CHAPTER 9 Nursing patients with disorders of the nervous system
Introduction
Many nurses may have contact with patients suffering from neurological disorders. Community nursing staff are increasingly involved in the care of patients recovering at home following acute neurosurgical interventions or with long-term neurological conditions. The National Service Framework for Long-Term (Neurological) Conditions (Department of Health 2005) has highlighted the need for quality care of patients with neurological conditions, regardless of the setting in which they are cared for (Box 9.1 outlines the experiences of living with a lifelong illness).
Box 9.1 Evidence-based practice
Living with a lifelong or long-term illness
‘Idiopathic normal pressure hydrocephalus (iNPH) is a complex and multifaceted disorder of cerebrospinal fluid (CSF) circulation. This paper presents the findings of grounded theory research undertaken to explore the health and illness experiences of individuals diagnosed with iNPH. Purposive and theoretical sampling was used to recruit 26 participants who all had a confirmed diagnosis of iNPH for at least 6 months before data collection. Data were collected through in-depth semi-structured recorded interviews (n = 15) and written personal biographies (n = 11) and analysed using the Glaserian grounded theory method. Four themes emerged from the data: hope, frustration, isolation and life-long illness, and are used to explore and explain the experiences of those living with iNPH. Greater understanding of patients’ experiences will help health professionals provide meaningful and effective care for patients and their families.’
Gelling L, McVicar A: Living with idiopathic normal pressure hydrocephalus: A grounded theory study, British Journal of Neuroscience Nursing 5(4):173–178, 2009.
This chapter considers the more common neurological and neurosurgical disorders and, where appropriate, makes reference to the less common disorders. The further reading suggestions at the end of the chapter provide more detailed information. It is hoped that the information contained here will raise awareness of this specialised field of nursing, and stimulate further discussion on how best to meet the needs of the patient with a neurological condition and of their family and/or significant others.
Anatomy and physiology
The nervous system is a complex, interrelated body system responsible for many functions including communication, coordination, behaviour and intelligence. It constantly receives data from the external and internal environments, interprets these, and then responds by adapting appropriately to demands.
The nervous system has two main divisions; the central nervous system (CNS), comprising the brain and spinal cord, and the peripheral nervous system (PNS), consisting of the cranial and spinal nerves. The PNS has two functional parts, the somatic (sensory and motor) and autonomic divisions (pp. 308–311).
Basic tissue structure
Nervous tissue consists of neuroglia (glial cells) and neurones (nerve cells). The neuroglia markedly outnumber the neurones and form a supportive, nutritive and protective network for the nervous system. In the PNS, supporting cells, called Schwann cells, form the myelin sheath as well as having a phagocytic role.
Myelin protects and electrically insulates nerve fibres from one another and speeds up nerve impulse transmission. Myelinated nerve impulses are transmitted by saltatory conduction, whereby the impulse jumps from one node of Ranvier to the next (Figure 9.1). Impulses in myelinated nerves are therefore transmitted very much faster than in unmyelinated nerves and require much less energy.
Figure 9.1 Structure of a multipolar neurone. It consists of three parts: (1) The nerve cell body, which is grey in colour. Each cell body is enclosed in a selectively permeable membrane, which also extends along the cell processes. The cell body contains a nucleus surrounded by cytoplasm which also contains other structures called organelles. (2) The dendrites are thread-like extensions of the cell body which increase the surface area available to receive signals from other neurones. (3) The axon is a single long process that conducts impulses away from the cell body. In many large peripheral axons, the axolemma is surrounded by another covering called the myelin sheath. This is a multiple-layered covering of fatty material which is white in colour. Its function is to insulate the neurone electrically and thus speed up the conduction of the nerve impulse, by segmentation. Each interruption of the sheath is known as a node of Ranvier and the speed of the impulse is increased by its ‘jumping’ from node to node. The axon and its collaterals branch into axon terminals, the ends of which form a bulb-like structure. These help to transmit an impulse from one neurone to another across the gap (synapse) between them or at the junctions with effector cells.
Neurones
Neurones are the structural and functional unit of the nervous system. They are capable of conducting impulses throughout the nervous system and to other excitable tissues, including muscles and glands. The structure of a typical multipolar neurone is shown in Figure 9.1.
