Severe head injury

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Chapter 67 Severe head injury

John A. Myburgh

Despite improvements in resuscitation and vital organ support, the management of patients with traumatic brain injury in the intensive care unit (ICU) presents a challenge to all members of the critical care team. As head injury is associated with a high mortality and morbidity, the benefits of intensive treatment and care may not become apparent until months or years later during rehabilitation after injury.

EPIDEMIOLOGY

Traumatic brain injury has been termed a ‘silent global epidemic’. It accounts for up to 30% of all trauma-related deaths and is the leading cause of death in young males in developed countries. The impact of mechanisation in developing countries has resulted in a sharp increase in the incidence and mortality from vehicular trauma.

In addition to this high mortality, the cost of survivors in these societies in emotional, social and financial terms is substantial as the effects of the original injury may persist for many years.

AETIOLOGY

Vehicular trauma, industrial accidents, falls and assaults account for the majority of head injury, with marked variations in patterns of injury across the world. For example, in Australasia, the incidence of head injury due to vehicular trauma is decreasing due to the success of preventive strategies such as restraint devices, speed control and stricter drink-driving legislation.1

DEMOGRAPHICS

The numbers of patients with traumatic brain injury presenting to hospitals vary widely in accordance with hospital admission policies and capabilities. Typical figures of all-cause head injury admissions in developed countries range from 200 to 300 per 100 000 patients.

Age and gender-specific data typically show two peaks: one in the second and third decades, with a male:female ratio of 2:1; the latter in the seventh to ninth decades with a more equivalent gender ratio.

PATTERNS OF INJURY

Traumatic brain injury represents a range of injury from mild head injury that may fully recover to severe injury associated with high mortality or high levels of disability.

Injury may be either blunt or penetrating, with the latter associated with a higher mortality.

Although the majority of head injuries (70–80%) are minor, a significant proportion of these patients may have poor functional outcomes due to secondary brain insults, missed injuries and comorbidities. Of the 20–30% who constitute moderate to severe head injury, approximately 10% of these are dead on admission whilst the remainder will usually require admission to the ICU for management in the first 7–10 days.

PATHOPHYSIOLOGY

Brain injury is a heterogenous pathophysiological process. It encompasses a spectrum of injury that includes the degree of brain damage at the time of injury (primary injury) in addition to insults that occur during the post-injury phase (secondary injury). These processes are depicted in Figure 67.1.

image

Figure 67.1 Pathophysiology of traumatic brain injury.

Both primary and secondary injuries are associated with the development of variable degrees of intracranial inflammation and disruption of cerebrovascular autoregulation.

An understanding of these processes is essential in order to quantify the severity of injury, direct appropriate management strategies and interpret information from clinical monitoring systems.

PRIMARY BRAIN INJURY

The severity of primary injury is determined by the degree of neuronal damage or death at the time of impact. This is a major determinant of outcome from traumatic brain injury and, with the exception of surgically evacuable mass lesions, is usually irreversible.

Primary brain injuries include all types of injury to the brain parenchyma and vasculature. Primary injuries that are associated with adverse outcome include traumatic subarachnoid haemorrhage and non-evacuable mass lesions, particularly in critical parts of the brain such as the posterior fossa.

SECONDARY BRAIN INJURY

Secondary brain insults are characterised by a reduction in cerebral substrate utilisation, particularly oxygen (Table 67.1). Of these insults, hypotension (defined as a systolic blood pressure of < 90 mmHg), hypoxia (oxygen saturation < 90% or PaO2 < 50 mmHg), hypoglycaemia, hyperpyrexia (temperature > 39°C) and prolonged hypocapnia (PaCO2 < 30 mmHg) have been shown to independently worsen survival following traumatic brain injury.

Table 67.1 Secondary brain insults following traumatic brain injury that are associated with increased morbidity and mortality

Systemic Intracranial
Hypoxia Seizure
Hypotension Delayed haematoma
Hypocapnia Subarachnoid haemorrhage
Hypercapnia Vasospasm
Hyperthermia Hydrocephalus
Hypoglycaemia Neuroinfection
Hyperglycaemia  
Hyponatraemia  
Hypernatraemia  
Hyperosmolality  
Infection  

Secondary insults may occur during initial resuscitation, transport both between and within hospitals, during anaesthesia and surgery, and subsequently in the ICU. These insults may initiate or propagate pathophysiological processes which may fatally damage neurones already rendered susceptible by the primary injury. Consequently, a vicious circle of secondary brain damage may develop with adverse outcomes.

INTRACRANIAL INFLAMMATION

As the brain is enclosed within the rigid skull and dura, small increases in intracranial volume result in sharp increases in intracranial pressure (Monro–Kelly doctrine). Consequently, the brain is a poorly compliant organ that has a limited capacity to accommodate pathological increases in intracranial pressure.

Traumatic brain injury invokes an inflammatory response characterised by the release of cytokines, freeradicals, excitatory amino acids and other mediators. The consequence of this response is disruption and alteration in the permeability of the blood–brain barrier, glial swelling and alterations in regional and global cerebral blood flow. The extent of this inflammatory process is an important determinant of intracranial pressure that may persist for some time following injury. Furthermore, alteration in blood–brain permeability may render the cerebral circulation susceptible to the effects of drugs that do not normally cross, such as osmotic diuretics and exogenous catecholamines.

CEREBRAL BLOOD FLOW AND AUTOREGULATION

Normally, cerebral blood flow is maintained at a constant rate in the presence of changing perfusion pressures by myogenic and metabolic autoregulation. These homeostatic mechanisms are impaired following head injury due to neuronal damage and intracranial inflammation. Distinct patterns of cerebral blood flow have been described following head injury that have direct clinical relevance with regard to management2 (Figure 67.2).

image

Figure 67.2 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.

THE HYPOPERFUSION PHASE

Cerebral blood flow is reduced by extrinsic and intrinsic mechanisms in the first 72 hours following injury, with resultant global and regional ischaemia. Because myogenic autoregulation is markedly impaired during this period, cerebral blood flow in the hypoperfusion phase is directly dependent on systemic blood pressure. Resultant neuronal ischaemia may result in ‘cytotoxic’ cerebral oedema and increased intracranial pressure.

In order to maintain cerebral perfusion, systemic blood pressure must be maintained during this phase so that cerebral perfusion pressure (defined as the difference between mean arterial pressure and intracranial pressure) is maintained between 60 and 70 mmHg.3

THE HYPERAEMIC PHASE

Following the initial hypoperfusion phase, autoregulatory mechanisms may start to recover with improved cerebral blood flow.

During this phase, intracranial inflammation and/or effects of medical therapies directed at maintaining adequate cerebral perfusion pressure may result in cerebral hyperaemia and increased intracranial pressure. The consequences of hyperaemia, inflammation and altered blood–brain permeability result in ‘vasogenic’ cerebral oedema.

This hyperaemic phase may persist for up to 7–10 days post injury and occurs in 25–30% patients. As there is restoration or increased cerebral blood flow during this phase, a range of cerebral perfusion pressure is recommended (50–70 mmHg).4

THE VASOSPASTIC PHASE

In a small cohort of patients (10–15%), particularly those with severe primary and secondary injuries or those with significant traumatic subarachnoid haemorrhage, a vasospastic phase characterised by typical cerebral blood flow patterns may persist. This phase represents a complex of cerebral hypoperfusion due to arterial vasospasm, posttraumatic hypometabolism and impaired autoregulation.5

RESUSCITATION

INITIAL ASSESSMENT

The resuscitation of head-injured patients should follow the principles outlined in the Advanced Trauma Life Support (ATLS®) guidelines for the early management of severe trauma.6

The initial emphasis is directed at assessing and controlling the airway, ensuring adequate oxygenation and ventilation, establishing adequate intravenous access and correcting haemodynamic inadequacy. Neurological assessment and brain-specific treatment should only follow once cardiorespiratory stability has occurred. Given the direct association between hypotension and hypoxia and adverse outcomes in traumatic brain injury, this is an absolute priority.

