Recently gained confusion, severe apathy, stupor or coma implies dysfunction of the cerebral hemispheres, the diencephalon and/or the upper brainstem.³ Focal lesions in supratentorial structures may damage both hemispheres, or may produce swelling that compresses the diencephalic activating system and midbrain, causing transtentorial herniation and brainstem damage. Primary subtentorial (brainstem or cerebellar) lesions may compress or directly damage the reticular formation anywhere between the level of the midpons and, (by upward pressure), the diencephalon. Metabolic or infectious diseases may depress brain functions by a change in blood composition or the presence of a direct toxin. Impaired consciousness may also be due to reduced blood flow (as in syncope or severe heart failure) or a change in the brain’s electrical activity (as in epilepsy). Concussion, anxiolytic drugs and anaesthetics impair consciousness without producing detectable structural changes in the brain.

Many of the enzymatic reactions of neurons, glial cells, and specialised cerebral capillary endothelium in the brain must be catalysed by the energy-yielding hydrolysis of adenosine triphosphate (ATP) to adenosine diphosphate (ADP) and inorganic phosphate. Without a constant and generous supply of ATP, cellular synthesis slows or stops, neuronal functions decline or cease, and cell structures quickly fall apart.⁴ The brain depends entirely on the process of glycolysis and respiration within its own cells to provide its energy needs. Even a short interruption of blood flow or oxygen supply threatens tissue vitality.

Seizures

A seizure is an uninhibited, abrupt discharge of ions from a group of neurons resulting in epileptic activity.⁵ The majority of patients experiencing seizures in the ICU do not have preexisting epilepsy, and their chances of developing epilepsy in the future are usually more dependent on the cause than on the number or intensity of seizures that they experience. However, because of other deleterious neuronal and systemic effects of seizures, their rapid diagnosis and suppression during a period of critical illness is necessary.

Seizures are classified depending on how they start as (a) partial or focal seizures, (b) generalised or full body seizures involving both cerebral hemispheres, or (c) partial seizures with secondary generalisation. A patient may still be conscious during a partial seizure whereas in generalised seizures they are not. As partial seizures may not always progress to tonic-clonic movement or alteration in consciousness, partial seizure represents one of the most elusive diagnoses in neurology and is often misdiagnosed. One of the most helpful points in the history of a partial seizure patient is the preepileptic event, the aura. The patient will describe the aura as a virtually identical sensation every time.

Aetiology of seizures

Seizures may either prompt the patient’s admission to ICU (because of status epilepticus) or develop as a complication of another illness.⁶ Seizures can be due to vascular, infectious, neoplastic, traumatic, degenerative, metabolic, toxic or idiopathic causes. Factors influencing the development of posttraumatic epilepsy include an early posttraumatic seizure, depressed skull fracture, intracranial haematoma, dural penetration, focal neurological deficit and posttraumatic amnesia (PTA) over 24 hours with the presence of a skull fracture or haematoma. Seizures in critically ill patients are most commonly due to drug effects; metabolic, infectious or toxic disorders; and intracranial mass lesions although they may be due to trauma or neoplasm.⁷ Conditions producing seizures tend either to increase neuronal excitation or to impair neuronal inhibition. A few generalised disorders (e.g. non-ketotic hyperglycaemia) may produce partial or focal seizures.

Alterations in Motor and Sensory Function

Alterations of motor and sensory function include skeletal muscle weakness and paralysis. They result from lesions in the voluntary motor and sensory pathways, including the upper motor and sensory neurons of the corticospinal and corticobulbar tracts, or the lower motor and sensory neurons that leave the CNS and travel by way of the peripheral nerve to the muscle and sensory receptors.

Muscle tone, which is a necessary component of muscle movement, is a function of the muscle spindle (myotatic) system and the extrapyramidal system, which monitors and buffers input to the lower motor neurons by way of the multisynaptic pathways.⁸ Upper motor neuron lesions produce spastic paralysis, and lower motor neuron lesions produce flaccid paralysis. Damage to the upper motor and sensory neurons of the corticospinal, corticobulbar and spinothalamic tracts is a common component of stroke.⁹ Polyneuropathies involve multiple peripheral nerves and produce symmetrical sensory, motor, and mixed sensorimotor deficits:

• Lesions of the corticospinal and corticobulbar tracts: result in weakness or total paralysis of predominantly distal voluntary movement, Babinski’s sign (i.e. dorsiflexion of the big toe and fanning of the other toes in response to stroking the outer border of the foot from heel to toe), and often spasticity (increased muscle tone and exaggerated deep tendon reflexes).

• Disorders of the basal ganglia: (extrapyramidal disorders) do not cause weakness or reflex changes. Their hallmark is involuntary movement (dyskinesia), causing increased movement (hyperkinesias) or decreased movement (hypokinesia) and changes in muscle tone and posture.

• Cerebellar disorders: cause abnormalities in the range, rate and force of movement. Strength is minimally affected.

Autonomic Nerve Dysfunction

Dysfunctions of the autonomic nervous system (ANS) or autonomic dysreflexia are recognised by the symptoms that result from failure or imbalance of the sympathetic or parasympathetic components of the ANS such as (i) increased (>120/min) or decreased (<50/min) heart rate, (ii) increased respiratory rate (>24/min), (iii) raised temperature (>38.5°C), (iv) increased (>160 mmHg) or decreased (<85 mmHg) systolic blood pressure, (v) increased muscle tone, (vi) decerebrate (extensor) or decorticate (flexor) posturing, and (vii) profuse sweating. For example, in spinal injury the presence of a noxious stimulus can be transmitted from the periphery to the spinal cord and activates dysfunctional sympathetic response.