Sensory (afferent) neurones
transmit impulses from receptors in the skin, sense organs and viscera to the brain and spinal cord. These are usually unipolar (cells with processes projecting from one pole), or bipolar, (processes project from two poles at opposite ends of the cell body). Bipolar neurones are found only in special sense organs, e.g. the retina of the eye.
The nerve impulse
A nerve impulse can be initiated by a stimulus such as a change in temperature, pressure or the chemical environment, or impulses can be generated spontaneously by pacemaker cells. The impulse is a self-propagating wave of electrical charge along the neuronal membrane.
At rest, the neurone has an unequal distribution of potassium and sodium ions on either side of the plasma membrane, which are necessary to maintain the chemical difference that produces an electrical difference: the inside of the cell is negatively charged in relation to the outside. This has been measured at −70 mV and is termed the resting membrane potential. This state is maintained by exchange of ions between the intracellular and extracellular fluids. A property of all neurones is their ability to produce an impulse when a stimulus is sufficient to initiate certain electrical and chemical changes within the cell membrane. These positive–negative changes occur in rapid succession, spreading to the end of the axon. (See Further reading, e.g. Marieb & Hoehn 2007.)
Generally, the larger the diameter of the axon, the quicker the nerve impulse travels, but the alternative device of saltatory conduction is found in myelinated neurones (Figure 9.2).
Neurotransmitters
The junctions between one neurone and another, and between neurones and muscles or glands, are known as synapses. Nerve impulses are transmitted across the gap at most synapses by chemical transmitters (neurotransmitters). The chemical is stored in vesicles in the expanded end of the axon and is released when the nerve impulse reaches this point. Several neurotransmitters have been identified, the most common ones being acetylcholine and noradrenaline. Many neurotransmitters are excitatory, resulting in the nerve impulse producing an effect such as contraction of muscle cells. Some, however, have an inhibiting effect and prevent the onward transmission of impulses, allowing, for example, muscle cells to relax. The effect of the neurotransmitter is terminated when it is destroyed by enzymes or reabsorbed into the neurone.
The central nervous system
The CNS consists of the brain and spinal cord.
The brain
The cerebrum
The cerebrum forms the bulk of the brain. The outer surface, the cortex (grey matter) consists of neuronal cell bodies. The surface area of the cerebral cortex is increased by folding into a series of grooves (sulci) and ridges (gyri). The deeper grooves are termed fissures and some form landmarks, e.g. the longitudinal fissure which almost splits the brain into left and right hemispheres (Figure 9.3).
Figure 9.3 The lobes and sulci of the cerebrum. Each of the lobes is bounded by ‘landmark’ fissures: the frontal lobe is separated from the parietal lobe by the central sulcus; the temporal lobe is separated from the frontal and parietal lobes by the lateral sulcus; and the occipital lobe is separated from the temporal and parietal lobes by the parietal–occipital sulcus.
Each hemisphere is subdivided into lobes, and each lobe is named according to the skull bones it underlies:
The cerebral cortex is responsible for three main functions:
Certain areas of the cerebral cortex have been identified as being responsible for specific functions, and can be mapped (Figure 9.4).
Relative size
The thumbs, fingers, lips, tongue and vocal cords are more sensitive than the trunk, due to the greater number of receptors found in them. The homunculus (Figure 9.5) illustrates how the various parts of the body are represented in the corresponding motor and sensory areas of the cerebral hemispheres, i.e. representation is proportional not to the relative size of the body parts, but to each part’s complexity of movement or the extent of its sensory innervation.
Cerebral dominance
Some functions (e.g. speech) are found in only one hemisphere, i.e. they are lateralised. Motor control is usually more highly developed in one cerebral hemisphere than in the other. This is referred to as dominance. Approximately 95% of the population are dominant in the left hemisphere and are right-handed. If the dominant hemisphere is damaged, the opposite hemisphere is capable of taking over and assuming a dominant role.
Association areas
Association areas are less well defined and are thought to be responsible for complex functions such as integration of the senses, memory, learning, thought processes, behaviour and emotion.
Connecting pathways
White matter containing myelinated axons lies below the outer cortical layer and forms connections between the cerebral cortex and other areas of grey matter in the CNS. Three types of connecting pathways have been identified:
Basal nuclei (commonly called basal ganglia)
Within the white matter of the cerebrum are paired islands of grey matter called the basal nuclei (N.B. ‘ganglia’ more properly describes structures in the PNS). They control subconscious movements, such as swinging the arms while walking, and regulating muscle tone for specific body movements, a function that is lost in Parkinson’s disease.
