- Clinical assessment
- Sport related head injury
Head trauma encompasses a wide spectrum of injury severity, and it is without doubt the most prevalent and feared cause of long term morbidity in the trauma patient. In terms of loss of function to the individual and cost to the community, the impact of head injuries is massive worldwide. It is one of the leading causes of death in children and young adults.
This chapter will deal with aspects of head injury in adults. Paediatric head injury is in many ways a different condition and will be dealt with in another chapter.
- The impact of head injuries is massive worldwide.
Head injured patients exhibit a wide spectrum of injury patterns and severity, ranging from trivial scalp lacerations to grossly disruptive, fatal brain injuries. The International Classification of Diseases requires multiple rubrics to adequately describe head injuries (World Health Organisation 1975). Subsequently, an all-encompassing definition is difficult and has limited usefulness. Optimum definitions derive from a combination of clinical and historical features. A history of blunt or penetrating trauma to the head, usually followed by a period of altered consciousness, and the presence of physical evidence of trauma, form the basic operational components of a head injury.
As such, a head injury may be defined as; the application and consequence of an external mechanical insult to the scalp, skull and intracranial contents.
Multiple classification systems exist for head injuries. The primary event may be described in terms of the anatomical structures involved and patterns of injury, or by the nature of the biomechanical stresses involved. Clinical, radiological, and pathological grading systems may be used to stratify the severity of a head injury.
Primary head injuries can be classified into three categories anatomically: scalp and bony injuries, focal intracranial injuries, and diffuse intracranial injuries (Table 4.1).
Scalp injuries vary from minor abrasions to extensive degloving injuries, but their magnitude correlates poorly with the degree of intracranial pathology. Bony injuries may be of the cranial vault or base of skull and occur with or without underlying brain injuries. Fractures may be linear or comminuted, depressed or undisplaced, closed or compound. Diastasis, another form of bony injury, refers to traumatic opening of suture lines.
Focal intracranial injuries are defined as macroscopically visible parenchymal damage limited to a well-defined area. They may be extraaxial, such as subdural or extradural haematomas, or intraaxial. Examples of the latter include cerebral contusion and intracerebral haemorrhage.
Diffuse intracranial injuries reflect widespread brain dysfunction, often in the absence of macroscopically evident damage, and result from a combination of mechanical and physiological disruption of neurones, and vascular injuries.
- Primary head injuries are classified into three categories anatomically (1) scalp and bony injuries (2) focal intracranial injuries and (3) diffuse intracranial injuries
Head injuries may be produced by direct contact with an object, by inertial acceleration-deceleration forces, or by some combination of these. (Table 4.2) This is discussed in greater depth below.
Grading of head injuries
Traumatic brain injury may be graded in terms of severity using a number of clinical grading systems. The most widely used of these is the Glasgow Coma Scale, which derives a score from 3 to 15 based on components of the neurological examination (Randell and Chesnut 1997, Teasdale and Jennett 1974). Best responses are recorded for eye opening, speech, and motor function, and the points tallied (see Table 4.3). Knowledge of the timing of examination is also important. The most accurate GCS is that obtained immediately post-resuscitation. For the paediatric population, a modified Glasgow Coma Scale is used. This caters for an age-appropriate verbal response and is also scored out of 15. By using this uniform, reproducible system, repeated examinations provide a clear guide to any change in the patients’ condition. It also enables unambiguous communication between clinicians regarding the level of injury.
Because the Glasgow Coma Scale provides a standardised method of describing the clinical status of a patient, it has become the basis of an arbitrary stratification of the head injuries into mild GCS 13-15, moderate 9-12, and Severe GCS 3-8. (Borzuk 1997)
The CT appearance in head trauma may also be graded. This gives a radiological correlate of injury severity, and has predictive value for outcome. It is particularly useful in diffuse head injuries. A widely used international classification system is based on the initial CT appearance (Table 4.4). The status of the mesencephalic cisterns, the degree of midline shift present, and the presence of a mass lesion are quantified. Diffuse brain injuries are stratified into 4 categories. Complete effacement of the basal cisterns and midline shift over 5mm in the absence of a surgical mass, define a subset of patients in whom the risk of development of severe intracranial hypertension and a fatal outcome is significantly higher (Marshall and Eisenberg 1991, Toutant and Klauber 1984).