There is strong evidence for numerous interactions among the central nervous system (CNS), peripheral nervous system (both sympathetic and parasympathetic branches), the endocrine system, and the immune system, hence ANS dysfunction is related to that complex triad.¹⁰ Autonomic nerve (AN) dysfunction ranges from alterations in the sympathetic–parasympathetic balance to almost complete cessation as occurs in spinal cord injury. As the ANS controls organ function AN dysfunction is related to all-organ alteration and failure. The immune system is connected to the nervous system through the ANS with many of the patients with infections, systemic inflammatory response and multi-organ failure exhibiting AN dysfunction. AN dysfunction is closely related to systemic inflammation hence those with conditions with increased levels of inflammatory markers such as chronic disease and obesity have predisposing AN dysfunction. AN dysfunction is assessed by time and spectral domain heart rate variability and is currently being researched as a neurological assessment technique.¹¹

Alterations in Cerebral Metabolism and Perfusion

For decades, impairment of cerebral metabolism has been attributed to impaired oxygen delivery, mediated by reduced cerebral perfusion in the swollen cerebral parenchyma. Accordingly, reduction of ICP is usually argued for restoration of previously compromised cerebral perfusion for improvement of cerebral metabolism. Although uncontrolled ICP elevation has been shown to be responsible for reduced oxygen delivery, non-ischaemic impairment of oxidative metabolism and mitochondrial damage has only recently been recognised as a prominent source of energy crisis triggered by brain injury in the presence of adequate cerebral blood flow.¹² Accumulating evidence has shown that the mitochondrion has a pivotal role in post traumatic neuronal death by integrating numerous noxious signals responsible for both structural and functional damage on one hand and by amplifying these signals through activation of several cellular signalling events leading to cell death. In addition, more complex processes with the alteration of cerebral perfusion, such as cerebral hypoperfusion, ischaemia, reperfusion injury, inflammation and oedema result in increased intracranial pressure (ICP).

Cerebral Ischaemia

Ischaemia is the inadequate delivery of oxygen, the inadequate removal of carbon dioxide from the cell, and an increase in the production of intracellular lactic acid. Ischaemia can be caused by an increase in nutrient utilisation by the brain in a hyperactive state, a decrease in delivery related to either cerebral or systemic complications, and/or a mismatch between delivery and demand.¹³ The ischaemic cascade is described in Figure 17.1. Inflammation, together with oxidative stress, excitotoxicity, disrupted calcium homeostasis and energy failure, is one of the key pathological changes in ischaemic brain damage.¹⁴ There is a significant inflammatory response in ischaemic brains, including leucocyte and monocyte infiltration into the brain, activation of microglia and astrocytes, elevated production of inflammatory cytokines and chemokines and increased expression and activity of adhesion molecules, complement and metalloproteinases. Of importance, brain ischaemia can lead to significant inflammatory responses in the central nervous system and can also cause significant changes in the peripheral immune system. There are two phases. In the relatively early phase, activated spleen cells and lymph nodes and blood mononuclear cells secrete significantly enhanced levels of TNF-α, IL-6 and IL-2. This then results in global immunosuppression affecting the spleen, lymph nodes, thymus and a significant decrease in the number of immune cells in the circulation.¹⁵ When cerebral blood flow (CBF) falls to about 40% of normal, EEG slowing occurs. When CBF falls below 10 mL/100 g/min (20%), the function of ionic pumps fails, which leads to membrane depolarisation. Cerebral ischaemia and reperfusion injury contribute to the cascade of physiological events, termed secondary brain injury. Recent studies have shown that low-dose paracetamol reduces inflammatory protein release from brain endothelial cells exposed to oxidant stress¹⁶ and that propofol protects against neuronal apotosis.¹⁷

FIGURE 17.1 Ischaemic cascade. In cerebral ischaemia, energy failure causes depolarisation of the neuronal membrane, and excitatory neurotransmitters such as glutamate are released together. A marked influx of Ca²⁺ into neurons then occurs, which provokes the enzymatic process leading to irreversible neuronal injury. Inflammation is also a contributing factor in the development of ischaemic damage.

Cerebral Oedema

Cerebral oedema is defined as increased brain water content. The brain is particularly susceptible to injury from oedema, because it is located within a confined space and cannot expand, and because there are no lymphatic pathways within the CNS to carry away the fluid that accumulates. The white matter is usually much more involved, as myelinated fibres have a loose extracellular space, while the grey matter has a much higher cell density with many connections and much less loose extracellular space.¹⁸ The two main subdivisions of cerebral oedema are extracellular and intracellular.

Intracellular (cytotoxic) oedema

Cellular swelling, usually of astrocytes in the grey matter, is generally seen after cerebral ischaemia caused by cardiac arrest or minor head injury.¹⁹ The blood–brain barrier (BBB) is intact and capillary permeability is not impaired. The cause of intracellular oedema is anoxia and ischaemia; it is usually not clinically significant, and is reversible in its early phases.

Extracellular (vasogenic) oedema

Extracellular oedema involves increased capillary permeability, and had been termed ‘BBB breakdown’.²⁰ Rises in brain water content with extracellular oedema are often quite dramatic, because the fluid that results from increased capillary permeability is usually rich in proteins, resulting in the spread of oedema and brain ischaemia. This can lead to cytotoxic oedema, and to the progressive breakdown of both astrocytes and neurons.¹⁹ While the classification of oedema is useful to define specific treatments, it is somewhat arbitrary, as cytotoxic and vasogenic oedema often occur concurrently. In fact, each of these processes may cause the other. Ultimately, these changes can lead to raised intracranial pressure and herniation.

Hydrocephalus

Hydrocephalus is the result of an imbalance between the formation and drainage of cerebrospinal fluid (CSF). Reduced absorption most often occurs when one or more passages connecting the ventricles become blocked, preventing movement of CSF to its drainage sites in the subarachnoid space just inside the skull.²¹ This type of hydrocephalus is called ‘non-communicating’. Reduction in absorption rate, called ‘communicating hydrocephalus’ can be caused by damage to the absorptive tissue. Both types lead to an elevation of the CSF pressure within the brain. A third type of hydrocephalus, ‘normal pressure hydrocephalus’, is marked by ventricle enlargement without an apparent rise in CSF pressure, which mainly affects the elderly.