With respect to head-injured patients, the following principles in the initial assessment apply.7,8

AIRWAY

All patients with severe head injury (traumatic coma), marked agitation or significant extracranial trauma require early oral endotracheal intubation.

Depending on the skill of the operator and available facilities, this should be performed using a rapid sequence induction with cricoid pressure and in-line immobilisation of the cervical spine.

All head-injured patients should be assumed to have a potential cervical spine injury, and should be immobilised in a rigid collar until that possibility is definitively excluded.

BREATHING (= VENTILATION)

Patients should be ventilated in 100% oxygen using 6–10 ml/kg tidal volumes until blood gas analysis is available.

Oxygenation should be maintained at at least 100 mmHg (13 kPa) and the ventilator adjusted to achieve a normal arterial carbon dioxide tension (35–40 mmHg; 4.5–5.0 kPa).

Non-depolarising muscle relaxants and narcotics such as fentanyl may facilitate ventilation in the immediate post-intubation period in combative patients.

Empirical hyperventilation during initial resuscitation is not indicated until adequate oxygenation, haemodynamic stability and urgent computed tomography have been achieved.9

CIRCULATION (= CONTROL OF SHOCK)

Prompt restoration of circulating blood volume and restoration of a euvolaemic state is critical.10

An emerging body of evidence recommends the use of crystalloids, specifically normal saline, for fluid resuscitation of patients with traumatic brain injury. The use of albumin for fluid resuscitation is associated with increased mortality and should be avoided.11 Hypertonic saline may have a role as a small-volume resuscitation fluid that is useful in expanding intravascular volume, with additional beneficial effects on cerebral blood flow and reduction of cerebral oedema,12 although there is no evidence of reduced mortality when used in the prehospital period.13

Early arterial monitoring for accurate measurement of mean arterial pressure and central venous catheter placement for providing a guide to volume replacement and administration of blood and drugs is essential. The placement of these lines must not delay volume resuscitation.

Inotropes, such as adrenaline (epinephrine) or noradrenaline (norepinephrine), or vasopressors such as phenylephrine or metaraminol, may be used to defend blood pressure once correction of hypovolaemia is underway or achieved.4 This may be necessary if sedatives or narcotics are coadministered.

The use of military antishock trousers (MAST suit) in traumatic brain injury is not recommended.

DISABILITY (= NEUROLOGICAL ASSESSMENT)

Assessment of neurological function following injury is important to quantify the severity of neurotrauma and to provide prognostic information. The level of function may be influenced by associated injuries, hypoxia, hypotension and/or drug or alcohol intoxication. Similarly, recording the mechanism of injury is important, as high velocity injuries are associated with a greater degree of neuronal damage. It is important to review ambulance and emergency personnel and records in order to obtain the most accurate information.

Level of consciousness

The ATLS® recommends an initial assessment during initial resuscitation based on the response to stimulation: Awake, Verbal, Pain, Unresponsive (AVPU). This provides a rapid and practical grading of function with severe head injuries defined as those who respond to pain only or who are unresponsive.

The Glasgow Coma Scale (GCS) has an established place in the management of traumatic brain injury and is the most widely accepted and understood scale.14 Whilst originally described as a prognostic index, it provides an overall assessment of neurological function, derived from three parameters: eye opening, verbal response and motor response (Table 67.2).

Table 67.2 The Glasgow Coma Scale.14 The best response following non-surgical resuscitation is scored

image

The best responses in the GCS components should be recorded following cardiorespiratory resuscitation and prior to surgical intervention in order to provide prognostic information. A GCS of 14–15 indicates a mild injury, 9–13 a moderate injury and 3–8 is classified as severe. In the severely injured, such as intubated patients or those with ocular or facial trauma, the motor response is the most useful.

Pupillary responses

Pupil size and reactivity are important when consciousness is impaired. Whilst not part of the GCS, pupillary function should always be assessed and recorded at the same time as the GCS, particularly prior to the administration of narcotics, sedatives or muscle relaxants.

In the absence of traumatic mydriasis, abnormalities of pupil size and reactivity may indicate compression of the third cranial nerve, suggesting raised intracranial pressure or impending herniation, particularly when associated with lateralising motor signs and depressed consciousness

Papilloedema is uncommon in the acute phase of head injuries.

Motor function

In addition to the motor response of the GCS, decerebrate or decorticate posturing, hemiparesis or lateralising signs, paraparesis and quadriparesis (given the high association with spinal injuries with traumatic brain injury) should be documented concurrently with the GCS and pupillary responses.

SECONDARY SURVEY

Once the initial assessment is complete and resuscitation underway, a thorough secondary survey adopting a ‘top-to-toe’ approach is mandatory. This is outlined in the ATLS® approach to the traumatised patient.6

The principles outlined in the initial assessment form the basis for prioritising interventions in the secondary survey in traumatic brain injury. Extracranial causes of hypoxia such as pulmonary contusion or haemo/pneumothorax must be excluded and promptly treated. Haemorrhage – both externally from fractures or lacerations and internally from major vascular disruption or visceral injuries – must be aggressively treated until circulatory stability is achieved. There is no place for ‘permissive hypotension’ in head-injured patients as has been advocated in selected cases of penetrating trauma.

Target mean arterial pressure should be estimated in the context of the patient’s premorbid blood pressure. Higher pressures may be necessary in hypertensive or elderly patients. The early use of inotropes such as adrenaline or noradrenaline may be necessary to achieve this.

An approach of ‘damage-control surgery’ is now advocated in head-injured patients to minimise secondary insults. In the initial 24–48 hours following injury, only life- or limb-threatening injuries should be addressed, following which patients are transferred to the ICU for stabilisation and monitoring. Thereafter, semi-urgent surgery such as fixation of closed fractures or delayed plastic repairs may be done. Patients with severe head injury undergoing prolonged emergency surgery should ideally have intracranial pressure monitoring placed as soon as possible.

Routine X-rays of the chest, pelvis and cervical spine and baseline blood tests (including blood alcohol level in appropriate cases) are part of the secondary survey.

BRAIN-SPECIFIC RESUSCITATION

The place of interventions and therapies specifically directed at reducing intracranial pressure has been extensively reviewed in evidence-based guidelines for the management of severe head injury. Whilst there is little evidence for the role of some therapies such as empirical hyperventilation and osmotherapy during resuscitation, they continue to be widely used in clinical practice.

HYPERVENTILATION

Ventilation-induced reductions in PaCO2 result in marked reductions in cerebral blood flow and consequently in intracranial pressure. However, as cerebral blood flow may be reduced during the initial period following injury, further reductions in cerebral perfusion will result if hyperventilation is used during this phase (Figure 67.2).

Hyperventilation is associated with reductions in cerebral oxygenation, particularly in areas of neuronal damage, potentially exacerbating cerebral hypoxia. The combination of induced cerebral ischaemia in the damaged brain therefore offsets any theoretical benefit of reducing intracranial pressure. Consequently, empirical hyperventilation is not indicated during initial resuscitation when cerebral blood flow is compromised.

However, hyperventilation remains a potent non-surgical clinical tool of reducing intracranial pressure. In the resuscitated head-injured patient with unequivocal clinical signs of raised intracranial pressure or impending tentorial herniation (pupillary dilatation, lateralising signs or a witnessed neurological deterioration), hyperventilation is an option.Reductions of PaCO2 to levels ≤30 mmHg (4 kPa) may be therefore considered prior to urgent imaging or surgery for evacuation of a mass lesion.9

OSMOTHERAPY

Osmotically active agents, such as mannitol, are widely used in the treatment of traumatic brain injury. Theoretically, mannitol is administered to increase plasma osmolality in order to cause net efflux of fluid from areas of damaged, oedematous brain, with resultant reduction in intracranial pressure. An intact blood–brain barrier is necessary for this to occur. Following intravenous administration of mannitol, an immediate plasma expanding effect that reduces haematocrit and viscosity ensues, which temporarily increases cerebral blood flow. Subsequent reductions in intracranial pressure probably result from restoration in cerebral perfusion pressure and rheological changes in cerebral blood flow, rather than specific cerebral dehydration.