Pathological grading following autopsy examination is used for ongoing research into head trauma and for epidemiological data collection.
- The Glasgow Coma Scale is a standardized and widely used of grading severity of head injuries.
Traumatic head injuries present a major public health issue globally. In Western countries trauma is the leading cause of death under the age of 45 and accounts for 10 to 20 deaths per 100 000 population annually (Jennett 1996, Palmer 1998). In the United States, over 100 000 patients suffer varying degrees of disability each year (Palmer 1998). The economic repercussions are vast. In the US alone, the annual cost of head injuries in terms of health care burden and loss of productivity exceeds 25 billion dollars (Borzuk 1997). Overall, 70 to 80% of patients seeking medical attention have mild head injuries. The remainder are divided equally into moderate and severe grades. Head injuries are responsible for almost half of trauma deaths, and they account for most of the long term morbidity (Jennett 1996).
- The majority of head injuries are minor with the remainder divided between moderate and severe grades.
- The economic repercussions of head injuries are great.
In terms of overall incidence and distribution of causes, extreme variation is seen both internationally and within geographically adjacent areas. This is illustrated by population studies showing markedly higher admission rates for head injuries in populous inner city areas, where assaults are prevalent, compared with predominantly rural areas where vehicular injuries are usually implicated and overall incidence of HI is low (Table 4.5).
The major impact of head injuries in all countries is on the younger population, typically 15 to 35 year olds (Jennett 1996). Age-specific mortality rates also peak in the elderly population, particularly in those over 70 years of age (Kraus et al. 1984). As a group they are involved in falls more frequently and often sustain significant injuries resulting in disability. There is also a high incidence of head injury in the very young, particularly those aged under 15 years (Brookes et al. 1990), but the great majority of these are mild. Overall they form the largest subgroup of age-specific attendees in emergency departments (Jennett 1996).
For most age groups world-wide there is an overwhelming male predominance in head injuries, in the order of 2 to1 (Kraus et al. 1984). The effect is less at either extreme of the age spectrum.
Recent research has shown an association between a polymorphism of the Apolipoprotein E (APO E) gene and outcome from head injury (Teasdale et al. 1997).
Apolipoprotein E is synthesized by reactive astrocytes and participates in the reparative response to acute brain injury by transporting lipids to regenerating neurons. Of the three isoforms of this protein in humans, APO E e4 is the least active in promoting repair, and may infact be detrimental by promoting the deposition of amyloid. The above study found patients with the APO E e4 allele were more than twice as likely as those without APO E e4 in their genotype to have an unfavourable outcome 6 months after head injury.
Patients with the APO E e4 polymorphism and who have a history of head injury are also at increased risk of developing Alzheimer’s disease (Mayeux et al. 1995).
- Apolipoprotein E e4 is correlated with unfavourable outcome after head injury.
B Causes of head injury
Motor vehicle accidents (MVA) are the most significant cause of head injuries world-wide, followed by falls and assault. Alcohol usage contributes to many of these. The relative contributions and incidence trends are however highly location-specific (Table 4.5).
Motor vehicle accidents predominate as a cause of severe head injury. In most cases, a vehicle occupant is injured. When pedestrians are involved they tend to sustain multiple injuries. Recent trends in developed countries suggest a reducing incidence of vehicular-related severe head injury (Table 4.6). The improved mortality rates correlate with the development of safer automobile design, improved traffic control, legislation to improve compliance with safety measures (e.g. wearing safety belts) and public prevention campaigns. One such preventative campaign targets the use of alcohol, with widespread random breath testing. The effect has been highly significant in the United Kingdom (HMSO 1995). In contrast to this is the sustained high incidence of severe head injury from motorbike accidents (MBA) in places like Taiwan, where traffic control is less vigorous. Here road traffic accidents account for 90% of all head injury admissions and vehicular deaths rose from 31 per 100 000 in 1977, to 37 per 100 000 in 1987 (Lee 1990). Comparatively, in united kingdom road deaths per 100 000 have decreased from 11 in 1980 to 7 in 1993. Other developed countries show similar trends (Table 4.6).