Cerebellum
The cerebellum is located below the posterior part of the cerebrum and is separated from it by a fold of dura mater (p. 305). It consists of two hemispheres separated by a narrow strip called the vermis. The cortex of the cerebellum consists of grey matter, folded to increase its surface area. The interior comprises white matter presented in a branching configuration termed the arbor vitae (tree of life). Links to the rest of the brain and spinal cord allow the cerebellum to receive sensory information and thereby to maintain equilibrium and modify voluntary movement, making it smooth and coordinated.
Pituitary gland
The pituitary gland is situated at the base of the brain in a depression or fossa in the sphenoid bone called the ‘sella turcica’. It is attached to the brain via a stalk which is continuous with the hypothalamus, and communication is by means of nerve fibres and blood vessels (see Ch. 5, Part 1).
Diencephalon
Three bilaterally symmetrical structures comprise the diencephalon:
The thalamus
consists of two oval-shaped masses, mainly consisting of grey matter, situated within the cerebral hemispheres just below the corpus callosum. Sensory impulses associated with pain, temperature, pressure and touch are conveyed to the thalamus, which acts as a ‘gateway’. Chaos would reign if all sensory information were allowed to reach the sensory cortex.
Brain stem
This comprises three structures: the medulla, the pons and the midbrain. Inferiorly the medulla is continuous with the spinal cord and connects with the pons above. The pons is continuous with the midbrain, which connects with the lower portion of the diencephalon.
The medulla
All the spinal pathways pass through the medulla. Descending motor pathways (corticospinal and corticobulbar) cross to the opposite side in triangular-shaped structures called the pyramids, a process known as decussation. The medulla:
Table 9.1 Outline of the cranial nerves
| Cranial NerveName And Number | Type | Functions |
|---|---|---|
| Olfactory (I) | Sensory | Smell (olfaction) |
| Optic (II) | Sensory | Vision |
| Oculomotor (III) | MotorSensory | Controls four of the extrinsic (external) muscles that move the eyeball, and the muscle that raises the upper eyelidSome fibres control the iris muscle that constricts the pupil, and the ciliary muscle, which changes lens shapeProprioception |
| Trochlear (IV) | MotorSensory | Controls the external muscle that moves the eyeball down and outwardsProprioception |
| Trigeminal (V) (three branches: ophthalmic, maxillary, mandibular) | MotorSensory | Motor to the muscles of chewing (mastication)Sensory to the face, mouth, teeth and the nose |
| Abducens (VI) | MotorSensory | Controls the extrinsic (external) muscle that moves the eyeball outwardsProprioception |
| Facial (VII) | MotorSensory | Controls the facial, scalp and some neck muscles – facial expression. Autonomic fibres to the lacrimal (tear), nasal and some salivary glands – lacrimation and salivationAlso controls the tiny stapedius muscle in the middle ear Taste |
| Vestibulocochlear (VIII) | Sensory | Hearing (audition) and balance |
| Glossopharyngeal (IX) | MotorSensory | Controls the pharyngeal muscles involved in swallowing. Autonomic fibres to some salivary glands – salivationTasteCarotid sinus – regulation of blood pressureProprioception |
| Vagus (X) | MotorSensory | Supplies external ear, heart, larynx, trachea, bronchi, lungs, pharynx, oesophagus, stomach, small intestine and proximal part of large intestine, the liver, gallbladder and pancreas – swallowing, digestive secretions and movement, etc.Taste and other sensory inputs from structures innervated |
| Accessory (XI) | MotorSensory | Controls muscles of the neck and shoulders – head movement, shoulder shrugging. The pharynx, soft palate and larynx – swallowingProprioception |
| Hypoglossal (XII) | MotorSensory | Tongue movements during speech and swallowingProprioception |
The pons
The pons is a bridge between the medulla and the midbrain. It comprises fibres that connect with the cerebellum and fibres that link between the spinal cord and the brain. It contains the nuclei of cranial nerves V to VIII inclusive (see Table 9.1, p. 309). Other important nuclei also exert an influence on respiration.