Hydrocephalus may be caused by: congenital brain defects; haemorrhage, in either the ventricles or the subarachnoid space; CNS infection (syphilis, herpes, meningitis, encephalitis or mumps); and tumours. Irritability is the commonest sign of hydrocephalus in infants and, if untreated, may lead to lethargy. Bulging of the fontanelle, the soft spot between the skull bones, may also be an early sign. Hydrocephalus in infants prevents fusion of the skull bones, and causes expansion of the skull. Symptoms of normal pressure hydrocephalus include dementia, gait abnormalities and incontinence.²² Treatment includes ventriculostomy drainage of CSF in the short term, or a surgical shunt for those with chronic conditions. Either is predisposed to blockage and infection.

Intracranial Hypertension

Intracranial pressure is the pressure exerted by the contents of the brain within the confines of the skull and the BBB. The Munro–Kelly hypothesis states that the contents of the cranium (60% water, 40% solid) are not compressible and thus an increase in volume causes a rapid rise in pressure and changes to the compensatory reserve and pulse amplitude, as illustrated in Figure 17.2.²³ Normal ICP is 0–10 mmHg, and a sustained pressure of >15 mmHg is termed intracranial hypertension, with implications for CBF.²⁴ Areas of focal ischaemia appear when ICP is >20 mmHg and global ischaemia occurs at >50 mmHg. ICP waveform contains valuable information about the nature of cerebrospinal pathophysiology. ICP increased to the level of systemic arterial pressure extinguishes cerebral circulation, which will restart only if arterial pressure rises sufficiently beyond the ICP to restore cerebral blood flow. Autoregulation of cerebral blood flow and compliance of the cerebrospinal system are both expressed in ICP. Methods of waveform analysis are useful, both to derive this information and to guide the management of patients.²⁵

FIGURE 17.2 The volume–ICP curve relationship.²¹

Initially, intracranial compliance allows compensation for rises in intracranial volume due to autoregulation. During a slow rise in volume in a continuous mode, the ICP rises to a plateau level at which the increased level of CSF absorption keeps pace with the rise in volume with ample compensatory reserve. This is expressed as an index, as shown in Figure 17.3.²⁶ Intermittent expansion causes only a transient rise in ICP at first. When sufficient CSF has been absorbed to accommodate the volume, the ICP returns to normal. The ICP finally rises to the level of arterial pressure which itself begins to rise, accompanied by bradycardia or other disturbances of heart rhythm (termed the Cushing’s response). This is accompanied by dilation of the small pial arteries and some slowing of venous flow, which is followed by pulsatile venous flow.

FIGURE 17.3 In a simple model, pulse amplitude of intracranial pressure (ICP) (expressed along the y-axis on the right side of the panel) results from pulsatile changes in cerebral blood volume (expressed along the x-axis) transformed by the pressure–volume curve. This curve has three zones: a flat zone, expressing good compensatory reserve, an exponential zone, depicting poor compensatory reserve, and a flat zone again, seen at very high ICP (above the ‘critical’ ICP) depicting derangement of normal cerebrovascular responses. The pulse amplitude of ICP is low and does not depend on mean ICP in the first zone. The pulse amplitude increases linearly with mean ICP in the zone of poor compensatory reserve. In the third zone, the pulse amplitude starts to decrease with rising ICP. RAP, index of compensatory reserve.²⁶

The respiratory changes depend on the level of brainstem involved. A midbrain involvement results in Cheyne-Stokes respiration. When the midbrain and pons are involved, there is sustained hyperventilation. There are rapid and shallow respirations with upper medulla involvement, with ataxic breathing in the final stages (see Figure 17.4).²⁷

FIGURE 17.4 Injury to the brainstem can result in various abnormal respiratory patterns.²⁷

Often, neurogenic pulmonary oedema may occur due to increased sympathetic activity as a result of the effects of elevated ICP on the hypothalamus, medulla or cervical spinal cord. The causes of intracranial hypertension are classified as acute or chronic. Acute causes include brain trauma, ischaemic injury and intracerebral haemorrhage. Infections such as encephalitis or meningitis may also lead to intracranial hypertension. Chronic causes include many intracranial tumours, such as ependymomas, or subdural bleeding that may gradually impinge on CSF pathways and interfere with CSF outflow and circulation. As the ICP continues to increase, the brain tissue becomes distorted, leading to herniation and additional vascular injury.²⁸

Neurological Therapeutic Management

This section explores cerebral perfusion, oxygenation and assessment. The objective of assessment is to identify and then initiate strategies in an attempt to prevent secondary insults and ischaemia. ICP monitoring is discussed in terms of therapeutic management.

Optimising Cerebral Perfusion and Oxygenation

Intracranial hypertension and cerebral ischaemia are the two most important secondary injury processes that can be anticipated, monitored and treated in the ICU. This applies to all aetiologies of brain injury including trauma. This section discusses the modalities of neuroprotection, including the management of intracranial hypertension, vasospasm and cerebral ischaemia. Nursing interventions for the prevention of secondary insults and promotion of cerebral perfusion are described in Table 17.1. Importantly, the aims of nursing management are based on published guidelines and are directed at optimising cerebral perfusion and metabolism by various initiatives.