Falls are a particularly significant aetiological factor for head injury in the elderly, who are generally more frail and poorly mobile, and in whom righting-reflexes are impaired. Very young, unsupervised toddlers who fall from a low height also comprise a substantial group. A head injury cause by a fall is more likely to require neurosurgical intervention than a head injury sustained in a motor vehicle accident. This is illustrated in Table 4.7.
Assaults are a major cause of admission for head injury in densely populated urban areas, particularly where large ethnic cultures coexist. In the New York Bronx or inner city Chicago up to 40% of significant head injuries are assault related. Assaults comprise almost half of all head injury admissions in Johannesburg but barely contribute to admissions in France. Head injuries caused by gunshot wounds are also significant in the United States where they account for about 1 in 20 of these admissions (Sosin et al. 1989).
Recreational and occupational accidents
Occupational and recreational accidents are also prevalent, and related injuries each account for about 10% of HI admissions (Baker et al. 1994).
Biomechanics of head injury
The biomechanics of head injury are complex due to the unique anatomical configurations of the brain being suspended in the bony cranium, and the head being connected to the trunk by the highly flexible cervical spine.
The 2 main forms of mechanical loading which result in tissue deformation, and thereby injury, are contact loading and inertial loading (motion or acceleration/deceleration forces) (Gennarelli and Meaney 1996). An impact to the head can result in both contact and inertial loading in varying degrees, however inertial loading can also occur without an impact to the head, such as deceleration of the head when a force is applied to the thorax of a moving person.
Each form of mechanical loading produces specific types of injuries, as indicated in Table 4.2. As can been seen from this Table, contact loading produces injuries by local skull bending, skull volume changes and shock wave propagation. Inertial loading produces injuries by relative motion between the skull and brain, and brain deformation.
The imparted energy from contact and/or inertial loading produces tissue deformation, and if this strain distorts the tissue beyond its functional or structural tolerance, an injury will result (Gennarelli and Meaney 1996). Tissue deformation can occur in the form of tension, compression or shearing forces. The degree of injury produced depends on factors such as the amount of force applied, the rate of its application and the mechanical properties of the tissue.
- Motor vehicle accidents combined with alcohol are the leading cause of severe head injuries.
Tissue deformation resulting from forces acting at the moment of impact constitute the primary injury. Impact and inertial forces are responsible in varying degrees for the different types of primary injuries. (Table 4.2)
Scalp and skull injuries
All degrees of scalp injuries are commonly seen in the head injured patient. Their importance lies both in the need for an adequate inspection and repair, and more importantly, in their role as a marker for potential underlying pathology. There is however only poor correlation between the presence of scalp injuries and intracranial pathology. A general knowledge of the anatomy is most helpful.
The scalp consists of five layers; skin, a dense connective tissue layer, the galea aponeurotica, a loose connective tissue layer, and the pericranium. The sensory nerves and arteries travel primarily in the layer of dense connective tissue. The arterial adventitia is intimately blended with the surrounding dense connective tissue, so that lacerated vessels are held open and may haemorrhage significantly (Welch and Boyne 1991). The venous drainage accompanies branches of the external carotid artery superficially, but there is also deep, transcranial drainage to the venous sinuses via emissary veins. The first three layers are intimately connected and can move freely over the pericranium, because of the loose connective tissue layer. Surgically they are considered as one layer (Bhattacharya et al. 1982).
Lacerations vary enormously in nature and extent, depending on the type and direction of forces applied. They may be small and superficial, or complex, stellate lesions involving most of the scalp. Scalp hair often obscures significant injuries.
Depending on the location, scalp contusions or haematomas, may bear great clinical significance and help direct the clinical and radiological examinations. Periorbital haematomas, often called 'racoon eyes' when present bilaterally, may reflect a base of skull fracture through the anterior cranial fossa. Similarly post-auricular bruising, known as 'Battle's sign', usually reflects a petrous base of skull fracture. This sign however may take days to develop.