The midbrain
The midbrain contains the centres for visual, auditory and postural reflexes. It is located above the pons and contains the nuclei of cranial nerves III and IV (see Table 9.1, p. 309). Cranial nerves I and II originate in the cerebrum.
The limbic system
A diffuse collection of nuclei, the limbic system, comprises an interconnected complex of structures, with links to the hypothalamus, cerebral cortex and the olfactory system. These are thought to be responsible for behaviour associated with emotions, subconscious motor and sensory drives and feelings of pain and pleasure.
The meninges
The brain and spinal cord are surrounded and protected by three meninges. From inside working out they are:
Pia mater
has its own blood supply and is a delicate layer that closely follows and adheres to the contours of the brain and spinal cord.
Arachnoid mater
is a fibrous layer between the pia and dura maters. It is separated from the pia mater by the subarachnoid space which contains cerebrospinal fluid (CSF). The arachnoid mater projects villi into the venous sinuses, which are responsible for the absorption of CSF.
Dura mater
is a double layer of dense fibrous tissue. It is separated from the arachnoid mater by the subdural space. The outer layer adheres closely to the underside of the cranial bones, whilst the inner, meningeal layer is much thinner. The spinal dura mater has only one layer, which corresponds to the meningeal layer of the cranium. The two layers of the dura mater separate at several locations and these spaces contain the venous sinuses, e.g. the falx cerebri and the tentorium cerebelli. The former forms an incomplete division dipping down between the two cerebral hemispheres (Figure 9.6). The tentorium cerebelli forms a division between the occipital lobes of the cerebrum and the cerebellum.
The ventricular system
The ventricular system of the brain comprises four fluid-filled irregular cavities (ventricles) interconnected by narrow pathways (Figure 9.7) and connected with the central canal of the spinal cord and the subarachnoid space. There are two lateral ventricles, one in each cerebral hemisphere, one ventricle (the third) located in the diencephalic region and the fourth located in the medulla.
Cerebrospinal fluid
circulates within the closed ventricular system. The normal features of CSF are:
The CSF production–absorption cycle is continuous and a fairly constant volume of 120–150 mL is maintained. When this process is interrupted and the volume is increased beyond normal limits, hydrocephalus occurs.
Most CSF is produced by the choroid plexus, a collection of specialised capillaries located within the lining of the ventricles, the largest amount being produced in the lateral ventricles. From here, the CSF passes through two interventricular foramina (foramen of Monro) to the third ventricle, then via the single cerebral aqueduct (aqueduct of Sylvius) to the fourth ventricle. Some CSF passes down into the central canal of the spinal cord but most passes up through the two lateral and one medial foramina in the roof of the fourth ventricle, to circulate round the brain and spinal cord in the subarachnoid space before being reabsorbed into the blood via the arachnoid villi.
Blood supply and drainage
The brain cannot survive without a constant supply of oxygen and glucose and receives 850 mL of oxygenated blood per minute. The blood supply to the head arises from the left and right common carotid arteries, which subdivide to form the internal and external carotid arteries. These supply blood to the anterior part of the brain, and the vertebral arteries supply the posterior part.
The greater part of the brain is supplied with blood by the arteries branching from the circulus arteriosus (circle of Willis), a ring of blood vessels located at the base of the brain (Figure 9.8).
Venous drainage is by small veins in the brain stem and cerebellum, and external and internal veins draining the cerebrum. Some of the external and internal veins empty into one large vein called the vein of Galen (great cerebral vein). Unlike other parts of the body, these veins do not correspond with their arterial supply. All these veins empty directly into a system of venous sinuses, including the superior and inferior sagittal, the straight, transverse, sigmoid and cavernous sinuses.
The blood–brain barrier
This selective barrier normally prevents many harmful substances crossing from the blood to the brain, e.g. microorganisms. The blood–brain barrier (BBB) is formed by the capillary endothelial cells which have ‘tight junctions’ and are supported by astrocytes (a type of neuroglial cells) to ensure that the capillary wall is relatively impermeable. The barrier allows the passage of oxygen, nutrients and metabolic waste, and some drugs, alcohol and other toxic substances.
The spinal cord
The spinal cord is an oval cylinder that lies within the spinal cavity of the vertebral column. In adults, it is approximately 45 cm long and extends from the medulla to the first or second lumbar vertebrae. Beyond this, the spinal nerves from the lumbar and sacral segments of the cord form the cauda equina, or ‘horse’s tail’. The lower part of the cord is attached to the coccyx by the filum terminale and is tapered in shape (Figure 9.9).
