Chapter 56 NURSING MANAGEMENT: acute intracranial problems
1. Identify the physiological mechanisms that maintain normal intracranial pressure.
2. Explain the aetiology of increased intracranial pressure, linking this to the clinical manifestations.
3. Describe the multidisciplinary care and nursing management of the patient with increased intracranial pressure.
4. Differentiate between types of head injury by mechanism of injury and clinical manifestations.
5. Describe the multidisciplinary care and nursing management of the patient with a head injury.
6. Compare the types, clinical manifestations and multidisciplinary care of brain tumours.
7. Discuss the nursing management of the patient with a brain tumour.
8. Analyse the nursing management of the patient undergoing cranial surgery.
9. Compare the primary causes, multidisciplinary care and nursing management of meningitis, encephalitis and brain abscess.
Acute intracranial problems include diseases and disorders that can increase intracranial pressure (ICP). This chapter discusses the mechanisms that maintain normal ICP, increased ICP, head injury, brain tumours and cerebral inflammatory disorders.
Intracranial pressure
It is important to understand the mechanisms associated with ICP when caring for patients with many different neurological problems. The skull is like a closed box with three essential volume components: brain tissue, blood and cerebrospinal fluid (CSF; see Fig 56-1). The total volume in the adult skull is 1900 mL. The intracellular and extracellular fluids of brain tissue make up approximately 78% of this volume; blood in the arterial, venous and capillary network makes up 12%; and the remaining 10% is CSF. Under normal conditions, in which intracranial volume remains relatively constant, the balance between these components maintains the ICP. Factors that influence ICP under normal circumstances are changes in: (1) arterial pressure; (2) venous pressure; (3) intraabdominal and intrathoracic pressures; (4) posture; (5) temperature; and (6) blood gases, particularly CO2 levels. The degree to which these factors increase or decrease the ICP depends on the ability of the brain to accommodate to the changes.
REGULATION AND MAINTENANCE OF INTRACRANIAL PRESSURE
Normal intracranial pressure
ICP is the hydrostatic force measured in the brain CSF compartment. Normal ICP is the pressure exerted by the total volume from the three components within the skull: brain tissue, blood and CSF. The modified Monro-Kellie doctrine describes the relatively constant volume of these three components within the rigid skull structure. If the volume of any one of the three components increases within the cranial vault and the volume from another component is displaced, the total intracranial volume will not change.1 This hypothesis is not applicable in situations in which the skull is not rigid (e.g. in neonates and in adults with unfused skull fractures or postsurgical craniectomy).
Normal compensatory adaptations
In applying the modified Monro-Kellie doctrine, the body can adapt to changes in the volume of components of the skull to maintain a normal ICP. Initial compensatory mechanisms include changes in the CSF volume due to altering CSF absorption or production, and displacement of CSF into the spinal subarachnoid space. Alterations in intracranial blood volume occur through the collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation and changes in venous outflow. Tissue brain volume compensates through distension of the dura or compression of brain tissue. Initially, an increase in volume produces no increase in ICP because of these compensatory mechanisms. However, these compensatory adaptations to changes in volume are limited; as the volume increase continues, the ICP rises and decompensation occurs, resulting in compression and ischaemia.2
Measuring ICP
ICP can be measured in the ventricles, subarachnoid space, subdural space, epidural space or brain parenchymal tissue using a water manometer or a pressure transducer. Normal ICP ranges from 0 to 15 mmHg. A sustained pressure above the upper limit is considered abnormal. ICP may become elevated because of head trauma; stroke; subdural, intracerebral or subarachnoid haemorrhage; brain tumour; inflammation; hydrocephalus; or brain tissue damage from other causes. Any patient who becomes acutely unconscious, regardless of the cause, is managed as if there were actual or potential elevations in the ICP. Patients with, or at risk of, elevated ICP usually receive invasive ICP monitoring in an intensive care unit (ICU), except those with irreversible problems or advanced neurological disease. Goals for nursing management of the patient with an elevated ICP include preservation of cerebral oxygenation and perfusion, early identification of neurological changes and prevention of complications.
CEREBRAL BLOOD FLOW
Cerebral blood flow (CBF) is the amount of blood in millilitres passing through 100 g of brain tissue in 1 minute. The global CBF is approximately 55 mL per minute per 100 g of brain tissue. There is a difference in flow between the white and grey matter of the brain. The white matter has a slower blood flow, approximately 25 mL per minute per 100 g, and the grey matter has a faster blood flow, approximately 75 mL per minute per 100 g.3 The maintenance of blood flow to the brain is critical because the brain requires a constant supply of oxygen and glucose. The brain uses 20% of the body’s oxygen and 25% of its glucose.
Autoregulation of cerebral blood flow
The brain has the ability to regulate its own blood flow in response to its metabolic needs in spite of wide fluctuations in systemic arterial pressure. Autoregulation is defined as the automatic alteration in the diameter of the cerebral blood vessels to maintain a constant blood flow to the brain during changes in systemic arterial pressure.3 The purpose of autoregulation is to ensure a consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure (CPP) within normal limits.
The lower limit of systemic arterial pressure at which autoregulation is effective in a normotensive person is a mean arterial pressure (MAP) of 50 mmHg. Below this, CBF decreases and symptoms of cerebral ischaemia, such as syncope and blurred vision, occur. The upper limit of systemic arterial pressure at which autoregulation is effective is a MAP of 150 mmHg.2 When this pressure is exceeded, the vessels are maximally constricted and further vasoconstrictor response is lost.
The CPP is the pressure needed to ensure blood flow to the brain. It is equal to the MAP minus the ICP (CPP = MAP – ICP; see the example in Box 56-1). This formula is clinically useful, although it does not consider the effect of systemic vascular resistance. Cerebral vascular resistance, generated by the arterioles within the cranium, links CPP and blood flow as follows:
BOX 56-1 Calculation of cerebral perfusion pressure
Example: systemic blood pressure = 122/84 mmHg
CPP, cerebral perfusion pressure; DBP, diastolic blood pressure; ICP, intracranial pressure; MAP, mean arterial pressure; SBP, systolic blood pressure.
CPP = flow × resistance
Non-invasive techniques used in intensive care to monitor changes in cerebrovascular resistance include transcranial Doppler studies.
As the CPP decreases, autoregulation fails and CBF decreases. Normal CPP is 70–100 mmHg. At least 50–60 mmHg is necessary for adequate cerebral perfusion. A CPP less than 50 mmHg is associated with ischaemia and neuronal death. A CPP below 30 mmHg results in cellular ischaemia and is incompatible with life. Under normal circumstances, autoregulation maintains an adequate CBF and CPP primarily by cerebral vasoreactivity and metabolic adjustments that affect the ICP. It is of paramount importance to maintain MAP when ICP is elevated. It should be remembered that CPP does not reflect perfusion pressure in all parts of the brain. There may be local areas of swelling and compression limiting regional perfusion pressure. Thus, a higher CPP may be needed for these patients to prevent localised tissue damage.
Pressure changes
The relationship of pressure to volume is depicted in the pressure–volume curve. The curve is affected by the brain’s elastance and compliance. Elastance is the brain’s ability to accommodate changes in volume. It represents the stiffness of the brain. With high elastance, large increases in pressure occur with small increases in volume.
Elastance = pressure/volume
Compliance is the inverse of elastance and is the expandability of the brain. It is represented as the volume increase for each unit increase in pressure. Low compliance is the same as high elastance. With low compliance, large changes in pressure result from small changes in volume.
Compliance = volume/pressure
The concept of the pressure–volume curve can be used to represent the stages of increased ICP (intracranial hypertension; see Fig 56-2). At stage 1 on the curve, there is high compliance and low elastance. The brain is in total compensation, with accommodation and autoregulation intact. An increase in volume (in any of the three volume components) does not increase the ICP. At stage 2, the compliance is lower and elastance is increasing. An increase in volume places the patient at risk of increased ICP. At stage 3, there is high elastance and low compliance. Any small addition of volume causes a great increase in pressure. Compensatory mechanisms fail, there is a loss of autoregulation and the patient may exhibit symptoms indicating increased ICP, such as changes in mentation or level of consciousness, headache or pupillary responsiveness. With a loss of autoregulation and a rise in systolic blood pressure (in an attempt to maintain cerebral perfusion), decompensation occurs. The patient’s response is characterised by systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and altered respirations. This is known as Cushing’s triad. As the patient enters stage 4, the ICP rises to terminal levels with little increase in volume. Herniation occurs as the brain tissue shifts from the compartment of greater pressure to a compartment of lesser pressure.
Factors affecting cerebral blood flow
Carbon dioxide, oxygen and hydrogen ion (H+) concentrations affect cerebral vessel tone. The partial pressure of arterial carbon dioxide (PaCO2) is a potent vasoactive agent. An increase in PaCO2 relaxes smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance and increases CBF. Alternatively, a decrease in PaCO2 reverses this process and decreases CBF. Cerebral oxygen tension below 50 mmHg results in cerebral vascular dilation. This dilation decreases cerebral vascular resistance, increases CBF and raises oxygen tension. However, if oxygen tension is not raised, anaerobic metabolism begins, resulting in an accumulation of lactic acid. As lactic acid increases and H+ accumulates, the environment becomes more acidic. Within this acidic environment, further vasodilation occurs in a continued attempt to increase blood flow. The combination of a severely low arterial oxygen pressure (PaO2) and an elevated H+ concentration (acidosis), which are both potent cerebral vasodilators, may produce a state wherein autoregulation is lost and compensatory mechanisms fail to meet tissue metabolic demands.2
Cerebral blood flow can be globally affected by cardiac or respiratory arrest, systemic haemorrhage and other pathophysiological states (e.g. diabetic coma, encephalopathies, infections, toxicities). Regional CBF can also be affected by trauma, tumours, cerebral haemorrhage or stroke. When regional or global autoregulation is lost, CBF is no longer maintained at a constant level but is directly influenced by changes in systemic blood pressure, hypoxia or catecholamines.
Increased intracranial pressure
Increased ICP is a life-threatening situation that results from an increase in any or all of the three components (brain tissue, blood, CSF) of the skull contents. Cerebral oedema is an important factor contributing to increases in ICP.
CEREBRAL OEDEMA
As shown in Box 56-2 there are a variety of causes of cerebral oedema (increased accumulation of fluid in the extravascular spaces of brain tissue). Regardless of the cause, cerebral oedema results in an increase in tissue volume that carries the potential for increased ICP. The extent and severity of the original insult are factors that determine the degree of cerebral oedema.
Three types of cerebral oedema have been distinguished: vasogenic, cytotoxic and interstitial oedema.4 More than one type may result from a single insult in the same patient.
Vasogenic cerebral oedema
Vasogenic cerebral oedema, the most common type of oedema, occurs mainly in the white matter and is attributed to changes in the endothelial lining of cerebral capillaries. These changes allow leakage of macromolecules from the capillaries into the surrounding extracellular space, resulting in an osmotic gradient that favours the flow of water from the intravascular to the extravascular space. A variety of insults, such as brain tumours, abscesses and ingested toxins, may cause an increase in the permeability of the blood–brain barrier and produce an increase in the extracellular fluid volume. The speed and extent of the spread of the oedema fluid are influenced by the systemic blood pressure, the site of the brain injury and the extent of the blood–brain barrier defect. This oedema may produce a continuum of symptoms ranging from focal neurological deficits to disturbances in consciousness, including coma (profound state of unconsciousness).
Cytotoxic cerebral oedema
Cytotoxic cerebral oedema results from local disruption of the functional or morphological integrity of cell membranes and occurs most often in the grey matter. Cytotoxic cerebral oedema develops from destructive lesions or trauma to brain tissue resulting in cerebral hypoxia or anoxia, sodium depletion and the syndrome of inappropriate antidiuretic hormone (SIADH). Cerebral oedema results as fluid and protein shift from the extracellular space directly into the cells, with subsequent swelling and loss of cellular function.
Interstitial cerebral oedema
Interstitial cerebral oedema is the result of periventricular diffusion of ventricular CSF in a patient with uncontrolled hydrocephalus. It can also be caused by enlargement of the extracellular space as a result of systemic water excess (hyponatraemia). Fluid moves into the cells to equilibrate with the hypotonic interstitial fluid. Regardless of the cause of cerebral oedema, manifestations of increased ICP result, unless compensation is adequate.
MECHANISMS OF INCREASED INTRACRANIAL PRESSURE
Elevated ICP (above the threshold of 20 mmHg) is clinically significant because it diminishes CPP, increases the risk of brain ischaemia and infarction, and is associated with a poor prognosis.4 Increased ICP can be caused by several clinical problems, including a mass lesion (e.g. haematoma, contusion, abscess, tumour), cerebral oedema (associated with brain tumours, hydrocephalus, head injury or brain inflammation) or metabolic insult. These cerebral insults may result in hypercapnia, cerebral acidosis, impaired autoregulation and systemic hypertension, which promote the formation and spread of cerebral oedema. This oedema distorts brain tissue, further increasing the ICP, which leads to even more tissue hypoxia and acidosis. Figure 56-3 illustrates the progression of increased ICP.
Crucial to the preservation of tissue is maintenance of CBF. Elevations in pressure that are more evenly distributed throughout the brain or slow increases in ICP (e.g. an enlarging brain lesion) preserve blood flow better than a rapid increase, as in primary brain injury. Sustained increases in ICP result in brainstem compression and herniation of the brain from one compartment to another.
Displacement and herniation of brain tissue cause a potentially reversible pathophysiological process to become irreversible. Ischaemia and oedema are further increased, compounding the pre-existing problem. Compression of the brainstem and cranial nerves may be fatal. Figure 56-4 illustrates herniations. Herniations force the cerebellum and brainstem downwards through the foramen magnum. If compression of the brainstem is unrelieved, respiratory arrest may occur.
CLINICAL MANIFESTATIONS
The clinical manifestations of increased ICP can take many forms, depending on the cause, location and rate at which the pressure increase occurs (see Fig 56-5). The earlier the condition is recognised and treated, the better the prognosis. The clinical manifestations of increased ICP are discussed below.