Osmotherapy is associated with a number of potentially adverse effects. Mannitol exerts an osmotic effect over a narrow range of plasma osmolality (290–330 mosm/l) above which theoretically beneficial effects may be negated. Mannitol will induce an osmolal gap between measured and calculated osmolality, so that regular measurements of serum osmolality are necessary to monitor the amount administered. This gap may be further increased by alcohol that is frequently present in the acute period. Mannitol will enter the brain where the blood–brain barrier is damaged, thereby potentially increasing cerebral oedema by increasing brain osmolality. Mannitol is a potent osmotic diuretic that may compromise haemodynamic stability by inducing an inappropriate diuresis in a hypovolaemic patient. Consequently, systemic hypotension may ensue which may cause further cerebral ischaemia or subsequent organ dysfunction such as acute renal failure. This effect may be exacerbated by the concomitant administration of catecholamines in order to defend systemic blood pressure.

Given the high risk with minimal benefit during resuscitation, the routine use of mannitol is not recommended in the absence of raised intracranial pressure and in patients where cerebral blood flow is compromised.15

Similarly to hyperventilation, mannitol is considered as an option only in resuscitated patients with unequivocal signs of raised intracranial pressure prior to imaging or evacuation of a mass lesion. Although doses are frequently quoted as 0.25–1.0 g/kg, lower doses are equally as effective as higher doses in terms of improving cerebral perfusion and are associated with a lower incidence of side-effects.

Hypertonic saline (3% solution) exerts similar osmotic plasma expanding effects to mannitol. These solutions do not exert an osmolal gap so that serum sodium reflects serum osmolality allowing easier titration. These solutions have been advocated as ‘small-volume resuscitation fluids’ that may be very effective in restoring systemic and cerebral perfusion in the acute phase following injury. In addition to reducing intracranial pressure, these solutions would appear to be superior to mannitol for resuscitation.16

EMERGENCY SURGICAL DECOMPRESSION (‘BURR HOLES’)

The advent of better equipped in-field resuscitation, medical retrieval, imaging and innovations such as teleradiology and telemedicine has largely superseded the need to perform urgent craniotomy in head-injured patients. In most instances, patients are resuscitated, stabilised and imaged with CT scans prior to any surgical intervention. This may involve transfer to a specialised trauma centre. CT scanning provides accurate information and directs the surgeon to a mass lesion that needs evacuation under optimal circumstances.

In remote communities without immediate access to CT scanning, surgical evacuation may be lifesaving in patients with a clear history of an expanding mass lesion such as an extradural or subdural haematoma. These include patients with low velocity injuries to the temporal region and an associated skull fracture that have clinical signs of intracranial herniation or a witnessed deterioration.

IMAGING

X-RAYS

All head-injured patients receive the routine ‘trauma series’ of X-rays, namely chest, pelvis and cervical spine (lateral, anteroposterior and peg views), although the last may be superseded by high resolution CT scan of the entire cervical spine.17

Skull X-rays have essentially been superseded by CT scanning and their routine use in the emergency evaluation of head-injured patients has been questioned.

COMPUTED TOMOGRAPHY (CT SCAN)

CT scanning is the most informative radiological technique in the evaluation of the acute head injury and is now standard in virtually all patients following head injury. CT scanning invariably requires moving the patient to a radiological suite. This must only be done once initial assessment and resuscitation are complete and the patient is stable enough to be transported by appropriately trained and equipped personnel.

The following patients should undergo CT head scan following traumatic brain injury:

• All patients with a history of loss of consciousness or traumatic coma.
• Combative patients where clinical assessment is masked by associated alcohol, drugs or extracranial injuries. These patients may require endotracheal intubation, sedation and ventilation to facilitate completion of CT scanning.

Technological advances in imaging now enable quick, high resolution digital images of the brain parenchyma and bony compartments. The most important role of CT scanning is prompt detection of mass lesion such as extradural or subdural haematomas. Thereafter, the degree of brain injury may be quantified by radiological criteria (Table 67.3 and Figure 67.3a).18

Table 67.3 Classification of CT scan appearance following traumatic brain injury.16 Examples are shown in Figure 67.3a

Category Definition
Diffuse injury (DI) I No visible intracranial pathology seen on CT scan
DI II (diffuse injury) Cisterns are present with midline shift 0–5 mm and/or Lesion densities present No high or mixed density > 25 mm May include bony fragments and foreign bodies
DI III (swelling) Cisterns are compressed or absent with midline shift 0–5 mm No high or mixed density > 25 mm
DI IV (shift) Midline shift > 5 mm No high or mixed density > 25 mm
Evacuated mass lesion Any lesion surgically evacuated
Non-evacuated mass lesion High or mixed density lesion > 25 mm, not surgically evacuated
image image image

Figure 67.3a Computed tomographic classification of diffuse axonal injury (Table 67.3).33 Panel (a) Diffuse injury II; Panel (b) Diffuse injury III; Panel (c) Diffuse injury IV.

These criteria are important for:

1 providing an index of injury severity
2 providing criteria for intracranial pressure monitoring
3 comparing the progression of injuries with subsequent scans
4 providing an index for prognosis

These criteria should be recorded following each CT scan, particularly when patients are transferred to secondary or tertiary centres. Examples of typical injuries appear in Figure 67.3a and 67.3b.

image image image

Figure 67.3b Intracranial haemorrhages. Panel (a) Acute subdural haematoma; Panel (b) Acute extradural haematoma; Panel (c) Acute traumatic subarachnoid haemorrhage.

The presence of traumatic subarachnoid haemorrhage should be recorded. This is an important index of severity of injury and is relevant for prognostication.19

CEREBRAL ANGIOGRAPHY

Cerebral angiography should be considered when a vascular injury, such as carotid artery dissection, is suspected in head-injured patients. This may be indicated by a large isodense lesion on CT scan or when the patient’s clinical condition is not consistent with the CT findings (e.g. a dense hemiparesis in the absence of a mass lesion).

MAGNETIC RESONANCE IMAGING

Magnetic resonance imaging (MRI) provides accurate detail of parenchymal damage, specifically small collections and non-haemorrhagic contusions. However, the information provided is not significantly better than that obtained from CT scanning to warrant routine use of MRI in the acute phase of injury. In addition, the placement and monitoring of an acute traumatised patient in an MRI scanner poses an additional risk that is not justified by the information provided.

MRI may have an important role in prognostication at a later stage in management, particularly in mild and moderate head injury.

INTERHOSPITAL TRANSFER

All severely head-injured patients should be managed in a specialised neurotrauma centre in close collaboration with intensive care physicians and neurosurgeons.20 This may involve intra- or interhospital transportation. This is a potentially hazardous exercise and has the potential to adversely affect outcome by causing secondary insults. Consequently, appropriately skilled and equipped personnel should only do this once resuscitation, stabilisation and initial imaging are completed.

A full primary and secondary survey and review of all documentation and investigation is required following transfer to a secondary or tertiary centre.

INTENSIVE CARE MANAGEMENT

There is no standard or uniform method of managing traumatic brain injury in the ICU. Most practices are determined by local preferences and experience, caseload and resources. The Brain Trauma Foundation of the American Association of Neurological Surgeons21 and the European Brain Injury Consortium22 have published evidence-based management guidelines for the management of severe brain injury. These publications provide very few standards by which to direct therapy and the majority of issues addressed are presented either as management guidelines or options.