The cord is segmented into five parts or regions, each corresponding to the specific vertebrae:
A labelling system identifies different levels within the spinal cord and vertebrae; the third cervical vertebra becomes C3, the fourth lumbar vertebra becomes L4 and so on.
Two enlargements of the spinal cord are seen: (i) from C4 to T1 containing the nerve supply for the upper limbs; and (ii) from L2 to S3 which supplies innervation to the lower limbs. Paired spinal nerves, part of the PNS, are attached by two short roots to the cord (see pp. 308, 309).
The structure of the spinal cord is illustrated in cross-section in Figure 9.10.
Figure 9.10 Cross-section of the spinal cord. The cord is incompletely divided into right and left halves by the posterior and anterior median fissures. In the centre is the central canal which contains CSF originating from the fourth ventricle. Extending the entire length of the cord, this is located within an H-shaped area of grey matter with posterior and anterior and, at some levels, lateral horns. The remainder of the cord is made up of white matter organised in columns in the posterior, lateral and anterior segments.
The spinal pathways are described as:
Each pathway has a name, derived from the spinal column in which it travels, the origin of the cell bodies and the termination of the axon.
Sensory pathways
Posterior column pathway
Each pathway comprises a chain of three neurones which transmit information such as discriminative touch and vibration sense from the appropriate receptors to the sensory cortex.
Spinothalamic pathways
are the lateral and anterior spinothalamic tracts. The first order neurone in both pathways connects the receptor with the spinal cord where it synapses with the second order neurone in the posterior grey horn. The pathway crosses over to the opposite side of the cord and ascends in either the lateral or anterior spinothalamic tract to the thalamus. The second order neurone synapses with the third order neurone, which then continues, terminating in the sensory cortex. Between them the spinothalamic tracts are responsible for conveying information about pain (see Ch. 19) and temperature, light touch and pressure.
Cerebellar pathways
are the posterior spinocerebellar and anterior spinocerebellar tracts. Both tracts convey impulses about joint position sense (proprioception) from muscles and joints, terminating in the cerebellum instead of the cerebral cortex. This time there are only two neurones involved, synapsing in the posterior grey horn.
Motor pathways
Once a motor process is initiated within the cerebral cortex, the impulses descend via two main motor pathways:
Upper and lower motor neurones
These are the functional units of the motor system and convey motor impulses. Damage to one or the other will result in very different functional impairment. Damage to an upper motor neurone results in spasticity, while damage to a lower motor neurone results in flaccid paralysis.
Upper motor neurones
extend from the motor cortex to either the cranial nerve nuclei in the brain stem or the anterior horn of the spinal cord. The upper motor neurone is contained entirely within the CNS.
The peripheral nervous system
The PNS has two functional parts:
The cranial nerves
The 12 pairs of cranial nerves pass from their origin, principally within the brain stem, out via small openings in the skull to innervate structures around the head and neck, and beyond (Table 9.1). Cranial nerves were formerly described as either motor or sensory, or mixed nerves; however, most motor nerves are now considered to be mixed, but with a dominance of motor or sensory fibres. (See Further reading, e.g. Tortora & Derrickson 2009.)
Spinal nerves
There are 31 pairs of spinal nerves, named and grouped according to the vertebrae with which they are associated. There are:
It should be noted that there is one more pair of cervical spinal nerves than there are vertebrae. This is because the first pair leave the vertebral canal between the occipital bone and the atlas, i.e. above C1, and the eighth pair leave below C7. Thereafter, the spinal nerves are named according to the vertebra immediately above.
Each spinal nerve has an anterior (motor nerve fibres) and a posterior root (sensory) (see Figure 9.10). The posterior root can be distinguished by its root ganglion, a cluster of nerve cell bodies.
Shortly after leaving the intervertebral foramina, both roots join together to form a mixed nerve. From here the spinal nerves continue to form a complex network all over the body, carrying motor signals to effectors such as the skeletal muscles and conveying sensory information such as touch to the CNS for interpretation. (See Further reading, e.g. Tortora & Derrickson 2009.)