Avulsion or degloving injuries represent a more severe type of the scalp injury. They occur when an appropriately directed force strips the mobile aponeurotic layer off the pericranium, the plain of cleavage being through the loose areolar connective tissue. Scalp vessels traversing this space may be torn producing a subgaleal haematoma. In the paediatric population, this is a potential cause for hypovolaemia.
The presence of a skull fracture reflects the degree of energy imparted at impact. They are found in 80% of all fatal head injuries (McCormick 1997). As discussed above, they may be open or closed, linear or depressed, and their presence greatly increases the likelihood of coexisting intracranial pathology. Fractures occur where local deformation of the vault exceeds regional bony tolerance. The nature of the fracture depends on the magnitude of the force applied, and also on the site impacted and the area over which the force is applied. Thin plated bone, such as that found in the pterional region, is far more susceptible to fracturing than is buttressed bone.
Linear fractures are a result of the outbending of bone at a distance from the impact site. The fracture line then takes the path of least resistance, usually running towards the point of contact. They are usually closed or 'simple'. Depressed skull fractures occur when contact forces are sufficiently concentrated. They are generally deemed to be significant when a fragment is displaced to a depth greater than the thickness of the skull. The degree of comminution and placement of bony fragments is highly variable. Compound injuries are defined by the presence of an overlying scalp laceration or by fracture extension through a nearby air sinus. If there has been a dural tear, the chance of infection is increased significantly.
Basilar skull fractures (BSF) describe fractures through the base of the skull, and may involve the anterior, middle or posterior cranial fossae. They are usually extensions of cranial vault fractures and frequently follow, but are not limited to, occipital or mandibular impacts. Pneumocephalus in the absence of a cranial vault fracture is essentially diagnostic of BSF. A subtype of BSF fracture is the hinge fracture. If the fracture line traverses the dorsum sellae, a transverse hinge fracture is produced. In this case the carotid canal is usually opened, and the tegman tympani is also frequently involved. A haemotympanum is a common accompaniment. Carotid dissections may also complicate this type of fracture.
Cranial nerves may be directly damaged in BSFs. Fractures of the cribriform plate and anterior cranial fossa (ACF) may cause olfactory and optic nerve injuries. With this type of fracture, there is also a risk that nasogastric tube insertion may lead to intracranial placement, with disastrous consequences (Wyler and Reynolds 1977). Petrous temporal bone involvement may lead to facial or vestibulocochlear nerve injury. CSF otorrhea or rhinorrhea, may result if the dural membrane is torn.
Diastasis refers to the traumatic opening of suture lines. This is most commonly seen at the coronal or lambdoid suture. A 'growing fracture' occasionally occurs when lacerated dura is wedged between the sides of a calvarial fracture, producing a leptomeningeal cyst. This tends to enlarge with time. They are predominantly a feature of the paediatric population and are seen most often in the parietal region.
Scalp injuries are commonly seen with intracranial head injuries, however there is poor correlation between the presence of scalp injuries and intracranial pathology
Racoon eyes' present bilaterally may reflect a base of skull fracture through the anterior cranial fossa.
Extradural haematomas (EDH) result from bleeding between the calvarium and dura mater. Meningeal vessels that groove the inner table of bone are usually implicated. The bleeding is typically arterial but the venous sinuses may also be implicated. The classic location is the temporoparietal region and results from middle meningeal artery disruption. However, about 18% occur in the anterior or posterior cranial fossae, and 10% are parasagittal (Jamieson and Yelland 1968). An overlying fracture is noted in about 90% of adults (Zimmerman and Bilaniuk 1982). Other intracranial pathology is expected in a third of patients (Blumberg 1998). Historically, only 20% of patients with traumatic EDHs experience a lucid interval (Jamieson and Yelland 1968).
Subdural haematomas may be classified as acute, subacute, or chronic, depending on the temporal profile of the lesion. Those presenting within 3 days of an injury are acute. Traumatic acute subdural haematomas (ASDHs) are seen in approximately 30% of severe head injuries. They are a poor prognostic sign, and depending on the timing of surgical evacuation, have mortality rates up to 90% (Seelig 1981). Most occur ipsilateral to the side of trauma, and about a third are contralateral (Lanksch 1979). They are also frequently associated with skull fractures. There are two types of acute subdural haematomas. The first type usually occurs in the context of a severe, diffuse type of traumatic brain injury and is continuous with contused, lacerated brain. The other type of ASDH is a result of ruptured superficial cerebral bridging veins that traverse the subdural space on their way to a venous sinus. They usually collect over the convexity but may also occur in the interhemispheric fissure and along the tentorium. The prognostic significance of ASDHs relates to the presence of both regional and global ischaemia, and unilateral hemispheric swelling, which is highly variable and is not related to the thickness of the haematoma (Bullock and Teasdale 1990).
