off a new electrical impulse in the next nerve. The same mechanism

activates muscles, where an efferent nerve fibre ends on a muscle – “the motor end plate”

Neurotransmitters include

Dopamine (low in Parkinson’s disease)

Serotonin

Acetylcholine (low in myasthenia gravis)

Adrenalin and nor-adrenaline

There are at least 50 neurotransmitters.

13

Fig 4

Activity:

What drugs do we use in critical care which affect chemical transmitters and in what situations? Write down as many as you can think of and read about how they act. Here is a starter:

1. Atracurium – a non-depolarising neuromuscular blocking drug used as a skeletal muscle

relaxant in rapid sequence induction for intubation. It blocks the effect of acetyl choline at

the motor endplate

2. ………………..

3. ………………..

4. ………………..

The peripheral nervous system.

14

This is divided into the autonomic nervous system which represents involuntary control of internal

organs such as blood vessels, cardiac muscles, smooth and visceral muscles; the ANS is further split

into the sympathetic and parasympathetic systems which work together to excite or inhibit

responses.

The somatic nervous system controls skeletal muscle, bones and joints.

Fig 5.

Organ Sympathetic System Parasympathetic System

Eye

Tear glands

Salivary glands

Lungs

Heart

Gut

Liver

Bladder

Dilates pupil

No effect

Inhibits saliva production

Dilates bronchi

Speeds up heart rate

Inhibits peristalsis

Stimulates glucose production

Inhibits urination

Constricts pupil

Stimulates tear secretion

Stimulates saliva production

Constricts bronchi

Slows down heart rate

Stimulates peristalsis

Stimulates bile production

Stimulates urination

Fig 6.

Somatic nervous system:

15

Reflex arc.

Fig 7. www.sciencegeek.net

The pain stimulus is transmitted up the afferent sensory neurone and then to the interneurone

within the spinal cord. The interneurone then relays the stimulus to the efferent motor neurone. The

muscle receives the stimulus and reacts. This reflex response can be elicited without the

involvement of the brain therefore does not reflect brain function and can be observed in a brain

dead patient. In order to increase reliability when testing a response to painful stimuli it is

recommended to locate a cranial nerve and exert pressure, this also increases reliability if there is a

high spinal injury.

16

Gross structures.

Fig 8

The brain and spinal cord are protected by bone (vertebrae and skull). Protection is further provided

by the meninges which exist in three membranous layers; the dural mater, arachnoid mater and pia

mater. In addition to these layers, the brain and spinal cord float in cerebrospinal fluid (CSF) which

circulates freely in the subarachnoid space. This fluid is produced at a rate of approximately 550ml

per day by the choroid plexus (about 70% of the total) and cells lining the ventricles. The fluid passes

out of the brain via the ventricles and there connecting channels, to pass over the surface of the

brain to be reabsorbed at the same rate into the venous sinuses. If there is a problem with

reabsorption such as blood from a subarachnoid haemorrhage clogging the system, then

hydrocephalus will develop (a build up of CSF). A lesion such as a tumour could also press down on

the communicating canals in the system and also cause hydrocephalus. A shunt can be inserted to

off load excess CSF. In the short term external ventricular drains can be used (EVD).

17

Fig 9 The CSF pathways.

The main network of arteries are found in the subarachnoid space. The four major arteries entering the skull are linked to form the Circle of Willis.

Fig 10. The Circle of Willis.

Cerebral aneurysms can form and if ruptured cause a subarachnoid haemorrhage.

The cerebrum.

The right and left cerebral hemispheres make up this structure. They are connected by the corpus

callosum. They receive afferent sensory information and send out efferent motor responses. The

cerebral cortex is a thin layer of cell nuclei (grey matter). White fibre tracts connect the nuclei to

synapse with other grey matter areas deeper in the brain.

18

http://www.bioon.com/book/biology/whole/image/1/1-6.tif.jpg Fig 11

Gyri are the worm like ridges which can be seen over the brain surface. Sulci are the grooves dividing

the gyri. Fissures are deeper divisions and there are fissures which are anatomically significant; the

Longitudinal fissure which divides the two hemispheres, the Transverse fissure which divides the

cerebellum from the cerebrum and the Sylvian fissure which divides the temporal lobe from the

frontal and parietal lobe.

The lobes of the brain.

Fig 12

19

Fig 13

Frontal Lobe

Primary motor cortex which controls motor movement of the opposite side of the body.

Fig 14

Representation of body of the motor strip of the frontal lobe. Not how the hands and feet and mouth have a larger representation.

20

Fig 15

Wernicke’s area (temporal lobe) – damage here would result in difficulty comprehending speech

(receptive dysphasia)

Broca’s area (frontal lobe) – Damage here would affect speech production although speech is

comprehended (expressive dysphasia)

The frontal lobe also controls emotions, regulates responses to social situations, controls executive decision making and goal directed problem solving.

The Parietal lobe.

Its major function is to integrate senses and provide spatial awareness. It processes tactile and

proprioceptive information, assists in visual cortex and motor communication, interprets taste

sensation. The body is represented in a sensory strip in a similar way to the motor strip:

21

Fig 16.

Note how the sensory parts of the body have a larger representation in the sensory strip of the

parietal lobe..

The occipital lobe.

This is the primary visual area. It interprets visual stimuli. The primary visual cortex processes size,

colour, light and motion.

The temporal lobe.

The main functions are; hearing, organisation and understanding language, memory formation and

retrieval.

All the lobes of the brain communicate with each other via feedback pathways. Further reading is

recommended to fully appreciate their functions.

The Diencephalon.

Within the brain are further structures with complex roles. The higher thought functions are to be

found nearer to the lobe surfaces and the more primitive and emotional functions can be found at

greater depths. Sometimes referred to as the ‘emotional brain’ this system is made up of grey

matter areas each with important roles. The Diencephalon is located above the brain stem.

22

Fig17

The AmygdalaStores emotional memories and has a role in producing and regulating hormone release for

emotional responses such as fight / flight .

The Hippocampus

Memory formation, classifying information, long-term memory storage, sense of space and location

are the main roles of this structure found deep in the temporal lobe.

The Hypothalamus

It is located deep within the brain and above the brain stem. It communicates closely with the

pituitary gland which controls many of the body’s functions via hormonal control. The Hypothalamus

has many roles:

Temperature regulation

Thirst and control of body water Appetite control

Endocrine control

Emotional reactions

Sleep and wakefulness

23

Stress response

The ThalamusThis is the relay station which receives afferent and efferent signals therefore the Thalamus the main

relay station in the brain. Most of the sensory signals; auditory, Visual, Somatosensory (from your

skin and internal organs), go through this region on their way to other parts of the brain for

processing. It also plays a function in motor control.

The basal ganglia.

Fig 18

Either side of the Thalamus are grey matter areas called the Basal Ganglia. The many areas have complex functions which include:

Control of the need to act upon an environmental stimuli such as hand washing when dirty, locking a door to keep safe.

Control of mood

Controlling automatic behaviours such as balancing when riding a bike

Control of movement

One of the main neuro transmitters used here is dopamine. It is degeneration in this area,

specifically the Substantia Nigra, which contributes to Parkinson’s disease.

24

The Brain Stem.

Fig 19

Mid brain

Pons

Medulla

Cranial Nerves III – XII have their nuclei in the brain stem.

Midbrain.

Is located above the pons and helps to regulate muscle tone, plays a role in auditory and visual

reflexes and co-ordination of movement.

Pons.

Main function is breathing regulation / respiratory drive.

Medulla Oblongata.

Merges into the spinal cord and includes important fiber tracts. It contains important control

centres:

Heart rate control

Blood pressure regulation

Breathing

Swallowing / gag

25

Cranial Nerves.

There are 12 pairs of cranial nerves. They do not cross over and so supply the same side of the body. III – XII originate in the brain stem.

Fig 20

Cranial Nerve: Major Functions:

I Olfactory smell

II Optic vision

III Oculomotor eyelid and eyeball movement, pupil constriction

IV Trochlear innervates superior obliqueturns eye downward and laterally

V Trigeminal chewing face & mouth touch & pain

VI Abducens turns eye laterally

VII Facial controls muscles of facial expression secretion of tears & salivataste

VIII Vestibulocochlear(auditory) hearing

26equilibrium, balance

IX Glossopharyngeal taste senses carotid blood pressure

X Vagus

senses aortic blood pressure slows heart rate stimulates digestive organstasteVocal cords

XI Spinal Accessory controls trapezius & sternocleidomastoidcontrols swallowing

XII Hypoglossal controls tongue movements

26

Key point: When brain stem death is suspected, the tests to diagnose brain death are focused upon examining the function of cranial nerves.

Activity:

Now log onto

www.aomrc.org. uk /.../42-a-code-of-practice-for-the-diagnosis-and-confirmation-of- death .

And read the document ‘A code of practice for the diagnosis and confirmation of death.’

Which cranial nerves are tested when confirming brain death?

……………………………………………………………………………………………………………..

…………………………………………………………………………………………………………….

…………………………………………………………………………………………………………….

…………………………………………………………………………………………………………….

Why is it important to monitor bloods and treat metabolic abnormalities such as a high sodium before carrying out brain stem tests?

……………………………………………………………………………………………………………….

……………………………………………………………………………………………………………….

What is the most important pre-condition for the diagnosis of brain death?

…………………………………………………………………………………………………..