TABLE 17.1 Nursing interventions for the promotion of cerebral perfusion in acute brain injury

Aim	Goal	Interventions
Maintain oxygenation	SaO₂ 98%, PaO₂ 100 mmHg, PbtO₂ >20	• Maintain airway. • Use 100% O₂ during initial resuscitation phase. • Intubate as soon as possible for Glasgow Coma Scale less than 8 or diaphragmatic respiratory insufficiency (C – spine number). • Obtain arterial blood gas and manipulate set FiO₂ to meet parameter goal. • Suction patient as needed. • Consider need for kinetic therapy, e.g. rotation/percussion therapy bed within spinal precautions. Use frequent subglottal suctioning, and maintain head of bed elevation at 30° or more to prevent VAP. • In recovery: assess for upper airway weakness and reflex (prevent aspiration), sputum retention and atelectasis.
Maintain PaCO₂	PaCO₂ 35–40 mmHg	• ABG assessment. • Adjust ventilator settings to obtain PaCO₂ of 35–40 mmHg. • Ensure optimal PaCO₂ for your patient: observe PbtO₂ and ICP during manipulation of PaCO₂. • Monitor end-tidal CO₂ continuously. • Observe for hypoventilation.
Maintain mean arterial pressure (MAP)	MAP 90 mmHg	• Maintain euvolaemia. • Give IV volume as prescribed to maintain CVP and PCWP within parameters. • Use noradrenaline once euvolaemic in order to optimise MAP. • Observe PbtO₂ for sedation-induced hypotension. • Transfuse to haematocrit of 33% or haemoglobin content 80–100 g/L. • Stroke: thrombolytic, embolic and ICH, MAP 90–120 mmHg
Maintain cerebral perfusion pressure 50–70 mmHg	CPP 50–70 mmHg	• Effectively reduce ICP while preserving or improving CPP • Position body with neck straight and no knee elevation in order to maintain venous outflow. • Make sure cervical collar and endotracheal tube ties are not too tight, especially behind the neck. • If patient has a ventriculostomy, drain per doctor’s orders.
Maintain intracranial pressure (CP) <20 mmHg	ICP <20 mmHg	• Elevate head of bed above the level of the heart to obtain optimal level of ICP and CPP. Monitor ICP, CPP and PbtO₂ to ensure optimal level for your patient (15–30°). • Sedate using propofol, morphine, fentanyl and/or lorazepam/midazolam • Mannitol prescription at 0.25–1.0 g/kg IV for ICP sustained at less than 20 mmHg (watch serum osmolality and consider holding for values >320 mOsmol/kg) OR Hypertonic Saline 7.5% prescription • Consider paralytics if positioning, cooling, sedation and mannitol does not resolve increased ICP. • Maintain the brain temperatures at 36–37°C, using cooling measures; prevent shivering (increases cerebral metabolic demands) • Prepare for surgical craniotomy if indicated.
Maintain environment/reduce stimulation	SjO₂ 50–75% PbtO₂ >20	• Group necessary interventions in a timely manner to allow for rest periods. • Screen visitors. • Minimise noise and lighting. • Avoid stimulation and prioritise interventions if ICP precarious. • Sedation as prescribed.
Maintain cerebral blood flow	PbtO₂ <20	• Optimise CPP to prescribed levels (60–70 mm Hg). • Optimise PaCO₂ as indicated to increase CBF. • Optimise sedation and consider paralytics. • Consider barbiturate prescription if above measures are not successful. • PaO₂ 100 mmHg and SaO₂ 98%. • Maintain CVP of 5–10 mmHg, and a PCWP of 10–15 mmHg. • Administer normal saline and/or colloids as prescribed to maintain parameters. • Transfuse to haematocrit of 33% or haemoglobin content 80–100 g/L. (Prescription to correct coagulopathies). • Monitor closely for signs and symptoms of neurogenic pulmonary oedema, especially in patients with cardiac history. • Maintenance of brain temperature at 36–37°C, with active cooling if necessary. • Transcranial Doppler image to check for vasospasm. • Non-traumatic SAH, administer IV nimodipine or magnesium infusion to prevent vasospasm as prescribed; consider components of HHH therapy. • Ischaemic stroke, administer tPA within 3 hours of event. • ICH, prevent rebleeding; administer prescribed recombinant factor VII, reduce hypertension.
Maintain nutrition		• Ensure early enteric feeding. • Oral enteric feeding tube (nasogastric contradicted in TBI). • Dietitian referral for metabolic requirements. • Stress ulcer prophylaxis.

Management of Cerebral Oxygenation and Perfusion

Cerebral monitoring in brain-injured patients has focused on the prevention of secondary injury to the brain owing to impaired perfusion. However, ICP monitoring and ICP manipulation does not equal cerebral oxygenation.²⁹ There are currently four techniques that can be used to assess cerebral oxygenation: jugular venous oxygen saturation, positron emission tomography, near-infrared spectroscopy, and brain tissue oxygenation monitoring (PbtO₂). Their strengths and weaknesses are the subject of several recent reviews.^30,³¹ The selection among these forms of oxygenation monitoring is focused on the appropriateness of focal or global monitoring, the location of the monitor in relation to the injury, and the intermittent or continuous nature of the monitoring. The use of PbtO₂, as assessed by the intraparenchymal polarographic oxygen probe, has the advantage of directly monitoring the zone of injury and thus earlier detection of perfusion abnormalities that may impact global cerebral oxygenation later. This may also allow the rescue of watershed areas of perfusion. However, there is controversy regarding the appropriate placement of such monitors. Insertion of the probe into non injured areas yields data equivalent to global assessments of cerebral oxygenation. Consequently, close attention should be paid to the location of the catheter in relation to the injury in interpretation and use of PbtO₂ results. Jugular venous oxygen saturation (SjO₂) is representative of global cerebral oxygen metabolism, but technically it is difficult to obtain reproducible results. Cerebral tissue oxygenation values of <20 mmHg are targeted for intervention based on Brain Trauma Foundation (BTF) guidelines but only at level III evidence.³² PbtO₂ can be increased by increasing the FiO₂/PaO₂ ratio and by reducing cerebral metabolic requirements for oxygen (CMRO₂) using brain temperature control with active cooling and metabolic rate control with sedation and adequate feeding. Additional interventions such as volume infusion, transfusion, and inotropic support directed at improving cardiac output can also be used to increase oxygen delivery.³³

Brain inflammation after injury contributes to impaired oxygenation and perfusion, but currently its management has not translated to successful clinical management. However, the use of cerebral microdialysis (MD) and the measurement of biochemical markers (lactate, glutamate, pyruvate, glycerol and glucose) of cerebral inflammation and metabolism do contribute towards early warnings of impending hypoxia/ischaemia and neurological deterioration, and this may allow timely implementation of neuroprotective strategies. Elevation of the lactate/pyruvate ratio is typically seen in cerebral ischaemia and mitochondrial dysfunction, and has been used to tailor therapy.³⁴ However, MD reflects only local tissue biochemistry and the accurate placement of the catheter is crucial. Furthermore, because there are wide variations in measured variables, trend data are more important than absolute values. Although MD is used routinely in a few centres it has not yet been introduced into widespread clinical practice and, at present, should be considered a research tool for use in specialist centres. MD has the potential to become established as a key component of multi-modality monitoring during management of acute brain injury during neurointensive care.