Subdural haematomas are classified as chronic when present for more than three weeks. However, the causative head injury is often very mild and in about 50% of cases a history of trauma is denied (Blumberg 1998). Important predispositions are age and underlying cerebral atrophy, particularly in alcoholics. Extensive brain distortion may be seen in the absence of a raised ICP when there is atrophy. Pathologically, a fibrovascular neomembrane develops at the margins of the haematoma. This begins on the dural surface and may give rise to repeated microhaemorrhages. When there has been delayed recurrent haemorrhages, lamination of the haematoma may be evident. The membrane may also be calcified.
Subacute subdural haematomas may be defined arbitrarily as lesions presenting between 3 days and 3 weeks after trauma. Their pathology shares features of both acute and chronic subdurals.
Subdural hygromas are thought to be caused by a traumatic tear in the arachnoid membrane, which allows for the passage of CSF into the subdural space. Their prevalence in the head injured patient is in the order of 6% (Blumberg 1998). They may be under high or low pressure, but usually resolve spontaneously. The radiological appearance of hygromas approximates that of a chronic SDH, but they are of lower density on CT.
Contusions are another type of focal injury. They are cortical bruises of the neural parenchyma, and usually affect the crown of a gyrus. If occurring at the site of impact a 'coup' lesion is produced. They result from direct disruption of cortical tissue and tearing of surface vessels. The final result is localised haemorrhage or necrosis. Complicated contusions or 'lacerations' involve disruption of the pial membrane and variable white matter disruption.
In moderate to severe injuries global skull shape changes may occur, which in addition to differential brain and skull movement during acceleration, create foci of low pressure sufficient to cause tissue disruption. When this leads to contusions opposite the site of impact, a 'contrecoup' lesion is produced. However, regardless of the injury, frontal and temporal locations are the most common sites affected (Adams 1980).
Intraparenchymal haemorrhage refers to focal haematomas over 2cm in size, deep to the cortical surface. This contrasts with areas of haemorrhagic contusion where blood diffuses into adjacent neural parenchyma. They are a result of deep vascular injury, and usually effect the frontal or temporal lobes where characteristic 'lobar' haemorrhages are produced. The basal ganglia are an uncommon site. The overall prevalence in severe head injuries is up to 1 to 3%, and in most cases they are accompanied by cortical contusions or an acute subdural haematoma (Rivano et al. 1980). They are associated with hypoperfusion to adjacent brain and in general a poor prognosis.
Intraventricualar haemorrhage is commonly associated with severe head injuries. This may result either from shearing of subependymal veins, from retrograde passage of subarachnoid blood, or from extension of an intracerebral haemorrhage. A frequent radiological feature of this type of haemorrhage is a blood fluid level in the occipital horns. In general it is a poor prognostic sign.
- Focal lesions include extradural haematomas, subdural haematomas, subdural hygromas, contusions, intraparenchymal haemorrhages and intraventricular haemorrhages.
- Subdural haematomas may be classified as acute, subacute, or chronic, depending on the temporal profile of the lesion
The brain may be damaged even without an impact. This occurs in 'impulsive loading' where pure inertial forces are applied to the brain. These may be translational, angular, rotational, or a combination. Under the influence of these forces differential movement of the skull and dura occurs relative to the brain, and also within different regions of the brain parenchyma. The resulting damage may be focal or diffuse. Axonal disruption and microvascular injury are the pathological hallmarks. Traditionally they have been associated only with the high velocity injuries seen in MVAs, but they are now a recognized complication of falls and blunt assault injuries.