Although management of head injury in the ICU will be considered in two sections – supportive therapy and brain-specific therapy – these occur simultaneously. The principles of management focus on the integration of all monitoring information in the context of the underlying injury so that secondary brain injury is prevented.

SUPPORTIVE THERAPY

Following initial resuscitation, good intensive care management forms the basis of head injury management and is regarded as a continuum of care. This takes priority over brain-specific therapies, which to date remain inconclusive in their efficacy.

HAEMODYNAMIC MANAGEMENT

Monitoring

Accurate measurement of systemic blood pressure is essential and should be measured via an arterial catheter referenced to the aortic root. A large artery such as the femoral artery should be considered in haemodynamically unstable patients as radial or dorsalis pedis arterial catheters may underestimate true systemic pressure in shocked patients. Given the importance of maintaining adequate systemic pressures, non-invasive measurement of bloodpressure is not recommended during the acute phase of monitoring.10

Therapy should be titrated to mean arterial pressure in accordance with the patient’s premorbid blood pressure – i.e. in older patients, higher mean arterial pressure (e.g. 80 mmHg) may be necessary.

Volume status should be assessed using clinical criteria, central venous pressure monitoring and hourly urine output.

Pulmonary artery catheterisation for the measurement of cardiac output and pulmonary artery pressures is rarely indicated in head-injured patients and is not recommended on current evidence.

Fluid management

The attainment of a euvolaemic state is essential throughout intensive care management. This is determined by standard measurements such as serum sodium and osmolality, urea and creatinine, pulse rate, right atrial and mean arterial pressure and urine output.

Resuscitative fluids depend on local preferences, as there is no evidence to recommend crystalloids over colloids.

Optimal rheology for the cerebral circulation requires a haematocrit of approximately 30%: patients should be transfused if actively bleeding or to maintain a haemoglobin between 8.5 and 10 g/l.

Maintenance fluids should be directed at maintaining a normal osmolality. As a general principle, glucose-containing solutions are not recommended; however, these may be required (i.e. as 5% dextrose in water) if patients become hyperosmolal (> 320 mosm/l).

Inotropic therapy

Inotropes such as adrenaline, noradrenaline or dopamine are frequently used to augment mean arterial pressure to attain an adequate cerebral perfusion pressure. These should only be commenced once volume resuscitation is actively underway or complete. The early use of inotropes is increasingly being advocated during resuscitation as an important strategy during the hypoperfusion phase.4

There are no conclusive trials to recommend one inotrope over another or combination of inotropes. Adrenaline, noradrenaline and dopamine are equally effective in augmenting cerebral perfusion pressure. The degree by which these agents directly affect the cerebral circulation following head injury is unknown, although there is some evidence suggesting that dopamine has both direct cerebrovascular and adverse neuroendocrine effects.23,24

Adrenaline is widely used as an initial inotropic agent in doses titrated to achieve a desired mean or cerebral perfusion pressure. Whilst effective, it may be associated with metabolic side-effects such as hyperlactataemia and hyperglycaemia, which may complicate metabolic management. For this reason, noradrenaline is currently regarded by many as the initial agent of choice for patients with traumatic brain injury.25

Doses may range widely and high doses may be required to attain a desired cerebral perfusion pressure, particularly if cerebral perfusion pressures are targeted for > 72 hours. It is important to prescribe inotropes in the context of the underlying injury. Lower cerebral perfusion pressure targets (i.e. 50–70 mmHg), and therefore doses of inotropes, may be necessary if patients develop cerebral hyperaemia. Titration of inotropes may require an index of cerebral blood flow such as jugular venous saturation monitoring during this phase.

Neurogenic hypertension

Neurogenic hypertension is common in the latter phases following injury (> 5 days) and is usually centrally mediated. It may be associated with ECG changes and/or supraventricular arrhythmias. It is usually self-limiting and correlates with the severity of injury. Treatment depends on the severity of the problem: β-blockers or centrally acting agents such as clonidine are usually effective; vasodilators are relatively contraindicated.

RESPIRATORY THERAPY

Monitoring

Continuous measurement of arterial oxygen saturation is essential.

Continuous measurement of end-tidal carbon dioxide is frequently performed, although the reliability is questionable and should be intermittently checked with arterial blood gases.

Monitoring of ventilatory parameters should be consistent with standard approaches and includes measurement of tidal volumes, respiratory rates, and inspiratory and expiratory airway pressures.

Ventilation

The majority of patients with severe head injury will require mechanical ventilation to ensure adequate oxygenation and to maintain an arterial carbon dioxide tension between 36 and 40 mmHg (4.8–5.3 kPa).

The principles of optimal ventilation, humidification and weaning are addressed elsewhere. Strategies such as ‘permissive hypercapnia’ that are advocated for selected patients with acute lung injury or acute respiratory distress syndrome do not have a role in head-injured patients due to the requirement to maintain normocapnia.

Positive end-expiratory pressure (PEEP) is recommended at low levels (5–10 cmH2O) to maintain functional residual capacity and oxygenation. Higher levels may compromise blood pressure, particularly in hypovolaemic patients, and should be used with caution. High levels of PEEP (> 15 cmH2O) may compromise cerebral venous return but adverse effects on intracranial pressure are uncommon.

Weaning from ventilation should commence once intracranial pathology has stabilised – resolution of cerebral oedema on CT scan, control of intracranial hypertension and adequate cerebral perfusion pressures.

Trials of extubation should be carefully considered so that subsequent hypoxic episodes do not occur, as these are potent secondary insults.

Patients with slow recovery of adequate consciousness should be considered for early tracheostomy, either percutaneously or surgically.

Neurogenic pulmonary oedema

This is a dramatic clinical syndrome that occurs in most patients with severe head injury and correlates with severity of injury. The underlying pathophysiological process is complex, but is primarily related to centrally mediated sympathetic overactivity. It is characterised by sudden onset of clinical pulmonary oedema, hypoxia, low filling pressures, poor lung compliance and bilateral lung infiltrates, usually within 2–8 hours following injury.

The process is usually self-limiting and treatment is primarily supportive, aimed at ensuring adequate oxygenation and ventilation. This usually requires endotracheal intubation and mechanical ventilation with the administration of PEEP. Ablation of sympathetic overactivity is effectively done with adequate sedation; β-blockade is usually unnecessary. Diuretics are effective but must be titrated against the volume status of the patient so that cerebral perfusion pressure is not compromised.26

The development of pulmonary oedema in patients with cardiac disease should be regarded as cardiogenic until proven otherwise.

Nosocomial pneumonia

Head-injured patients who require prolonged ventilation are at increased risk of nosocomial pneumonia. This is associated with secondary brain injury and an increased mortality.27 Risk factors include barbiturate and hypothermia therapy. Diagnosis and treatment are discussed elsewhere.

SEDATION, ANALGESIA AND MUSCLE RELAXANTS

There are no standards for sedation and analgesia in head injured patients – protocols will depend on local preferences and resources. The level of sedation and analgesia required for head-injured patients depends on the degree of traumatic coma, haemodynamic stability, intracranial pressure and systemic effects of the head injury itself.

During the resuscitation phase, where cerebral hypoperfusion is common, sedation should be titrated to cause the least effect on systemic blood pressure. During this period, short-acting narcotics such as fentanyl are useful, particularly if patients have associated extracranial injuries. These agents have relatively little adverse effect on haemodynamics and have the additional benefit of tempering systemic sympathetic surges that frequently occur after injury. As narcotics affect pupillary responses, these must be documented before administration, and CT scan should be performed soon afterwards to define baseline intracranial pathology. Short-term muscle relaxants such as vecuronium are useful during this phase to control combative patients following intubation, ventilation and sedation.