Management of Intracranial Hypertension

Raised ICP is treated by removing mass lesions and/or increasing the volume available for expansion of injured tissue. This may be achieved by reducing one of the other available intracranial fluid volumes:

1. CSF by ventricular drainage (as discussed previously)

2. cerebral blood volume by hyperventilation, osmotic diuretic therapy or hypothermia

3. brain tissue water content by osmotic diuretic therapy

4. removing swollen and irreversibly injured brain

5. increasing cranial volume by craniotomy decompression.

Each modality will be discussed in terms of its physiological effect, efficacy and potential use for prevention of secondary brain injury.

Hyperventilation

Hyperventilation reduces PaCO₂ and will reduce ICP by vasoconstriction induced by alkalosis but it also decreases cerebral blood flow.³⁵ The fall in ICP parallels the fall in CBV. Hyperventilation decreases regional blood flow to hypoperfused areas of the brain. Thus, generally PaCO₂ should be maintained in the low normal range of about 35 mmHg. Hyperventilation should be utilised only when ICP elevations are refractory to other methods and when brain tissue oxygenation is in the normal range.³⁶ The BTF Guidelines recommend hyperventilation therapy only for brief periods when there is no neurological deterioration or for longer periods when ICP is refractory to other therapies.³²

Osmotherapy

Acute administration of an osmotic such as mannitol or hypertonic saline produces a potent antioedema action, primarily on undamaged brain regions with an intact BBB. This treatment causes the movement of water from the interstitial and extracellular space into the intravascular compartment, thereby improving intracranial compliance or elastance. In addition to causing ‘dehydration’ of the brain, osmotic agents have been shown to exert beneficial non-osmotic cerebral effects, such as augmentation of cerebral blood flow (by reducing blood viscosity, resulting in enhanced oxygen delivery), free radical scavenging, and diminishing CSF formation and enhancing CSF reabsorption.³⁷

The BTF recommends mannitol in intracranial hypertension in bolus administration, keeping the serum osmolarities greater than 320 mOsm/L, plasma Na+ <160 mmol/L and avoiding hypovolaemia. Urine output after mannitol administration needs to be replaced, generally with normal saline. Brain free water is increased with 5% dextrose and hyperglycaemia; hence these need to be avoided. The use of frusemide in conjunction with mannitol promotes a synergistic action, particularly in patients refractory to mannitol alone. Recent studies now suggest that mannitol and frusemide have antiepileptic properties ³⁸ and that mannitol has a role in ischaemic stroke.

Intravenous hypertonic saline (HTS) increases cerebral perfusion and decreases brain swelling and inflammation more effectively than conventional resuscitation fluids. HTS behaves like 20% mannitol in acute cerebral oedema but maintains haemodynamic status. However, unlike HTS, mannitol induces a diuresis, which is relatively contraindicated in patients with both TBI and hypovolaemia as it may worsen intravascular volume depletion and decrease cerebral perfusion. Therefore, despite theoretical advantages of HTS resuscitation in patients with TBI, an Australian randomised controlled trial ³⁹ found no difference in outcome between HTS and other resuscitation fluids in prehospital resuscitation. However, in many Australian and New Zealand intensive care units, HTS is used as a preferred alternative to mannitol in patients with raised ICP.

Normothermia

Hyperthermia occurs in up to 40% of patients with ischaemic stroke and intracerebral haemorrhage and in 40–70% of patients with severe TBI or aneurysmal subarachnoid haemorrhage. Hyperthermia is independently associated with increased morbidity and mortality after ischaemic and haemorrhagic stroke, and in subarachnoid haemorrhage and TBI patients temperature elevation has been linked to raised intracranial pressure. Temperature elevations as small as 1–2°C above normal can aggravate ischaemic neuronal injury and exacerbate brain oedema.⁴⁰ Mild hypothermia protects numerous tissues from damage during ischaemic insult.⁴¹ The use of paracetamol, cooling blankets, ice packs, evaporative cooling and new cooling technologies may be useful in maintaining normothermia. Hyperaemia (increased blood flow) may occur during rewarming, resulting in acute brain swelling and rebound intracranial hypertension.⁴² In an original study, Marion and colleagues.⁴³ demonstrated a higher mortality rate than in more recent trials,⁴⁴ possibly due to rapid rewarming and rebound hyperaemia and cerebral oedema.

Maintenance of body temperature at 35°C may be optimal.⁴⁵ Intracranial pressure falls significantly at brain temperatures below 37°C but no difference was observed at temperatures below 35°C. Cerebral perfusion pressure peaks at 35–36°C and decreases with further falls in temperature.⁴⁵ At a temperature below 35°C, both oxygen delivery and oxygen consumption decrease. Cardiac output decreases progressively with hypothermia. Therefore, cooling to 35°C may reduce intracranial hypertension and maintain sufficient CPP without associated cardiac dysfunction or oxygen debt.⁴⁶ As the temperature is lowered from 34°C to 31°C, the volume of IV fluid infusion and inotrope requirements increase substantially and, despite such interventions, mean arterial pressure decreases. At 31°C serum potassium, white blood cell count and platelet counts are diminished.⁴⁷ Thus, it seems that hypothermia to 35°C may be optimal.