Change in level of consciousness
The level of consciousness is a sensitive and important indicator of the patient’s neurological status. Changes in the level of consciousness are a result of impaired CBF, which affects the cells of the cerebral cortex and the reticular activating system (RAS). The RAS is located in the brainstem with neural connections to many parts of the nervous system. An intact RAS can maintain a state of wakefulness even in the absence of a functioning cerebral cortex.
Interruptions to impulses from the RAS or alteration of the functioning of the cerebral hemispheres can cause unconsciousness (abnormal state of complete or partial unawareness of self or environment). The patient’s state of consciousness is defined by both the behaviour and the pattern of brain activity recorded by an electroencephalogram (EEG). The change in consciousness may be dramatic, as in coma, or subtle, such as a flattening of affect, change in orientation or decrease in level of attention. In the deepest state of unconsciousness (i.e. coma), the patient does not respond to painful stimuli. Corneal and pupillary reflexes are absent. The patient cannot swallow or cough and is incontinent of urine and faeces. The EEG pattern demonstrates decreased or absent neuronal activity.
It is often difficult to identify increased ICP as the cause of coma. Loss of consciousness also confuses the interpretation of clinical signs, which makes it difficult to follow the progression of the increasing ICP.
Changes in vital signs
Changes in vital signs are caused by increasing pressure on the thalamus, hypothalamus, pons and medulla. Manifestations such as Cushing’s triad, consisting of increasing systolic pressure (widening pulse pressure), bradycardia with a full and bounding pulse, and irregular respiratory pattern, may be present but often do not appear until ICP has been increased for some time or is markedly increased suddenly (e.g. head trauma). A change in body temperature may also be noted due to increased ICP affecting the hypothalamus.
Ocular signs
Compression of the oculomotor nerve (cranial nerve [CN] III) results in dilation of the pupil ipsilateral (same side) to the mass or lesion, sluggish or no response to light, inability to move the eye upwards and ptosis of the eyelid. These signs can be the result of a shifting of the brain from the midline, a process that compresses the trunk of CN III, paralysing the pupil sphincter. A fixed, unilaterally dilated pupil is a neurological emergency that indicates herniation of the brain. Other cranial nerves may also be affected, such as the optic (CN II), trochlear (CN IV) and abducens (CN VI) nerves. Signs of dysfunction of these cranial nerves include blurred vision, diplopia and changes in extraocular eye movements. Central herniation may initially manifest as sluggish but equal pupil response. Uncal herniation may cause a dilated unilateral pupil. Papilloedema, a choked optic disc seen on retinal examination, is also noted and is a non-specific sign associated with persistent increased ICP.
Decrease in motor function
As the ICP continues to rise, the patient manifests changes in motor ability. A contralateral (opposite side) hemiparesis or hemiplegia may be seen, depending on the location of the source of the increased ICP. If painful (noxious) stimuli are used to elicit a motor response, the patient may exhibit localisation to the stimuli or a withdrawal from the stimuli. Decorticate (flexor) and decerebrate (extensor) posturing are reflex responses that may also be elicited by noxious stimuli (see Fig 56-6). Decorticate posture consists of internal rotation and adduction of the arms with flexion of the elbows, wrists and fingers as a result of interruption of voluntary motor tracts. Extension of the legs may also be seen. A decerebrate posture may indicate more serious damage and results from disruption of motor fibres in the midbrain and brainstem. In this position, the arms are stiffly extended, adducted and hyperpronated. There is also hyperextension of the legs with plantar flexion of the feet.
Figure 56-6 Decorticate and decerebrate posturing. A, Decorticate response. Flexion of arms, wrists and fingers with adduction in upper extremities. Extension, internal rotation and plantarflexion in lower extremities. B, Decerebrate response. All four extremities in rigid extension, with hyperpronation of forearms and plantarflexion of feet. C, Decorticate response on right side of body and decerebrate response on left side of body. D, Opisthotonic posturing.
COMPLICATIONS
The major complications of uncontrolled increased ICP are inadequate cerebral perfusion and cerebral herniation (see Fig 56-4). To understand cerebral herniation better, two important structures in the brain must be described. The falx cerebri is a thin wall of dura that folds down between the cortex, separating the two cerebral hemispheres. The tentorium cerebelli is a rigid fold of dura that separates the cerebral hemispheres from the cerebellum (see Fig 56-4). It is called the tentorium (meaning tent) because it forms a tent-like cover over the cerebellum. Tentorial herniation occurs when a mass lesion in the cerebrum forces the brain to herniate downwards through the opening created by the brainstem. Uncal herniation occurs when there is lateral and downward herniation. Cingulate herniation occurs when there is lateral displacement of brain tissue beneath the falx cerebri.
DIAGNOSTIC STUDIES
Diagnostic studies are aimed at identifying the presence and the underlying cause of increased ICP (see Box 56-3). Magnetic resonance imaging (MRI) and computed tomography (CT) have revolutionised the diagnosis of increased ICP. These tests are used to differentiate the many conditions that can cause increased ICP and to evaluate therapeutic options. Other tests that may be used include cerebral angiography, EEG, cerebral blood flow measurement, transcranial Doppler studies, near-infrared spectroscopy for regional cerebral oxygenation and evoked potential studies. Positron emission tomography (PET) is also used to diagnose the cause of increased ICP. In general, a lumbar puncture is not performed when increased ICP is suspected because of the possibility of cerebral herniation from the sudden release of pressure in the skull from the area above the lumbar puncture.
BOX 56-3 Increased intracranial pressure
MULTIDISCIPLINARY CARE
Diagnostic studies
History and physical examination
Vital signs, neurological assessments, ICP measurements
Skull, chest and spinal X-ray studies
MRI, CT scan, PET, EEG, angiography
Laboratory studies, including FBC, coagulation profile, electrolytes, creatinine, ABGs, ammonia level, general drug and toxicology screen, CSF analysis for protein, cells, glucose
Collaborative therapy
Elevation of head of bed to 30° with head in a neutral position
Intubation and mechanical ventilation
Maintenance of PaO2 at 100 mmHg (13.5 kPa) or greater
Maintenance of fluid balance and assessment of osmolality
Maintenance of systolic arterial pressure between 100 and 160 mmHg
Maintenance of cerebral perfusion pressure >70 mmHg
Reduction of cerebral metabolism (e.g. high-dose barbiturates)
ABGs, arterial blood gases; CSF, cerebrospinal fluid; CT, computed tomography; ECG, electrocardiogram; EEG, electroencephalogram; FBC, full blood count; GI, gastrointestinal; ICP, intracranial pressure; MRI, magnetic resonance imaging; PaO2, partial pressure of arterial oxygen; PET, positron emission tomography.
MEASUREMENT OF INTRACRANIAL PRESSURE
Indications for intracranial pressure monitoring
ICP monitoring is used to guide clinical care when the patient is at risk of or has elevations in ICP. It may be used in patients with a variety of neurological insults, including haemorrhage, stroke, tumour, infection or traumatic brain injury. ICP should be monitored if patients are admitted with a Glasgow Coma Scale (GCS) score of 8 or less and an abnormal CT scan (haematomas, contusion, oedema or compressed basal cisterns).5
Methods of measuring intracranial pressure
Multiple methods and devices are available to monitor ICP (see Fig 56-7). The gold standard is the ventriculostomy, whereby a catheter is inserted into the lateral ventricle and coupled to an external transducer.5 This technique directly measures the pressure within the ventricles, facilitates removal and/or sampling of CSF and allows for intraventricular drug administration. As with fluid-coupled blood pressure monitoring systems, signals can be distorted by excessive tube length or bubbles in the line. In these systems, the transducer is external and its position must remain constant with respect to the patient’s head to produce comparable pressures. An alternative technology, the fibreoptic catheter, has a sensor transducer located within the catheter tip. The sensor tip is placed within the ventricle or the brain tissue and provides a direct measurement of brain pressure. Other less commonly used transducers include pneumatic systems and intracranial strain gauges. Similar to the fibreoptic system, these systems produce excellent quality waveforms, do not require repositioning with patient movement and usually cannot be re-zeroed.
Figures 56-7 Coronal section of brain showing potential sites for placement of ICP monitoring devices.
Technology is now available to measure cerebral oxygenation and cerebral ischaemia. This technology offers an indirect assessment of cerebral oxygenation and perfusion. Two such devices are currently being used in ICU settings: the LICOX brain tissue oxygenation catheter and the jugular venous bulb catheter. The LICOX catheter is placed in the frontal white matter of the brain and provides continuous brain tissue PO2 (PbtO2) monitoring; the normal range for PbtO2 is 37–47 mmHg.6 A lower than normal PbtO2 level is indicative of ischaemia. The jugular venous bulb catheter is placed in the internal jugular vein and positioned so that the catheter tip is located in the jugular bulb; placement is verified by a lateral skull X-ray. This catheter provides a measurement of SjvO2, which indicates total venous brain tissue extraction of oxygen, a measure of cerebral oxygen supply and demand.6 The normal SjvO2 range is 60–80%. Values of <50–56% demonstrate impaired cerebral oxygenation. With the use of either device, interventions can be specifically focused to improve brain tissue oxygen levels. The use of both approaches remains under debate.6
Infection is a serious consideration with ICP monitoring. Infection rates are highest in fluid-coupled systems, with incidence rates commonly cited as being between 1% and 20%.7 Over the last few years much research has been focused on reducing the level of infection. One recent study reported that the use of antibiotic-impregnated ventriculostomy catheters resulted in a reduction of ventriculostomy infections from 6.1% to 0.2% and recommended their use in the adult neurosurgical population.8 Factors that contribute to the development of infection include ICP monitoring for more than 5 days, use of a ventriculostomy, the presence of a CSF leak and a concurrent systemic infection. Routine care may include regular diagnostic testing for CSF organism growth.
ICP should be measured as a mean pressure at the end of expiration. If a CSF drainage device is in place, the drain must be closed for at least 6 minutes to ensure an accurate reading. The waveform strip should be recorded along with other pressure monitoring waveforms. The normal ICP waveform is shaped somewhat like an arterial pressure trace (see Fig 56-8), although the pressures are in a much lower range. This is because arterial pressure is transmitted to the choroid plexus and then to the CSF in the ventricular and subarachnoid spaces. When the waveform is monitored so that components in synchrony with the cardiac cycle can be visualised, the normal ICP waveform has three phases (see Table 56-1).
Figure 56-8 Intracranial pressure (ICP) monitoring can be used to continuously measure ICP. The ICP tracing shows normal, elevated and plateau waves. At high ICP the P2 peak is higher than the P1 peak, and the peaks become less distinct and plateau.
Source: Copstead LC, Banasik JL. Pathophysiology. 3rd edn. Philadelphia: Saunders; 2005.
TABLE 56-1 Normal ICP waveforms*
| Waveform | Meaning |
|---|---|
| P1 percussion wave | Represents arterial pulsations |
| P2 rebound wave | Reflects intracranial compliance |
| P3 dicrotic wave | Follows dicrotic notch; represents venous pulsations |
*See figure 56-8.
The nurse should monitor the ICP waveform, as well as mean CPP. It has been noted that when P2 is higher than P1, the intracranial space may be non-compliant and the patient may be at risk of developing elevated ICP (see Fig 56-8). It is important to consider the rate that change occurs and the patient’s clinical condition. Neurological deterioration may not occur until ICP elevation is pronounced and sustained. Any indication of ICP elevation, either as a mean increase in pressure or as an abnormal waveform configuration, should be reported to the medical team immediately.
Inaccurate ICP readings can be caused by CSF leaks around the monitoring device, obstruction of the intraventricular catheter or bolt (from tissue or blood clot), a difference between the height of the bolt and the transducer, and kinks in the tubing. In fluid-coupled systems, bubbles or air in the tubing also dampen the waveform.
CSF drainage
With the ventricular catheter and certain fibreoptic systems, it is possible to control ICP by removing CSF. To do this, a Y connector is inserted in the line (see Fig 56-9).
Figure 56-9 Intermittent drainage system. Cerebrospinal fluid (CSF) is drained via a ventriculostomy when intracranial pressure exceeds the upper pressure parameter set by the doctor. The three-way stopcock is opened to allow CSF to flow into the draining bag for brief periods (30–120 seconds) until the pressure is below the upper pressure parameter.
Using a closed system, elevations in ICP are controlled by removing CSF by gravity drainage and by adjusting the height of the drip chamber and drainage bag relative to the patient’s ventricular reference point. Typically, a point 15 cm above the ear canal (foramen of Monroe) is selected. Raising the system diminishes drainage, whereas lowering the system increases drainage volume. Careful monitoring of the volume of CSF drained is essential, keeping in mind that normal adult CSF production is about 20–30 mL per hour, with a total CSF volume of 90–150 mL within the ventricles and subarachnoid space. The level of the ICP to initiate drainage, the amount of fluid to be drained, the height of the system and the frequency of drainage are generally ordered by the patient’s doctor. Preventing infection by using strict aseptic technique during dressing changes or sampling of CSF is imperative. The system must remain intact to ensure that the ICP readings are accurate, because treatment is initiated based on the level of the pressures.
Complications of this type of drainage system include ventricular collapse, infection and herniation or subdural haematoma formation from rapid decompression. Although it is generally recognised that CSF removal decreases ICP and improves CPP, guidelines for CSF removal are not universally accepted and are typically based on institution or medical preference.6
MULTIDISCIPLINARY CARE
The goals of multidisciplinary care (see Box 56-3) are to identify and treat the underlying cause of increased ICP and to support brain function. A careful history is an important diagnostic aid that can direct the search for the underlying cause.
The first step in the management of increased ICP is to ensure adequate oxygenation to support brain function. An endotracheal tube or tracheostomy may be necessary to maintain adequate ventilation. Arterial blood gas (ABG) analysis guides the oxygen therapy. The goal is to maintain the PaO2 at 100 mmHg (13.5 kPa) or greater. It may be necessary to maintain the patient on a mechanical ventilator to ensure adequate oxygenation.