During the intensive care phase, the requirements for sedation are different. Sedation should be titrated to have the patient sedated as lightly as possible to allow clinical assessment of neurological function and to facilitate mechanical ventilation. The level of sedation will depend on haemodynamic stability and the degree of intracranial pressure. Infusions of narcotics and benzodiazepines (e.g. morphine and midazolam) are useful in providing moderate to deep levels of sedation and are effective in controlling surges of intracranial pressure. However, these agents may accumulate, resulting in a delay in return of consciousness or, if used for prolonged periods, may be associated with an emergence delirium state.

The use of propofol as a sole sedating agent has become popular.28 It provides deep levels of sedation, which is effective in controlling systemic sympathetic swings and rises in intracranial pressure. It is rapidly reversible on cessation allowing prompt assessment of neurological status and does not accumulate. In addition, pupillary responses are not directly affected. Propofol should be used with caution in haemodynamically unstable patients, as it is a potent negative inotrope. The prolonged use of propofol is associated with tachyphylaxis and significant caloric loading from the lipid vector. Concerns have been raised about myocardial depression and sudden cardiac death, particularly if large doses are administered.29

The routine use of muscle relaxants is not recommended either to facilitate sedation or to control raised intracranial pressure. The prolonged use of these agents is associated with adverse outcome in traumatic brain injury and prolonged use of non-depolarising muscle relaxants is associated with polyneuromyopathies.

BODY POSITION

Patients should be nursed at 30–45° head elevation to facilitate ventilation, improve oxygenation, and reduce the risk of aspiration. The head should be kept in a neutral position.30

PHYSIOTHERAPY

Physiotherapy has an important role to play in the removal of lung secretions, prevention of contractures and venous thrombosis. Patients with raised intracranial pressure may require boluses of sedation before chest physiotherapy to prevent acute rises in intracranial pressure.

METABOLIC MANAGEMENT

Routine measurement of biochemistry is essential with the aim of keeping all parameters within normal limits. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) and diabetes insipidus may occur following head injury. Management is discussed elsewhere.

Hyperglycaemia is common following severe head injury and is usually centrally mediated and transient. Blood sugar levels should be maintained within normal limits with insulin infusions. The role of ‘tight’ glycaemic control (i.e. 4.0–6.0 mmol/l) in patients with traumaticbrain injury has not been determined and as hypoglycaemia is a recognised secondary insult, normal blood sugar levels (i.e. 8.0–10.0 mmol/l) are recommended.

Core temperature should be routinely monitored as hyperthermia has been identified as a cause of secondary injury. However, the real incidence of hyperpyrexic secondary brain damage may be underestimated as a temperature gradient of 1–2°C between core and brain temperature has been demonstrated and efforts should be directed at maintaining core temperature at 37.5°C.

NUTRITION

The caloric needs of head-injured patients must be addressed as soon as possible following resuscitation. Early enteral feeding is recommended.31

Placement of a nasogastric and/or enteral feeding tubes in head-injured patients is usually via the oral route until an anterior cranial fossa (fractured cribriform plate) is excluded. Thereafter, post-pyloric tubes, via the oral, nasal or percutaneous route, are recommended as gastroparesis is common following head injury.

STRESS ULCER PROPHYLAXIS

The incidence of gastric erosions and ‘stress ulceration’ has markedly decreased with better resuscitation and early enteral feeding. Head-injured patients are at no more risk than other critically ill patients for developing stress ulceration.

H2 antagonists, such as ranitidine, should be used in ventilated patients until enteral feeding is established, following which they may be ceased.

Patients with a previous history of peptic ulceration should remain on antacid therapy for the duration of the intensive care stay.

THROMBOPROPHYLAXIS

Head-injured patients, particularly those requiring prolonged ventilation and sedation, or with extracranial injuries, are at increased risk for developing thromboembolism. The use of anticoagulants such as fractionated or low molecular weight heparins is contraindicated in patients with intracranial haemorrhage. Consequently, the role of thromboprophylactic agents in head injury is difficult and there are no standards for their use.32

As a general rule, anticoagulants should not be used in head-injured patients with any evidence of destructive intracranial pathology or haemorrhage, until there is resolution of these processes on CT scan.

Non-pharmacological methods of thromboprophylaxis such as elastic stockings or pneumatic calf compressors are unproven, but provide a reasonable alternative. Frequent surveillance using Doppler ultrasound of the iliofemoral veins in high-risk patients, such as those with pelvic fractures, should be performed. Patients who develop deep-vein thromboses and who cannot be anticoagulated should be considered for inferior vena caval filters. The use of anticoagulants in head-injured patients with proven pulmonary embolism will depend on the relative risk to the patients’ life.

ANTIBIOTICS

These should be used sparingly and in accordance with accepted microbiological principles. Prophylactic antibiotics should only be prescribed to cover insertion of intracranial pressure monitors and are not recommended for basal skull fractures.33 Frequent cultures of leaking or draining cerebrospinal fluid should be taken and infection treated specifically.

BRAIN-SPECIFIC MONITORING

The most accurate assessment of brain function following traumatic brain injury is a full clinical neurological examination in the absence of drugs or sedatives. However, this is often not possible for the majority of head-injured patients managed in the ICU.

Ideally, neuromonitoring should provide accurate and integrated information about intracranial pressure–volume relationships (elastance), patterns and adequacy of cerebral perfusion, and an assessment of cerebral function. No such monitor exists, although each of these parameters may be monitored in various ways with variable levels of accuracy and clinical utility.

CLINICAL ASSESSMENT

Regular assessments of GCS, pupillary signs and motor responses (see above) should be made and recorded in the ICU flow chart. Concomitant sedation may influence the level of consciousness and this should be recorded. Initially, these assessments are recorded hourly, but this may change as patients become more stable.

A witnessed deterioration in GCS, especially the motor response, or the development of new lateralising signs should be regarded as life-threatening intracranial hypertension or tentorial herniation until proven otherwise.

INTRACRANIAL ELASTANCE

Intracranial pressure monitoring

The recognition that raised intracranial pressure is associated with adverse outcome led to the measurement of this parameter in order to quantify the degree of injury and to assess the response to treatments directed at reducing intracranial pressure.

The Brain Trauma Foundation guidelines recommend intracranial pressure monitoring in patients with traumatic coma (severe head injury: GCS = 8 following non-surgical resuscitation)34 with either:

• abnormal CT scan:

• diffuse injury II–IV (Table 67.3) or
• high or mixed density lesions > 25 mm

• normal CT scan with two or more of the following features.

• age > 40 years
• unilateral or bilateral motor posturing
• significant extracranial trauma with systolic hypotension (< 90 mmHg)

Coagulopathy is a contraindication to intracranial pressure monitoring. Measurement of intracranial pressure35 with an intraventricular catheter is the most accurate and clinically useful method. It has the advantages of zero calibration, cerebrospinal fluid drainage for raised intracranial pressure and allows dynamic testing of pressure–volume relationships. Disadvantages include technical difficulty with insertion, particularly in patients with cerebral oedema and compression of the lateral ventricles, and an increased incidence of infection.

Solid state systems such as fibreoptic (e.g. Camino®) or strain gauge tipped catheters (e.g. Codman®) may be placed intraparenchymally or intraventricularly. These systems transduce intracranial pressure to provide high fidelity waveforms. They are small calibre and although requiring a small craniotomy (burr hole) for insertion, may be inserted at the bedside. Disadvantages include inability to perform zero calibration after insertion and baseline drift that may be clinically significant after 5 days.

Fluid-filled subdural catheters have been used for many years. However, these are no longer recommended due to the development of more accurate solid state systems. Subdural pressures do not accurately reflect global intracranial pressure, particularly in the presence of a craniectomy. Pressure readings may also be affected by local clot formation within the catheter.