Cerebellum

Fig 21

27

Is located in the posterior fossa of the skull. It is a vital part of the brain that communicates with the

higher brain and the peripheral nervous system by relays with the basal ganglia, being particularly

concerned with motor control, learned movements and balance. The final motor output from the

brain is from the motor cortex, through the thalamus (integrating the modulating inputs from the

cerebellum) to the upper motor neurones in the Pyramidal tract which cross in the front of the brain

stem (Pyramidal decussation) finally connecting via the corticospinal pathway to the lower motor

neurons in the anterior part of the spinal cord (lower brain stem for the cranial nerves).

The motor-cortico-spinal tracts cross over at the level of the medulla; the sensory pathways in the spinal cord. Many cerebellar functions are ipsilateral (control the same side of the body)

28

The main functions of this primitive part of the brain are:

Maintenance of Equilibrium

balance

posture

eye movement

Coordination of walking

Adjustment of Muscle Tone

Motor Leaning – Motor Skills

Cognitive Function

The posterior fossa structures lie beneath a tough shelf of dura around the level of the ear called the Tentorial Shelf. Above the shelf lie the four lobes. The area below the shelf is referred to as infratentorial or the posterior fossa. Because of the location of the cranial nerves in this area it is important to ensure the gag reflex and swallow are intact before allowing a patient to eat and drink if they have pathology or have had surgery in this location.

The Pituitary Gland

The master gland of the body sits in a central location in the brain and controls many body functions. It secretes hormones to maintain homeostasis including hormones that stimulate other endocrine glands in the body. Lesions on this gland can have devastating effects. Raised intracranial pressure can cause diabetes insipidus. This is not sugar diabetes; it is a disruption of water balance in the body. Antidiuretic hormone is no longer released and the body looses water at a rapid rate. Clinical features are:

Thirst

High urine output with a low specific gravity

Rising serum sodium

Rising blood osmolality

Low urine osmolality

The sodium in the body has not increased; it is simply the loss of water from the body that

causes sodium to be more concentrated. The treatment for diabetes insipidus is to administer

29

antidiuretic hormone, replace intravascular volume and also investigate and reverse the primary

cause which may be a tumour, infection or raised intracranial pressure.

The pituitary gland controls many hormones in the body and therefore disease of this gland can

manifest in many ways:

Thyroid dysfunction

Reproductive dysfunction

Growth dysfunction

Adrenal dysfunction

Fig 22

The Pineal Gland

A small structure in a central location in the brain. It is commonly calcified in adults. Briefly, the

role of this gland includes:

Melatonin production

Timing of sexual maturity

Circadian rhythm

30

Salt and Water Balance.

The brain communicates with the vascular system and renal system to regulate water balance in

the body. It is no surprise that damage to the brain can result in syndromes that result in an

imbalance of salt and water. We have already looked at diabetes insipidus, however, there are

other manifestations of imbalances which can also be life threatening.

SIADH

Syndrome of inappropriate antidiuretic hormone release. The blood osmolality is low because

water is being retained. Antidiuretic hormone release reduces water loss via the kidneys. Sodium

in the blood will appear low and the blood is more dilute. Normally ADH is secreted when

osmoreceptors pick up a high serum osmolality which signals dehydration. The kidney retains

water. If there is an inappropriate secretion of ADH water is retained. Urine output will be low,

the patient may be confused, lethargic and have signs of water toxicity. Low serum sodium could

result in seizures, cerebral oedema and eventually death.

Serum osmolality will be less than 270, CVP may be high.

The treatment includes; fluid restriction, sodium replacement, diuretics, treat reversible causes.

Low sodium should be gradually increased over days as rapid correction can cause pontine

demyelination.

Cerebral Salt Wasting Syndrome.

CSW means that the body is excreting salt in the urine. Salt has a high osmotic action so carries

water with it. This results in a large diuresis in addition to a low serum sodium. The patient will

be dehydrated, confused, hypotensive and deteriorating. Treatment includes fluid replacement,

sodium replacement and treatment of reversible causes.

Neuro intensive care units will have a chart like this one to aid diagnosis. Sometimes the patient is

referred to an endocrinologist for an opinion because syndromes can be hard to diagnose and have

complex presentations.

31

Epilepsy and the Intensive care

There is a high risk of developing seizures in any patient who is neurologically compromised. A

seizure represents an uncontrolled electrical spasm of activity within the cerebral cortex, causing

a massive increase in cerebral metabolic demand so that damage due to hypoxia may occur. The

brain is very sensitive to change. Seizures may manifest because of the trauma, tumour, CNS

infection, sub-dural empyema, electrolyte, metabolic imbalance or pre-existing epilepsy.

Seizures must be controlled as a matter of urgency. When there has been a witnessed seizure

following trauma, a loading dose of anticonvulsant will be prescribed and then the drug

continued regularly at a maintenance dose. If the patient has known epilepsy then urgent re-

assessment of medication is required. Anticonvulsant levels should be assessed regularly and

reversible causes of the seizure should be sought out. If the seizure activity does not terminate

this could mean airway compromise and the patient should be admitted to intensive care for

airway protection and seizure control.

Status Epilepticus is manifested by unrelenting and resistant seizures. These are potentially

lethal and control must be gained. Cerebral metabolism therefore oxygen consumption will be

high and could cause irreversible damage such as ischaemia. Because of the increased muscle

32

activity and brain activity a rise in lactate levels will be seen and body temperature which can

mimic sepsis. Treatment, if not terminated by loading with anticonvulsant is deep barbiturate

coma. Thiopental Sodium is used to ‘rest’ the brain and terminate the seizure activity while the

cause is reversed. Since this will also arrest respiration it is always accompagnied by intubation

and artificial ventilation. Usually this will also mean observation of brain wave activity using a

cerebral function monitor. This is a simple form of EEG and allows the intensive care team to

measure efficacy of treatment. Too much barbiturate will over suppress activity, and depress

cardiac function (therefore bloodpressure) and too little will not be effective. Barbiturate can

also interfere with pupil size and reactivity and can confound this neurological observation. It

also takes a prolonged period to wear off once the drug has been stopped.

Anticonvulsants such as phenytoin have a narrow therapeutic index and are protein bound, this

means that there is a high risk of toxicity and that plasma levels must be adjusted to albumin

levels. Some of the toxic side effects – eg problems with balance - are irrelevant in ITU in a

ventilated patient, and the priority is to halt the status epilepticus.

Activity

Look up and write the equation used to adjust phenytoin level to albumen:

33

Neurological conditions which may require critical care admission:

Guillian Barre Syndrome is an example of a neurological illness which can result in an intensive care

admission. This is an autoimmune disease which results in the destruction of the myelin sheath

(demyelination). This disruption slows the impulse and could actually cause cell body death if severe

resulting in permanent disability. Breathing difficulties and autonomic dysfunction mean severe

cases of this disease require intensive therapy. Treatment includes steroids, immunoglobulins and

plasmapheresis plus respiratory support. Guillian Barre syndrome may be triggered by a minor

illness such as a respiratory infection.

Symptoms:

Bilateral muscle weakness commonly starting in the legs (ascending).

Numbness and parasthesia

Clumsiness

Reduced reflexes

Deterioration in lung function

Severe cases my result in total paralysis at the height of the disease process. The patient will be

aware and very frightened. Sedation for tolerance during this phase is essential. Treatment is aimed

at removing harmful auto antibodies in the plasma (plasmapheresis), steroids to reduce

inflammation and IV immunoglobulins to reduce the effects of the autoantibodies attacking the

nerve sheath. Total recovery is possible, however, severe forms of the disease may result in

34

permanent disability. As the nerves re-gain function the patient can experience severe pain and

critical care teams may require specialist advice on pain management.

Specific nursing considerations:

Monitoring of forced expiratory volumes regularly is essential to detecting respiratory deterioration

in non ventilated patients. Be aware of swallowing difficulties and the risk of aspiration. Be aware of

severe pain as function improves. This disease can result in severe autonomic dysfunction; swings in

blood pressure, tachy / bradycardia can pose a threat as they can be difficult to treat due to

unpredictability.

Activity:

Visit http://www.nhs.uk/conditions/Guillain-Barre-syndrome/Pages/Introduction.aspx

And read about this syndrome.

Myasthenia Gravis

Is a neuromuscular disorder which means the nerve / muscle interface is affected (neuromuscular

junction). This is also a form of autoimmune disease. Myasthenia Gravis causes poor transmission

across the synapse, the receptor sites for the neurotransmitter acetylcholine (neurotransmitter) are

attacked / blocked by auto antibodies. Treatment includes pyridostigmine and steroids. A severe

deterioration may result in requiring respiratory support whilst steroids and immunoglobulins and

in some cases plasmapheresis are administered and adjustment of medication is made.

35

Pyridostigmine is an anticholonesterase which helps to increase the duration of transmission by

enhancing the effect of acetylcholine. There is no cure for this disease therefore symptom control is

the focus of treatment. In some cases a tumour of the Thymus gland plays a role in the disease

(detected by CT of the chest). The Thymus gland has a role in normal immune function. It is thought

that developing immune cells may receive the ‘wrong’ instructions and attack the receptor sites at

the synapse.

Specific nursing care considerations:

Monitoring forced expiratory volumes in non ventilated patients is essential to detect the trend of

deterioration. Be aware of swallowing difficulties and the risk of aspiration. Be aware that muscle

weakness can improve with rest and worsen with activity. Diarrhoea can be a problem as a specific

side effect of pyridostigmine.

Activity:

Visit the National Institute for Neurological Disorders and Stroke (www.ninds.nh.gov) and read

about myasthenia gravis.

36

The Spine.

This section is brief as there is a separate work book on this subject.

Fig 23

There are 31 pairs of spinal nerves.

37

Fig 24

The anterior (front) horn is where the efferent motor pathways exit the spine on their way to the body. Anterior horn cell disease is effectively motor neurone disease. The posterior horn (back) is where the sensory neurones enter the central nervous system to carry the afferent messages to the brain.

