Neurological assessment of head injuries using the Glasgow ...
[pic]
Cheshire and Mersey Critical Care Network
Neuro Critical Care Work Book
Workbook Series
Number: xx
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
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
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
Learning Outcomes
• Having completed this pack you will be able to: -
1 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.
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 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.
- 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
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:
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
[pic] fig 1 (.uk)
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.
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.
[pic]Fig 2
()
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?
[pic]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.
[pic]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.
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.
[pic]Fig 5.
|Organ |Sympathetic System |Parasympathetic System |
|Eye |Dilates pupil |Constricts pupil |
|Tear glands |No effect |Stimulates tear secretion |
|Salivary glands |Inhibits saliva production |Stimulates saliva production |
|Lungs |Dilates bronchi |Constricts bronchi |
|Heart |Speeds up heart rate |Slows down heart rate |
|Gut |Inhibits peristalsis |Stimulates peristalsis |
|Liver |Stimulates glucose production |Stimulates bile production |
|Bladder |Inhibits urination |Stimulates urination |
Fig 6.
Somatic nervous system:
Reflex arc.
[pic]Fig 7.
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.
Gross structures.
[pic]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).
[pic]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.
[pic]
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.
[pic]
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.
[pic]
Fig 12
[pic]Fig 13
Frontal Lobe
Primary motor cortex which controls motor movement of the opposite side of the body.
[pic]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.
[pic]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:
[pic]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.
[pic]Fig17
The Amygdala
Stores 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
Stress response
The Thalamus
This 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.
[pic]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.
The Brain Stem.
[pic]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
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.
[pic]Fig 20
|Cranial Nerve: | |Major Functions: |
| | | |
|I Olfactory | |smell |
| | | |
|II Optic | |vision |
| | | |
|III Oculomotor | |eyelid and eyeball movement, pupil constriction |
| | | |
|IV Trochlear | |innervates superior oblique |
| | |turns 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 & saliva |
| | |taste |
|VIII Vestibulocochlear | |hearing |
|(auditory) | |equilibrium, balance |
|IX Glossopharyngeal | |taste |
| | |senses carotid blood pressure |
|X Vagus | |senses aortic blood pressure |
| | |slows heart rate |
| | |stimulates digestive organs |
| | |taste |
| | |Vocal cords |
|XI Spinal Accessory | |controls trapezius & sternocleidomastoid |
| | |controls swallowing |
|XII Hypoglossal | |controls tongue movements |
| | | |
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
.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
[pic]Fig 21
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).
[pic]
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)
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 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
[pic]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
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.
[pic]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 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:
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 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
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.
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 (ninds.) and read about myasthenia gravis.
The Spine.
This section is brief as there is a separate work book on this subject.
[pic]Fig 23
There are 31 pairs of spinal nerves.
[pic]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.
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:
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
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.
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
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.
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 assessor
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 |Vigilance of the nursing team is vital for early detection and |