Corticosteroids

Excessive inflammation has been implicated in the progressive neurodegeneration that occurs in multiple neurological diseases, including cerebral ischaemia. The efficacy of glucocorticoids is well established in ameliorating oedema associated with brain tumours and in improving the outcome in subsets of patients with bacterial meningitis. Despite encouraging experimental results, clinical trials of glucocorticoids in ischaemic stroke, intracerebral haemorrhage, aneurysmal subarachnoid haemorrhage and traumatic brain injury have not shown a definite therapeutic effect. Furthermore, the CRASH (corticosteroid randomisation after significant head injury) trial demonstrated an increased risk of death from use of steroids from all causes within two weeks of injury, and was stopped early.⁴⁸ Consequently, the BTF Guidelines state that the use of steroids is not recommended for TBI.³²

The evidence supporting glucocorticoid therapy for spinal cord injury is controversial; however, methylprednisolone continues to be widely employed in this setting (this is discussed further below under Spinal injury management).

Barbiturates and sedatives

The BTF Guidelines state that high-dose barbiturate therapy may be considered in haemodynamically-salvageable severe TBI patients with intracranial hypertension refractory to maximal medical and surgical interventions.⁴⁹ The utilisation of barbiturates for the prophylactic treatment of ICP has not been indicated. Barbiturates exert cerebral protective and ICP-lowering effects through alteration in vascular tone, suppression of metabolism and inhibition of free radical-mediated lipid peroxidation. Barbiturates may effectively lower cerebral blood flow and regional metabolic demands. The lower metabolic requirements decrease cerebral blood flow and cerebral volume. This results in beneficial effects on ICP and global cerebral perfusion. Barbiturates within the BTF guidelines are now included under the heading of Anaesthetics, Analgesics and Sedatives and these also recommend (Level II) that it is beneficial to minimise painful or noxious stimuli as well as agitation as they may potentially contribute to elevations in ICP. Therefore propofol is recommended for the control of ICP, but does not improve mortality or six-month outcome. High dose propofol should be avoided as it can produce significant morbidity.⁴⁹

Surgical interventions

The European TBI Guidelines suggest that operative management be considered for large intracerebral lesions within the first four hours of injury. The use of unilateral craniectomy after the evacuation of a mass lesion, such as an acute subdural haematoma or traumatic intracerebral haematoma, is accepted practice. Surgery is also recommended for open compound depressed skull fractures that cause a mass effect.⁵⁰

Decompressive craniectomy, for refractory intracranial hypertension, has been performed since 1977, with a significant reduction in ICP for both TBI ⁵⁰ and ischaemic stroke.⁵¹ In 2011 a multi-centre prospective randomised trial of early decompressive craniectomy in patients with severe traumatic brain injury reported that in adults with severe diffuse traumatic brain injury and refractory intracranial hypertension, early bifrontotemporoparietal decompressive craniectomy decreased intracranial pressure and the length of stay in the ICU but surprisingly was associated with more unfavorable outcomes at both 6 and 12 months using the Extended Glasgow Outcome Scale.⁵²

Prevention of Cerebral Vasospasm

Cerebral vasospasm is a self-limited vasculopathy that develops 4–14 days after subarachnoid haemorrhage (SAH) and/or TBI (see Figure 17.5). Oxyhaemoglobin, a product of haemoglobin breakdown, probably initiates vasoconstriction, leading to smooth-muscle proliferation, collagen remodelling and cellular infiltration of the vessel wall. The resulting vessel narrowing can lead to ischaemia. SAH patients develop cerebral vasospasm, and about one-third develop symptomatic vasospasm, which is associated with neurological signs and symptoms of ischaemia. Posttraumatic brain injury cerebral vasospasm occurs in approximately 10–15% of patients.

FIGURE 17.5 Pathophysiology of traumatic brain injury.

Calcium antagonists, such as nimodipine, have not been effective in TBI subarachnoid haemorrhage with vasospasm, and recent studies have suggested that calcium antagonists even prevent neurogenesis after TBI. Nimodipine has demonstrated effectiveness in the treatment of vasospasm in aneurysmal SAH and is now an option for recommended practice. An initial study of nimodipine in patients with TBI demonstrated no difference in outcome, and a Cochrane Systematic Review supports this conclusion.⁵³

Magnesium may prevent cerebral vasospasm through several mechanisms. Increased ATP entry into cells could decrease ischaemic depolarisation and limit infarction size. Magnesium also both inhibits the presynaptic release of excitatory amino acids and is a non-competitive antagonist to postsynaptic NMDA receptors. The drug can also cause vasodilation by inhibiting calcium channel-mediated smooth muscle contraction. Finally, magnesium increases cardiac contractility, which may improve cerebral perfusion in dysautoregulated brain tissue. TBI animal studies have demonstrated promising neuroprotection, but this is still to be confirmed in clinical trials.⁵⁴ Magnesium, however, does not cross the intact BBB easily, limiting its effect to injury and disease with leaky BBB. A randomised clinical trial of aneurysmal SAH patients receiving magnesium found that IV magnesium infusion reduced the frequency of delayed cerebral ischaemia in patients with aneurysmal SAH and subsequent poor outcome.⁵⁵

In SAH, more aggressive intravascular volume expansion and induced hypertension are used in conjunction with haemodynamic monitoring. By maintaining haematocrit at 30–33%, a shift in the oxygen dissociation curve is avoided.⁵⁶ Haemodilutional therapy increases collateral circulation at the site of haemorrhage, while reducing aggregation of erythrocytes where small vessel spasm has occurred. However, there is some emerging physiological data suggesting that normovolaemic hypertension may be the component most likely to increase cerebral blood flow after subarachnoid haemorrhage. In contrast, hypervolaemic haemodilution is associated with increased complications and might also lower the haemoglobin to excessively low levels.⁵⁶ Also in aneurysmal SAH, endovascular therapies, such as intra-arterial papaverine infusion, are employed. Papaverine acts immediately and increases arterial calibre and cerebral blood flow, but its effects are short-lived. Balloon angioplasty is particularly effective as a durable means of alleviating arterial narrowing and preventing stroke in patients with symptomatic vasospasm after aneurysmal SAH. The timing of endovascular intubation and use of inotropes in patients with cardiac dysfunction are unresolved issues.⁵⁷

Other Neuroprotective Measures

Many promising animal studies have not transferred to successful human clinical trials and there have been a plethora of different mechanisms that block single molecular processes but do not address the complex molecular processes involved in brain injury. Currently there is interest in antioxidants (Tirilazad mesylate), leukocyte adhesion inhibition (Enlimomab), and continued interest in erythropoietin, progesterone and their metabolites and receptors as neuroprotective targets and treatments.