Spinal injury can be devastating and not only result in motor weakness but also autonomic dysfunction. Injury can change the way the body responds to certain drugs and therapies. A separate package on the spine will complement this learning resource.

Activity

Look up the term ‘autonomic dysreflexia’ in relation to spinal injury. Write a brief account below on how this may impact on stability and nursing activities.

38

End of Section Activity.

Maybe the deep structures within your brain have retained the information; time to find out.

1. What are the two main divisions of the nervous system?

A.

b.

2. Name the three types of nerves found in the nervous system

a.b.c.

3. Name the neurones that make up the afferent pathways

4. Name the neurones that make up the efferent pathways

5. What is the difference between efferent and afferent?

6. Which section of the spinal cord holds efferent fibres?

a. Anterior horn

b. Posterior horn

7. Name the divisions of the peripheral nervous system:

8. Name the four lobes of the brain:

39

a.

b.

c.

d.

9. Name three functions for each of these lobes:

a.

b.

c.

d.

10. If the patient had a lesion in Wernicke’s area what might be observed?

11. If the patient had a lesion in Broca’s area what might be observed?

12. What is the name of the main ‘relay’ station deep within the brain?

13. Name at least three functions of the hypothalamus

14. How many pairs of cranial nerves are there?

15 Name six functions of the brain stem

40

a.

b.

c.

d.

e.

f.

16 Fill in the missing words:

The Cerebellum is located in the ..........................of the skull. It is a vital part of the brain that

communicates with the higher brain and the peripheral nervous system by relaying to

the................ ................, .................... and ..................... neurones via a pathway called

the .............. ...............

17 A patient with Guillian Barre syndrome may require intensive care. Why would this patient have muscle weakness?

a. The brain has been attacked by antibodies and cannot function

b. The myelin sheath made of protein has been attacked by auto antibodies and cannot transmit.

c. There are multiple lesions in the spinal cord

d. There is a lack of neurotransmitter

18 What is the name of the gap between the cells which must be traversed by the nerve impulse?

19 Name three neurotransmitters.

41

a.

b.

c.

20 A patient with Myasthenia Gravis may require intensive care because of muscle weakness. Why are the muscles weak?

a. The myelin sheath is being broken down by auto antibodies.

b. The receptor sites of the nerve receiving the message across synapse are not effective

c. A stroke in the motor strip of the frontal lobe

21 The Pituitary gland is the master gland of the body. It has many complex functions. Name four ways in which disruption of pituitary function can manifest

a.

b.

c.

d.

22. SIADH can be characterised by:

a. High urine output and low sodium

b. Low urine output and low sodium

c. High urine output and high sodium

23. A low sodium and high urine output could be:

a. SIADH

b. DI

c. CSW

42

43

Neurological Observation in Critical Care

Well done. You have completed a whistle stop tour of the nervous system. Now it is time to look at the patient. How much do you know about the Glasgow Coma Scale. Are you confident to use it and interpret what you are seeing? Time to find out!

The following section is set out in a simple fashion so that the information can be read easily alongside rationale. Using your new knowledge of A&P You will now be able to make more sense of the observations you do.

Objectives for this section:

a. Understand the GCS observation tool and its limitations

b. Apply the tool and interpret results

c. Demonstrate an understanding of further clinical signs of raised intracranial pressure and how to detect them

The traumatic brain injury learning session follows the neurological observation session. It is following this section that you will be tested on your ability to tie the sections together and relate the information to patient care.

44

Neurological Assessment

‘ASSESSING AND RECORDING CONSCIOUS LEVEL FORMS A MAJOR PART OF NURSING ACTIVITIES…A RECORD OF NURSES’ OBSERVATIONS IS GREATLY SUPERIOR TO ANYTHING PRODUCED BY CONNECTING THE PATIENT TO A MACHINE.’ Teasdale 1975.

Developed by Teasdale and Jennett (1974), the Glasgow Coma Scale (GCS) is the tool used in most hospital and pre-hospital settings to assess level of consciousness (Dawes, et al 2007). The scale is not designed to be used in isolation but forms a major component of in-depth observation required for timely detection of neurological deterioration (NICE, 2007).

Frequent observation and recording of GCS concurrently with limb responses, pupil responses to light, blood pressure, pulse rate, oxygen saturation, respiratory rate, temperature and blood glucose monitoring complete this vital data set.

Differing techniques are often practised amongst nurses (Waterhouse, 2008), however, it is essential that assessment of the GCS is carried out using the same method to increase accuracy and control observer bias (Edwards, 2001).

The Glasgow Coma scale is comprised of evaluating three components each of which receive a score:

E = Eye opening (maximum = 4)

M = Motor response (best recorded) (maximum = 6)

V = Verbal response (maximum = 5)

MILD HEAD INJURY GCS 13 – 15

MODERATE HEAD INJURY GCS 9 – 12

SEVERE HEAD INJURY GCS 3 - 8

The highest point on the scale score is 15; the patient will be alert, orientated and have full limb power. The lowest point score is 3; there will be no response at all from each component. A base line GCS, pupil and vital sign assessment must be carried out at triage for all head injured patients. Regular monitoring thereafter will aid detection of deterioration which may be subtle over time. Prevention of secondary brain injury has primacy in the management of neurologically vulnerable patients; early detection and reporting of changes is a key role of the nurse (Hickey, 2009).

Limitations of the GCS:

If the patient is intubated / sedated

Tracheostomy – patient cannot speak

Local injury – eyes closed due to swelling

Focal neurological deficit – patient has expressive dysphasia

If the patient does not speak the same language as the assessor45

If the patient has taken analgesia/medication/alcohol

If the patient has learning difficulties (or a child)

Remember it is a scale and not a score – you should cite the result for each category, and although commonly, indeed routinely and mistakenly done it is not valid to add up the scores, or do any arithmetic on the values. Technically it is a non-parametric scale.

ACTION RATIONALE

Frequency of neurological observations

GCS assessment will be carried out by a

practitioner who has received training in the

techniques and has been passed as competent.

Observations should be performed and

recorded on a half-hourly basis until GCS equal

to 15 has been achieved.

Following assessment in A&E The minimum

frequency of observations for patients with GCS

equal to 15 should be as follows:

half-hourly for 2 hours

then 1-hourly for 4 hours

then 2-hourly thereafter.

If a patient with GCS equal to 15 deteriorates at

any time after the initial 2-hour period,

observations should revert to half-hourly and

follow the original frequency schedule (NICE,

2007).

This includes the full vital sign set: Bp, SA02,

pulse, resps, temp, GCS & pupil size and

reaction.

Inform medical staff of any deterioration without

delay.

It is recommended that nurses who are handing

Vigilance of the nursing team is vital for early

detection and treatment of deterioration thus

prevention of secondary brain injury and

improved prognosis.

The frequency of neurological observations is

determined by professional judgement

(Edwards, 2001). It is therefore essential that

decisions are made by a trained and competent

practitioner.

The condition of the patient, combined with

clinical judgement, should determine frequency.

The patient in A&E who has sustained a brain

injury must be observed frequently as early

intervention may prevent secondary injury.

Deterioration can be subtle in onset and the

patient requires detailed and frequent

observation.

If the patient is deteriorating there must be

assessment by an anaesthetist. Aspiration,

airway obstruction and subsequent lung

infiltration leads to hypoxia and secondary brain

injury therefore increased length of stay in

hospital and poor outcome.

46

over a patient perform the GCS together so a

‘shift change deterioration’ is not recorded.

In addition to a deteriorating GCS signs of raised

ICP include: headache, vomiting, seizure.

ACTION

A patient who is deteriorating and requires

transfer to CT / a specialist centre or has a GCS

less than 8 should be intubated.

RATIONALE

EYE OPENING –

Spontaneously 4 To speech 3 To pain 2 None 1 Eyes closed by swelling = C

Assess for eye opening by observing the patient

as you approach: eyes open spontaneously,

score 4.

If the patient’s eyes remain closed, say

something to elicit a response: eyes open,

score 3.

Speech, touch and finally pain is utilised.

If there is no response to speech, touch the

patient on hand, arm or shoulder and

shake, shout louder to elicit a response:

eyes open, score 3.

If there is no response, exert a peripheral painful

stimulus to the side of the finger nail.

eyes open, score 2.

If there is no eye opening following the

Assesses wakefulness, a function of structures

within the brainstem (Lindsay et al, 2004;

Waterhouse, 2005).

Spontaneous eye opening is an indication that

the arousal mechanisms within the brain are

Functioning (Teasdale, 1976).

If neuronal pathways are impaired due to

trauma or a rise in intracranial pressure, a

greater sensory stimulus is needed to evoke eye

opening (Edwards, 2001).

‘Central’ painful stimulus may result in the

patient grimacing and eye closure may persist

therefore pressure to the side of the nail of the

finger is used to determine ability to eye open.

(Waterhouse, 2005)

Peripheral pain may be applied to the side of the

finger not the nail bed to prevent damage

(Edwards, 2001).

47

application of painful stimulus, score 1.

ACTION

VERBAL RESPONSE

Orientated 5

Disorientated 4

Inappropriate words 3

Incomprehensible sounds 2

None 1

Endotracheal tube or tracheostomy = T

Ask questions to assess orientation to time, place

and person, e.g. ask the patient the month or

year, where they are and who they are.

Avoid questions that elicit a yes/no response.

Dysphasic patients cannot be assessed

accurately for orientation.

If correct answers are elicited to all 3 questions,

score 5.

If the patient cannot answer the above questions

correctly but is able to engage in conversation,

score 4.