The autonomic nervous system
The ANS comprises the nerves carrying motor impulses to the internal organs; thus it is exclusively peripheral and motor. Its activity is influenced by many factors, including sensory information from the internal organs, numerous peptides and hormones, and signals from higher control centres such as the hypothalamus. It is described as having two divisions, the sympathetic and parasympathetic, each imposing different effects (Figures 9.11, 9.12). (See Further reading, e.g. Tortora & Derrickson 2009.)
Figure 9.11 The sympathetic outflow, the main structures supplied and the effects of stimulation. Solid lines, preganglionic fibres; broken lines, postganglionic fibres.
Neurological investigations
Patients may undergo a range of neurological investigations depending on their condition. Pre-procedure preparation and post-procedure care is identified in Table 9.2. The specific investigations performed for each condition are detailed throughout the chapter.
Head injury and raised intracranial pressure
In 2006/2007 almost 156 000 people were admitted to hospital in England as a result of head injury, the majority of whom were young males. These figures have risen significantly since the implementation of the NICE head injury guidelines in 2003, which were updated in 2007 (Goodacre 2008). The majority of head injuries are mild (Glasgow coma scale [GCS] 13–15) but moderate (GCS 9–12) or severe injuries (GCS 3–8) are more likely to result in morbidity and mortality (see Ch. 28).
Falls (24–43%) and assaults (30–50%) are the most common causes of mild head injury in the UK, followed by road accidents (25%), although these account for a far greater proportion of moderate to severe head injuries. Alcohol may be implicated in up to 65% of all adult head injuries (NICE 2007a).
Pathophysiology
The adult skull can be considered as a rigid box divided into two major compartments, containing non-compressible components. A uniform pressure, called intracranial pressure (ICP), is maintained, defined as the pressure exerted within the cerebral ventricular system. When an individual sustains a head injury or there is some abnormal pathology, e.g. a tumour, it can cause ICP to rise.
Three intracranial components contribute to maintaining ICP:
The brain tissue contributes 80% of the content. The remaining 20% is taken up in equal proportion by the CSF and the blood. Under normal circumstances, ICP is maintained within normal limits (0–15 mmHg), but when there is an increase in the volume of one of these components within the confined space of the skull a rise in ICP may occur. Transient rises in pressure occur with activities such as coughing or sneezing and this is a normal physiological response.
Changes to the brain and its associated structures following trauma may cause ICP to rise to a dangerous level, resulting in coma and leading to permanent brain damage or even death.
The causes and presenting symptoms of raised ICP
A raised ICP can be due to intracerebral or extracerebral causes (Box 9.2).
A rise in ICP can develop over a number of months in a slow-growing brain tumour, with the patient hardly noticing any symptoms, or it can occur in a matter of minutes following severe head injury, when the patient becomes immediately unconscious. A distinct correlation exists between ICP and conscious level; as ICP rises, conscious level deteriorates.
A relationship exists between the volume of a lesion inside the head and ICP, represented by the pressure–volume curve (Figure 9.13).
During the initial rise in ICP, compensatory mechanisms come into play. The cerebral ventricular system can reduce the volume of CSF by displacing it into a distensible spinal dural sac. A reduction in cerebral blood volume also occurs as a result of autoregulation, the ability of blood vessels to constrict according to local conditions. This is represented by the flattened part of the curve. However, this is only a temporary measure and, as the volume of the expanding lesion increases, compensation is overcome and the steep part of the curve is entered. Then for every small increase in volume, the corresponding rise in ICP is dramatic. This process has four identifiable stages (Box 9.3).
Stages of volume–pressure relationship in raised intracranial pressure
Other factors which have an influence on this complex process include cerebral blood flow and cerebral oedema. (See Further reading, e.g. Woodward & Mestecky 2011.)
Herniation
The skull has two compartments:
Herniation is the process by which tissue in a high-pressure compartment is compressed and forced through an available opening into an adjoining low-pressure compartment. Such a situation can exist in the patient with raised ICP.
The opening that permits trans-tentorial herniation is the tentorial notch, and that which permits tonsillar herniation is the foramen magnum.
Subfalcine herniation
involves the herniation of brain tissue across the midline from one side of the head to the other, under the falx cerebri.
Trans-tentorial herniation
involves the downward displacement of the cerebral hemispheres, diencephalon and midbrain (central herniation). The nerves and posterior cerebral arteries are stretched and compression of the oculomotor nerve (IIIrd cranial nerve) occurs, resulting in a non-reactive pupil that may also be dilated. These and other structures are displaced into the posterior fossa.