Central Nervous System Disorders

CNS disorders include brain and/or spinal injury from trauma, infection or immune conditions. The pathophysiology and aetiology of these disorders are discussed here, including management of these conditions.

Traumatic Brain Injury

Head injury is a broad classification that includes injury to the scalp, skull or brain. Traumatic brain injury (TBI) is the most serious form of head injury. The range of severity of TBI is broad, from concussion through to post coma unresponsiveness. The Australian age-standardised incidence rate of TBI in 2004/5 was about 150 per 100,000 population. Approximately 90,211 Australians ^58,⁵⁹ and 16,000–22,500 New Zealanders⁶⁰ are hospitalised for TBI every year. Males aged 15–19 years have the highest incidence rates and suffer TBI at a rate almost three times that of women. The very young (0–4 years) and the very old (over 85 years) are also at increased risk.⁶¹ Indigenous Australians suffer TBI at almost three times the rate (410 per 100,000) of non-Indigenous Australians.⁶² It is estimated that 40,000 Australians are living with a disability as a result of TBI.⁶³ Despite definition issues relating to TBI epidemiology, there was an average annual decline of 5% in the TBI rate to 1997/98 but the incidence has increased since then. An Australian and new Zealand epidemiological study⁶⁴ of TBI (see Research vignette) found that the mean age was 41.6 years; 74.2% were men; 61.4% were due to vehicular trauma, 24.9% were falls in elderly patients, and 57.2% had severe TBI (Glasgow Coma Scale score ≤8). Twelve-month mortality was 26.9% in all patients and 35.1% in patients with severe TBI.

Aetiology

In Australia, motor vehicle-related trauma accounts for about two-thirds of moderate and severe TBI, with falls and assaults being the next most common causes. New Zealand has a higher proportion of recreational injuries compared to vehicle-related trauma. Sporting accidents and falls account for a far greater percentage of mild injuries. Alcohol is associated with up to half of all cases of TBI. In Australia and New Zealand, blunt trauma (falls and vehicle-related), rather than penetrating (stabbing and firearms) or blast, is the predominant mechanism of injury.⁶³ The transfer of energy to the brain tissue actually causes the damage and is a significant determinant in the severity of injury (and routinely noted in ED on admission). In the past 10 years, the introduction of safer car designs, airbags and other road traffic initiatives (e.g. redesigning hazardous intersections, driver education campaigns, random breath testing and reducing speed limits) have decreased the overall number of road fatalities; improvements in retrieval, neurosurgery and intensive care in the past few decades have enabled many people to survive injuries that would previously have been fatal. Research into and prevention of falls and shaken-baby syndromes has had a small impact on incidence reduction.^65,⁶⁶

Pathophysiology of TBI

TBI is a heterogeneous pathophysiological process (see Figure 17.5). The mechanisms of injury forces inflicted on the head in TBI produce a complex mixture of diffuse and focal lesions within the brain.⁶⁷ Damage resulting from an injury can be immediate (primary) or secondary in nature. Secondary injury results from disordered autoregulation and other pathophysiological changes within the brain in the days immediately after injury. Urgent neurosurgical intervention for intracerebral, subdural or extradural haemorrhages can mitigate the extent of secondary injury. Scalp lesions can bleed profusely and quickly lead to hypovolaemic shock and brain ischaemia. Cerebral oedema, haemorrhage and biochemical response to injury, infection and increased ICP are among the commonest physiological responses that can cause secondary injury. Tissue hypoxia is also of major concern and airway obstruction immediately after injury contributes significantly to secondary injury. Poor cerebral blood flow, as a result of direct (primary) vascular changes or damage, can lead to ischaemic brain tissue, and eventually neuronal cell death.⁶⁸ Systemic changes in temperature, haemodynamics and pulmonary status can also lead to secondary brain injury (Figure 17.6). In moderate to severe and, occasionally in mild, injury, cerebral blood flow is altered in the initial 2–3 days, followed by a rebound hyperaemic stage (days 4–7) leading to a precarious state (days 8–14) of cerebral vessel unpredictability and vasospasm.⁶⁴ More than 30% of TBI patient have AN dysfunction characterised by episodes of increased heart rate, respiratory rate, temperature, blood pressure, muscle tone, decorticate or decerebrate posturing, and profuse sweating.⁷⁰ Lack of insight into these processes and implementing early weaning of supportive therapies can lead to significant secondary insults.

FIGURE 17.6 Conceptual changes in cerebral blood flow and intracranial pressure (ICP) over time following traumatic brain injury: (A) cytotoxic oedema; (B) vasogenic oedema; (C) cerebral blood flow CPP = cerebral perfusion pressure; MAP = mean arterial pressure.

Focal injury

Because of the shape of the inner surface of the skull, focal injuries are most commonly seen in the frontal and temporal lobes, but they can occur anywhere. Contact phenomena are commonly superficial and can generate superficial or contusional haemorrhages through coup and contrecoup mechanisms.⁷¹ Cerebral contusions are readily identifiable on CT scans, but may not be evident on day 1 scans, becoming visible only on days 2 or 3. Deep intracerebral haemorrhages can result from either focal or diffuse damage to the arteries.