If single word answers are given or if the patient

is unable to form a sentence; inappropriate

words,

score 3.

If only noises such as grunting sounds are made,

RATIONALE

Determines comprehension, cognition and

reflects the ability to process thoughts into

words. Be aware that confusion can be subtle

and only detected in conversation after a few

minutes. The patient may learn responses if

corrected following frequent observation

therefore variation of questions can be useful.

Core elements must be correct, the patient must

know who he/she is, where he/she is and the

date (Teasdale, 1976)

Focal lesions may cause speech difficulties such

as expressive/receptive dysphasia/aphasia and

may not indicate impaired consciousness

(Teasdale,1976):

Aphasia description:

Receptive aphasia: Inability to process written or spoken language

Expressive aphasia: Inability to express written or spoken language

Global aphasia: Inability to receive language or express using written or spoken language

Dysphasia description:

Receptive dysphasia: Inability or difficulty in

understanding the spoken word: due to damage

48

score 2.

If the patient makes no attempt to speak and no

sounds are made, score 1.

At this stage responses may not be elicited by

talking to the patient and a painful stimulus may

be required (Waterhouse, 2005).

If no verbal response is possible due to an

endotracheal tube or tracheostomy (without

a speaking valve) write ‘T’ against ‘none’.

to Wernicke’s area responsible for

comprehension of speech

Expressive dysphasia: Inability or difficulty in

putting thoughts into words: due to damage in

Broca’s area. The patient can understand what

has been said to them, but cannot find the right

words to reply.

Dysarthria: Slurred speech

(Lindsay et al, 2004).

Teasdale and Jennett (1974) recommended

descriptive narration beside the chart when

difficulties in categorising the patient are

experienced.

Motor response

Obey commands 6

Localise to pain 5

Flexion to pain 4

Flexion abnormal 3

Extension 2

None 1

Record the best arm response. Do not ask to

squeeze hands. Request a specific action, i.e;

‘raise your arms, wriggle your fingers, pull me

towards you, push me away.’ If the patient

cannot respond ask them to stick the tongue

out / move eyes to the left, right.

Assesses areas of the brain that identify sensory

input and ability to translate this into a motor

response (Lindsay, 2004).

The ability to follow a command indicates that

the patient can process instructions (Fischer

and Mathieson, 2001).

Grasping is a primitive reflex and may happen

spontaneously and not in response to command

(Teasdale, 1976)

Patients with a spinal lesion or neurological

condition may not be able to move limbs but

may be awake and able to move the tongue or

49

If no motor response to loud speech or touch is made: A painful stimulus should be used, pressure

applied over the supra-orbital nerve (except for

suspected facial fractures) or to the spinal

accessory nerve lying under the trapezius muscle

(except for high cervical fractures). Essentially

the painful stimulus should be located on or as

near to the head as possible and above the

clavicle.

Methods of applying central pain stimuli.

Trapezium squeeze (cervical spine C3-4): Use

thumb and two fingers as pincers. Feel for the

trapezium muscle and twist or squeeze.

Significant pressure is exerted for no longer than

20 seconds and any verbal and non verbal

responses noted.

Supraorbital pressure (trigeminal V): Under the

eyebrow edge feel for a notch. Press hard with

the thumb for a maximum of 30 seconds.

eyes to command.

Painful Stimuli

Painful stimuli can be central evoking a response

from the brain, or peripheral evoking primarily a

response from the spine (Edwards, 2001). There

may be contraindications for applying central

stimulus to the orbit (Lowry, 1998; Edwards,

2001; Waterhouse, 2005) therefore these

techniques should only be used by practitioners

trained and competent.

Orbit pressure should not be applied if facial

fractures are present or suspected.

‘Central’ painful stimuli is a more reliable

indicator of brain function because it stimulates

a cranial nerve and not a reflex arc.

Peripheral pain may evoke a spinal reflex action

and is therefore not as reliable (Lindsay et al,

2004; Edwards, 2001).

Localising to pain is a deliberate movement of

the arm across the midline of the body in an

attempt to push away from the source of the

painful stimuli (Fischer and Mathieson, 2001).

The patient may be spontaneously localising to

an irritant such as an oxygen mask. The patient

therefore demonstrates an awareness of

environment.

Flexion to pain is an indication of more severe

dysfunction (Lindsay et al, 2004; Fischer and

Mathieson, 2001). Abnormal flexion (arms

withdraw up and wrists rotate inwards) may be

50

Not to be used if facial fractures are suspected or

confirmed. Use if a high cervical insult or injury

suspected.

If there is no localising response then peripheral

pain to the finger may be used. Assess each limb

separately and record the best response.

an indication of a lesion in the cerebral

hemisphere or internal capsule (Fischer and

Mathieson, 2001).

Extension (arms push down) indicates severe

cerebral damage below the level of the red

nucleus

(Lindsay et al, 2004).

No response may indicate a spinal cord lesion or

late stage raised intracranial pressure.

ACTION RATIONALE

PUPIL REACTIONS

(See appendix p 16 – 17)

Determine patient history that may affect pupil

reactions e.g. cataracts, iridectomy or recent

drug therapy that may dilate or constrict the

pupil.

Note the size, shape, equality and position of the

pupils (both eyes simultaneously).

Using a pen torch, shine the light moving from

Abnormal reactions can indicate raised

intracranial pressure and/or damage to the

oculomotor nerve (see A&P). Both pupils should

react at the same time if light is directed at one

eye. This is called a consensual response.

Progressive dilatation and loss of pupil reaction

on one side can be due to pressure on the

oculomotor nerve on the same side. Damage can

be caused by a variety of lesions, however, if

pressure continues, the nerve on the other side

can also be compressed resulting in bilaterally

unreactive, dilated pupils; a sign of severe

51

the outer towards the inner aspect of the eye.

Observe the size shape and reaction of the pupil

and record brisk reactions as + and sluggish

reactions as ‘S’.

Wait a few seconds before repeating the

procedure in the other eye.

TESTING LIMB POWER

damage and brain herniation (Lindsay et al,

2004).

Both pupils should be assessed at the same time

to observe and compare reaction.

IDENTIFICATION OF FOCAL DEFICIT

ACTION RATIONALE

LIMB POWER

(recorded on limb section of chart)

Each limb will be assessed

Arm strength.

Ask the patient to close their eyes and hold their

arms out in front of them, palms facing up. If the

patient can maintain this position, record the

power as normal.

The power of each limb should be recorded

separately on the lower section of the

assessment chart.

The best response is charted on the GCS graph at

the top of the chart using one dot.

If an arm drifts downwards record that limb as

mildly weak. The mildest response is that the

palm rotates to a downward position known as

pronator drift.

Limb responses may give clues to the origin of

the neurological dysfunction (Lindsay et al,

2004); eg, a weak limb on the right side will

indicate damage to the left motor strip, or

ipsilateral spinal cord

The GCS is the total score of the best responses;

however, it is essential to reveal any weakness

and difference in power. Clinical examination of

the limbs may be carried out to aid clarity. Each

limb may be scored out of 5:

5 normal

4 move against some resistance

3 move against gravity only

2 Can move with gravity eliminated

1 Flicker

0 nothing

Assessment of strength is then transcribed onto

the limb assessment section of the observation

52

If the patient is unable or has extreme difficulty

in lifting their arms off the bed but can make

some movement (eg move fingers) record as

severely weak.

If the patient is unable to move their arms, apply

pain and record the response

(see figure on posturing)

Leg strength.

Ask the patient to raise their legs off the bed or

place hand on the sole of the foot and ask the

patient to push, then place hand on top of the

patients foot and ask them to pull their foot

upwards. Place hands on both knees and ask the

patient to push the knees up hard. Record

whether the power of each leg is normal or

mildly weak if the patient can comply.

If the patient cannot lift their legs easily but can

make some movement, record as severely weak.

If the patient cannot move the legs the response

to painful stimulus will be documented as

described.

chart

normal strength - full movement against both gravity and resistance.

mild weakness - limb moves against gravity but not against resistance (no push/pull).

severe weakness – limb is able to move but unable to lift against gravity.

Lower limb response to peripheral painful stimuli

is not reliable due to involvement of spinal

reflexes therefore the best limb response

charted on the GCS will be from the arms

(Hickey, 2009;Lindsay et al,2004).

ACTION

VITAL SIGNS

Will be monitored and recorded concurrently

with neurological assessment:

RATIONALE

GCS is one component of assessment. Vital signs

complete the full complement of data on which

treatment and intervention can be based.

53

Temperature

Investigate and treat cause of temperature.

Septic screen

liaise with microbiology team

Fluid from ear / nose which tests positive for

glucose may be cerebrospinal fluid

Pulse –

Blood Pressure

Beat to beat real time invasive monitoring will

be used for all patients requiring intubation and

for patients who are deteriorating:

ECG

Invasive Bp

Blood gas analysis

On going ABCDE assessment

Base of skull fracture and CSF

rhinorrhoea/otorrhoea (CSF drip from nose/ear)

increase risk of infection.

A patient who has sustained a severe head

injury may have localised damage to the

temperature regulating centre in the

hypothalamus. As the patient’s temperature

rises vasodilation of the cerebral blood vessels

takes up more room in the closed box of the

skull (Waterhouse, 2005; Lindsay et al, 2004). A

raised temperature will also increase metabolic

demands on the brain.

Bradycardia – the heart rate may drop as low as

35-50 beats per minute in the later stages of

raised intracranial pressure (Lindsay et al,2004).

Tachycardia – can occur where there is damage

to the hypothalamus and in the terminal stages

of raised ICP (Lindsay et al, 2004).