Diffuse Axonal Injury (DAI) is so named because of the presence of widespread damage to axons throughout the brain and brainstem. It is usually seen in the context of severe, high speed traumatic brain injury where angular and rotational forces are causative. This type of injury accounts for roughly a third of deaths from head injury and most of the persistent neurological deficits seen in survivors (Teasdale 1998). The effect depends on the direction of the force applied and on local gyral geometry. It tends to be more severe if it occurs in the coronal plane. At a microscopic level axonal bulbs or retraction balls are seen with various degrees of parenchymal dehiscience (Blumberg 1998). Sites particularly susceptible include:
Superior cerebellar peduncles;
Subcortical white matter;
Other areas of the brainstem.
The best macroscopic and radiological markers of DAI are haemorrhage in the corpus callosum and in one or both superior cerebellar peduncles. Grading is to some extent predictive of outcome and, as discussed above, an internationally recognised grading system has been formulated based on CT appearance. (Table 4.4)
Trauma is the most common cause of subarachnoid haemorrhage. On CT scan it is seen as high density change in the sulci, major fissures, or basal cisterns. The multiple potential sites of origin for the haemorrhage include damaged pial vessels, extensive intraventricular haemorrhage, and haemorrhagic cortical contusions. The significance of this type of injury lies in the potential difficulty in distinguishing it from an aneurysmal source of haemorrhage with certainty, and the potential for developing communicating hydrocephalus as a delayed complication.
Primary brain stem lesions include contusions, shearing injuries, and various 'rents' or separations. They typically occur as part of a diffuse brain injury. Brainstem contusions are often associated with basilar fractures, usually of the clivus, and may coexist with superficial lacerations. Pontomedullary tears or rent is another brainstem lesion characteristic of severe trauma. They are most often due to marked hyperextension of the head and neck and rarely occur without a skull or upper C-spine fracture (McCormick 1997). Other well recognised injuries to the brainstem include tears and separations of the mesenchephalic-pontine and spinal-medullary junctions. These injuries are lethal, and fortunately uncommon.
- The brain may be damaged even without an impact through inertial forces.
Vascular injuries are a common feature of head injuries involving significant inertial forces, such as high speed motor vehicle accidents, but may also be seen in less severe types of trauma. They may be classified as parenchymal or extraparenchymal and can effect all vessels types, including dural sinuses. (Table 4.8)
Traumatic aneurysms are a well known complication of head injury, and may occur on branches of the external and internal carotid arteries. They are usually 'false' and result from complete mural rupture with organised surrounding haematoma. Superficial middle cerebral branches are the most common sites involved, followed by peripheral branches of the anterior cerebral artery (McCormick 1997). When major vessels at the base of the brain are involved the distinction between traumatic and non-traumatic causation is difficult. Certain angiographic features such as, location away from branch points and absence of a definable neck, suggest the former.
Lesser forms of arterial disruption such as arterial dissection are more common, and may complicate all grades head injury. Pathologically there is tearing of the intimal lining and variable disruption of the other vessel wall components. Exposure of subendothelial tissues and altered local haemodynamics predisposes to thrombosis. This may give rise to distal emboli or cause complete occlusion.
All segments of the internal carotid artery may be affected, but the extracranial portion above the bifurcation is the most common site. Traumatic vertebral dissections usually involve the distal extracranial portion of the artery between the axis and base of skull (Zee and Go 1998). Symptoms vary from a low grade head or neck ache to massive stroke, but in many patients they are asymptomatic.
Lacerations to the dural sinuses, or thrombosis, usually results from penetrating injuries or depressed skull fractures. Traumatic carotid-cavernous fistulas occur in 1 to 2% of patients with severe head injuries (McCormick 1997). They are usually associated with a base of skull fracture, particularly those affecting the sphenoid bone.
- Vascular lesions such as traumatic aneurysms are well known complications of severe head injury.
Secondary brain injury refers to all cerebral insults that follow the primary injury. It may result directly from the pathophysiological processes initiated by the primary insult, or it may be due to the extraneous effects of trauma such as hypoxia or systemic hypotension. The major forms of secondary injury seen are hypoxia, hypotension, disordered cerebral blood flow, and the commonly related pathologies of cerebral oedema and raised intracranial pressure. They may act in isolation, but more commonly there is a combination of interacting mechanisms that contribute to the secondary insult in a given patient. The importance of these secondary injuries lies in their potential for prevention, and reversibility.