|received training in the techniques and has been passed as |treatment of deterioration thus prevention of secondary brain injury|
|competent. |and improved prognosis. |
| | |
|Observations should be performed and recorded on a half-hourly basis|The frequency of neurological observations is determined by |
|until GCS equal to 15 has been achieved. |professional judgement (Edwards, 2001). It is therefore essential |
|Following assessment in A&E The minimum frequency of observations |that decisions are made by a trained and competent practitioner. |
|for patients with GCS equal to 15 should be as follows: |The condition of the patient, combined with clinical judgement, |
|half-hourly for 2 hours |should determine frequency. The patient in A&E who has sustained a |
|then 1-hourly for 4 hours |brain injury must be observed frequently as early intervention may |
|then 2-hourly thereafter. |prevent secondary injury. Deterioration can be subtle in onset and |
|If a patient with GCS equal to 15 deteriorates at any time after the|the patient requires detailed and frequent observation. |
|initial 2-hour period, observations should revert to half-hourly and|If the patient is deteriorating there must be assessment by an |
|follow the original frequency schedule (NICE, 2007). |anaesthetist. Aspiration, airway obstruction and subsequent lung |
|This includes the full vital sign set: Bp, SA02, pulse, resps, temp,|infiltration leads to hypoxia and secondary brain injury therefore |
|GCS & pupil size and reaction. |increased length of stay in hospital and poor outcome. |
|Inform medical staff of any deterioration without delay. |A patient who is deteriorating and requires transfer to CT / a |
|It is recommended that nurses who are handing over a patient perform|specialist centre or has a GCS less than 8 should be intubated. |
|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. |RATIONALE |
| | |
|ACTION | |
|EYE OPENING – | |
| |Assesses wakefulness, a function of structures within the brainstem |
|Spontaneously 4 |(Lindsay et al, 2004; Waterhouse, 2005). |
|To speech 3 | |
|To pain 2 | |
|None 1 |Spontaneous eye opening is an indication that the arousal mechanisms|
|Eyes closed by swelling = C |within the brain are |
| |Functioning (Teasdale, 1976). |
| | |
|Assess for eye opening by observing the patient as you approach: |If neuronal pathways are impaired due to trauma or a rise in |
|eyes open spontaneously, |intracranial pressure, a greater sensory stimulus is needed to evoke|
|score 4. |eye opening (Edwards, 2001). |
| | |
|If the patient’s eyes remain closed, say something to elicit a | |
|response: eyes open, |‘Central’ painful stimulus may result in the patient grimacing and |
|score 3. |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) |
|Speech, touch and finally pain is utilised. | |
|If there is no response to speech, touch the patient on hand, arm or|Peripheral pain may be applied to the side of the finger not the |
|shoulder and |nail bed to prevent damage (Edwards, 2001). |
|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 application of painful | |
|stimulus, score 1. | |
| | |
|ACTION |RATIONALE |
| | |
|VERBAL RESPONSE |Determines comprehension, cognition and reflects the ability to |
| |process thoughts into words. Be aware that confusion can be subtle |
|Orientated 5 |and only detected in conversation after a few minutes. The patient |
|Disorientated 4 |may learn responses if corrected following frequent observation |
|Inappropriate words 3 |therefore variation of questions can be useful. |
|Incomprehensible sounds 2 |Core elements must be correct, the patient must know who he/she is, |
|None 1 |where he/she is and the date (Teasdale, 1976) |
|Endotracheal tube or tracheostomy = T | |
| |Focal lesions may cause speech difficulties such as |
|Ask questions to assess orientation to time, place and person, e.g. |expressive/receptive dysphasia/aphasia and may not indicate impaired|
|ask the patient the month or year, where they are and who they are. |consciousness (Teasdale,1976): |
| | |
|Avoid questions that elicit a yes/no response. | |
| |Aphasia description: |
|Dysphasic patients cannot be assessed accurately for orientation. | |
| |Receptive aphasia: Inability to process written or spoken language |
|If correct answers are elicited to all 3 questions, | |
|score 5. |Expressive aphasia: Inability to express written or spoken language |
| | |
|If the patient cannot answer the above questions correctly but is |Global aphasia: Inability to receive language or express using |
|able to engage in conversation, |written or spoken language |
|score 4. | |
| |Dysphasia description: |
|If single word answers are given or if the patient is unable to form| |
|a sentence; inappropriate words, |Receptive dysphasia: Inability or difficulty in understanding the |