Tachycardia also indicates a need for fluid

resuscitation and further investigation of the

cause and subsequent treatment must be

initiated without delay.

Hypertension – a rising systolic blood pressure

combined with a widening pulse

pressure is a late sign of increasing ICP (Lindsay

et al, 2004). Treatment of hypertension must be

discussed with a senior medical colleague as

sudden lowering of blood pressure may result in

secondary injury (infarct) because the CPP has

been reduced when the ICP has been high.

Hypotension – if autoregulation is impaired by a

54

Pupil assessment

Cerebral perfusion = mean arterial pressure

(MAP) – intracranial pressure (ICP)

HYPOXIA & HYPOTENSION PREVENTION – ABCDE

MAP > 80 PO2 > 13 PCO2 4.5 – 5

SAO2 > 97 TIMELY INTUBATION

Respirations

cerebral event hypotension results in decreased

blood flow and therefore oxygen supply to the

brain.

Cerebral perfusion (CPP) must be maintained to

prevent secondary injury.

Hypotension may also be caused by

hypovolaemia, sepsis, sedative drugs etc. Causes

of hypotension must be treated immediately.

The target cerebral perfusion pressure is 60 – 70

mmHg. CPP below 60 carries a risk of secondary

brain injury through infarction and cerebral

oedema.

ICP is not electronically monitored in A&E. In

order that perfusion of the brain is protected it is

recommended that an MAP of > 80 should be

achieved (see Walton Centre guidelines). It is

vital that blood pressure below this level is

treated urgently.

Respiration assessment is a vital early warning

sign of reducing consciousness. Respiratory

depression and loss of airway protection will

occur as the GCS score falls.

If the patient is deteriorating there must be

assessment by an anaesthetist

if GCS falls to 13 or less.

Intubation is essential at GCS 8 or less.

Aspiration and subsequent lung

infiltration leads to hypoxia and

secondary brain injury and increased

length of stay in critical care & poor

55

prognosis.

Follow local care plan, guidelines and care bundles for care of the unconscious patient & artificially ventilated patient.

ACTION

Urine output will be monitored hourly.

Insert a urinary catheter if GCS is 12 or less.

If urine output exceeds 3oo ml per hour for two consecutive hours perform urine specific gravity, paired urine and serum osmolality. Report results to medical colleagues.

RATIONALE

Diabetes insipidus (DI) indicated by excessive urine output, low urine osmolality and rising serum osmolality and serum sodium.

Normally the pituitary gland secretes antidiuretic hormone (ADH) when blood osmolality rises. This function is disrupted due to rising ICP. Large volumes of water are passed and the sodium concentration in the blood is raised. This is not to be confused with therapeutic diuresis which follows the administration of mannitol used to treat high ICP. It is essential to have the diagnosis made by a senior medical colleague. Treatment is the administration of antidiuretic hormone (DDAVP).(Hickey, 2009)

ACTION

Avoid neck flexion

keep the body in alignment.Nurse head up by 20 - 30 degrees.

If spinal injury is suspected – tilt the bed end down to achieve position whilst maintaining alignment.

RATIONALE

Cerebral venous drainage will be impeded by neck flexion and poor body positioning. This will cause a rise in ICP. Intra-abdominal pressure may also cause a rise in ICP therefore hips should not be bent at an acute angle (Hickey, 2009).Risk of aspiration into the lungs is increased in intubated patients if nursed at an angle less than 30 degrees (ventilator care bundle).

ACTION

Observe for seizure activity

When the patient is sedated and artificially ventilated seizure activity is difficult to detect but may be manifested by tachycardia, pupil changes and cardiovascular instability.

RATIONALE

A,B,C,D,E protocol. Seizure control immediately. Seizures increase cerebral metabolism and increase ICP therefore risk of secondary brain injury.

ACTION

Specific fluid balance:A detailed hourly fluid balance account will be maintained.Aim for a neutral balance.

RATIONALE

Blood volume must be maintained to prevent hypotension and maintain cerebral blood flow.Water balance between the intravascular space and brain tissue depends upon an osmotic

56

Avoid use of hypOtonic solutions and 5% glucose.Monitor serum sodium determine cause if low.

Mannitol will be administered by expert request to manage high ICP

Hypertonic saline administration may be requested (refer to Walton Centre guidelines)

gradient. Glucose contained within crystalloid infusion will be metabolised and the remaining water will infiltrate the brain tissue & contribute to cerebral oedema.Traumatic brain injury can cause disorders of sodium balance (see above section).Mannitol is an osmotic diuretic and will cause excess diuresis. Intravascular volume must be maintained using colloid.

Hypertonic saline reduces brain water and increases intravascular volume. Serum sodium will rise and serum osmolality will rise. This is the therapeutic nature of hypertonic saline (Refer to Walton Centre ICP management guidelines).

ACTION

Blood gases – specific value ranges

Maintain PO2 > 13 kpaMaintain CO2 4.5 – 5 kpaPre-oxygenation with 100% O2 for 60 seconds prior to suctioning ET tube.

(refer to Walton Centre ICP management protocol)

RATIONALE

Maintain oxygenation of the damaged brain.

CO2 can cause vasodilatation of cerebral vessels which will then take up more room in the confines of the skull (see appendix). ICP will rise.

Sedation of the artificially ventilated patient specifics

In acute stages of head injury management sedation must be adequate to prevent coughing and bucking on the endotracheal tube spontaneously and when suction is applied.Sedation holds (ventilator care bundle) should not be performed in acute ICP management.

RATIONALE

Coughing and straining will increase ICP.

Ventilator mode:

Ventilator modes which give predictable tidal volumes are recommended

RATIONALE

Sudden rises in CO2 due to poor compliance with pressure limited modes may occur.

Abnormal posturing.

57

Afferent = impulse in from environment

Efferent = impulse from the brain

REFERENCES

58

Responses to external stimulus cannot be modified by the control centres in the brain as the connections are damaged. Extension instead of flexion in the muscle is seen.

Dawes, E. Lloyd, H. Durham, L (2007) ‘Monitoring and recording patient’s neurological observations.’ Nursing Standard. 22 (10) pp 40 – 45

Dougherty, L and Lister, S (Eds) (2004) The Royal Marsden Hospital Manual of Clinical NursingProcedures 6th Ed London: Blackwell

Edwards, S L (2001) Using the Glasgow Coma scale: analysis and limitations British Journal ofNursing Vol. 10 No. 2 pp. 93-101

Fischer,J and Mathieson, C (2001) The history of the Glasgow Coma Scale: implications for practice.Critical Care Nursing Quarterly. Vol 23 No 4 pp. 52-57

Hickey, J V (2009) The Clinical Practice of Neurological and Neurological and Nursing. Philadelphia:Lippincott-Raven

Lindsay, K, W. Bone, Callander (2004) Neurology and Neurosurgery Illustrated. 4th Ed. London. Churchill Livingstone.

Lowry, M (1999) The Glasgow Coma Scale in clinical practice: a critique. Nursing Times Vol. 95 No.22 pp. 40-42

National Institute for Clinical Excellence (2007) ‘Head Injury: Triage, Assessment and Early Management of Head Injury in Children, Infants and Adults.’ www.nice.org.uk/CG056 (accessed June 2010)

Shah, S (1999) Neurological Assessment. Nursing Standard Vol. 13 No. 22 pp. 49-56

Stewart, N (1996) Neurological Observations. Professional Nurse Vol. 11 No. 6 pp 377-378

Teasdale, G. (1976) ‘Assessment of Head Injuries.’ British Journal of Anaesthesia. Vol 48. Pp 761 - 766

Teasdale, G. Jennett, B. (1974) ‘Assessment of coma and impaired consciousness: a practical scale.’ The Lancet. 2, 7282, pp 81 - 84

Waterhouse, C (2005) The Glasgow Come Scale and other neurological observations. (learningzone: neurological assessment) Nursing Standard Vol. 19 No. 33 pp. 56

Waterhouse, C. (2008) ‘An audit of nurses’ conduct and recording of observations using the Glasgow Coma Scale.’ British Journal of Neuroscience Nursing. Vol 4 No 10. Pp 492 - 499

59

FURTHER READING

Dootson, S (1990) Critical Care: Sensory Imbalance and Sleep Loss Nursing Times Vol. 86 No. 35pp. 26-29.

Ellis, A and Cavanagh, SJ (1992) Aspects of Neurological Assessment using the Glasgow ComaScale. Intensive Critical Care Nursing Vol. 8 No.2 pp 94 - 99

Hickey, J V (2009) The Clinical Practice of Neurological and Neurological and Nursing. Philadelphia:Lippincott-Raven

Hudak, C, Gallo, B, Morton, P (1998) Critical Care Nursing. Philadelphia: Lippincott

Lindsay, K, W. Bone, Callander (2004) Neurology and Neurosurgery Illustrated. 4th Ed. London. Churchill Livingstone.

Mooney, G and Comerford, DM (2003) Neurological Observations. Nursing Times Vol. 99 No. 17 pp.24-25

Price, T (2002) Painful stimuli and the Glasgow Coma Scale. Nursing in Critical Care Vol. 7 No. 1pp. 19-23

Teasdale, G M and Murray, L (2000) Revisiting the Coma Scale and Coma Score. Intensive CareMedicine Vol. 26 No. 2 pp 153-154

Woodward S (1997) Practical Procedures for Nurses. Neurological Observations Nursing Times Vol. 93 Nos. 45-48 parts 5.1 – 5.4

Pictures sourced from:

www.mstrust.org.uk

www.faculty.washington.net

www.bioon.com

www.sciencegeek.net

www.medicalook.com

www.biologymad.com

TRAUMATIC BRAIN INJURY

60

Each year, an estimated 1 million people in the UK go to hospital as a result of a head injury.