If the condition is caused by a mass, such as a tumour or haematoma, surgical removal of the mass is the best management (see the sections on brain tumours and cranial surgery later in the chapter). Non-surgical intervention for the reduction of tissue volume related to cerebral tissue swelling and cerebral oedema includes the use of diuretics and corticosteroids.
Drug therapy
Drug therapy plays an important part in the management of increased ICP. Mannitol and oral glycerol are used as osmotic diuretics. Mannitol (25%) is the most widely used agent and is given intravenously.9 Mannitol acts to decrease the ICP in two ways: plasma expansion and osmotic effect. Mannitol has an immediate plasma-expanding effect that reduces the haematocrit and blood viscosity, thereby increasing CBF and cerebral oxygen delivery. A vascular osmotic gradient is created by mannitol, moving fluid from the tissues into the blood vessels. The ICP is thus reduced by a decrease in the total brain fluid content. Fluid and electrolyte status must be monitored when osmotic diuretics are used. Mannitol may be contraindicated if renal disease is present and if serum osmolality is elevated.9
Loop diuretics, such as frusemide, bumetanide and ethacrynic acid, may be used in the management of increased ICP. These diuretics inhibit sodium and chloride reabsorption in the ascending limb of the loop of Henle and thus reduce blood volume and, ultimately, tissue volume. In addition, they cause a reduction in the rate of CSF production, which also contributes to the reduction in ICP.3
Corticosteroids (e.g. dexamethasone) are thought to control the vasogenic oedema surrounding tumours and abscesses but appear to have limited value in the management of patients with head injuries. The mode of action of corticosteroids is not completely known. It is theorised that they act by their stabilising effect on the cell membrane and by inhibiting the synthesis of arachidonic acid from cell membranes, thus preventing the formation of pro-inflammatory mediators. Corticosteroids are also thought to improve neuronal function by improving cerebral blood flow and restoring autoregulation.
Complications associated with the use of corticosteroids include hyperglycaemia, increased incidence of infections, gastrointestinal (GI) bleeding and hyponatraemia. Fluid intake and sodium and glucose levels should be monitored regularly. Patients receiving corticosteroids should concurrently be given antacids, histamine H2-receptor antagonists (e.g. ranitidine) or proton pump inhibitors (e.g. omeprazole) to prevent GI ulcers and bleeding.
Drug therapy for reducing cerebral metabolism may be an effective strategy to control ICP. The reduction in the metabolic rate decreases the CBF and therefore the ICP. High-dose barbiturates (e.g. thiopentone) are used in patients with increased ICP refractory to treatment. Barbiturates produce a decrease in cerebral metabolism and a subsequent decrease in ICP. A secondary effect is a reduction in cerebral oedema and production of a more uniform blood supply to the brain.3 Capabilities to monitor the patient’s ICP, blood flow, EEG and metabolism should be available when this treatment is used. Antiseizure drugs such as phenytoin may be used because seizures can further increase ICP.
Hyperventilation therapy
In the past, aggressive hyperventilation (PaCO2 <25 mmHg [<3.4 kPa]) was a mainstay treatment of elevated ICP. The lowering of the PaCO2 leads to constriction of the cerebral blood vessels, reducing CBF and thereby decreasing the ICP. More recent evidence suggests that aggressive hyperventilation increases the risk of focal cerebral ischaemia and may adversely affect outcomes.4 Prolonged aggressive hyperventilation therapy should be avoided in the absence of increased ICP, particularly during the first 24 hours following a head injury or when CBF is low. Brief periods of hyperventilation therapy may be useful for refractory intracranial hypertension.4,5
Nutritional therapy
All patients must have their nutritional needs met regardless of their state of consciousness or health. Early feeding following brain injury improves outcomes.8 The patient with increased ICP is in a hypermetabolic and hypercatabolic state, which increases the need for glucose to provide the necessary fuel for metabolism of the injured brain. If the patient cannot maintain an adequate oral intake, other means of meeting nutritional requirements, such as enteral feedings or total parenteral nutrition, should be initiated. Nutritional replacements should begin within 3 days after injury in order to reach full nutritional replacement within 7 days after injury.9 Because malnutrition promotes continued cerebral oedema, maintaining optimal nutrition is imperative. (Nutritional therapy is discussed in Ch 39.) Feedings or supplements should be guided by the patient’s fluid and electrolyte status, as well as the patient’s metabolic needs.
Therapy is directed at keeping the patient normovolaemic.10 The use of fluid restriction to reduce tissue volume should be evaluated on the basis of clinical factors such as urine output, insensible fluid loss, serum and urine osmolality (concentration of particles in the fluid [serum or urine]) and the condition of the patient. Intravenous (IV) 0.45% or 0.9% sodium chloride is the preferred solution for administration of piggyback medications because a lowering of serum osmolality and an increase in cerebral oedema occur if 5% dextrose in water is used.10
NURSING MANAGEMENT: INCREASED INTRACRANIAL PRESSURE
Nursing assessment
Subjective data about the patient with increased ICP can be obtained from the patient or family or others who are familiar with the patient. The nurse must learn appropriate assessment techniques and describe the level of consciousness by noting the specific behaviours observed. When a deviation from the normal state of consciousness occurs, a more structured method of observation should be initiated. This type of systematic approach to nursing assessment is illustrated in Figure 56-10 and consists of assessing the level of consciousness using the Glasgow Coma Scale (see Table 56-2) and by body functions. Adequate circulation and respiration are the most vital and should always be the first body functions assessed.
Glasgow Coma Scale
The GCS was developed in 1974 in response to the lack of clarity and ambiguity about assessment of altered states of consciousness.11 It is a quick, practical and standardised system for assessing the degree of impaired consciousness. The three areas assessed in the GCS are the ability of a patient to speak, obey commands and open the eyes when a verbal or painful stimulus is applied.11 Specific assessments evaluate the patient’s response to varying degrees of stimuli. Three indicators of response are evaluated: (1) opening of the eyes; (2) the best verbal response; and (3) the best motor response (see Table 56-2). The specific behavioural responses to the testing stimuli in each of the three areas are given a numerical value and can be plotted on a graph. The nurse’s responsibility is to elicit the best response on each of the scales: the higher the score, the higher the level of brain functioning. A graph can be used to determine whether the patient is stable, improving or deteriorating. The subscale scores are particularly important if a patient is untestable in one area—for example, severe periorbital oedema may make eye opening impossible. The total GCS score is the sum of the numerical values assigned to each of the three areas evaluated. The highest score is 15 for a fully alert person, and the lowest possible score is 3. A score of 8 or less is generally indicative of coma.12
The GCS offers several advantages in the assessment of the unconscious patient. It is specific and structured, allowing different healthcare professionals to arrive at the same conclusion about the patient’s status. It saves time for the assessor because the ratings are done with numbers rather than with lengthy descriptions. It has been well validated and has been in constant use since its development. Nevertheless, in order to use the scale correctly, nurses need to be properly trained it its use. This ensures that there is consistency between each practitioner in terms of approach and expectations.
Yet, assessing individual responses to painful stimuli, especially central nervous system response, is an area that continues to be controversial.13 There is clear consensus about how peripheral pain should be assessed and the steps that need to be taken to assess whether patients are aware of their surroundings.14 First, peripheral pain stimulus should be applied to the extremities only if the patient fails to respond to verbal commands, gentle touch or shaking. Second, the level of painful intensity should be increased gradually. Finally, pain should be elicited by applying pressure with a pen or pencil to the lateral outer aspect of the second or third interpharangeal (finger) joint (the nail bed should not be used).14 However, there is no consensus about the appropriate method that should be used to elicit a response from the central nervous system, although the use of the trapezius squeeze seems to be the one favoured by many practitioners.15 While an observational study conducted in 2008 found that the sternal rub is still favoured by many nurses,16 the National Neuroscience Benchmarking group in the UK recommends the use of supraorbital pressure in its unpublished guidelines.15 Within Australia and New Zealand the method used to elicit a response to painful stimulus tends to be governed by hospital or departmental policy. The National Guidelines in New Zealand17 and Australia18 advocate the use of the GCS, but do not provide any guidance as to how the pain stimulus should be administered. The GCS is specific enough to discriminate between different or changing states, and nurses need to ensure that they adhere to institutional policy with regard to applying painful stimuli to patients to ensure that assessments are consistent and reliable.
Other components of the neurological assessment include checks of the pupils (see Fig 56-11), extremity strength testing and, if appropriate, corneal reflex testing.
Neurological assessment
The pupils are compared to one another for size, movement and response (see Fig 56-11). If the oculomotor nerve is compressed, the pupil on the affected side (ipsilateral) becomes larger until it dilates fully. If ICP continues to increase, both pupils dilate.
Pupillary reaction is tested with a pen torch. The normal reaction is brisk constriction when the light is shone directly into the eye. A consensual response (a slight constriction in the opposite pupil) should be noted at the same time. A sluggish reaction can indicate early pressure on CN III. A fixed pupil shows no response to light stimulus, which usually indicates increased ICP. It is important to note that there are other causes of a fixed pupil, including direct injury to the oculomotor nerve (CN III), previous eye surgery/injury and use of mydriatic eye drops.
Evaluation of other cranial nerves can be included in the neurological check. Eye movements controlled by CNs III, IV and VI can be examined in the patient who is awake and can be used to assess the function of the brainstem. In the unconscious patient, extraocular eye movements are not specifically tested. Testing the corneal reflex gives information on the functioning of cranial nerves V and VII. If this reflex is absent, routine eye care should be initiated to prevent corneal abrasion. Eye movements of the uncooperative or unconscious patient can be elicited by reflex with the use of head movements (oculocephalic) and caloric stimulation (oculovestibular) (see Chs 20 and 21). To test the oculocephalic reflex (doll’s head or doll’s eyes phenomenon), the nurse rotates the patient’s head briskly while holding the eyelids open. A positive response is movement of the eyes across the midline in the opposite direction to that of the rotation. Next, the nurse quickly flexes and then extends the neck. Eye movement should be opposite to the direction of head movement: up when the neck is flexed and down when it is extended. Abnormal responses can aid in locating the intracranial lesion. This test should not be attempted if a cervical spine problem is suspected.
Motor strength is tested by asking the patient who is awake to squeeze the nurse’s hands to compare strength in the hands. The palmar drift test is an excellent measure of strength in the upper extremities. The patient raises the arms in front of the body with the palmar surfaces facing upwards. If there is any weakness in the upper extremity, the palmar surface turns downwards and the arm drifts downwards. Asking the patient to raise the foot from the bed or to bend the knees up in bed is a good assessment of lower extremity strength. All four extremities should be tested for strength and evaluated for any asymmetry in strength or movement.
The motor strength of the unconscious or uncooperative patient can be assessed by observing spontaneous movement. If no spontaneous movement is possible, a pain stimulus should be applied to the patient and the response noted. Resistance to movement during passive range-of-motion exercises is another measure of strength.
The vital signs (e.g. blood pressure, pulse, respiratory rate, temperature) should be systematically recorded. The nurse must be aware of Cushing’s triad as this indicates severe increased ICP. Besides recording respiratory rate, the nurse should also note the respiratory pattern (see Fig 56-12).
Nursing diagnoses
Nursing diagnoses for the patient with increased ICP include, but are not limited to, those presented in NCP 56-1.
Planning
The overall goals are that the patient with increased ICP will: (1) maintain a patent airway; (2) have ICP within normal limits; (3) demonstrate normal fluid and electrolyte balance; and (4) have no complications secondary to immobility and decreased level of consciousness.
Nursing implementation
Acute intervention
Nursing management care during the acute phase focuses on maintaining physiological homeostasis, protecting the patient from harm and providing emotional support.
Respiratory function
Maintaining a patent airway is critical in the patient with increased ICP and is a primary nursing responsibility. As the level of consciousness decreases, the patient is at increased risk of airway obstruction from the tongue falling back and occluding the airway or from accumulation of secretions. Altered breathing patterns may become evident (see Fig 56-12). Airway patency can be aided by keeping the patient lying on one side, with frequent position changes. Snoring sounds, which may indicate obstruction, should be noted. Accumulated secretions should be removed by suctioning, as needed. An oropharyngeal airway facilitates breathing and provides an easier suctioning route in the comatose patient. In general, any patient with an altered level of consciousness who is unable to maintain a patent airway or effective ventilation needs intubation and mechanical ventilation.
The nurse must use measures to prevent hypoxaemia and hypercapnia. Proper positioning of the head is important. Elevation of the head of the bed by 30° enhances respiratory exchange and aids in decreasing cerebral oedema. Suctioning and coughing can cause transient decreases in the PaO2 and increases in the ICP. Suctioning should be kept to a minimum and should be less than 10 seconds in duration, with administration of 100% oxygen before and after to prevent decreases in the PaO2.19 To avoid cumulative increases in the ICP with suctioning, it should be limited to two passes per suction procedure. Patients with elevated ICP are at risk of lower CPP during suctioning.19 The CPP must be maintained above 60 mmHg to preserve cerebral perfusion.
Abdominal distension can interfere with respiratory function and should be prevented. Insertion of a nasogastric tube to aspirate the stomach contents can prevent distension, vomiting and possible aspiration. However, in patients with facial and skull fractures, a nasogastric tube is contraindicated and oral insertion of an orogastric tube is preferred.
Pain, anxiety and fear from the initial injury, therapeutic procedures or noxious stimuli can increase ICP and blood pressure, complicating the management and recovery of the patient with a brain injury. The appropriate choice or combination of sedatives, paralytics and analgesics for symptom management presents a challenge to members of the intensive care team. Administration of these agents may alter the neurological state, masking true neurological changes. It may be necessary to suspend pharmacological therapy temporarily in order to assess neurological status appropriately. The choice, dose and combination of agents may vary depending on the patient’s history, neurological state and overall clinical presentation.