Measurements are used to calculate cerebral perfusion pressure: mean arterial pressure minus intracranial pressure. For this calculation, both measurements should be referenced to the external auditory meatus (equivalent to the circle of Willis).

Intracranial pressure monitoring should be continued until the patient can be assessed clinically, intracranial pressure has stabilised (< 20–25 cmH2O) and cerebral oedema has resolved on CT scan. This occurs in the majority of patients within 7 days. Patients with refractory intracranial hypertension may require monitoring for longer periods, although this may be complicated by drift (with solid state systems), infection (with intraventricular catheters) or occlusion (subdural catheters). In this situation, intracranial pressure monitors may need to be replaced or removed and patients assessed by serial CT scan or clinically.

CEREBRAL BLOOD FLOW

Currently, there is no method of routinely measuring cerebral blood flow at the bedside. Technological advances such as mapping with labelled xenon under computed tomography and laser Doppler flowmetry provide useful imaging of regional and cerebral blood flow. However, these techniques are intermittent, labour intensive and limited to research-based units.

A number of qualitative measurement techniques are available that provide an indirect assessment of cerebral blood flow that may be useful, particularly when used in conjunction with other modalities such as intracranial pressure monitoring and CT scanning. Interpretation of these measurements must be taken within the clinical context, particularly the time course of the underlying injury (Figure 67.2).

Jugular bulb oximetry

Measurement of oxygen saturation in the jugular bulb by the retrograde placement of a fibreoptic catheter provides an indirect assessment of cerebral perfusion. Low jugular venous saturations (< 55%) may be indicative of cerebral hypoperfusion due to systemic hypotension or hypocapnia. High levels of jugular venous saturation (> 85%) may be indicative of cerebral hyperaemia or inadequate neuronal metabolism, such as occurs during the hyperaemic phase or during the evolution of brain death. Both low and high jugular venous saturation are associated with adverse outcomes.36

There are insufficient data to provide evidence-based indications for the routine use of jugular bulb oximetry. Its use is limited to experienced units when an index of cerebral blood flow is required during adjunctive therapies in patients with intracranial hypertension – for example, cerebral perfusion pressure augmentation with catecholamines, barbiturate coma, hyperventilation or hypothermia.

Transcranial Doppler

Transcranial Doppler ultrasonography with a 2 MHz pulsed Doppler probe allows non-invasive, intermittent or continuous assessment of the velocity of blood flow through large cerebral vessels. Insonation through a naturally occurring acoustic window such as the transtemporal approach allows insonation of the anterior, middle and posterior cerebral arteries, terminal internal carotid artery and anterior and posterior communicating arteries.37

Measured indices of flow include systolic, mean and diastolic flow velocities. Distinct patterns associated with normal, hyperaemic, vasospastic and absent flow are recognised. Derived indices such as the Gosling pulsatility index (systolic/diastolic difference divided by the mean velocity) and Lindegaard ratio (between middle cerebral artery to extracranial internal carotid artery) may assist in differentiating these flow patterns.

Despite increasing use of transcranial Doppler to diagnose posttraumatic hyperaemia and vasospasm, there are insufficient data to provide evidence-based indications for the routine use of transcranial Doppler.

Continuous measurements and trends of transcranial Doppler provide a better assessment of flow/velocity patterns than intermittent or daily measurements. The technique is operator-dependent and there may be significant variations in velocity patterns during the course of the injury. Consequently, interpretation of intermittent measurements should be made in conjunction with other variables such as CT scan appearance, intracranial pressure and, where applicable, jugular venous saturation.

CEREBRAL FUNCTION AND METABOLISM

Electroencephalography

Electroencephalography has been used for many years to assess seizure activity that may be masked by sedatives or muscle relaxants and to provide an objective estimate of the degree of electrical neuronal depression with barbiturate therapy. Whilst seizures may not be clinically apparent in a proportion of patients, and may constitute an important secondary insult, the accuracy and reliability of electroencephalography in ICUs is questionable due to outside electrical interference from monitors and ventilators.38

The development of bispectral index (BIS monitoring) as a measurement of depth of anaesthesia has led to the suggestion that this may be an alternative to the use of electroencephalography with barbiturate or sedative therapy in traumatic brain injury. Bispectral index has not been validated in this context and cannot be recommended as a titration end-point.39

Other forms of electroencephalography such as processed electroencephalography and integrated cerebral function monitors have a limited role in head-injured patients due to the amount of data generated and the need for skilled personnel to acquire and interpret the data.

Evoked potentials

Measurement of evoked potentials, assessing the integrity of sensory and motor pathways, may provide diagnostic and prognostic information; however, because of the complexity of the technique, it is not recommended for general use.40 The reliance of one variable, such as evoked potentials, to predict outcome from traumatic brain injury is not recommended.

Neuronal function

Research developments in microprobe technology have resulted in specific electrodes that may be placed into the brain parenchyma to measure brain oxygen, pH and carbon dioxide tensions. These may be individual electrodes or combined with other sensors such as pressure monitors to form multimodal tissue monitors.

Cerebral microdialysis is a technique that measures brain extracellular fluid metabolites. Dialysate is obtained through a microdialysis catheter inserted through the same burr hole as an intracranial pressure monitor to measure concentration and fluxes of markers of intracranial inflammation (e.g. lactate, pyruvate and purines).41

Whilst these systems provide highly specific information about the biochemical milieu of focal areas of brain tissue, their clinical utility is limited to research centres.

BRAIN INJURY SURVEILLANCE

Serial assessment of the anatomical injury is an essential part of monitoring head injury. This is done by serial CT scanning at frequent intervals depending on the neurological status of the patient.

Any patient who develops an unexplained neurological deterioration or significant validated deviation of monitored parameters should have a CT scan so that new or delayed intracranial mass lesions are identified.

CT scans should be assessed and scored according to the classification outlined in Table 67.3. The progression or resolution of axonal injury, cerebral oedema, contusion and haemorrhages should be recorded. Other parameters such as intracranial pressure and jugular venous saturation should be interpreted in accordance with the CT scan appearance.

However, as CT scanning requires transport of the patient to a radiology suite, this should only be done by experienced personnel when the patient is stable.

BRAIN-SPECIFIC THERAPY

Treatment options directed at ameliorating brain injury are limited. Despite intensive research into defining the pathobiological processes in primary injury, studies analysing therapies designed to modulate intracranial inflammation have not been successful. These include aminosteroids, calcium channel blockade and N-methyl-D-aspartic acid (NMDA) antagonists.42

Brain-specific or ‘targeted’ therapy is directed at maintaining cerebral perfusion pressure and minimising intracranial pressure. Whilst there is an inherent relationship between these two principles, priorities are different depending on the time course of the underlying injury. This is important as strategies directed at one may have adverse effects in the other (Figure 67.2).

DEFENCE OF CEREBRAL PERFUSION PRESSURE

The pathophysiological principles outlined on p. 765 are important in defining strategies to optimise cerebral perfusion pressure following injury. Whilst the Brain Trauma Foundation guidelines recommend a cerebral perfusion pressure of 60–70 mmHg, this figure may not be applicable over the entire time course following injury.3

This requires a change from a ‘set and forget’ philosophy to one of ‘titration against time’ in order to prescribe desirable therapeutic targets.

Hypoperfusion phase (0–72 hours)

Cerebral hypoperfusion is present in the majority of patients with severe head injury (GCS = 8). During this phase, augmentation of cerebral perfusion pressure is paramount and should be done by maintaining adequate haemodynamic function.

The principles outlined above on ‘Haemodynamic management’ become the mainstay of defence of cerebral perfusion pressure. This phase should be regarded as an extension of resuscitation and supportive treatment. During this period, a cerebral perfusion pressure of at least 60 mmHg is recommended. In addition to reduced cerebral blood flow, intracranial pressure may be increased by mass lesions or ‘cytotoxic’ cerebral oedema. The latter will usually respond to restoration of cerebral perfusion pressure.

