Severe head injury

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.

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, free radicals, 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 management ² (Figure 67.2).

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

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

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.

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Jul 7, 2016 | Posted by admin in CRITICAL CARE | Comments Off

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