Opioids, such as morphine sulphate and fentanyl, are rapid-onset analgesics with minimal effect on the CBF or oxygen metabolism. The IV anaesthetic sedative propofol has gained popularity in the management of pain and anxiety in the ICU because of its rapid onset, short half-life and oxygen-saving properties. Unlike opioids, it decreases the ICP, the CBF and oxygen metabolism. Non-depolarising neuromuscular blocking agents (e.g. vecuronium, cisatracurium) are useful for ventilatory management and for treatment of refractory intracranial hypertension. Because these agents paralyse muscles without blocking pain or noxious stimuli, they are used in combination with sedatives, analgesics or benzodiazepines. Benzodiazepines, although useful for symptom management and for ventilatory support, are usually avoided in the management of the patient with increased ICP because of the hypotension effect and long half-life, unless used as an adjunct to neuromuscular blocking agents.
ABGs should be measured and evaluated regularly (see Ch 25). The nurse should frequently monitor the ABG values and maintain the levels within prescribed or acceptable parameters. The appropriate ventilatory support can be ordered on the basis of the PaO2 and PaCO2 values.
Fluid and electrolyte balance
Fluid and electrolyte disturbances can adversely affect the ICP. IV fluids should be monitored closely with the use of a limited-volume device or a volume-control apparatus for accuracy. Intake and output, with insensible losses and daily weights taken into account, are important parameters in the assessment of fluid balance.
Electrolyte determinations should be made daily and any abnormal values should be discussed with the doctor. It is especially important to monitor serum glucose, sodium and potassium levels and osmolality. Urinary output is monitored to detect problems related to diabetes insipidus (e.g. increased urinary output related to a decrease in antidiuretic hormone secretion) and SIADH, which results in decreased urinary output. Besides urinary output, the serum sodium level and osmolality are also used to diagnose diabetes insipidus and SIADH. Diabetes insipidus may result in severe dehydration unless treated. The usual treatment is fluid replacement, vasopressin or desmopressin acetate (see Ch 48). SIADH results in a dilutional hyponatraemia that may produce cerebral oedema, changes in level of consciousness, seizures and coma.
Monitoring intracranial pressure
The measurement of ICP enhances clinical decision making by detecting early signs of intracranial hypertension and response to therapy. ICP monitoring is used in combination with other physiological parameters to guide the care of the patient and assess the patient’s response to routine care. The Valsalva manoeuvre, coughing, sneezing, hypoxaemia and arousal from sleep are factors that can increase ICP. Nurses should be alert to these factors and should attempt to minimise them. Nursing management of the patient with increased ICP is one of the most important aspects of the care provided to these patients.
Body position
The patient with increased ICP should be maintained in the head-up position.20 The nurse must take care to prevent extreme neck flexion, which can cause venous obstruction and contribute to elevated ICP. The body position should be adjusted to decrease the ICP maximally and to improve the CPP. Traditional practice has been to elevate the head of the bed to 30°, unless a concurrent cervical neck injury has been identified. Research now suggests there is an inconsistent response of the ICP and the CPP to head elevation.20 Elevation of the head of the bed reduces sagittal sinus pressure, promotes venous drainage from the head via the valveless jugular system and decreases the vascular congestion that can produce cerebral oedema. However, raising the head of the bed above 30° may decrease the CPP by lowering systemic blood pressure. Careful evaluation of the effects of elevation of the head of the bed on both the ICP and the CPP is required. The bed should be positioned so that it lowers the ICP while optimising the CPP and other indices of cerebral oxygenation. Care should be taken to turn the patient with slow, gentle movements because rapid changes in position may increase the ICP. Caution should be used to prevent discomfort in turning and positioning the patient because pain or agitation also increases pressure. Increased intrathoracic pressure contributes to increased ICP by impeding the venous return. Thus coughing, straining and the Valsalva manoeuvre should be avoided. Extreme hip flexion should be avoided to decrease the risk of raising the intraabdominal pressure, which can restrict movement of the diaphragm and cause respiratory distress. The patient should be turned at least every 2 hours.
Decorticate or decerebrate posturing is a reflex response in some patients with increased ICP. Turning, skin care and even passive range of motion can elicit the posturing reflexes. Attempts should be made to provide the necessary physical care activities to minimise complications of immobility, such as atelectasis and contractures. In cases of severe posturing reflexes, these activities may have to be done less frequently because posturing can cause increases in ICP.
Protection from injury
The patient with increased ICP and a decreased level of consciousness needs protection from self-injury. Confusion, agitation and the possibility of seizures can put the patient at risk of injury. Restraints should be used judiciously in the agitated patient. If restraints are absolutely necessary to keep the patient from removing tubes or falling out of bed, they should be secure enough to be effective, and the skin area under the restraints should be observed regularly for irritation. Agitation may increase with the use of restraints, which indicates the need for other measures to protect the patient from injury. Light sedation with agents such as haloperidol or lorazepam may be needed. Asking a family member to stay with the patient may have a calming effect. For the patient with seizures or the patient at risk of seizure activity, seizure precautions should be instituted. These include padded side rails, an airway at the bedside, accurate and timely administration of antiseizure drugs, and close observation.
The patient can benefit from a quiet, non-stimulating environment. The nurse should always use a calm, reassuring approach. Touching and talking to the patient, even one who is in a coma, is always appropriate care. The nurse must create a balance between sensory deprivation and overload for the patient with increased ICP.
Psychological considerations
Besides the carefully planned physical care provided to the patient with increased ICP, the nurse must also be aware of the psychological wellbeing of the patient and family. Anxiety over the diagnosis and the prognosis for the patient with neurological problems can be distressing to the patient, the family and the nursing staff. The nurse’s competent and assured manner in performing the care needed by the patient is reassuring to everyone involved. Short, simple explanations are appropriate and allow the patient and family to acquire the amount of information they desire. There is a need for support, information and education of both patients and families. The nurse should assess family members’ desires and needs to assist in providing care for the patient and allow their participation as appropriate.
Head injury
Head injury includes any trauma to the scalp, skull or brain. Head trauma is used primarily to signify cranio-cerebral trauma, which includes an alteration in consciousness, no matter how brief.
Statistics about the occurrence of head injuries are incomplete because many victims die at the scene of the accident or because the condition is considered minor and healthcare services are not sought. In Australia, more than 22,710 people with traumatic brain injury (TBI) are treated in hospital emergency departments.21 In New Zealand, between 22,000 and 33,000 people experience a TBI every year.22 Stroke and TBI are leading causes of morbidity, disability and mortality in New Zealand: together, they account for the second largest share of total disability-adjusted life years lost and premature mortality (8.5% and 11.7%, respectively).22 Survival rates from TBI in Australia and New Zealand are not readily available but are probably similar to those from the US, where 22% of patients die.23 There has been a 5% annual decline in the rate of TBI in the past decade due to safer motor vehicles and improved first-line management. Motor vehicle accidents and falls are the most common causes of head injury. Higher-risk groups for TBI are 15–24-year-olds (from motor vehicle accidents, assaults), people older than 65 years (from falls) and males (twice the risk due to risk-taking behaviour). Alcohol is associated with up to half of all TBI cases. Other causes of head injury include assaults, sports-related injuries, firearm injury and recreational accidents.
Head trauma has a high potential for poor outcome.23 Deaths from head injury occur at three separate points in time after the injury: immediately after the injury, within 2 hours after the injury and approximately 3 weeks after the injury. Factors that predict a poor outcome include the presence of an intracranial haematoma, the increasing age of the patient, abnormal motor responses, impaired or absent eye movements or pupil light reflexes, early sustained hypotension, hypoxaemia or hypercapnia, and ICP levels higher than 20 mmHg.24 The majority of deaths occur immediately after the injury, either from the direct head trauma or from massive haemorrhage and shock. Deaths occurring within 2 hours of the trauma are caused by progressive worsening of the head injury or by internal bleeding. Immediate notice of changes in neurological status and surgical intervention are critical in preventing deaths at this point. Deaths occurring 3 weeks or more after injury result from multisystem failure. Expert nursing care, in conjunction with care from the rest of the multidisciplinary team, is crucial in decreasing mortality in the weeks following the injury.
TYPES OF HEAD INJURIES
Scalp lacerations
Scalp lacerations are the most minor of the head traumas. Because the scalp contains many blood vessels with poor constrictive abilities, most scalp lacerations are associated with profuse bleeding. The major complication associated with scalp laceration is infection.
Skull fractures
Skull fractures frequently occur with head trauma. There are several ways to describe skull fractures: (1) linear or depressed; (2) simple, comminuted or compound; and (3) closed or open (see Table 56-3). Fractures may be closed or open, depending on the presence of a scalp laceration or extension of the fracture into the air sinuses or dura. The type and severity of fracture depend on the velocity, the momentum, the direction of the injuring agent and the site of impact.
The location of the fracture alters the presentation of the manifestations (see Table 56-4). For example, a basilar skull fracture is a specialised type of linear fracture that occurs when the fracture involves the base of the skull and can evolve over several hours. Manifestations include facial paralysis, Battle’s sign (see Figs 56-13 and 56-14, B) and conjugate deviation of gaze. This fracture generally crosses a sinus and tears the dura (e.g. the frontal or the temporal) and is associated with leakage of CSF. Rhinorrhoea (CSF leakage from the nose) (see Fig 56-14, A) or otorrhoea (CSF leakage from the ear) generally confirms that the fracture has traversed the dura (see Fig 56-14).
TABLE 56-4 Clinical manifestations of different types of skull fractures
| Location | Syndrome or sequelae |
|---|---|
| Frontal fracture | Exposure of the brain to contaminants through frontal air sinus, possible association with air in forehead tissue, CSF rhinorrhoea or pneumocranium |
| Orbital fracture | Periorbital ecchymosis (raccoon eyes) |
| Temporal fracture | Boggy temporal muscle because of extravasation of blood, oval-shaped bruise behind ear in mastoid region (Battle’s sign), CSF otorrhoea |
| Parietal fracture | Deafness, CSF or brain otorrhoea, bulging of tympanic membrane caused by blood or CSF, facial paralysis, loss of taste, battle’s sign |
| Posterior fossa fracture | Occipital bruising resulting in cortical blindness, visual field defects; rare appearance of ataxia or other cerebellar signs |
| Basilar skull fracture | CSF or brain otorrhoea, bulging of tympanic membrane caused by blood or CSF, battle’s sign, tinnitus or hearing difficulty, facial paralysis, conjugate deviation of gaze, vertigo |
CSF, cerebrospinal fluid.
Figure 56-14 A, Raccoon eyes and rhinorrhoea. B, Battle’s sign (postauricular ecchymosis) with otorrhoea. C, Halo or ring sign (see text).
Two methods of testing can be used to determine whether the fluid leaking from the nose or ear is CSF. The first method is to test the leaking fluid with a Dextrostix or Tes-Tape strip to determine whether glucose is present. CSF gives a positive reading for glucose. If blood is present in the fluid, testing for the presence of glucose is unreliable because blood contains glucose. In this event, the nurse should look for the ‘halo’ or ‘ring’ sign (see Fig 56-14, C). To perform this test, the nurse allows the leaking fluid to drip onto a white pad or towel and observes the drainage. Within a few minutes the blood coalesces into the centre and a yellowish ring encircles the blood if CSF is present. The colour, appearance and amount of leaking fluid must be noted because both tests can give false-positive results.
The major potential complications of skull fractures are intracranial infections and haematoma, as well as meningeal and brain tissue damage.
Minor head trauma
Brain injuries are categorised as being minor or major. Concussion (a sudden transient mechanical head injury with disruption of neural activity and a change in the level of consciousness) is considered a minor head injury. The patient may or may not lose total consciousness with this injury.
Signs of concussion include a brief disruption in level of consciousness, amnesia about the event (retrograde amnesia) and headache. The manifestations are generally of short duration. If the patient has not lost consciousness or if the loss of consciousness lasts less than 5 minutes, the patient is usually discharged from the care facility with instructions to see their local doctor or return to the emergency department if symptoms persist or if behavioural changes are noted.
Postconcussion syndrome is seen anywhere from 2 weeks to 2 months after concussion. Symptoms include persistent headache, lethargy, personality and behavioural changes, shortened attention span, decreased short-term memory and changes in intellectual ability. This syndrome can significantly affect a patient’s ability to perform the activities of daily living.
Although concussion is generally considered benign and is usually resolved spontaneously, the symptoms may be the beginning of a more serious, progressive problem. At the time of discharge, it is important to give the patient and family instructions for observation and accurate reporting of symptoms or changes in neurological status.
Major head trauma
Major head trauma includes cerebral contusions and lacerations. Both injuries represent severe trauma to the brain. Contusions and intracerebral lacerations are generally associated with closed injuries.
A contusion is the bruising of the brain tissue within a focal area that maintains the integrity of the pia mater and arachnoid layers. A contusion develops areas of necrosis, infarction, haemorrhage and oedema. A contusion frequently occurs at the site of a fracture. With contusion, the phenomenon of coup–contrecoup injury is often noted (see Fig 56-15). Damage from coup–contrecoup injury occurs because of mass movement of the brain inside the skull. Contusions or lacerations occur both at the site of the direct impact of the brain on the skull (coup) and at a secondary area of damage on the opposite side away from injury (contrecoup), as the brain is thrown from side-to-side, leading to multiple contused areas. The prognosis is dependent upon the amount of bleeding, which can range from minimal to severe. Neurological assessment may demonstrate focal findings as well as generalised findings, depending on the level of consciousness. Seizures are a common complication of brain contusion.
Figure 56-15 Coup–contrecoup injury. After the head strikes the wall, a coup injury occurs as the brain strikes the skull (the primary impact). The contrecoup injury (the secondary impact) occurs when the brain strikes the skull surface opposite the site of the original impact.
Lacerations involve actual tearing of the brain tissue and often occur in association with depressed and compound fractures and penetrating injuries. Tissue damage is severe and surgical repair of the laceration is impossible because of the texture of the brain tissue. If bleeding is deep into the brain parenchyma, focal and generalised signs are noted.
When major head trauma occurs, many delayed responses are seen, including haemorrhage, haematoma formation, seizures and cerebral oedema. Intracerebral haemorrhage is generally associated with cerebral laceration. This haemorrhage manifests as a space-occupying lesion accompanied by unconsciousness, hemiplegia on the contralateral side and a dilated pupil on the ipsilateral side. As the haematoma expands, symptoms of increased ICP become more severe. Prognosis is generally poor for the patient with a large intracerebral haemorrhage. Subarachnoid haemorrhage and intraventricular haemorrhage can also occur secondary to head trauma.