|score 3. |spoken word: due to damage to Wernicke’s area responsible for |
|If only noises such as grunting sounds are made, |comprehension of speech |
|score 2. |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 |
|If the patient makes no attempt to speak and no sounds are made, |words to reply. |
|score 1. | |
|At this stage responses may not be elicited by talking to the |Dysarthria: Slurred speech |
|patient and a painful stimulus may be required (Waterhouse, 2005). | |
| |(Lindsay et al, 2004). |
|If no verbal response is possible due to an endotracheal tube or | |
|tracheostomy (without |Teasdale and Jennett (1974) recommended descriptive narration beside|
|a speaking valve) write ‘T’ against ‘none’. |the chart when difficulties in categorising the patient are |
| |experienced. |
| | |
| | |
|Motor response |Assesses areas of the brain that identify sensory input and ability |
|Obey commands 6 |to translate this into a motor response (Lindsay, 2004). |
|Localise to pain 5 | |
|Flexion to pain 4 | |
|Flexion abnormal 3 |The ability to follow a command indicates that the patient can |
|Extension 2 |process instructions (Fischer |
|None 1 |and Mathieson, 2001). |
| |Grasping is a primitive reflex and may happen spontaneously and not |
|Record the best arm response. Do not ask to squeeze hands. Request a|in response to command (Teasdale, 1976) |
|specific action, i.e; ‘raise your arms, wriggle your fingers, pull |Patients with a spinal lesion or neurological condition may not be |
|me towards you, push me away.’ If the patient cannot respond ask |able to move limbs but may be awake and able to move the tongue or |
|them to stick the tongue out / move eyes to the left, right. |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|
|If no motor response to loud speech or touch is made: |to the orbit (Lowry, 1998; Edwards, 2001; Waterhouse, 2005) |
|A painful stimulus should be used, pressure applied over the |therefore these techniques should only be used by practitioners |
|supra-orbital nerve (except for suspected facial fractures) or to |trained and competent. |
|the spinal accessory nerve lying under the trapezius muscle (except |Orbit pressure should not be applied if facial fractures are present|
|for high cervical fractures). Essentially the painful stimulus |or suspected. |
|should be located on or as near to the head as possible and above |‘Central’ painful stimuli is a more reliable indicator of brain |
|the clavicle. |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 |
|Methods of applying central pain stimuli. |midline of the body in an attempt to push away from the source of |
| |the painful stimuli (Fischer and Mathieson, 2001). The patient may |
|Trapezium squeeze (cervical spine C3-4): Use thumb and two fingers |be spontaneously localising to an irritant such as an oxygen mask. |
|as pincers. Feel for the trapezium muscle and twist or squeeze. |The patient therefore demonstrates an awareness of environment. |
|Significant pressure is exerted for no longer than 20 seconds and |Flexion to pain is an indication of more severe dysfunction (Lindsay|
|any verbal and non verbal responses noted. |et al, 2004; Fischer and Mathieson, 2001). Abnormal flexion (arms |
| |withdraw up and wrists rotate inwards) may be an indication of a |
|Supraorbital pressure (trigeminal V): Under the eyebrow edge feel |lesion in the cerebral hemisphere or internal capsule (Fischer and |
|for a notch. Press hard with the thumb for a maximum of 30 seconds. |Mathieson, 2001). |
|Not to be used if facial fractures are suspected or confirmed. Use | |
|if a high cervical insult or injury suspected. |Extension (arms push down) indicates severe cerebral damage below |
| |the level of the red nucleus |
|If there is no localising response then peripheral pain to the |(Lindsay et al, 2004). |
|finger may be used. Assess each limb separately and record the best|No response may indicate a spinal cord lesion or late stage raised |
|response. |intracranial pressure. |
| | |
| | |
| | |
| | |
| | |
| | |
| | |
| | |
| | |
| | |
| | |
| | |
|ACTION |RATIONALE |
| |Abnormal reactions can indicate raised intracranial pressure and/or |
|PUPIL REACTIONS |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 |
|(See appendix p 16 – 17) |consensual response. |
| |Progressive dilatation and loss of pupil reaction on one side can be|
|Determine patient history that may affect pupil reactions e.g. |due to pressure on the oculomotor nerve on the same side. Damage can|
|cataracts, iridectomy or recent drug therapy that may dilate or |be caused by a variety of lesions, however, if pressure continues, |
|constrict the pupil. |the nerve on the other side can also be compressed resulting in |
| |bilaterally unreactive, dilated pupils; a sign of severe damage and |