Males are more likely to have a head injury than females and the age group most at risk is

between 15 and 29 years of age.

GOALS FOR THIS SECTION:

1. Understand that traumatic brain injury is a process, not an event

2. Understand the pathophysiological mechanisms involved in traumatic brain injury

Definition: Severe Head trauma associated with a Glasgow Coma Score of ≤ 8 after resuscitation

EYE OPENING VERBAL RESPONSE MOTOR RESPONSE

(please refer to GCS section)

TBI is a process, not one event

Primary injury is that directly caused by the trauma; secondary by the effects afterwards, such as brain swelling. Secondary injury can be more damaging than primary injury. The main mechanisms of brain injury are:

◦ Extracranial injuries causing hypoxia, hyoptension

◦ Brain Contusion

◦ Increased intracranial pressure ( ICP) due to brain swelling or itracranial blood clots

◦ Diffuse Axonal Injury (DAI)

CT reveals a left sided subdural haematoma and frontal haemorrhagic contusions. There is mid line shift. On examination his right pupil is 5mm in size and fails to constrict to light.

Bp = 95 / 60

MAP = 77

ICP = 25 and is set to rise as a heamatoma expands and contusions swell.

61

MAP 77 – ICP 25 = CPP 52

Cerebral perfusion is not being met and infarction occurs. Urgent surgical action is required!

Autoregulation.

Cerebral auto regulation is the mechanism for maintaining a constant cerebral blood flow in the face

of changes in systemic blood pressure. The control of this process is quite complex, as is the control

of systemic blood pressure, and relies on both neural and metabolic (chemical) mechanisms

controlling the diameter of peripheral blood vessels, both venous and arterial and arterioles, and the

force, volume and rate of cardiac contractions. Baroreceptors detecting blood volume are located

in the atria, great veins, pulmonary vessels, aortic arch and carotid sinus. The carotid body via the

glossopharyngeal nerve detects the influence of systemic oxygenation – the chemosensitve parts of

the brain stem detect changes due to acidosis – such as rising carbon dioxide levels, or lactic acidosis

from ischaemia producing efferent responses from the brain stem via the parasympathetic (primarily

vagus nerve) and sympathetic systems. These systems – via sympathetic innervation of brain blood

vessels , together with the local microchemical environment influence the diameter of these vessels

resulting in autoregulation – a constant cerebral blood, though set to the metabolic needs of the

brain – thus blood flow is higher when the patient is awake, and locally when a particular part of the

brain is active - such as Broca’s area when the patient is talking. It is this local effect that is

measured by functional MRI scans. This system, in particular the level of acidosis in the respiratory

centre in the brain stem also plays a major role in the control respiratory function, though in

ventilated patients on ITU these responses will not be apparent.

Autoregulation may fail in disease states particularly head injury and sub-arachnoid haemorrhage. In

this circumstance falls in perfusion pressure will then produce a fall in blood flow and ischaemic

damage results. It is therefore critical to maintain adequate CPP in these circumstances.

The blood brain barrier.

62

Endothelial cells within the capillary bed make up the blood brain barrier (BBB). Together with other

cells such as astrocytes, they provide an interface between the blood and brain tissue via tight

junctions between the cells. Transport of gases and nutrients, protection from toxic substances and

protection from changes in oncotic pressure are functions of the BBB thus homeostasis is maintained

(Tortora, Grabowski, 2000). However, the BBB will not be intact after TBI. Disruption of the blood

brain barrier will lead to transcapillary leakage and cerebral oedema, and loss of cerebral

autoregulation (Nordström 2003).

These are the reasons why it is vital to maintain the CPP. In the absence of ICP monitoring the MAP

must be maintained at 80mmHg while a specialist neuro intensive care bed is secured.

63

CEREBRAL PERFUSION PRESSURE

INTRACRANIAL PRESSURE

This graph demonstrates a loss of autoregulation following TBI. CPP is reduced by increases in ICP.

64

The oculomotor III nerve is compressed and the pupil fixes and dilates

The brain stem is compressed producing the Cushing response – BP up, HR down

Herniation schematic from Robbins and Cotran. Pathologic Basis of Disease. 7th ed. Philadelphia: Elselvier; 2005.

The key concept of the non compressible box of the skull is a vital point to appreciate as secondary injury results in this evolving scenario. The brain stem is compressed as the cerebellar tonsils herniate through the foramen magnum. Brain death is imminent.

THINK AHEAD

Triage History Imaging Neurosurgical referral Keep communicating

A SSESSMENT & TIMELY ACCESS TO NEUROSURGICAL ADVICE

TRIAGE REFERAL ON GOING GCS & pupil assessment EWS & 2 WAY COMMUNICATION

HYPOXIA & HYPOTENSION PREVENTION – ABCDE

MAP > 80 PO2 > 13 PCO2 4.5 – 5 SAO2 > 97 TIMELY INTUBATION

EARLY IMAGING & REPORTING < 1 HOUR WHEN GCS 13 OR LESS

Consider trauma series CT head, C0 – T5, chest, image pelvis & abdomen

AMBULANCE TRANSFER TO NEUROSURGICAL CENTRE < 4 HOURS FROM TRIAGE

65

Pre-warn ambulance service of impending emergency transfer

DECISION MAKING BY SENIOR DOCTOR IN BOTH HOSPITALS

Consultant involvement to support timely decisions

It is imperative that the patient with an expanding lesion is identified early and is transported to expert help without delay.

Treatment Options:

Surgical Management:

Evacuation of space occupying lesion (haematoma, abscess, tumour)

Evacuation of contusions and removal of bone flap = decomrpessive craniectomy

Insertion of an extraventricular drain (EVD) to off load CSF and decrease ICP (Lumbar puncture contraindicated with expanding Space Occupying Lesion!)

Medical Management:

Protection of airway

Control of CO2 & PO2

MAP > 80mmhg

ICP less than 20, CPP between 60 – 70

Euvolaemia

Body alignment

Sedation

Control of seizures

Consider prophylactic anticonvulsant

Antibiotics / antivirals for CNS infections

Steroids for tumour

66

Normothermia

Glucose control

Haemostasis

Homeostasis

Therapeutic hypothermia

Barbiturate coma

REFERENCES:

The Brain Trauma Foundation. (2007), Guidelines for the management of traumatic

brain injury, Journal of Neuro Trauma, vol 24, Supplement 1, Pp S- 59 S

- 64. p 17-23. p 47-74.

Nordström CH. (2003), Assessment of critical thresholds for cerebral perfusion pressure by bedside

monitoring of regional energy metabolism. Neurosurg Focus;15:5.

Tortora G J, Grabowski S R, (2000) Principles of anatomy and physiology. John Wiley & sons, inc. New

York. 9th ed. p 447 – 448. ISBN 0-471-36692-7

67

Activity 7. END OF SECTION TEST:

Now you have read and absorbed the contents of this section using the structures in your brain, it is

time to see if you have retained the information and can relate this to how you care for a patient

who requires intensive care because they are neurologically compromised. Good luck.

1. CPP STANDS FOR: .............................................................

2. Complete the equation:

CPP = ...........................................................................

Your patient has a BP of 100/60 and an ICP of 26 what is the cerebral perfusion pressure?

68

3. Name four mechanisms of brain injury:

4. What range is a normal ICP?

5. What MAP would be an ideal target for a patient without an intracranial pressure monitor?

6. How would you apply painful stimuli to assess limb reponses of the patient cannot obey

commands?

7. How can you differentiate between flexion and extension of a limb?

8. What is the name for this posture? The patient pushes the arms down.

69

9. What is the name for this posture?

10. Describe a normal pupil response to light.

70

11. What is consensual response to light?

12. If there is a dilated pupil which does not respond to light, what could be the clinical

significance?

13. Once the patient is intubated is it necessary to continue to assess the pupils?

a. Yes

b. No

14. How can a carbon dioxide above 5kpa affect intracranial pressure?

a. Causes vasoconstriction

b. Causes vasodilatation and a raised ICP

c. Causes a higher urine output

15. What is the difference between afferent and efferent?

71

16. What could happen to the serum sodium if the patient has diabetes insipidus?

a. It would be rising

b. It would be reducing

c. There would be no change

17. What would happen to the urine output if the patient had diabetes insipidus?

a. It would be low

b. It would be high

c. There would be no change

18. What would happen to the serum osmolality if the patient had diabetes insipidus?

a. It would rise

b. It would fall

c. It would not change

72

19. What is the treatment for diabetes insipidus?

20. Why is it important to avoid neck flexion in a head injured patient?

You have a growing body of knowledge. Why not put yourself to the test with a virtual patient?

Activity.

The THINK AHEAD e-learning package Online.edgehill.ac.uk

73

The ‘Think Ahead’ learning package has been developed to support and educate medical and nursing staff involved in the delivery of care to head injured patients in the acute setting, including emergency departments, surgical and medical assessment centres and observation wards.

Think Ahead is an interactive and intuitive package which offers a multi-media learning experience and more information is available at: online.edgehill.ac.uk.

An insight into the use of sedation in Neuro critical care

Helen Jones

Therapeutic sedation is administered in the critical care setting for a wide range of reasons. It is used

to contribute to the control of intracranial pressure, agitation, stress, delirium and to keep the

patient from self harm (Bion,1999). In the general intensive care setting, sedation with analgesia is

used to achieve compliance and comfort during therapeutic mechanical ventilation. A ‘tube tolerant’

state is achieved utilising a sedation scoring tool such as the Ramsay Scale or Richmond Agitation

Sedation Scale, in combination with a sedation protocol.