PATHOPHYSIOLOGY
Diffuse axonal injury (DAI) is widespread axonal damage occurring after a mild, moderate or severe TBI. The damage occurs primarily around axons in subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus and brainstem.25 Initially, DAI was believed to occur from the tensile forces of trauma that sheared axons, resulting in axonal disconnection. There is increasing evidence that axonal damage is not preceded by an immediate tearing of the axon from the traumatic impact but rather the trauma changes the function of the axon, resulting in axon swelling (axonal ballooning) and disconnection. This process takes approximately 12–24 hours to develop and may persist longer. The clinical signs and symptoms include decreased level of consciousness, increased ICP, decerebration or decortication, and global cerebral oedema. Approximately 90% of patients with DAI remain in a persistent vegetative state.
COMPLICATIONS
Epidural haematoma
An epidural haematoma (extradural haematoma) results from bleeding between the dura and the inner surface of the skull. An epidural haematoma is a neurological emergency and is usually associated with a linear fracture crossing a major artery in the dura, causing a tear (see Figs 56-16 and 56-17). It can have a venous or an arterial origin. Venous epidural haematomas are associated with a tear of the dural venous sinus and develop slowly. In arterial haematomas, the middle meningeal artery lying under the temporal bone is often torn. Haemorrhage occurs into the epidural space, which lies between the dura and the inner surface of the skull (see Fig 56-17). Because this is an arterial haemorrhage, the haematoma develops rapidly and under high pressure. Symptoms typically include unconsciousness at the scene, with a brief lucid interval followed by a decrease in level of consciousness. Other symptoms may be a headache, nausea and vomiting, or focal findings. Rapid surgical intervention to prevent cerebral herniation dramatically improves outcomes. Patients over 65 years of age with increased ICP have a higher mortality rate than younger patients.22
Subdural haematoma
A subdural haematoma occurs from bleeding between the dura mater and the arachnoid layer of the meningeal covering of the brain. A subdural haematoma usually results from injury to the brain substance and its parenchymal vessels (see Fig 56-16). The veins that drain from the surface of the brain into the sagittal sinus are the source of most subdural haematomas. Because a subdural haematoma is usually venous in origin, the haematoma is much slower to develop into a mass large enough to produce symptoms. However, a subdural haematoma may be caused by an arterial haemorrhage, in which case it develops more rapidly. Subdural haematomas may be acute, subacute or chronic (see Table 56-5).
An acute subdural haematoma manifests signs within 48 hours of the injury. The signs and symptoms are similar to those associated with brain tissue compression in increased ICP and include decreasing level of consciousness and headache. The patient appears drowsy and confused. The ipsilateral pupil dilates and becomes fixed if the ICP is significantly increased.
A subacute subdural haematoma usually occurs within 2–14 days of the injury. Failure to regain consciousness may point to this possibility. After the initial bleeding, a subdural haematoma may appear to enlarge over time as the breakdown products of the blood draw fluid into the subdural space to reach isotonicity.
A chronic subdural haematoma develops over weeks or months after a seemingly minor head injury. The peak incidence of chronic subdural haematoma is in the sixth and seventh decades of life when a potentially larger subdural space is available as a result of brain atrophy. With atrophy, the brain remains attached to the supportive structures but tension is increased, and it is subject to tearing. The larger size of the subdural space also accounts for the presenting complaint being focal symptoms, rather than the signs of increased ICP. Chronic alcoholics are prone to cerebral atrophy and subsequent development of subdural haematoma.
Delay in diagnosis of a subdural haematoma in the older adult can be attributed to symptoms that mimic other health problems in this age group, such as vascular disease and senile dementia. Somnolence, confusion, lethargy and memory loss are associated with health problems other than subdural haematoma.
Intracerebral haematoma
Intracerebral haematoma occurs from bleeding within the parenchyma and occurs in approximately 16% of head injuries. It usually occurs within the frontal and temporal lobes, possibly from the rupture of intracerebral vessels at the time of injury. A ‘burst’ lobe is an intracerebral or intracerebellar haematoma that is an extension of a subarachnoid haemorrhage. This type of intracerebral haematoma is thought to result from haemorrhage of supracortical vessels. The size and location of the haematoma is a key determinant of prognosis.
DIAGNOSTIC STUDIES AND MULTIDISCIPLINARY CARE
CT scan is considered the best diagnostic test to determine craniocerebral trauma because it allows rapid diagnosis and intervention. MRI, PET and evoked potential studies may also be used in the diagnosis and differentiation of head injuries. An MRI scan is more sensitive in detecting small DAI lesions than a CT scan because of the lack of gross pathological changes in brain tissue. Transcranial Doppler studies allow the measurement of CBF velocity. A cervical spine X-ray may also be indicated. In general, the diagnostic studies are similar to those used for a patient with increased ICP (see Box 56-3). The GCS can be used to classify head injury as mild (score of 13–15), moderate (score of 9–12) or severe (score of 3–8).
Emergency management of the patient with a head injury is presented in Table 56-6. In addition to measures to prevent secondary injury by treating cerebral oedema and managing increased ICP, the principal treatment of head injuries is timely diagnosis and surgery if necessary. For the patient with concussion and contusion, observation and management of increased ICP are the primary management strategies.
The treatment of skull fractures is usually conservative. For depressed fractures and fractures with loose fragments, a craniotomy is necessary to elevate the depressed bone and remove the free fragments. If large amounts of bone are destroyed, the bone may be removed (craniectomy) and a cranioplasty will be needed at a later time (see the section on cranial surgery later in the chapter).
In cases of acute subdural and epidural haematomas, the blood must be removed. A craniotomy is usually done to visualise the bleeding vessels so that the bleeding can be controlled. Burr-hole openings may be used in an extreme emergency for a more rapid decompression, followed by a craniotomy to stop all bleeding. A drain is generally placed postoperatively for several days to prevent any re-accumulation of blood.
NURSING MANAGEMENT: HEAD INJURY
Nursing assessment
The patient with a head injury is always considered to have the potential for developing increased ICP. Increased ICP is associated with higher mortality rates and poorer functional outcomes.7 The most important aspects of the objective data are noting the GCS score (see Table 56-2), assessing and monitoring the neurological status (see Fig 56-10) and determining whether a CSF leak has occurred.
Nursing diagnoses
Nursing diagnoses and potential complications for the patient who has sustained a head injury may include, but are not limited to, the following:
• ineffective tissue perfusion (cerebral) related to interruption of CBF associated with cerebral haemorrhage, haematoma and oedema
• hyperthermia related to increased metabolism, infection and loss of cerebral integrative function secondary to possible hypothalamic injury
• acute pain related to headache, nausea and vomiting
• impaired physical mobility related to decreased level of consciousness and treatment-imposed bed rest
• anxiety related to abrupt change in health status, hospital environment and uncertain future
• potential complication: increased ICP related to cerebral oedema and haemorrhage.
Planning
The overall goals are that the patient with an acute head injury will: (1) maintain adequate cerebral perfusion; (2) remain normothermic; (3) be free from pain, discomfort and infection; and (4) attain maximal cognitive, motor and sensory function.
Nursing implementation
Health promotion
One of the best ways to prevent head injuries is to prevent car, bicycle and motorcycle accidents. The nurse can be active in campaigns that promote safe driving and can speak to driver education classes about the dangers of unsafe driving and of driving after drinking alcohol. Using a seat belt in a car and wearing a helmet when riding a bicycle or motorcycle are the most effective measures for increasing survival after accidents. Legislation requiring the compulsory wearing of fitted seat belts in cars and protective helmets for cyclists and motorcyclists and their pillion passengers for both children and adults has served to reduce the severity of injuries substantially. The nurse should be familiar with data on outcomes of using safety devices when promoting occupational health and safety (OHS) to different groups in the community.
Acute intervention
Management at the scene of the accident can have a significant impact on the outcome of the head injury. Emergency management of head injury is discussed in Table 56-6.
The general goal of nursing management of the patient with a head injury is to maintain cerebral perfusion and prevent secondary cerebral ischaemia. Surveillance or monitoring for a change in neurological status is critically important because the patient’s condition may deteriorate rapidly, which will necessitate emergency surgery. Appropriate preoperative and postoperative nursing interventions are initiated if surgery is anticipated. Because of the close association between haemodynamic status and cerebral perfusion, the nurse must be aware of any coexisting injuries or conditions. In the acute injury period, treating other life-threatening conditions (i.e. haemorrhage, hypoxia) may take initial priority in nursing care.
The nurse should explain the need for frequent neurological assessments to both the patient and the family. Behavioural manifestations associated with head injury can result in a frightened, disoriented patient who is combative and resists help. The nurse’s approach should be calm and gentle. A family member may be available to stay with the patient and thus prevent increasing anxiety and fear.26 Other teaching points are presented in Box 56-4.
PATIENT & FAMILY TEACHING GUIDE
Teaching guidelines for the patient and family during the initial 2–3 days after a head injury include the following:
1. Notify your healthcare provider immediately if experiencing signs and symptoms that may indicate complications. These include:
2. Have someone stay with the patient.
4. Check with your healthcare provider before taking drugs that may increase drowsiness, including muscle relaxants, tranquillisers and opioid pain medications.
5. Avoid driving, using heavy machinery, playing contact sports and taking warm baths.
The nurse should perform neurological assessments at intervals based on the patient’s condition. The GCS is useful in assessing the level of arousal (see Table 56-2). Indications of a deteriorating neurological state, such as a decreasing level of consciousness or lessening of motor strength, should be reported to the doctor, and the patient’s condition should be monitored closely.
The major focus of nursing care for the brain-injured patient relates to increased ICP (see NCP 56-1). However, there may be specific problems that require nursing intervention.
Eye problems may include loss of the corneal reflex, periorbital ecchymosis and oedema, and diplopia. Loss of the corneal reflex may necessitate administering lubricating eye drops, taping the eyes shut or suturing the eyelids to prevent abrasion. Periorbital ecchymosis and oedema disappear spontaneously but cold and, later, warm compresses provide comfort and hasten the process. Diplopia can be relieved by the use of an eye patch.
Hyperthermia may occur from infection or injury to the hypothalamus. Elevations in body temperature can result in increased CBF, cerebral blood volume and ICP.4 Increased metabolism secondary to hyperthermia increases metabolic waste, which in turn produces further cerebral vasodilation. The nurse should attempt to control hyperthermia and maintain normothermia in the patient. There is some evidence to suggest that therapeutic hypothermia (32–35°C) may be beneficial during the first 24 hours following injury.4
If CSF rhinorrhoea or otorrhoea occurs, the nurse should inform the doctor immediately. The patient should lie flat in bed unless this is contraindicated because of increased ICP. The head of the bed may be raised to decrease CSF pressure so that a tear can seal. A loose collection pad may be placed under the nose or over the ear. No dressing should be placed into the nasal or ear cavities. The patient should be cautioned not to sneeze or blow the nose. Nasogastric tubes should not be used and nasotracheal suctioning should not be performed on these patients.
Nursing measures specific to the care of the immobilised patient, such as those related to bladder and bowel function, skin care and infection, are also indicated. Nausea and vomiting may be a problem and can be alleviated by antiemetic drugs. Headache can usually be controlled with paracetamol alone or combined with small doses of codeine.
If the patient’s condition deteriorates, intracranial surgery may be necessary. A burr-hole opening or craniotomy may be indicated, depending on the underlying injury that is causing the symptoms. The emergency nature of the surgery may hasten the usual careful preoperative preparation. The nurse should consult with the neurosurgeon to determine specific preoperative nursing measures. The patient is often unconscious before surgery, making it necessary for a family member to sign the consent form for surgery. This is a difficult and frightening time for the patient’s family and requires sensitive nursing management. The suddenness of the situation makes it especially difficult for the family to cope.
Ambulatory and home care
Once the condition has stabilised, the patient is usually transferred for acute rehabilitation management to prepare them for re-entry into the community. As with any craniocerebral problem, there may be chronic problems related to motor and sensory deficits, communication, memory and intellectual functioning. Many of the principles of nursing management of the patient with a stroke are appropriate (see Ch 57). Conditions that may require nursing and collaborative management include poor nutritional status, bowel and bladder management, spasticity, dysphagia, neurogenic heterotopic ossification (overgrowth of bone), deep vein thrombosis and hydrocephalus. With time and patience, many of the chronic problems subside or disappear. The patient’s outward appearance is not a good indicator of how well they will function in the home or work environment.
Seizure disorders are seen in approximately 5% of patients with a non-penetrating head injury. The most vulnerable time for seizures to develop is during the first week after the head injury, but some patients may not develop a seizure disorder until years after the initial injury. Some doctors recommend that antiseizure drugs be used prophylactically. Others may not institute treatment until a seizure is witnessed or an EEG demonstrates seizure activity. Phenytoin is the antiseizure drug of choice in posttraumatic seizure activity.
The mental and emotional sequelae of brain trauma are often the most incapacitating problems. Many patients with head injuries who have been comatose for more than 6 hours undergo some personality change. They may suffer loss of concentration and memory and defective memory processing. Personal drive may decrease; apathy and apparent laziness may increase. Euphoria and mood swings, along with a seeming lack of awareness of the seriousness of the injury, may occur. The patient’s behaviour may indicate a loss of social restraint, judgement, tact and emotional control.
Family members often have unrealistic expectations of the patient as the coma begins to recede and expect full return to pre-trauma status. In reality, the patient experiences a reduced awareness and ability to interpret environmental stimuli. The nurse must prepare the family for the patient’s emergence from the coma and explain that the process of awakening often takes several weeks.