During this phase, medical therapies directed at raised intracranial pressure such as osmotherapy or hyperventilation should only be used if cerebral perfusion pressure is maintained at an appropriate level and the patient is adequately monitored.

Assessment of adequacy of the response to augmentation of cerebral perfusion pressure is made by intracranial pressure trends, CT scan appearance and, where possible, neurological assessment. If patients appear to have stabilised, sedation may be reduced with the aim of extubation.

Hyperaemic phase (3–7 days)

Approximately 25–30% of patients will develop clinical signs of cerebral hyperaemia, characterised by raised intracranial pressure, persistent cerebral oedema on CT scan and possibly confirmed by high jugular venous saturations.43 This may be due to vasogenic cerebral oedema caused by intracranial inflammation or by catecholamine infusions often used to augment cerebral perfusion pressure.

The diagnosis of catecholamine-induced cerebral hyperaemia is difficult. This should be suspected in patients who require progressively increasing doses of catecholamines (e.g. > 20 μg/min of adrenaline or noradrenaline) to attain a prescribed cerebral perfusion pressure of 60 mmHg. This phenomenon is due to tachyphylaxis to prolonged catecholamine infusions and may be responsible for iatrogenically increasing intracranial pressure.

If CT appearance is unchanged, cerebral perfusion pressure targets may be lowered in order to use lower doses of inotropes. This exercise may be facilitated by jugular venous saturation monitoring or transcranial Doppler to provide an index of adequate cerebral blood flow for the lower cerebral perfusion pressure.

If patients continue to have raised intracranial pressure, strategies directed at reducing intracranial pressure should be considered.

REDUCTION OF INTRACRANIAL PRESSURE

In the absence of intracranial mass lesions, raised intracranial pressure is usually an indicator of severity of the underlying injury and represents exhausted intracranial elastance.

The most effective methods of reducing raised intracranial pressure are mechanical interventions such as removal of mass lesions, drainage of cerebrospinal fluid or decompressive craniectomy.

A number of medical strategies directed at reducing intracranial pressure have been used for many years. Despite widespread use and firmly held beliefs, there is little evidence to support the routine use of these therapies.44

Intracranial pressure should be maintained at < 25 cmH2O.45 Trends of intracranial pressure are equally as important and should be assessed within the context of cerebral perfusion pressure and the methods used to defend it.

Surgical evacuation of mass lesions

The prompt detection and evacuation of mass lesions causing raised intracranial pressure is the most effective method of relieving intracranial hypertension. Although the majority of these lesions will be present immediately after injury and will be treated during the resuscitative phase, approximately 10% patients will develop delayed intracranial haematomas. These are detected by sudden unexplained rises in intracranial pressure or by CT scan surveillance.

Close liaison and coordination with neurosurgeons is essential.

Cerebrospinal fluid drainage

Drainage of cerebrospinal fluid through an intraventricular catheter is an effective method of reducing intracranial pressure. If present, these catheters should be placed 5–10 cm above the head and opened for drainage every 1–4 hours.

Decompressive craniectomy

Wide, bilateral, frontoparietal craniectomies are increasingly being advocated to reduce intracranial pressure in patients with refractory intracranial hypertension. Whilst there are numerous case series demonstrating dramatic improvements, there are no conclusive outcome-based trials to make firm recommendations.46

Recent experience in paediatric patients is encouraging and the role of pre-emptive decompressive craniectomy in high-risk patients is yet to be determined.47

Osmotherapy

The rationale and role of osmotherapy using mannitol or hypertonic solution is addressed on p. 780. The same principles during resuscitation apply during intensive care management.

Mannitol or hypertonic saline should only be used in patients with validated intracranial hypertension who are euvolaemic, haemodynamically stable, with a serum osmolality < 320 mosm/l.

There is no evidence that osmotherapy or induced dehydration improves outcome or is more effective in cytotoxic than vasogenic cerebral oedema.15

Hyperventilation

The role of hyperventilation during intensive care management is limited to the indications outlined on p. 780.

The routine prolonged use of hyperventilation in head-injured patients is associated with a worse outcome than patients ventilated to normocapnia. This is probably due to reductions of cerebral blood flow and secondary brain ischaemia.

Current evidence-based guidelines do not recommend the use of routine hyperventilation.9

Hypothermia

Induced hypothermia has been used for many years to reduce cerebral metabolism and thereby raised intracranial pressure. A sound theoretical benefit exists in experimental models where hypothermia is induced immediatelyfollowing injury with prompt reduction in raised intracranial pressure. However, these benefits have not translated into improved outcomes in a number of clinical trials.48

Induced hypothermia (to temperatures of 30–33°C) is associated with prolonged ventilation and increased susceptibility to nosocomial infection, and may be associated with increased morbidity and mortality in head-injured patients.

Currently, hypothermia is regarded as a ‘second tier’ option in patients with refractory intracranial hypertension, but on current evidence, cannot be recommended.

Barbiturate coma

The role of barbiturates in traumatic brain injury is similar to hypothermia. Despite experimental evidence that barbiturates reduce cerebral metabolism and reduce intracranial pressure, no definitive studies have shown a benefit in clinical trials. Barbiturates have invariably been used in patients with refractory intracranial hypertension where a positive outcome was unlikely, making interpretation of these trials difficult.

Titration of barbiturate coma to burst suppression on an electroencephalograph is suggested as a reasonable end-point. However, this is often difficult to obtain and measure.

Barbiturates may cause hypotension and reduce cerebral blood flow, potentially exacerbating secondary insults in patients with cerebral oligaemia. Prolonged use of barbiturates will delay awakening and predispose the patient to nosocomial infection.

Barbiturates are a ‘second tier’ option in patients with refractory intracranial hypertension and not recommended on current evidence.49

Steroids

Steroids have been advocated for many years to ameliorate intracranial inflammation, thereby reducing intracranial pressure. A large international study has provided conclusive evidence that steroids may be associated with adverse outcomes in traumatic brain injury, and therefore have no place in management.50,51

Cerebral blood volume regulation

Following resuscitation and stabilisation, a strategy reducing cerebral perfusion pressure to > 50 mmHg using colloids, β-blockade, clonidine and dihydroergotamine may be effective in minimising secondary cerebral hyperaemia and vasogenic oedema. This strategy requires a measurement of cerebral blood flow to demonstrate adequate cerebral perfusion.52

CEREBRAL VASOSPASM

Posttraumatic cerebral vasospasm occurs in approximately 10–15% of patients. It is associated with a high morbidity and mortality. It is frequently present in patients with traumatic subarachnoid haemorrhage and is a marker of severity of injury.

Cerebral angiography and transcranial Doppler are frequently used to diagnose vasospasm, although false positives and negatives exist with both techniques and the true incidence of clinically significant vasospasm is uncertain.

Treatment options remain limited. Calcium antagonists, such as nimodipine, have not been shown to be effective in traumatic subarachnoid haemorrhage. Strategies that have been used in aneurysmal subarachnoid haemorrhage such as ‘triple H’ therapy (induced hypertension, hypervolaemia and haemodilution) or chemical angioplasty have not been evaluated in traumatic subarachnoid haemorrhage and are not recommended.5

SEIZURE PROPHYLAXIS

Seizures are infrequent following traumatic brain injury and usually present at the time of injury. These should be treated with anticonvulsants (e.g. diazepam, midazolam) when they occur. Subsequent prophylaxis with phenytoin is recommended only in patients with destructive parenchymal lesions on CT scan and continued for 10 days following injury. Short-term seizure prophylaxis does not prevent late onset posttraumatic epilepsy.53

OUTCOME AND PROGNOSIS

Patient factors that determine outcome from traumatic brain injury include severity of primary and secondary injuries, low GCS on presentation,54 advanced age (> 60 years)55 and comorbidities. Prediction of outcome is difficult and must be made with circumspection as significant functional improvements, particularly in young patients, may occur over time.