74

There has been a critical re-evaluation of sedation techniques in the last ten years and the goal of

heavily sedated and comatose patients on mechanical controlled modes of ventilation has been

replaced by the concept of the awake yet compliant, comfortable patient who can interact with the

environment and exercise the muscles of respiration. This, together with the practice of sedation

holds (Kress and Pohlman et al, 2000) has led to reduced length of stay and better outcome

following critical illness (Jackson and Proudfoot et al, 2010). Important in this process is the ability to

assess the level of sedation the patient requires and administer appropriate agents to achieve

therapeutic effect by following an evidence based pathway.

A survey of 192 critical care units in the UK revealed that 88% utilised a sedation scoring tool, 66.4%

of which used the Ramsay Sedation Score. 80% used an evidence based sedation protocol for

guidance. Propofol was the preferred agent for sedation in the first 24 hours and for weaning from

mechanical ventilation..

The pharmacological properties of propofol allow for rapid weaning from ventilation and its use in

critical care has been correlated with reduced length of stay and increased critical care capacity

(Krishnan et al, 2004). Propofol has been used widely in neuro-intensive care because it allows rapid

assessment of neurology after the infusion has been stopped; this has obvious benefits as the critical

care team can assess the patient’s neurological function in a timely fashion. It has also been reported

to have neuro-protective properties and has been shown to reduce intracranial pressure (ICP) in

several studies (Hutchens et al, 2006). However, the potentially lethal but rare propofol-related

infusion syndrome (PRIS) has been highlighted in an increasing volume of case reports and a large

prospective study (Roberts et al, 2009), administration through the guidance of protocol is therefore

essential. The study by Roberts et al (2009) revealed that the syndrome can manifest soon after the

infusion has started and at low doses. Critically ill adults were recruited from 11 critical care units in

the US. Of the 1017 patients 35% were neurosurgical. All patients were administered propofol

beyond 24 hours and monitored for manifestation of PRIS associated symptoms. A patient was

deemed to have PRIS if they developed metabolic acidosis and cardiac dysfunction together with

one or more significant symptoms; rhabdomyolysis, elevated triglyceride levels or renal failure. 1.1%

of the 1017 developed PRIS as defined by the study. None of the 1.1% developed rhabdomyolysis or

Brugada ecg patterns. Of the 11 patients who were diagnosed with PRIS two developed symptoms

within the first day of administration of propofol and 10 developed symptoms within 3 days. There

were two deaths and these were also the only patients who received a propofol dose exceeding 83

ug/kg/min. Due to the early onset of PRIS symptoms in their cohort of patients the authors advised

that clinical signs of PRIS should be monitored from the commencement of the agent.

75

This was the first large trial which debated this complex and poorly defined syndrome although

many case studies have been published. The authors stated that among 71 previously published case

studies 86% received a dose exceeding 83 ug/kg/min. Despite increasing reports of the syndrome

there remains a lack of international consensus on definition.

PRIS results in impairment of fatty acid chain oxidation and inhibits oxidative phosphorylation in the

mitochondria (vernooy and Delhaas et al, 2006).

PRIS symptoms:

Acidosis

Lactic acid build up

Raised CK

Raised triglyceride levels

Urine myoglobin

Dark urine

Bradyarrhythmias

Pyrexia

Raised potassium

Most of these elements are monitored routinely in critical care. Indeed, these clinical signs can

reflect the state of critical illness, organ failure and sepsis. However, triglyceride levels could be

added to routine screening for patients receiving propofol infusion to aid detection of PRIS. In

addition, attention must be drawn to ecg changes such as Brugada ecg patterns:

electrocardiographic changes which herald sudden death due to PRIS are typically ST-segment

elevation in leads V1 – V3 (Vernooy and Delhaas et al, 2006).

Administration of sedation for intracranial pressure (ICP) control is essential. Full compliance with

artificial ventilation must be achieved to facilitate manipulation of carbon dioxide levels and to

prevent coughing which will increase the ICP. Under this condition, higher doses of sedation will be

used to achieve maximal therapeutic effect. In addition sedation suppresses the cerebral metabolism

which reduces blood flow ; therefore blood volume and consequently also ICP. Once cerebral

76

metabolism is maximally suppressed there is no further advantage in increasing the dose of

sedation, though in practice this level is rarely reached except in total barbiturate coma. EEG control

maybe used to assess the suppression, or its simpler derivatives such as the Cerebral Function

Monitor, or BIS. Conversion from propofol infusion to midazolam infusion would seem desirable if

ICP continues to be monitored and weaning from ventilation is not clinically advised. A sedation

scoring system would not be practical in this situation; however, it is necessary to know how much

sedation is required in order to limit the negative effects of sedation: hypotension, accumulation,

increased dependence on vasopressors, organ dysfunction and increased length of stay in critical

care.

Response to sedation can depend upon: body mass index, age, alcohol and drug use, hepatic and

renal function. The amount of sedation required to achieve therapeutic effect can therefore vary

greatly. It is essential to have knowledge of all these factors when considering the use of sedation.

In control of intracranial pressure:

Assess body mass index

Use a protocol to guide choice of agent – propofol not to exceed 24 hours if weaning is not

clinically advised – assess triglyceride levels daily and monitor for symptoms of PRIS.

BIS monitoring

Concomitant use of analgesia

Exempt from sedation hold element of ventilator care bundle

In achieving tube tolerance and control of agitation where ICP is not actively managed:

Assess body mass index

Use of sedation score tool

Concomitant use of analgesia

Pain relief scoring tool

Consider remifentanil as alternative to propofol

The use of sedation protocols can reduce weaning time from ventilation and therefore reduce length

of stay in critical care (Chanques et al, 2006; Quenot et al, 2007). It is therefore appropriate to

develop and introduce such protocols.

77

Manufacturers of sedative agents continue to develop products for the acute setting. Propofol has

been used widely in all critical care settings because of its short duration of action and ease of use

for weaning from mechanical ventilation. Remifentanil is also a short acting agent which has been

used in weaning with good results (Di Nardo et al, 2005) and may be used to achieve a tube tolerant

state.

Considering the diversity of symptoms for PRIS and the heterogeneity of the critically ill patient it is

clearly difficult to diagnose with a significant degree of confidence. The reported cases may be the

‘tip of an iceberg’ or may not have been PRIS because symptoms cross over with many critical care

conditions such as sepsis. In order to increase patient safety it seems appropriate to limit the use of

propofol by the following methods:

Introduction of sedation pathway which can be nurse led

Introduction of sedation scoring tool used concurrently with pain scoring

THE RAMSAY SEDATION SCALE

Level 1: Patient anxious and agitated, restless or both.

Level 2: Patient cooperative, orientated and tranquil.

Level 3: Patient responds to commands only

Level 4: Patient exhibits a response to a light glabellar tap or a loud auditory stimulus.

Level 5: Patient exhibits a sluggish response to a light glabellar tap or loud auditory

stimulus.

Level 6: No response to a light glabellar tap or loud auditory stimulus.

The Ramsay Sedation Score has two clearly defined categories. 1-3 assess wakefulness, 4-6

assess degrees of sleep. This does not replace the use of the Glasgow Coma Scale assessment of

patients. A Ramsay sedation score of 2 would be the target for patients sedated to maintain

‘tube tollerance’ and a reduction in agitation. However, the ‘orientated’ descriptor may not be

78

applicable for patients who are neurologically compromised. This element is also difficult to

assess when the trachea is intubated. The scale has been validated for clinical use and is utilised

in a significant percentage of UK critical care units.

The Richmond Agitation Scale (RASS)

A scale with a range from +4 to -5. A score of 0 is the desired level of sedation. The RASS is linked to

the CAM ICU work sheet for the diagnosis of delirium and is therefore a commonly used scale in

critical care units. It could be argued that the RASS, because of it’s detailed and abundant

descriptors, is more sensitive when applied to patients with complex neurology would also link

more effectively with risk assessments.

Score Term Description

+4 Combative Overtly combative or violent, immediate

danger to staff

+3 Very agitated Pulls on or removes tubes or catheters or has

aggressive behavior toward staff

+2 Agitated Frequent nonpurposeful movement or patient

ventilator dyssynchrony

+1 Restless Anxious or apprehensive but movements not

aggressive or vigorous

0 Alert and calm

-1 Drowsy Not fully alert, but has sustained (more than 10

seconds) awakening, with eye contact/eye

opening to voice

-2 Light sedation Briefly (less than 10 seconds) awakens with

eye contact to voice

-3 Moderate sedation Any movement (but no eye contact) to voice

79

-4 Deep sedation No response to voice, but any movement to

physical stimulation

-5 Unarousable No response to voice or physical stimulation

Key Learning Points:

Sedation scoring reduces anxiety therefore can reduce the incidence of delirium and post

traumatic stress which impact upon recovery / morbidity.

Sedation scoring enables the patient to continue to interact and move limbs and muscles of

breathing therefore reducing length of stay in critical care.

Improved psychotropic medication use will reduce side effects of sedation

References:

Bion, J. (1999) Intensive Care Medicine: Fundamentals of anaesthesia and acute medicine. BMJ

publishing. London.

Chanques G, Jaber S, Barbotte E. et al (2006). ‘Impact of systematic evaluation of pain and agitation

in an intensive care unit.’ Crit Care Med. 34:1691-1699.

Di Nardo, M. Paperini, A. Mosca, C et al (2005) ‘Weaning from mechanical ventilation using

remifentanil versus midazolam-morphine analgo sedation: our experience.’ Critical Care. 9 (supp 1). P

135. Available at: www.http://ccforum.com/content/9/s1/p135

80

Hutchens, M, P. Memtsoudis, S. Sadovinkoff, N. (2006) ‘Propofol for sedation in neuro-intensive

care.’ Neurocritical Care. 4 (1). Pp 54-62.