Progressive recovery may continue for 6 months or more before a plateau is reached and a prognosis for recovery can be made. Specific nursing management in the posttraumatic phase depends on specific residual deficits. In all cases the family must be given special consideration. They need to understand what is happening and be taught appropriate interaction patterns. The nurse must give guidance and referrals for financial aid, child care and other personal needs and must assist the family in involving the patient in family activities whenever possible. Assisting the patient and family in developing and maintaining hope and keeping communication open are strategies perceived as supportive by families.26
When the time for discharge planning arrives, the patient and family may benefit from very specific post-discharge instructions to avoid family–patient friction.27 Special ‘no’ policies that may be appropriately suggested by the neurosurgeon, neuropsychologist and nurse include no drinking of alcoholic beverages, no driving, no work with hazardous implements and machinery, and no unsupervised smoking. Family members, particularly spouses, go through role transition as the role changes from one of spouse to that of carer.26,27 Referral to a brain injury support group may help the family and the patient to make the necessary adjustments to their lives.
CLINICAL PRACTICE
Situation
The emergency nurse receives a radio call from the ambulance service about a young man who has been involved in a motorcycle crash. The patient was not wearing a helmet and has a large open skull fracture with obvious grey matter oozing from the area. Transport from the accident scene was delayed by 45 minutes as a result of a severe thunderstorm and traffic congestion. On the way to the hospital the patient’s pupils become fixed and dilated and he has a cardiac arrest. Estimated arrival at the hospital is still an additional 45 minutes as a result of the severe weather. The ambulance officers request permission to stop cardiopulmonary resuscitation (CPR) efforts.
Important points for consideration
• Brain death occurs when the cerebral cortex stops functioning or is irreversibly destroyed.
• Since technology has been developed that assists in supporting life, controversies have arisen related to an exact definition of death.
• Criteria for brain death include coma or unresponsiveness, absence of brainstem reflexes and apnoea (see Ch 9). Specific assessments by a doctor are required to validate each of the criteria.
• The patient’s clinical manifestations indicate that brain death has occurred.
• Brain death criteria do not address patients in a permanent vegetative state because the brainstem activity in these patients is adequate to maintain heart and lung function.
Critical thinking questions
1. What factors should be considered in terms of possible organ donation by this young man if he is assessed as being brain dead?
2. What are your feelings about the cessation of brain function versus the cessation of heart and lung function as the criteria for the death of a patient?
3. What are the laws or practices regarding ambulance officers stopping CPR efforts in the field?
4. What should the nurse do on receiving a request like this? Who is ultimately responsible for making this kind of decision and on what basis?
Brain tumours
The incidence of brain tumours is estimated as 4.6 per 100,000 in Australia and 4.4 per 100,000 in New Zealand, with the number of deaths related to brain tumours estimated as 10 per 100,000 in Australia and 205 per year in New Zealand.28 Brain tumours rank fourth as a cause of death from cancer in individuals 35–54 years of age.28 Survival at 5 years from brain tumours is approximately 23%. The incidence of brain tumours has remained relatively static over the past 10 years.28
The causes of brain tumours are not fully understood. In those without known risk factors such as family history, the only known causes are prior exposure to therapeutic ionising radiation and long-term depression of the immune system, as seen in people with organ transplants or those with AIDS. Because no one really knows what causes brain tumours, little can be done to prevent their occurrence.29
TYPES
Brain tumours can occur in any part of the brain or spinal cord. Tumours of the brain may be primary, arising from tissues within the brain, or secondary, resulting from metastasis from a malignant neoplasm elsewhere in the body. Secondary brain tumours are the most common type. Brain tumours are generally classified according to the tissue from which they arise. The most common primary brain tumours originate in astrocytes. These tumours are called gliomas and account for 65% of primary brain tumours (see Table 56-7): glioblastoma multiforme is the most common primary brain tumour, followed by meningioma and astrocytoma. A glioblastoma and meningioma are depicted in Figure 56-18. More than half of all brain tumours are malignant; they infiltrate the brain parenchyma and are not amenable to complete surgical removal. Other tumours may be histologically benign but are located such that complete removal is not possible. Brain tumours are more commonly seen in middle-aged people but they may occur at any age.
Figure 56-18 A, Glioblastoma. A large glioblastoma (G) arises from one cerebral hemisphere and has grown to fill the ventricular system. B, Meningioma. These two different sections from different levels in the same brain show a meningioma (M) compressing the frontal lobe and distorting the underlying brain.
Unless treated, all brain tumours eventually cause death from increasing tumour volume leading to increased ICP. Brain tumours rarely metastasise outside the central nervous system (CNS) because they are contained by structural (meninges) and physiological (blood–brain) barriers. Table 56-7 compares the major brain tumours.
CLINICAL MANIFESTATIONS
The clinical manifestations of brain tumours depend mainly on the location and size of the tumour. The rate of growth and the appearance of manifestations depend on the location, size and mitotic rate of the cells and the tissue of origin. Figure 56-19 illustrates the functional areas of the cerebral cortex and can be used as a guide to correlate manifestations with the location of the tumour.
Wide ranges of possible clinical manifestations are associated with brain tumours. Headache is a common problem. Tumour-related headaches tend to be worse at night and may awaken the patient. The headaches are usually dull and constant but are accompanied occasionally by throbbing. Seizures are common in gliomas and brain metastases. Brain tumours can cause nausea and vomiting from increased ICP. Cognitive dysfunction, including memory problems and mood or personality changes, is another common manifestation, especially in patients with brain metastases. Muscle weakness, sensory losses, aphasia and visual spatial dysfunction are also manifestations of brain tumours. As the brain tumour expands, it may produce manifestations of increased ICP, cerebral oedema or obstruction of the CSF pathways. Manifestations may clearly indicate the location of the tumour by an alteration in the function controlled by the affected area (see Table 56-8).
COMPLICATIONS
If the tumour mass obstructs the ventricles or occludes the outlet, ventricular enlargement (hydrocephalus) can occur. Surgical treatment is necessary to relieve the pressure and involves placement of a ventriculoatrial or a ventriculoperitoneal shunt. A catheter with one-way valves is placed in the lateral ventricle and then tunnelled through the skin to drain CSF into the right atrium or the peritoneum. Rapid decompression of ICP can cause prostration and headache, which may be prevented by gradually introducing the patient to the upright position. The patient should be instructed to avoid contact sports that may result in a blow to the valve or shearing of the catheter. The doctor should be notified if signs of increased ICP occur, such as decreasing level of consciousness, restlessness, headache, blurred vision or vomiting without nausea. Signs of an infected shunt, such as high fever, persistent headache and stiff neck, warrant investigation.
DIAGNOSTIC STUDIES
An extensive history and a comprehensive neurological examination must be part of the diagnostic examination of a patient with a suspected brain tumour. A careful history and physical examination may provide data with respect to location. Diagnostic studies are similar to those used for a patient with increased ICP (see Box 56-3). The sensitivity of techniques such as MRI and PET allows detection of very small tumours and may provide more reliable diagnostic information. CT and brain scanning are used to diagnose the location of the lesion. Other tests include magnetic resonance spectroscopy, functional MRI, PET scans and single photon emission CT (SPECT). The EEG is useful but of less importance. A lumbar puncture is seldom diagnostic and carries with it the risk of cerebral herniation. Angiography can be used to determine blood flow to the tumour and further localise the tumour. Other studies are done to rule out a primary lesion elsewhere in the body. Endocrine studies are helpful when a pituitary adenoma is suspected (see Ch 49).
The correct diagnosis of a brain tumour can be made by obtaining tissue for histological study. In most patients, tissue is obtained at the time of surgery. Computer-guided stereotactic biopsy is also an option if complete resection is not possible or practical. A smear or frozen section can be performed in the operating room for a preliminary interpretation of the histological type. With this information, the neurosurgeon can make a better decision about the extent of surgery. In some cases, immunohistochemical stains or electron microscopy may be necessary to ascertain the correct diagnosis. Determination of the MIB-1 index, a measure of mitotic rate, is often helpful in assessing the mitotic activity of a given tumour.
MULTIDISCIPLINARY CARE
Treatment goals are aimed at: (1) identifying the tumour type and location; (2) removing or decreasing tumour mass; and (3) preventing or managing increased ICP.
Surgical therapy
Surgical removal is the preferred treatment for brain tumours. Stereotactic surgical techniques are used with greater frequency to perform a biopsy and remove small brain tumours. The outcome of surgical therapy depends on the type, size and location of the tumour. Meningiomas and oligodendrogliomas can usually be completely removed, whereas the more invasive gliomas and medulloblastomas can be only partially removed. Computer-guided stereotactic biopsy, ultrasound, functional MRI and cortical mapping can be used to localise brain tumours intraoperatively. Complete surgical removal is not always possible because the tumour is not always accessible or has involved vital parts of the brain. Surgery can reduce tumour mass, which decreases ICP and provides relief of symptoms with an extension of survival time. Tumours located in the deep central areas of the dominant hemisphere, the posterior corpus callosum or the upper brainstem cause extensive neurological damage and are usually considered inoperable.
Radiation therapy and radiosurgery
Radiation therapy (see Ch 15) is commonly used as a follow-up measure after surgery. Radiation seeds can also be implanted into the brain. Cerebral oedema and rapidly increasing ICP may be a complication of radiation therapy but they can be managed with high doses of corticosteroids (dexamethasone, prednisone or methylprednisolone).
Stereotactic radiosurgery is a method of delivering a highly concentrated dose of radiation precisely directed at a location within the brain. Stereotactic radiosurgery may be used when conventional surgery has failed or is not an option because of the tumour location.
Chemotherapy
The effectiveness of chemotherapy has been limited by difficulty getting drugs across the blood–brain barrier, tumour cell heterogeneity and tumour cell drug resistance. A group of chemotherapeutic drugs called the nitrosoureas (e.g. carmustine, lomustine) are particularly effective in treating brain tumours. Normally the blood–brain barrier prohibits the entry of most drugs into the brain. The most malignant tumours cause a breakdown of the blood–brain barrier in the area of the tumour, allowing chemotherapeutic agents to be used to treat the malignancy. Chemotherapy-laden biodegradable wafers implanted at the time of surgery can deliver chemotherapy directly to the tumour site. Other drugs being used include methotrexate and procarbazine. Two methods used to deliver chemotherapeutic drugs directly to the CNS are via an Ommaya reservoir and intrathecal administration.
Temozolomide is the first oral chemotherapeutic agent found to cross the blood–brain barrier. In contrast with many of the traditional chemotherapies, which require metabolic activation to exert their effects, temozolomide has the ability to convert spontaneously to a reactive agent that directly interferes with tumour growth. It does not interact with other drugs commonly taken by patients with brain tumours, such as anticonvulsants, corticosteroids and antiemetics.30
Many techniques to control and treat brain tumours are being investigated. These include radium implants in the tumour bed, local hyperthermia and biological therapy. Although progress in treatment has increased the length and quality of survival of patients with gliomas, outcomes still remain poor.31
NURSING MANAGEMENT: BRAIN TUMOURS
Nursing assessment
The initial assessment should be structured to provide baseline data of the neurological status and the information needed to design a realistic, individualised care plan. Areas to be assessed include the level of consciousness, motor abilities, sensory perception, integrated function (including bowel and bladder function), balance and proprioception, and the coping abilities of the patient and family. Watching a patient perform activities of daily living and listening to the patient’s conversations are convenient ways to perform part of the neurological assessment. Asking the patient or family to explain the problem can be helpful in determining the patient’s limitations and can provide information about the patient’s insight into the problem. All initial data should be accurately recorded to provide a baseline for comparison to determine whether the patient’s condition is improving or deteriorating.
Interview data are as important as the actual physical assessment. Questions concerning medical history, intellectual abilities and educational level, and history of nervous system infections and trauma should be asked. Determining the presence of seizures, syncope, nausea and vomiting, headaches or other pain is important in planning care for the patient.
Nursing diagnoses
Nursing diagnoses for the patient with a brain tumour may include, but are not limited to, the following:
• impaired tissue perfusion (cerebral) related to cerebral oedema
• acute pain (headache) related to cerebral oedema and increased ICP
• self-care deficits related to altered neuromuscular function secondary to tumour growth and cerebral oedema
• anxiety related to the diagnosis and treatment
• potential complication: seizures related to abnormal electrical activity of the brain
• potential complication: increased ICP related to the presence of the tumour and the failure of normal compensatory mechanisms.
Planning
The overall goals are that the patient with a brain tumour will: (1) maintain normal ICP; (2) maximise neurological functioning; (3) be free from pain and discomfort; and (4) be aware of the long-term implications with respect to prognosis and cognitive and physical functioning.
Nursing implementation
A primary or metastatic tumour of the frontal lobe can cause behavioural and personality changes. Loss of emotional control, confusion, disorientation, memory loss and depression may be signs of a frontal lobe lesion. These behavioural changes are often not perceived by the patient but can be disturbing and even frightening to the family. These changes may also cause a distancing to occur between the family and the patient. Assisting the family in understanding what is happening to the patient and supporting the family through this diagnostic phase are important roles for the nurse.
The confused patient with behavioural instability can be a challenge. Protecting the patient from self-harm is an important part of nursing care.30 At times when the patient manifests rage and aggression, the nurse must also be concerned about self-protection. Close supervision of activities, use of side rails, judicious use of restraints, padding of the rails and the area around the bed, and a calm reassuring approach to care are all essential techniques in the care of such patients.
Perceptual problems associated with frontal lobe and parietal lobe tumours contribute to a patient’s disorientation and confusion. Minimising environmental stimuli, creating a routine and using reality orientation can be incorporated into the care plan for the confused patient.
Seizures often occur with brain tumours. These are managed with antiseizure drugs. Seizure precautions should be instituted for the protection of the patient. Some behavioural changes seen in the patient with a brain tumour are a result of seizure disorders and can improve with control of the seizures by means of drugs (see Ch 58).
Motor and sensory dysfunctions are problems that interfere with the activities of daily living. Alterations in mobility must be managed and the patient should be encouraged to provide as much self-care as physically possible. Self-image often depends on the patient’s ability to participate in care within the limitations of the physical deficits.
Language deficits can also occur in patients with brain tumours. Motor (expressive) or sensory (receptive) dysphasia may occur. The disturbance in communication can be frustrating for the patient and may interfere with the nurse’s ability to meet the patient’s needs. Attempts should be made to establish a communication system that can be used by both the patient and the staff.