Diffuse injury

Diffuse (axonal) injury (DAI) refers to the shearing of axons and supporting neuroglia; it may also traumatise blood vessels and can cause petechial haemorrhages, deep intracerebral haematomas and brain swelling.⁷¹ DAI results from the shaking, shearing and inertial effects of a traumatic impact. Mechanical damage to small venules as part of the BBB can also trigger the formation of haemorrhagic contusions. This vascular damage may increase neuronal vulnerability, causing post-traumatising perfusion deficits and the extravasation of potentially neurotoxic blood-borne substances. The most consistent effect of diffuse brain damage, even when mild, is the presence of altered consciousness. The depth and duration of coma provide the best guide to the severity of the diffuse damage. The majority of patients with DAI will not have any CT evidence to support the diagnosis. Other clinical markers of DAI include the high speed or force strength of injury, absence of a lucid interval, and prolonged retrograde and anterograde amnesia. Figure 17.7 contrasts CT scans with haematoma formation and DAI.

FIGURE 17.7 Extradural haematoma and a subtle subdural haematoma (left), subdural haematoma (middle left), diffuse axonal injury (middle right), and combination injuries (right).

Mild TBI

Mild TBI often presents as a component of multitrauma or sports injury and can be overlooked at the expense of other peripheral injuries. Risk factors such as vomiting, dizziness, facial and skull fractures; including the loss of CSF from the nose or the ear, will categorise those needing further surveillance. Routine head CT and assessment of PTA are recommended to exclude mass lesions and DAI. Diagnosis and management in the acute phase of mild TBI is as crucial to functional outcome and rehabilitation as in moderate-to-severe TBI.⁷²

Skull fractures

Skull fractures are present on CT scans in about two-thirds of patients after TBI. Skull fractures can be linear, depressed or diastatic, and may involve the cranial vault or skull base. In depressed skull fractures the bone fragment may cause a laceration of the dura mater, resulting in a cerebrospinal fluid leak.⁷³ Basal skull fractures include fractures of the cribriform plate, frontal bones, sphenoid bones, temporal bone and occipital bones. The clinical signs of a basal skull fracture may include: CSF otorrhoea or rhinorrhoea, haemotympanum, postauricular ecchymoses, periorbital ecchymoses, and injury to the cranial nerves: VII (weakness of the face), VIII (loss of hearing), olfactory (loss of smell), optic (vision loss) and VI (double vision).

Nursing Practice

The surveillance and prevention of secondary injury is the key to improving morbidity and mortality outcomes ⁶⁹ (see Table 17.1). It should be noted that in a post hoc in analysis of saline critically ill patients with TBI, fluid resuscitation with albumin was associated with higher mortality rates than was resuscitation with saline.⁷⁴ Interventions are targeted at maintaining adequate cerebral blood flow and minimising oxygen consumption by the brain in order to prevent ischaemia. The anticipation and prevention of systemic complications are also of vital importance. Assessment is vital to establish priorities in care and is discussed in Chapter 16.

Nursing management of the neurologically impaired, immobilised, mechanically ventilated patient is described in Table 17.2 and is an adaptation of the current guidelines³² (see Table 17.3) to clinical practice (see Online resources for TBI-related protocols). In all TBI multitrauma patients, disability and exposure/environmental control assessment includes the routine trauma series of X-rays, namely chest, pelvis and cervical spine (lateral, anteroposterior and odontoid peg views). These should be reviewed by a radiologist and areas of concern, particularly in the upper and lower regions of the cervical spine, should be clarified with further investigations such as CT scans. Isolated TBI requires CT scanning of the head and upper spine. The management of TBI should include spinal precautions until spinal injury is definitively excluded.

TABLE 17.2 Nursing management of the neurologically impaired, immobilised, mechanically-ventilated patient

Nursing domain	Nursing outcome	Nursing interventions
Ventilation and oxygenation	• Airway patent. • Arterial pH, PaO₂, PbtO₂, SaO₂ within normal range. • PaCO₂ & ETCO₂ within normal range. • Lungs clear to auscultation. • No evidence of atelectasis or aspiration. • Chest X-ray clear of pathology.	• Assess ventilation parameters: ensure ET patency and position. • Assess bilateral chest movement: listen for airway obstruction or ET cuff leak; auscultate for air entry. • Assess chest X-ray. • Adequate sedation and ventilation to maintain PbtO₂, ICP, CPP. • Suction only as necessary: preoxygenate, avoid prolonged coughing; effective technique. • Avoid ICP complications of PEEP. • Position to avoid aspiration. • Provide meticulous oral hygiene.
Mobility/safety	• Cerebral blood flow uncompromised. • Minimal and transient changes in PbtO₂–ICP–CPP and return to desired parameters within 5 min of nursing intervention. • Patient integument maintained and infection free: skin, mucous membranes, cornea, wounds, invasive lines • Complications of immobility prevented: DVT, pneumonia, muscle strength. • Patient safety enabled, preventing nosocomial infection, secondary brain injury, self-harm. • Nutrition prescribed according to patient need. • Healing defined and uneventful.	• Haemodynamic stability maintained. Brain ischaemia and intracranial hypertension controlled. • Nursing interventions planned for minimal disturbance; efficient intervention. • Pressure-relieving mattress: allows minimal position changes for integument protection, with minimal CMRO₂ requirement, sequential compression device for venous return. • Hygiene maintained: assess integument, assess cornea, assess mucous membranes. • Maintain infection control interventions with invasive devices and wounds. • Administer preventive plan of treatment with vigilance and prediction. • Enable communication with other health professionals. • Chemical and physical restraint applied per assessment and prescription, within institutional policy. < div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Resourcing Critical Care Recovery and Rehabilitation Resuscitation Cardiovascular Assessment and Monitoring Stay updated, free articles. Join our Telegram channel Tags: ACCCNs Critical Care Nursing Jul 11, 2016 \| Posted by admin in NURSING \| Comments Off on Neurological Alterations and Management Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access

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