Lateral trans-tentorial herniation occurs in the presence of an expanding lesion located close to the temporal lobe. The medial part of the temporal lobe (the uncus) is forced downwards and can subsequently develop into a central herniation (Figure 9.14).
Medical/surgical management
Common presenting symptoms
The head-injured patient with raised ICP may be fully alert and orientated, but consciousness is usually impaired. Neurological deficits can be found, e.g. limb weakness or occurrence of a seizure. Answers to the questions listed below should be obtained as they have an influence on the management and outcome:
Early signs and symptoms of raised ICP include reduction in level of consciousness and focal neurological deficits (e.g. limb weakness or speech deficits), followed by pupil changes and finally systemic changes (Cushing’s triad – bradycardia, hypertension and reduced/irregular respiratory rate). Hyperthermia may also occur due to compression of the hypothalamus and loss of the ability to autoregulate temperature.
Investigations
In the head-injured patient, skull X-ray may reveal a fracture and computed tomography (CT) or magnetic resonance imaging (MRI) may demonstrate cerebral contusions or lacerations and/or an intracranial haematoma (Hickey 2002) (Box 9.4).
Brain injuries
Contusions
Contusions are bruising of the cerebral tissue, most commonly affecting the frontal, occipital and undersurface of the temporal lobes.
Lacerations
Brain tissue is lacerated as a result of, for example, a skull fracture, resulting in disruption to cellular activity which will produce focal neurological deficits such as hemiparesis (weakness on one side of the body).
ICP monitoring
One of the most important diagnostic measures is the monitoring of ICP. This is an invasive technique involving direct measurement of ICP. A typical system comprises a fibreoptic transducer-tipped catheter, which can be placed in the lateral ventricle, subdural or extradural space. The level of ICP is then transmitted to a digital data display as a waveform. A pulsatile waveform will be demonstrated along with a pressure level indicating if the patient’s ICP is within normal limits (≤15 mmHg) (Figure 9.15).
Treatment
In the past, the treatment of head injury focused primarily on the interventions required to reduce ICP. However, greater emphasis is now placed on maintaining cerebral perfusion pressure (CPP) which is the pressure needed to perfuse the brain with blood, at more than 70 mmHg (Box 9.5). Those patients with a high ICP, low blood pressure and low CPP make a poorer recovery. The means by which this is achieved are varied according to circumstances.
Hyperosmolar agents
An intravenous infusion of 100 mL of 20% mannitol over 15 min will reduce ICP by establishing an osmotic gradient between the plasma and brain tissue, thus removing water from the oedematous brain tissue to the blood. This will ‘buy’ time to allow the patient to be prepared for transfer to a specialist unit or for surgery. Repeated boluses may be administered over 24 hours, but may lead to a rebound increase in ICP.
Controlled ventilation
In the past it was recommended that the reduction of PaCO2 would reduce ICP. However, it also causes vasoconstriction, thus reducing cerebral blood volume. The resultant reduction in cerebral blood flow may itself cause ischaemic brain damage (Lindsay & Bone 2004) so patients are ventilated to keep PaCO2 within normal limits. Maintaining the blood pressure and CPP appear to be as important, if not more important, than lowering ICP.
Fluid management
Dextrose infusions should not be given to patients with head injuries. Due to disruption to the BBB, administration of dextrose could exacerbate cerebral oedema. 0.9% sodium chloride is the fluid of choice initially.
Sedatives
If ICP fails to respond to standard measures then sedation, under carefully controlled conditions, may help by reducing cerebral metabolism and thus offering a degree of protection for the brain (Lindsay & Bone 2004).
Surgical intervention
Surgery may be performed to remove a focal lesion such as an expanding haematoma and this may be combined with decompression. Withdrawal of small amounts of CSF via a ventricular catheter results in a reduction of ICP, but this provides only temporary relief. To be effective, drainage would require to be continuous, but this is often impractical.