Nutritional intake may be decreased because of the patient’s inability to eat, loss of appetite or loss of desire to eat. Assessing the patient’s nutritional status and ensuring adequate nutritional intake are important aspects of care.30 The patient may need encouragement to eat or, in some cases, may have to be fed orally, parenterally, by gastrostomy or nasogastric tube, or by total parenteral nutrition. The patient with a brain tumour who undergoes cranial surgery requires complex nursing care. This is discussed in the next section.
Evaluation
The expected outcomes are that the patient with a brain tumour will:
• be free of pain, vomiting and other discomforts
• maintain ICP within normal limits
• demonstrate maximal neurological function (cognitive, motor, sensory) with regard to the location and extent of the tumour
• maintain optimal nutritional status
• accept the long-term consequences of the tumour and its treatment.
Cranial surgery
The cause or indication for cranial surgery may be related to a brain tumour, CNS infection (e.g. an abscess), vascular abnormalities, craniocerebral trauma, epilepsy or intractable pain (see Table 56-9).
TYPES
Various types of cranial surgical procedures are presented in Table 56-10.
TABLE 56-10 Types of cranial surgery
| Type | Description |
|---|---|
| Burr hole | Opening into the cranium with a drill; used to remove localised fluid and blood beneath the dura |
| Craniotomy | Opening into the cranium with removal of a bone flap and opening the dura to remove a lesion, repair a damaged area, drain blood or relieve increased intracranial pressure |
| Craniectomy | Excision into the cranium to cut away a bone flap |
| Cranioplasty | Repair of a cranial defect resulting from trauma, malformation or previous surgical procedure; artificial material used to replace damaged or lost bone |
| Stereotactic procedure | Precision localisation of a specific area of the brain using a frame or a frameless system based on three-dimensional coordinates; the procedure is used for biopsy, radiosurgery or dissection |
| Shunt procedure | Alternative pathway to redirect cerebrospinal fluid from one area to another using a tube or implanted device; examples include ventriculoperitoneal shunt and ommaya reservoir |
Craniotomy
Depending on the location of the pathological condition, a craniotomy may be frontal, parietal, occipital, temporal or a combination of any of these. A set of burr holes is drilled and a saw is used to connect the holes to remove the bone flap. Sometimes operating microscopes are used to magnify the site. After surgery the bone flap is wired or sutured. Sometimes drains are placed to remove fluid and blood. Patients are usually cared for in ICU until stable.
Stereotactic surgery
Stereotactic surgery is neurosurgery using a precision apparatus (often computer-guided) to assist the surgeon to target an area of the brain precisely (see Fig 56-20). Stereotactic biopsy can be performed to obtain tissue samples for histological examination. CT scanning and MRI are used to image the targeted tissue. With the patient under general or local anaesthesia, the surgeon drills a burr hole or creates a bone flap for an entry site and then introduces a probe and biopsy needle. Stereotactic procedures are used for removal of small brain tumours and abscesses, drainage of haematomas, ablative procedures for extrapyramidal diseases (e.g. Parkinson’s disease) and repair of arteriovenous malformations. A major advantage of the stereotactic approach is a reduction in damage to surrounding tissue.
Stereotactic radiosurgery is a procedure that involves closed-skull destruction of an intracranial target using ionising radiation focused with the assistance of an intracranial guiding device. A sophisticated computer program is used while the patient’s head is held still in a stereotactic frame. Radiosurgical techniques can use a linear accelerator or a gamma knife. In the gamma knife procedure, a high dose of cobalt radiation is delivered to precisely targeted tumour tissue. The dose of radiation can be delivered over a single 4–6-hour treatment time. In some situations, some tumours are treated over several weeks.
In combination with stereotactic procedures to identify and localise tumour sites, surgical lasers can be used to destroy tumours. Stereotactic procedures are used to identify the tumour site. Three surgical lasers currently used include the carbon dioxide, argon and neodymium: yttrium-aluminium-garnet (Nd:YAG) lasers. All three work by creating thermal energy, which destroys the tissue on which it is focused. Laser therapy also provides the benefit of reducing damage to surrounding tissue.
NURSING MANAGEMENT: CRANIAL SURGERY
Nursing assessment
The nursing assessment of the patient undergoing cranial surgery is similar to that for the patient with increased ICP (see NCP 56-1).
Nursing diagnoses
Nursing diagnoses for the patient with cranial surgery are similar to those for the patient with increased ICP and may include, but are not limited to, those presented in NCP 56-1.
Planning
The overall goals are that the patient with cranial surgery will: (1) return to normal consciousness; (2) be free from pain and discomfort; (3) maximise neuromuscular functioning; and (4) be rehabilitated to maximum ability.
Nursing implementation
Acute intervention
The general preoperative and postoperative nursing care for the patient undergoing cranial surgery is similar regardless of the cause. Nursing management is presented in NCP 56-1. The patient (if conscious and coherent) and the family will be gravely concerned about the potential physical and emotional problems that can result from surgery. The uncertainty regarding prognosis and outcome requires compassionate nursing care in the preoperative period.
Preoperative teaching is important in allaying the fears of the patient and family and also in preparing them for the postoperative period. They should be given general information about the type of operation that will be performed and what can be expected immediately after the operation. The neurosurgeon needs to explain the procedure and the likely outcomes to the patient and family prior to surgery. The nurse should explain that some hair is shaved to allow better exposure and to prevent contamination: this explanation should help prevent unnecessary concern over this task. The hair is usually removed in the operating room after induction of anaesthesia. The family should also be informed that the patient will be taken to ICU or to a special care unit after the operation.
The primary goal of care after cranial surgery is the prevention of increased ICP. Frequent assessment of the patient’s neurological status is essential during the first 48 hours. In addition to neurological functions, fluids, electrolyte levels and osmolality are monitored closely to detect changes in sodium regulation, the onset of diabetes insipidus or severe hypovolaemia. Turning and positioning of the patient sometimes depend on the site of the operation. If the surgical approach is in the posterior fossa, the patient is generally kept flat or at a slight elevation (10–15°). Lying on the back should be prevented as much as possible and flexion of the neck should be avoided to protect the suture line. The maximum swelling in the operative area occurs within 24–48 hours after the surgery.
The dressing is usually in place for 3–5 days. With an incision over the skull in the anterior or middle fossa, the patient will return from the operating room with the head elevated at an angle of 30–45°. If a bone flap has been removed (craniectomy), care should be taken not to position the patient on the operative side. The dressing should be observed for colour, odour and amount of drainage. The surgeon must be notified immediately of any excessive bleeding or clear drainage. Checking drains for placement and assessing the area around the dressing are also important. Scalp care should include meticulous care of the incision to prevent wound infection. The area should be cleansed and treated in accordance with hospital protocol or the neurosurgeon’s orders. Once the dressing is removed, use of an antiseptic soap for washing the scalp may also be beneficial. The psychological impact of hair removal can be alleviated by using a wig, turban, scarves or cap after the incision has completely healed. For the patient who is receiving radiation, using a sun block and head covering should be advocated if any exposure to the sun is anticipated.
Ambulatory and home care
The rehabilitative potential for a patient after cranial surgery depends on the reason for the surgery, the postoperative course and the patient’s general state of health. Nursing interventions must be based on a realistic appraisal of these factors. An overall goal for the nurse is to foster independence for as long as possible and to the highest degree possible.
Specific rehabilitation potential cannot be determined until cerebral oedema and increased ICP subside postoperatively. Care must be taken to maintain as much function as possible through measures such as careful positioning, meticulous skin and mouth care, regular range-of-motion exercises, bowel and bladder care, and adequate nutrition.
Referrals may be made to other specialists on the healthcare team. For example, a speech therapist may be helpful to the patient who has a speech problem or a physiotherapist may provide an exercise plan to regain functional deficits. The needs and problems of each patient should be addressed individually because many variables affect the plan.
The patient’s mental and physical deterioration, including seizures, personality disorganisation, apathy and wasting, is difficult for both the family and healthcare professionals to watch. Mental and emotional residual deficits are often more difficult for the patient and family to accept than are motor and sensory losses. Although progress is continuously being made to help patients with brain tumours by means of chemotherapy, conventional and interstitial radiation, and biological therapies, the prognosis remains grim.22 The nurse can provide much help and support during the adjustment phase and in long-term planning.
Evaluation
The expected outcomes are that the patient who has had cranial surgery will:
CLINICAL PRACTICE
Situation
A 26-year-old patient in a permanent vegetative state is diagnosed with her fifteenth bladder infection. The community nurse needs to determine whether or not to seek antibiotics for this infection. The family members have said that no heroic measures should be used to extend the life of their daughter and sister but they have been unwilling to withdraw the existing treatment, which is enteral nutrition through a gastrostomy tube. Should antibiotics be withheld?
Important points for consideration
• Patients in a persistent vegetative state do not recover.
• Providing nutrition and hydration, even if by artificial means, can have significant cultural, religious and psychological meaning to patients and families.
• Clarification with the family about the goals of treatment and the patient’s wishes, when she was competent and if they are known, is imperative. It is important to know whether treatment for an infection would be considered heroic based on the family’s perspective of what the patient would want.
• The family’s concerns about pain, suffering and quality of life for the patient must be explored within the context of the overall plan of care.
• Withholding treatment is morally acceptable when a competent patient consents to it, if there is no medical benefit to the patient, if the treatment merely prolongs life or if the burden of treatment outweighs the benefit to the patient.
INFLAMMATORY CONDITIONS OF THE BRAIN
Meningitis, encephalitis and brain abscesses are the most common inflammatory conditions of the brain and spinal cord. Meningitis is an acute inflammation of the pia mater and the arachnoid membrane surrounding the brain and spinal cord and includes the CSF; encephalitis is an inflammation of the brain; and a brain abscess is a collection of infective cells in part of the brain. Inflammation can be caused by bacteria, viruses, fungi and chemicals (e.g. contrast media used in diagnostic tests or blood in the subarachnoid space) (see Table 56-11). CNS infections may occur via the bloodstream, by extension from a primary site, or along cranial and spinal nerves. The mortality rate is approximately 2–30% in the general population, with higher rates in elderly patients.32 Up to 40% of those who recover may have long-term neurological deficits, including hearing loss.33
TABLE 56-11 Comparison of cerebral inflammatory conditions
CSF, cerebrospinal fluid; CT, computed tomography; EEG, electroencephalogram; HSV, herpes simplex virus; ICP, intracranial pressure; MRI, magnetic resonance imaging; PCR, polymerase chain reaction; PET, positron emission tomography; PMN, polymorphonuclear cells; WBC, white blood cell.
Bacterial meningitis
AETIOLOGY AND PATHOPHYSIOLOGY
Bacterial meningitis is considered a medical emergency and untreated it has a mortality rate approaching 100%. The organisms usually gain entry to the CNS through the upper respiratory tract or the bloodstream but they may enter by direct extension from penetrating wounds of the skull or through fractured sinuses in basal skull fractures.32
Bacterial meningitis usually occurs in the autumn, winter or early spring and is often secondary to viral respiratory disease. Older adults and those who are debilitated are more often affected than is the general population. Streptococcus pneumoniae and Neisseria meningitidis are the leading causes of bacterial meningitis. Haemophilus influenzae was once the most common cause. However, the use of H. influenzae vaccine has resulted in a significant decrease in bacterial meningitis related to this organism.
The inflammatory response to the infection tends to increase CSF production, with a moderate increase in ICP. In bacterial meningitis the purulent secretions produced quickly spread to other areas of the brain through the CSF. If this process extends into the brain parenchyma or if concurrent encephalitis is present, cerebral oedema and increased ICP become more of a problem. All patients with bacterial meningitis must be observed closely for manifestations of increased ICP, which is thought to be a result of swelling around the dura, and increased CSF volume.
CLINICAL MANIFESTATIONS
Fever, severe headache, nausea, vomiting and nuchal rigidity (resistance to flexion of the neck) are key signs of bacterial meningitis. A positive Kernig’s sign (severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90°), a positive Brudzinski’s sign (where flexion of the neck causes flexion of the patient’s hip and knees), photophobia, decreased level of consciousness and signs of increased ICP may also be present. Coma is associated with a poor prognosis and occurs in 5–10% of patients with bacterial meningitis. Seizures occur in approximately one-third of all cases.32 The headache of bacterial meningitis will become progressively worse and may be accompanied by vomiting and irritability. If the infecting organism is a meningococcus, a skin rash is common and petechiae may be seen.
COMPLICATIONS
The most common acute complication of bacterial meningitis is increased ICP. More than 90% of patients will have increased ICP and it is the major cause of unconsciousness. Another complication of bacterial meningitis is residual neurological dysfunction. Cranial nerve dysfunction often occurs with CNs III, IV, VI, VII or VIII in bacterial meningitis. The dysfunction usually disappears within a few weeks. However, hearing loss may be permanent after bacterial meningitis.
Cranial nerve irritation can have serious sequelae. The optic nerve (CN II) is compressed by increased ICP. Papilloedema is often present, and blindness may occur. When the oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves are irritated, ocular movements are affected. Ptosis, unequal pupils and diplopia are common. Irritation of the trigeminal nerve (CN V) is evidenced by sensory losses and loss of the corneal reflex, and irritation of the facial nerve (CN VII) results in facial paresis. Irritation of the vestibulocochlear nerve (CN VIII) causes tinnitus, vertigo and deafness.
Hemiparesis, dysphasia and hemianopsia may also occur. These signs usually resolve over time. If resolution does not occur, a cerebral abscess, subdural empyema, subdural effusion or persistent meningitis is suggested. Acute cerebral oedema may occur with bacterial meningitis, causing seizures, CN III palsy, bradycardia, hypertensive coma and death.
A non-communicating hydrocephalus may occur if the exudate causes adhesions that prevent the normal flow of the CSF from the ventricles. CSF reabsorption by the arachnoid villi may also be obstructed by the exudate. Surgical implantation of a shunt is the only treatment.