|Note the size, shape, equality and position of the pupils (both eyes|brain herniation (Lindsay et al, 2004). |
|simultaneously). |Both pupils should be assessed at the same time to observe and |
| |compare reaction. |
|Using a pen torch, shine the light moving from 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. |IDENTIFICATION OF FOCAL DEFICIT |
| | |
| | |
| | |
| | |
| | |
|TESTING LIMB POWER | |
|ACTION |RATIONALE |
| | |
| | |
|LIMB POWER |Limb responses may give clues to the origin of the neurological |
| |dysfunction (Lindsay et al, 2004); eg, a weak limb on the right side|
|(recorded on limb section of chart) |will indicate damage to the left motor strip, or ipsilateral spinal |
| |cord |
|Each limb will be assessed |The GCS is the total score of the best responses; however, it is |
| |essential to reveal any weakness and difference in power. Clinical |
|Arm strength. |examination of the limbs may be carried out to aid clarity. Each |
| |limb may be scored out of 5: |
|Ask the patient to close their eyes and hold their arms out in front|5 normal |
|of them, palms facing up. If the patient can maintain this position,|4 move against some resistance |
|record the power as normal. |3 move against gravity only |
| |2 Can move with gravity eliminated |
|The power of each limb should be recorded separately on the lower |1 Flicker |
|section of the assessment chart. |0 nothing |
| | |
|The best response is charted on the GCS graph at the top of the |Assessment of strength is then transcribed onto the limb assessment |
|chart using one dot. |section of the observation chart |
| | |
|If an arm drifts downwards record that limb as mildly weak. The |normal strength - full movement against both gravity and resistance.|
|mildest response is that the palm rotates to a downward position | |
|known as pronator drift. | |
| |mild weakness - limb moves against gravity but not against |
|If the patient is unable or has extreme difficulty in lifting their |resistance (no push/pull). |
|arms off the bed but can make some movement (eg move fingers) record| |
|as severely weak. |severe weakness – limb is able to move but unable to lift against |
|If the patient is unable to move their arms, apply pain and record |gravity. |
|the response | |
|(see figure on posturing) | |
| | |
| |Lower limb response to peripheral painful stimuli is not reliable |
| |due to involvement of spinal reflexes therefore the best limb |
|Leg strength. |response charted on the GCS will be from the arms (Hickey, |
| |2009;Lindsay et al,2004). |
|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. | |
|ACTION |RATIONALE |
| | |
|VITAL SIGNS | |
| |GCS is one component of assessment. Vital signs complete the full |
|Will be monitored and recorded concurrently with neurological |complement of data on which treatment and intervention can be based.|
|assessment: | |
| |Base of skull fracture and CSF rhinorrhoea/otorrhoea (CSF drip from|
|Temperature |nose/ear) increase risk of infection. |
|Investigate and treat cause of temperature. |A patient who has sustained a severe head injury may have localised |
|Septic screen |damage to the temperature regulating centre in the hypothalamus. As |
|liaise with microbiology team |the patient’s temperature rises vasodilation of the cerebral blood |
|Fluid from ear / nose which tests positive for glucose may be |vessels takes up more room in the closed box of the skull |
|cerebrospinal fluid |(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). |
|Pulse – |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 |
|Blood Pressure |the ICP has been high. |
| |Hypotension – if autoregulation is impaired by a cerebral event |
|Beat to beat real time invasive monitoring will be used for all |hypotension results in decreased |
|patients requiring intubation and for patients who are |blood flow and therefore oxygen supply to the brain. |
|deteriorating: |Cerebral perfusion (CPP) must be maintained to prevent secondary |
|ECG |injury. |
|Invasive Bp |Hypotension may also be caused by hypovolaemia, sepsis, sedative |
|Blood gas analysis |drugs etc. Causes of hypotension must be treated immediately. |
|On going ABCDE assessment | |
|Pupil assessment | |
| |The target cerebral perfusion pressure is 60 – 70 mmHg. CPP below 60|
|Cerebral perfusion = mean arterial pressure (MAP) – intracranial |carries a risk of secondary brain injury through infarction and |
|pressure (ICP) |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. |
|HYPOXIA & HYPOTENSION PREVENTION – ABCDE | |
|MAP > 80 PO2 > 13 PCO2 4.5 – 5 |If the patient is deteriorating there must be assessment by an |
|SAO2 > 97 TIMELY INTUBATION |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 prognosis. |
| | |
| | |
|Respirations | |
Follow local care plan, guidelines and care bundles for care of the unconscious patient & artificially ventilated patient.