Nursing management and health promotion: head injury
Head injury is preventable. This is an area in which nurses should exercise their health promotion skills, e.g. by emphasising the dangers associated with head injury and its detrimental effects when communicating with patients who have experience of minor head injury with good recovery, and with their families. This may include consideration of driver behaviour or unsafe work practices. The use of seatbelts for the driver and all car passengers has led to a reduction in head injuries, as has the use of protective headgear for motorcyclists and horse riders (Headway 2004). Because a common contributing factor in head injury is alcohol intake, where appropriate, the patient can be encouraged to consider personal lifestyle and the consumption of alcohol.
Immediate priorities
The immediate nursing aim is to prevent further damaging rises in ICP, and the first priority is to identify any alteration in respiratory function due to an inability to maintain an airway (Box 9.6). The nurse should be aware of the presence of other injuries, e.g. if the patient has been in a road traffic accident (see Chs 18, 27 for detail of assessment and interventions).
Respiratory care priorities in a patient with raised intracranial pressure
Assessment of neurological status
This is performed in order to:
Any deterioration in neurological status may be an early indication that ICP is rising further, thus increasing the likelihood of herniation (Mestecky 2007). Neurological assessment is important, as this may be the only indication that the patient’s condition is deteriorating and a standardised method of monitoring neurological status enhances this process. The gold standard method is the Glasgow Coma Scale (NICE 2007a) (Ch. 28).
The nurse, as the health care professional who normally spends most time with the patient, should learn to observe changes in the patient’s behaviour which may herald an impending change in neurological status, e.g. the patient who does not answer questions so readily or who is becoming agitated and restless (Box 9.7).
The expert neurosurgical nurse will be alert to the early warning signs that must be reported so that treatment can be carried out as soon as possible (p. 314).
Cardiovascular assessment
The final life-threatening concern in a patient with a rising ICP is the effect of alterations to systemic and cerebral circulation, due to shock and cardiovascular instability. Unless requested by medical staff to do otherwise, the nurse should always report if:
Readings which are outwith these parameters will render the patient more susceptible to brain damage as a result of raised ICP and lowered CPP. The recognition of the vulnerable patient has been greatly facilitated by the use of early warning system charts.
Surgery
Pre-operative care
Urgent surgery (e.g. craniotomy) may be indicated on admission or in response to subsequent deterioration. The nurse may need to prepare the patient in a very short time and also provide adequate explanation and reassurance (see Ch. 26).
Postoperative care
The overall priorities for patients following neurosurgery are:
Table 9.3 outlines the main complications of neurosurgery.
Table 9.3 Complications of neurosurgery
| Complications | Cause | Interventions |
|---|---|---|
| Altered conscious level | Increased ICP due to cerebral haemorrhage/oedema | Frequent assessment of neurological status |
| Onset of seizures | Cerebral irritation | Observation of seizures. Appropriate interventions if they occur (see section on epilepsy) |
| Limb weakness | Increased ICP due to cerebral haemorrhage/oedema | Frequent assessment of limb movements |
| Speech problems | Increased ICP due to cerebral haemorrhage/oedema | Frequent assessment of verbal responses |
| Respiratory problems | Increased ICP due to cerebral haemorrhage/oedema | Frequent assessment of respiratory status |
| Loss of swallowing reflex | Increased ICP due to cerebral haemorrhage/oedema | Assessment of swallowing and keep nil by mouth |
| Loss of corneal reflex | Increased ICP due to cerebral haemorrhage/oedema | Eye care. Keep eyes closed to protect cornea |
| Periorbital oedema | Direct result of surgery | Observe for swollen/bruised periorbital tissues |
As the patient progresses, their needs will require to be reassessed and the nursing interventions adjusted accordingly. The aim of care is to ensure optimal function and the early detection of complications.
Subsequent considerations
All of the nursing interventions identified in Chapter 26 will apply. Only those interventions specific to the patient who is unconscious due to raised ICP are included here. The main aim of care remains that of preventing further rises in ICP.
The patient care outlined in the following sections uses the Roper et al (1980) framework of the activities of living model.
Communicating
Unpleasant stimuli are known to increase ICP, so the nurse should take a calm, reassuring approach. Relatives should be encouraged to talk to the patient and, although they may feel rather foolish at first, they will be encouraged if they see the nurse doing this. They should, however, be warned to avoid discussing potentially upsetting topics as the unconscious patient may still be able to hear (Hickey 2002) and this may cause their ICP to rise.
Any investigations or care to be performed should be explained to the patient and their family who will be anxious and distressed at this time, particularly as outcomes may be uncertain.
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