Jackson, D, L. Proudfoot, C. Cann, K. Et al. (2010) ‘A systematic review of sedation practice in the ICU

on resource use, costs and patient safety.’ Critical Care. 14. R59

Available at: www.http://ccforum.com/content/14/2/R59

Kress J,P. Pohlman A,S. O'Connor M,F, et al. (2000) ‘ Daily interruption of sedative infusions in

critically ill patients undergoing mechanical ventilation’. N Engl J Med.342:1471–1477. doi:

10.1056/NEJM200005183422002.

Krishnan, J, A. Moore, D. Robeson, C. Et al. (2004) ‘A prospective, controlled trial of a protocol based

strategy to discontinue mechanical ventilation.’ American Journal of Respiratory and Critical care

Medicine. 169. 673-678.

Quenot J,P. Ladoire S. Devoucoux, F et al (2007) ‘Effect of a nurse-implemented sedation protocol on

the incidence of ventilator-associated pneumonia’ Crit Care Med .35:2031-2036.

Reschreiter, H. Maiden, M. Kapilla, A. (2008). ‘Sedation practice in the intensive care unit: a UK

national survey.’ Critical Care. 12. Available at:

www.http://ccforum.com/content/12/6/R152

Roberts, R, J. Barletta, J, F. Fong, J. Et al. (2009) ‘Incidence of propofol-related infusion syndrome in

critically ill adults: a prospective, multicenter study.’ Critical Care. 13. Available at:

www.http://ccforum.com/content/13/5/R169

81

Vernooy, K. Delhaas, T. Cremer, O. et al (2006) ‘Electrocardiographic changes predicting sudden

death in propofol-related infusion syndrome.’ Heart Rhythm. 3 (2). Pp 131-137.

Subarachnoid Haemorrhage.

Prior to reading this section it is essential to revise the anatomy and physiology section of this work

book, specifically the subarachnoid space, CSF pathways and Circle of Willis. Please use

supplementary reading material to enhance your learning as you work through the section. Useful

websites include:

www.nhs.uk/conditions/ Subarachnoid - haemorrhage

www.brainandspine.org.uk/.../ subarachnoid _ haemorrhage /

www.avmsupport.org.uk

82

A haemorrhage into the space where the cerebrospinal fluid circulates is called a Subarachnoid

Haemorrhage (SAH). This is commonly caused by the rupture of a cerebral aneurysm located in the

main Circle of Willis or one of the branches or an arteriovenous malformation.

SAH is graded in severity using the WFNS scale – the poorer the grade the worse the prognosis and

the higher the treatment risk:

World Federation of Neurosurgery grading system (Teasdale et al)

Grade GCS Focal neurological defict

I 15 None

II 13/14 - None

III 13/14 Present

IV 7-12 Present or absent

V 6 or less Present or absent

An older scale, called the Hunt and Hess scale was used in the past – it differs from the WFNS scale

in taking into consideration meningism which is due to irritation of the meninges by the blood, and

believed to correlate with cerebral vasospasm, in which circumstance treatment of the aneurysm is

thought to have a higher risk of post-procedural ischaemic deficit.

Hunt and Hess scale:

83

It is difficult to classify those ventilated as they cannot be assessed, and it may be undesirable to

reverse the ventilation in order to assess the patient as this may produce its own secondary insult..

The initial rupture of an aneurysm can result in a sudden loss of consciousness as the cerebral

circulation is disrupted. The level of consciousness may improve subsequently. Emergency care

must be focused upon protecting the airway and addressing immediate threats to life. Diagnosis is

determined by a CT scan in the first instance and then a lumbar puncture. Once the diagnosis has

been made referral to a neurosurgical expert will follow. Depending upon the severity of the bleed

the patient will either be transferred to a ward at the local neurosurgical centre or critical care.

Further imaging to aid detection of the culprit vessel will be completed once the patient is stable.

These include:

CT angiogram

Digital subtraction angiography (DSA)

84

The vessels of the brain are highlighted by dye and the bleeding point and type of abnormality is

detected.

Appropriate treatment can then be planned. Options include:

Image guided insertion of coils into the aneurysm to seal it.

Clipping of the aneurysm (only usually performed if the surgeon is evacuating an associated

intracerebral clot – often this is secondary to a middle cerebral artery aneurysm).

Surgical removal of an arteriovenous malformation, or treatment with stereotactic

radiosurgery either alone or sometimes combined with embolisation. This is usually

performed electively after recovery from the effects of the haemorrhage.

Unfortunately these measures to prevent re-bleeding do not prevent other side effects of bleeding

into the subarachnoid space. Hydrocephalus may develop as blood blocks the re-absorption system

in the CSF circulation (see A&P section). The treatment is the insertion of an extraventricular drain

(EVD). This drain is inserted into a ventricle and acts as an escape for the CSF that will build up. It is a

gravity drain and the amount drained can be controlled by adjusting the height of the chamber in

relation to the external auditory meatus or bridge of the nose (the anatomical zero point at which

CSF exits the ventricles through the foramen of monro and circulates). The blood will eventually

break down and the CSF system will return to function and the drain may be removed. If there are

on-going problems with hydrocephalus an internal shunt may be required.

85

Prevention of secondary injury is paramount. Spasm of cerebral vessels in response to the free blood

can cause devastating problems relating to cerebral perfusion. Spasm is most likely to develop

between day 3 and day 12 following the bleed. Risks of spasm gradually reduce until 21 days post

bleed when the risk is negligible. The treatment to ameliorate or prevent vessel spasm is a calcium

channel blocker called Nimodipine. 60 mg 4 hrly must be continued for the 21 day period. If the

patient cannot absorb the tablet form the IV is available in a 0.02% solution, both have the same

efficacy.

Prior to and following the securing of the aneurysm it is essential to maintain cerebral perfusion.

Before the aneurysm is secured the MAP must be maintained for perfusion (see head injury

management) as hypotension will cause reduced cerebral blood flow, however, hypertension may

be associated with a greater risk of re-bleed. Once the aneurysm is secured hypertensive therapy

86

may be required to maintain perfusion. This therapy must be guided by a neurosurgeon / neuro-

vascular intervention specialist.

Adequate circulating volume is also essential to cerebral perfusion therefore strict observation of

fluid balance and avoidance of dehydration is vital.

Patients who have had a SAH may suffer from disorders of sodium balance (see previous notes on

this subject). Any change in serum sodium, urine output must be investigated.

Subarachnoid haemorrhage – Activity 9.

Label the layers of the brain in this diagram

87

The Circle of Willis is ……….……………………….. found in the ………………………….

Space

Label the Ventricles:

88

Name at least two causes of SAH:

Label the main arteries in the Circle of Willis: 1, 2, 6, 9, 12, 17

89

6. Describe common symptoms of a SAH

90

7. A SAH is graded in severity using the ……………………………………scale

Briefly describe the 1 – 5 scale and conscious level / deficits expected in each

8. Name at least two diagnostic tests used to detect a SAH

91

9. List 4 complications of SAH

10. Nimodipine can reduce complications, which one?

a. Stroke

b. Re-bleed

c. Low sodium

d. High sodium

11.Side effects of Nimodipine include:

92

12.A drop in GCS could be caused by:

14. EVD stands for E V D

15. An EVD is the treatment for a complication of SAH, which one?

16.Why would we monitor sodium levels closely in this patient group?

17.What treatment is there available? Name three.

93

a/

b/

c/

18.What does HHH stand for?

COMPETENCIES & RECORDS OF SUPERVISED PRACTICE

94

- There are a number of clinical competencies that can be achieved associated with this

area of practice. Please refer to the national competency folder and documentation.

STANDARDS FOR ASSESSMENT

95

COMPETENCY ASSESSMENT CRITERIA

Stage 0 Not applicable

Stage 1 Foundation

Can demonstrate basic skills that contribute to the activity under direct supervision of a competent practitioner

Applies to a practitioner gaining experience and developing skills and knowledge Developing knowledge of relevant policies, procedures and guidelines

Stage 2 Intermediate

Can demonstrate acceptable performance in the activity, but requires some supervision and guidance

Relies on some instruction Demonstrates knowledge and understanding of relevant policies, procedures and

guidelines

Stage 3 Proficient

Can demonstrate competent performance in the activity to specific criteria without direct supervision

Can supervise and instruct others in a range of activities related to roles and responsibilities

Consistently applies knowledge and understanding of any relevant policies, procedures and guidelines to the activity

Stage 4 Advanced

Can demonstrate skilled activity with advanced theoretical knowledge and understanding based on current research/best practice, relevant policies, procedures and guidelines

96

Can problem solve through critical analysis and evaluate in more complex situations

Stage 5 Expert

Can demonstrate skilled performance based on intuition, expert knowledge and established practice

Can solve problems through critical analysis and evaluation in more complex situations

Can identify new areas for research and change, and leads in the development of practice/service delivery

Ref. Adapted from

Storey L., Howard J., Gilles A. (2002)

Radcliffe Medical

RECORD OF SUPERVISED PRACTICE

Supervised practice of undertaking care of a head injured patient

The minimum standard to be achieved is stage 3 ‘Proficient’ and level 1 of the national competencies relating to neuro critical care

97

Procedure Comments Standard Achieved

Date

98

Learner Signature:……………… Preceptor/Assessor Signature:……………………

RECORD OF SUPERVISED PRACTICE

Procedure Comments Standard Date

99

Achieved

100

Learner Signature:……………… Preceptor/Assessor Signature:……………………

101

102