There are patients in whom the prognosis is clearly very poor or hopeless. A proportion of these patients will become brain dead and may be considered for organ donation. This is discussed elsewhere. In other patients, it may be appropriate to withdraw active treatment. This increasingly complex process requires time, careful consideration and consensus with all members of the health care and relatives.

Outcomes from traumatic brain injury are difficult to quantify. Whilst mortality is an easy end-point to measure, functional outcome is an equally important measurement, as the effects of traumatic brain injury on psychosocial recovery and duration of rehabilitation often take extended periods of time.

The future challenge facing the intensive care management of traumatic brain injury is to determine whether standards of practice and innovations improve mortality and functional survival. There is a responsibility to ensure that accurate outcome data are collected both at institution and regional levels. This will define the epidemiology and provide the basis for future studies.

REFERENCES

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3 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Guidelines for cerebral perfusion pressure. J Neurotrauma. 2000;17:497-506.

4 Myburgh JA. Driving cerebral perfusion pressure with pressors: how, which, when? Crit Care Resusc. 2005;7:200-205.

5 Oertel M, Boscardin WJ, Obrist WD, et al. Posttraumatic vasospasm: the epidemiology, severity, and time course of an underestimated phenomenon: a prospective study performed in 299 patients. J Neurosurg. 2005;103:812-824.

6 American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors. Chicago IL: American College of Surgeons, 1997.

7 BTF Guidelines. The Brain Trauma Foundation. The American Association of Neurological Surgeons. Initial management. J Neurotrauma. 2000;17:463-470.

8 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Resuscitation of blood pressure and oxygenation. J Neurotrauma. 2000;17:471-478.

9 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Hyperventilation. J Neurotrauma. 2000;17:513-520.

10 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Hypotension. J Neurotrauma. 2000;17:591-595.

11 SAFE Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350:2247-2256.

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13 Cooper DJ, Myles PS, McDermott FT, et al. Prehospital hypertonic saline resuscitation of patients with hypotension and severe traumatic brain injury: a randomized controlled trial. JAMA. 2004;291:1350-1357.

14 Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974;2:81-84.

15 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Mannitol. J Neurotrauma. 2000;17:521-526.

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18 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Computed tomography scan features. J Neurotrauma. 2000;17:597-627.

19 Servadei F, Murray GD, Teasdale GM, et al. Traumatic subarachnoid hemorrhage: demographic and clinical study of 750 patients from the European brain injury consortium survey of head injuries. Neurosurgery. 2002;50:261-267.

20 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Trauma systems. J Neurotrauma. 2000;17:457-462.

21 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Management and prognosis of severe traumatic brain injury. J Neurotrauma. 2000;17:449-554.

22 Maas AI, Dearden M, Teasdale GM, et al. EBIC-guidelines for management of severe head injury in adults. European Brain Injury Consortium. Acta Neurochir (Wien). 1997;139:286-294.

23 Myburgh JA, Upton RN, Grant C, et al. A comparison of the effects of norepinephrine, epinephrine, and dopamine on cerebral blood flow and oxygen utilisation. Acta Neurochir Suppl (Wien). 1998;71:19-21.

24 Van den Berghe G, de Zegher F. Anterior pituitary function during critical illness and dopamine treatment. Crit Care Med. 1996;24:1580-1590.

25 Ract C, Vigue B. Comparison of the cerebral effects of dopamine and norepinephrine in severely head-injured patients. Intensive Care Med. 2001;27:101-106.

26 McManis P, Lee C, Morgan M, et al. Neurogenic pulmonary oedema. Aust N Z J Med. 2000;30:514.

27 Ewig S, Torres A, El Ebiary M, et al. Bacterial colonization patterns in mechanically ventilated patients with traumatic and medical head injury. Incidence, risk factors, and association with ventilator-associated pneumonia. Am J Respir Crit Care Med. 1999;159:188-198.

28 Kelly DF, Goodale DB, Williams J, et al. Propofol in the treatment of moderate and severe head injury: a randomized, prospective double-blinded pilot trial. J Neurosurg. 1999;90:1042-1052.

29 Cremer OL, Moons KGM, Bouman ACB, et al. Long-term propofol infusion and cardiac failure in adult head-injured patients. Lancet. 2001;357:117-118.

30 Winkelman C. Effect of backrest position on intracranial and cerebral perfusion pressures in traumatically brain-injured adults. Am J Crit Care. 2000;9:373-380.

31 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Nutrition. J Neurotrauma. 2000;17:539-548.

32 Hammond FM, Meighen MJ. Venous thromboembolism in the patient with acute traumatic brain injury: screening, diagnosis, prophylaxis, and treatment issues. J Head Trauma Rehabil. 1998;13:36-50.

33 Jacobs DG, Westerband A. Antibiotic prophylaxis for intracranial pressure monitors. J Natl Med Assoc. 1998;90:417-423.

34 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Indications for intracranial pressure monitoring. J Neurotrauma. 2000;17:479-492.

35 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Recommendations for intracranial pressure monitoring technology. J Neurotrauma. 2000;17:497-506.

36 Macmillan CS, Andrews PJ, Easton VJ. Increased jugular bulb saturation is associated with poor outcome in traumatic brain injury. J Neurol Neurosurg Psychiatry. 2001;70:101-104.

37 Castillo MA. Monitoring neurologic patients in intensive care. Curr Opin Crit Care. 2001;7:49-60.

38 Procaccio F, Polo A, Lanteri P, et al. Electrophysiologic monitoring in neurointensive care. Curr Opin Crit Care. 2001;7:74-80.

39 Myles PS, Cairo S. Artifact in the bispectral index in a patient with severe ischemic brain injury. Anesth Analg. 2004;98:706-707.

40 Carter BG, Butt W. Review of the use of somatosensory evoked potentials in the prediction of outcome after severe brain injury. Crit Care Med. 2001;29:178-186.

41 Peerdeman SM, Girbes AR, Vandertop WP. Cerebral microdialysis as a new tool for neurometabolic monitoring. Intensive Care Med. 2000;26:662-669.

42 Maas AI, Steyerberg EW, Murray GD, et al. Why have recent trials of neuroprotective agents in head injury failed to show convincing efficacy? A pragmatic analysis and theoretical considerations. Neurosurgery. 1999;44:1286-1298.

43 Marmarou A, Fatouros PP, Barzo P, et al. Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients. J Neurosurg. 2000;93:183-193.

44 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Critical pathway for the treatment of established intracranial hypertension. J Neurotrauma. 2000;17:537-538.

45 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Intracranial pressure treatment threshold. J Neurotrauma. 2000;17:493-495.

46 Munch E, Horn P, Schurer L, et al. Management of severe traumatic brain injury by decompressive craniectomy. Neurosurgery. 2000;47:315-322.

47 Taylor A, Butt W, Rosenfeld J, et al. A randomized trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension. Childs Nerv Syst. 2001;17:154-162.

48 Clifton GL, Miller ER, Choi SC, et al. Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med. 2001;344:556-563.

49 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Use of barbiturates in the control of intracranial hypertension. J Neurotrauma. 2000;17:527-530.

50 Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury – outcomes at 6 months. Lancet. 2005;365:1957-1959.

51 Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet. 2004;364:1321-1328.

52 Eker C, Asgeirsson B, Grande PO, et al. Improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation. Crit Care Med. 1998;26:1881-1886.

53 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Role of antiseizure prophylaxis following head injury. J Neurotrauma. 2000;17:549-554.

54 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Glasgow Coma Scale Score. J Neurotrauma. 2000;17:563-572.

55 BTF Guidelines. Brain Trauma Foundation. American Association of Neurological Surgeons. Age. J Neurotrauma. 2000;17:573-582.

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