Waterhouse-Friderichsen syndrome is a complication of bacterial meningitis caused by meningococcal bacteria. It manifests as petechiae, disseminated intravascular coagulation (DIC) and adrenal haemorrhage. DIC is a serious complication of bacterial meningitis.33 DIC is the cause of death in about 1% of patients with bacterial meningitis.
DIAGNOSTIC STUDIES
When a patient presents with manifestations suggestive of bacterial meningitis, a blood culture should be done. Diagnosis is usually verified by doing a lumbar puncture and analysis of the CSF. Variations in the CSF depend on the causative organism. Protein levels in the CSF are usually elevated and are higher in bacterial than in viral meningitis (see the discussion on viral meningitis below). Decreased CSF glucose concentration is common in bacterial meningitis and may be normal in viral meningitis. The CSF is purulent and turbid in bacterial meningitis; it may be the same or clear in viral meningitis. The predominant white blood cell type in the CSF during bacterial meningitis is polymorphonuclear cells (see Table 56-11). Specimens of the CSF, sputum and nasopharyngeal secretions are taken for culture before the start of antibiotic therapy to identify the causative organism. A Gram stain is done to detect bacteria.
X-rays of the skull may demonstrate infected sinuses. CT scans and MRI may be normal in uncomplicated meningitis. In other cases, CT scans may reveal evidence of increased ICP or hydrocephalus.
MULTIDISCIPLINARY CARE
Bacterial meningitis is a medical emergency. Rapid diagnosis based on a history and physical examination is crucial because the patient is usually in a critical state when healthcare is sought. When bacterial meningitis is suspected, antibiotic therapy is instituted after the collection of specimens for cultures, even before the diagnosis is confirmed (see Box 56-5). The fundus of the eye should be examined for papilloedema before lumbar puncture to assess possible increased ICP.
MULTIDISCIPLINARY CARE
Collaborative therapy
Cephalosporin (e.g. cefotaxime, ceftriaxone)
Paracetamol or aspirin for temperature above 38°C
CSF, cerebrospinal fluid; CT, computed tomography; FBC, full blood count; IV, intravenous; MRI, magnetic resonance imaging; PET, positron emission tomography; WBC, white blood cell.
Ampicillin, penicillin, cefuroxime, cefotaxime, ceftriaxone and ceftazidime are the drugs of choice for treating bacterial meningitis. These drugs are effective because of their ability to penetrate the blood–brain barrier.
NURSING MANAGEMENT: BACTERIAL MENINGITIS
Nursing assessment
Initial assessment should include vital signs, neurological evaluation, fluid intake and output, and evaluation of the lungs and skin (see Fig 56-10).
Nursing diagnoses
Nursing diagnoses for the patient with bacterial meningitis may include, but are not limited to, those presented in NCP 56-2.
Planning
The overall goals are that the patient with bacterial meningitis will have: (1) return to maximal neurological functioning; (2) resolution of infection; and (3) decreased pain and discomfort.
Nursing implementation
Health promotion
Prevention of respiratory tract infections through vaccination programs for pneumococcal pneumonia and influenza should be supported by nurses.25 Early and vigorous treatment of respiratory tract and ear infections is important. People in close contact with anyone who has bacterial meningitis should be given prophylactic antibiotics.
Acute intervention
The patient with bacterial meningitis is usually acutely ill. The fever is high and head pain is severe. Irritation of the cerebral cortex may result in seizures. The changes in mental status and level of consciousness depend on the degree of increased ICP. Assessment of vital signs, neurological evaluation, fluid intake and output, and evaluation of lung fields and skin should be performed at regular intervals based on the patient’s condition and recorded carefully.
Head pain and neck pain secondary to movement require attention. Codeine provides some pain relief without undue sedation for most patients. The patient should be assisted to a position of comfort, often curled up with the head slightly extended. The head of the bed should be slightly elevated, when permitted after lumbar puncture. A darkened room and a cool cloth over the eyes relieve the discomfort of photophobia.
For the delirious patient, additional low lighting may be necessary to decrease hallucinations. All patients suffer some degree of mental distortion and hypersensitivity and may be frightened and misinterpret the environment. Every attempt should be made to minimise environmental stimuli and prevent injury. Restraints should be avoided. Arm boards, secured with multiple layers of stretch gauze, protect the IV infusion site. The presence of a familiar person at the bedside has a calming effect. The nurse must be efficient with care but also should project an attitude of caring and unhurried gentleness. The use of touch and a soothing voice to give simple explanations of activities is helpful. If seizures occur, appropriate observations should be made and protective measures should be taken. Antiseizure drugs such as phenytoin are administered as ordered. Problems associated with increased ICP are also managed.
Fever must be vigorously managed because it increases cerebral oedema and the frequency of seizures. In addition, neurological damage may result from an extremely high temperature over a prolonged time. Paracetamol or aspirin may be used to reduce fever. However, if the fever is resistant to aspirin or paracetamol, more vigorous means are necessary, such as an electric cooling blanket. Care should be taken not to reduce the temperature too rapidly because shivering may result, causing a rebound effect and increasing the temperature. The extremities should be wrapped in sheepskin, soft towels or a blanket covered with a sheet to protect them from ‘frostbite’. Care of the skin should be frequent to prevent breaks in the skin. If a cooling blanket is not available or desirable, tepid sponge baths with water may be effective in lowering the temperature. The skin must be protected from excessive drying and injury.
Because high fever greatly increases the metabolic rate and thus insensible fluid loss, the patient should be assessed for dehydration and adequacy of fluid intake. Diaphoresis further increases fluid losses, which should be estimated and included in an intake and output record. Replacement fluids should be calculated as 800 mL per day for respiratory losses and 100 mL for each degree of temperature above 38°C. Supplemental feeding to maintain adequate nutritional intake via tube or oral feedings may be necessary. The designated antibiotic schedule must be followed to maintain therapeutic blood levels. Observations should be made for side effects of the drugs used.
In most cases, bacterial meningitis does not require isolation, with the exception of those caused by meningococcal bacteria. However, the use of standard precautions is essential to protect the patient and the nurse.
Ambulatory and home care
After the acute period has passed, the patient requires several weeks of convalescence before normal activities can be resumed. In this period, good nutrition should be stressed, with an emphasis on a high-protein, high-kilojoule diet in small, frequent feedings.
Muscle rigidity may persist in the neck and the backs of the legs. Progressive range-of-motion exercises and warm baths are useful. Activity should be gradually increased as tolerated, but adequate bed rest and sleep should be encouraged.
Residual effects are uncommon in meningitis caused by meningococcal bacteria. However, infection with pneumococcal bacteria can result in sequelae such as dementia, seizures, deafness, hemiplegia and hydrocephalus. Vision, hearing, cognitive skills, and motor and sensory abilities should be assessed after recovery, with appropriate referrals as indicated. Meningitis in infancy may have ‘silent’ neurological sequelae, which are manifested as learning and behavioural problems when the child reaches school age.
Throughout the acute and convalescent periods the nurse should be aware of the anxiety and stress experienced by individuals close to the patient.
Evaluation
The expected outcomes for the patient with bacterial meningitis are addressed in NCP 56-2.
Viral meningitis
The most common causes of viral meningitis are enteroviruses, arboviruses, human immunodeficiency virus (HIV) and herpes simplex virus (HSV). Viral meningitis usually presents as a headache, fever, photophobia and stiff neck. The fever may be moderate or high. There are usually no symptoms of brain involvement.
The most important diagnostic test is examination of the CSF. The typical finding is lymphocytosis (see Table 56-11). Organisms are not seen on Gram stain or acid-fast smears. Polymerase chain reaction used to detect viral-specific deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) is the most important method for diagnosing CNS viral infections.32,33
Viral meningitis is managed symptomatically because the disease is self-limiting. Antiviral therapy is not used. Full recovery from viral meningitis is expected. Rare sequelae include persistent headaches, mild mental impairment and uncoordination.
Encephalitis
Encephalitis, an acute inflammation of the brain, is a serious and sometimes fatal disease.
AETIOLOGY AND PATHOPHYSIOLOGY
Encephalitis is usually caused by a virus. Many different viruses have been implicated in encephalitis, some of them associated with certain seasons of the year and endemic to certain geographic areas. Ticks and mosquitoes transmit epidemic encephalitis. Examples include Murray Valley encephalitis (MVE), Kunjin (KUN) virus and Japanese encephalitis. Non-epidemic encephalitis may occur as a complication of measles, chickenpox or mumps. HSV encephalitis is the most common cause of acute non-epidemic viral encephalitis. Cytomegalovirus (CMV) encephalitis is one of the common complications in patients with acquired immunodeficiency syndrome (AIDS).
MVE was first isolated in 1951, although ‘Australian encephalitis’ has been recorded as early as 1911. Birds are the hosts for the mosquito Culex annulirostris, which carries the virus. Cases vary in severity from mild to severe, with only 1 in 500 cases leading to significant illness. Symptoms including flu-like symptoms and brain dysfunction can occur after a few days.
CLINICAL MANIFESTATIONS AND DIAGNOSTIC STUDIES
The onset of infection is typically non-specific with fever, headache, nausea and vomiting. It can be acute or subacute. Signs of encephalitis appear on day two or three and may vary from minimal alterations in mental status to coma. Virtually any CNS abnormality can occur, including hemiparesis, tremors, seizures, cranial nerve palsies, personality changes, memory impairment, amnesia and dysphasia.
Early diagnosis and treatment of viral encephalitis are essential for favourable outcomes. Diagnostic findings related to viral encephalitis are shown in Table 56-11. Brain imaging techniques include MRI and PET. Polymerase chain testing tests for HSV-DNA and RNA levels in CSF allow early detection of HSV viral encephalitis.34
The clinical distinction between meningitis and encephalitis is based on brain function. Patients with meningitis may be uncomfortable, lethargic or distracted by headache but their cerebral function remains normal. In encephalitis, however, abnormalities in brain function are common, including altered mental status, motor or sensory deficits, and speech or movement disorders.
NURSING AND MULTIDISCIPLINARY CARE: VIRAL ENCEPHALITIS
To prevent encephalitis, mosquito control should be practised, including removing water where mosquitoes can breed. In addition, insect repellent should be used as necessary.
Collaborative and nursing management of encephalitis is symptomatic and supportive. Cerebral oedema is a major problem and diuretics (mannitol) and corticosteroids (dexamethasone) are used to control it. In the initial stages of encephalitis, many patients require intensive care.
Aciclovir is used to treat encephalitis caused by HSV infection. Use of aciclovir has been shown to reduce mortality rates, although neurological complications may not be reduced. For maximal benefit, antiviral agents should be started before the onset of coma. Seizure disorders should be treated with antiseizure drugs. Prophylactic treatment with antiseizure drugs may be used in severe cases of encephalitis. Treatment of CMV encephalitis in AIDS patients is discussed in Chapter 14.
Brain abscess
Brain abscess is an accumulation of pus within the brain tissue that can result from a local or a systemic infection. Direct extension from ear, tooth, mastoid or sinus infection is the primary cause. Other causes include spread from a distant site (e.g. pulmonary infection, bacterial endocarditis), skull fracture and a prior brain trauma or surgery. Streptococci and Staphylococcus aureus are the primary infective organisms.
Manifestations are similar to those of meningitis and encephalitis and include headache, fever, and nausea and vomiting. Signs of increased ICP may include drowsiness, confusion and seizures. Focal symptoms may be present and reflect the local area of the abscess. For example, visual field defects or psychomotor seizures are common with a temporal lobe abscess, whereas an occipital abscess may be accompanied by visual impairment and hallucinations. Quantitative CT and MRI are used to diagnose a brain abscess.
Antimicrobial therapy is the primary treatment for brain abscess. Other manifestations are treated symptomatically. If drug therapy is not effective, the abscess may need to be drained, or removed if it is encapsulated. In untreated cases, the mortality rate approaches 100%. Nursing measures are similar to those for management of meningitis or increased ICP. If surgical drainage or removal is the treatment of choice, nursing care is similar to that described under cranial surgery.
Other infections of the brain include subdural empyema, osteomyelitis of the cranial bones, epidural abscess and venous sinus thrombosis after periorbital cellulitis.
The patient with a head injury
CASE STUDY
Patient profile
Adrian Li is a 23-year-old man who was riding a motorcycle that ran into a car. He was sedated, paralysed and intubated by paramedics at the scene before being transported to hospital by helicopter. He was brought to the emergency department with a diagnosis of closed head injury with skull fracture.
Diagnostic studies
• CT of the head was positive for left skull fracture, left subdural haematoma, bilateral intraventricular and subarachnoid haemorrhage, and cerebral oedema
• CT of the abdomen/pelvis showed a lacerated liver, multiple infarcts to the right kidney, fluid around the duodenum and pancreas, and multiple left pelvic fractures
• Chest X-ray showed a right lung contusion and pneumomediastinum and subcutaneous emphysema
CRITICAL THINKING QUESTIONS
1. What could be the cause of this patient’s hypoxia, hypotension and tachycardia?
2. How could the injuries impact on his neurological condition?
3. What area of the brain does this patient’s clinical manifestations suggest may be injured?
4. What nursing interventions should be implemented? What are the priorities? Why?
5. Based on the assessment data presented, write one or more nursing diagnoses. Are there any collaborative problems?
1. Vasogenic cerebral oedema increases intracranial pressure (ICP) by:
2. A patient with ICP monitoring has a pressure of 12 mmHg. The nurse understands that this pressure reflects:
3. The nurse plans care for the patient with increased ICP with the knowledge that the best way to position the patient is to:
4. The nurse is alerted to a possible acute subdural haematoma in the patient who:
5. During admission to the emergency department of a patient with a severe head injury, the nurse places the highest priority on assessment for:
6. A patient is suspected of having a cranial tumour. The signs and symptoms include memory deficits, visual disturbances, weakness of right upper and lower extremities, and personality changes. The nurse recognises that the tumour is most likely located in the:
7. Nursing management of a patient with a brain tumour includes:
8. The primary goal of nursing care after a craniotomy is:
9. A nursing measure that is indicated to reduce the potential for seizures and increased ICP in the patient with bacterial meningitis is:
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