|ACTION |RATIONALE |
| | |
| | |
|Urine output will be monitored hourly. |Diabetes insipidus (DI) indicated by excessive urine output, low |
| |urine osmolality and rising serum osmolality and serum sodium. |
|Insert a urinary catheter if GCS is 12 or less. | |
| |Normally the pituitary gland secretes antidiuretic hormone (ADH) |
|If urine output exceeds 3oo ml per hour for two consecutive hours |when blood osmolality rises. This function is disrupted due to |
|perform urine specific gravity, paired urine and serum osmolality. |rising ICP. Large volumes of water are passed and the sodium |
|Report results to medical colleagues. |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 |RATIONALE |
| | |
|Avoid neck flexion |Cerebral venous drainage will be impeded by neck flexion and poor |
| |body positioning. This will cause a rise in ICP. Intra-abdominal |
|keep the body in alignment. |pressure may also cause a rise in ICP therefore hips should not be |
|Nurse head up by 20 - 30 degrees. |bent at an acute angle (Hickey, 2009). |
| |Risk of aspiration into the lungs is increased in intubated patients|
|If spinal injury is suspected – tilt the bed end down to achieve |if nursed at an angle less than 30 degrees (ventilator care bundle).|
|position whilst maintaining alignment. | |
|ACTION |RATIONALE |
| | |
|Observe for seizure activity |A,B,C,D,E protocol. Seizure control immediately. |
| |Seizures increase cerebral metabolism and increase ICP therefore |
|When the patient is sedated and artificially ventilated seizure |risk of secondary brain injury. |
|activity is difficult to detect but may be manifested by | |
|tachycardia, pupil changes and cardiovascular instability. | |
| ACTION |RATIONALE |
| | |
|Specific fluid balance: |Blood volume must be maintained to prevent hypotension and maintain |
|A detailed hourly fluid balance account will be maintained. |cerebral blood flow. |
|Aim for a neutral balance. |Water balance between the intravascular space and brain tissue |
|Avoid use of hypOtonic solutions and 5% glucose. |depends upon an osmotic gradient. Glucose contained within |
|Monitor serum sodium determine cause if low. |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. |
|Mannitol will be administered by expert request to manage high ICP | |
| |Hypertonic saline reduces brain water and increases intravascular |
|Hypertonic saline administration may be requested (refer to Walton |volume. Serum sodium will rise and serum osmolality will rise. This |
|Centre guidelines) |is the therapeutic nature of hypertonic saline |
| |(Refer to Walton Centre ICP management guidelines). |
|ACTION |RATIONALE |
| | |
|Blood gases – specific value ranges |Maintain oxygenation of the damaged brain. |
| | |
|Maintain PO2 > 13 kpa |CO2 can cause vasodilatation of cerebral vessels which will then |
|Maintain CO2 4.5 – 5 kpa |take up more room in the confines of the skull (see appendix). ICP |
|Pre-oxygenation with 100% O2 for 60 seconds prior to suctioning ET |will rise. |
|tube. | |
| | |
|(refer to Walton Centre ICP management protocol) | |
| | |
|Sedation of the artificially ventilated patient specifics |RATIONALE |
| | |
|In acute stages of head injury management sedation must be adequate | |
|to prevent coughing and bucking on the endotracheal tube |Coughing and straining will increase ICP. |
|spontaneously and when suction is applied. | |
|Sedation holds (ventilator care bundle) should not be performed in | |
|acute ICP management. | |
|Ventilator mode: |RATIONALE |
| | |
|Ventilator modes which give predictable tidal volumes are |Sudden rises in CO2 due to poor compliance with pressure limited |
|recommended |modes may occur. |
Abnormal posturing.
[pic]
Afferent = impulse in from environment
Efferent = impulse from the brain
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Waterhouse, C (2005) The Glasgow Come Scale and other neurological observations. (learning
zone: 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
FURTHER READING
Dootson, S (1990) Critical Care: Sensory Imbalance and Sleep Loss Nursing Times Vol. 86 No. 35
pp. 26-29.
Ellis, A and Cavanagh, SJ (1992) Aspects of Neurological Assessment using the Glasgow Coma
Scale. 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. 1
pp. 19-23
Teasdale, G M and Murray, L (2000) Revisiting the Coma Scale and Coma Score. Intensive Care
Medicine 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:
.uk
faculty.
TRAUMATIC BRAIN INJURY
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.
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.
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.
[pic]
This graph demonstrates a loss of autoregulation following TBI. CPP is reduced by increases in ICP.
[pic]
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
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
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
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?
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.
[pic]
9. What is the name for this posture?
[pic]
10. Describe a normal pupil response to light.
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?
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
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
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.
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.
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 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.
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 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
-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:
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:
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:
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:
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:
nhs.uk/conditions/Subarachnoid-haemorrhage
.uk/.../subarachnoid_haemorrhage/
.uk
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:
[pic]
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)
[pic]
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.
[pic]
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 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
The Circle of Willis is ……….……………………….. found in the …………………………. Space
Label the Ventricles:
[pic]
Name at least two causes of SAH:
Label the main arteries in the Circle of Willis: 1, 2, 6, 9, 12, 17
[pic]
6. Describe common symptoms of a SAH
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
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:
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.
a/
b/
c/
18. What does HHH stand for?
COMPETENCIES & RECORDS OF SUPERVISED PRACTICE
- 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
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
• 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
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Learner Signature:……………… Preceptor/Assessor Signature:……………………
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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.
INTRACRANIAL PRESSURE
CEREBRAL PERFUSION PRESSURE
The brain stem is compressed producing the Cushing response – BP up, HR down
The oculomotor III nerve is compressed and the pupil fixes and dilates
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