Hypoxic insults are known to significantly worsen outcome in traumatic brain injuries, and hypoxia is present in almost 50% of fatal head injuries (Chesnut et al. 1993). In the early post-injury phase, it is the most prevalent form of secondary insult.
A normally functioning cerebral vasculature is highly sensitive to hypoxia, and responds to this by vasodilatation, thereby increasing cerebral blood flow and maintaining oxygen delivery (Fortune et al. 1992). This is illustrated in Fig 4.1 which demonstrates the usual increase in cerebral blood flow and oxygen delivery seen with hypoxia for any given PaCO2, in the non head-injured patient. However, in the setting of a traumatic brain injury there is amelioration of this protective effect, and profound vulnerability to hypoxia. The major causes of hypoxia in the trauma patient are respiratory dysfunction resulting in asphyxia or inadequate ventilation, and impaired oxygen delivery. Another significant cause of relative or absolute hypoxia is increased metabolic demand, where energy expenditure exceeds oxygen dependent production. Seizures are one such cause of increased metabolic demand, and may result in complete consumption of cellular energy.
Physiologically, hypoxia is defined as an arterial partial pressure of oxygen (PaO2) less than 60mmHg. At this level of PaO2 and below, the haemoglobin saturation with oxygen rapidly declines, causing a reduction in the arterial oxygen content. The end result is impaired oxygen delivery and a low tissue oxygen tension. As a result, there is cellular conversion from aerobic to anaerobic metabolism and reduced total energy production. Tissue damage will result if the insult is of sufficient severity or duration.
The cellular effects of hypoxia are complex and varied, and are best understood in terms of the basic physiology. For normal neuronal survival and function, a continuous supply of energy in the form of Adenosine triphosphate (ATP) is essential. The basic building blocks for this are Adenosine diphosphate (ADP), O2, and glucose, and of these it is the ADP that is usually the limiting substrate. The production of ATP may take place either in the cytoplasm, where the anaerobic glycolytic pathway occurs, or in the mitochondria, where the critical oxygen-dependent respiratory chain enzymes reside and where the Krebs cycle takes place. The latter aerobic pathway is far more powerful, but requires a critical level of tissue oxygen tension. An important by-product of the former pathway is Lactate and Hydrogen ions. This means that in hypoxic conditions where oxygen is lacking, but where glucose and other substrate supplies are unaltered, ATP production occurs predominantly via the anaerobic glycolytic pathway, resulting in acidosis and disturbed cellular function (Siesjo 1992). In particular, there is inhibition of phosphpofructokinase, a key enzyme in the glycolytic pathway, and widespread protein conformational change and dysfunction (Popp et al. 1997). With disruption of anaerobic pathways and the further depletion of energy levels, there is a degradation in all areas of cellular homeostasis, and in particular, transmembrane ion gradients. The main primary active transport system is the Na-K ATPase. It is electrogenic and highly energy dependent, and through the generation of the transmembrane Na+ gradient it provides the energy for many of the secondary active transport systems, such as the Na-H+ and Na-Ca2+ exchangers. In hypoxic conditions, where energy stores are depleted, there is a progressive failure of this pump and a loss of the Na+ gradient (Popp et al. 1997). This leads to the accumulation of intracellular Na+ and a reduced drive for Na+ dependent secondary active transport systems. There is intracellular acidosis and accumulation of calcium. This in turn leads to the activation of Ca++ dependent proteases, resulting in cellular organelle and membrane injury, and further amplification of the process.
- Hypoxic insults significantly worsen outcome in traumatic brain injuries
Cerebral blood flow and hypotension
A critically low cerebral blood flow may result from any cause of systemic hypotension or raised intracranial pressure, and profoundly influences outcome in the head injured patient. The effect depends on the nature and severity of the insult.
Under normal conditions there are effective and highly sensitive physiological control systems operating to maintain adequate and appropriate global and regional cerebral blood flow (CBF), to compensate for fluctuations in blood pressure and brain activity. The normal CBF approximates 55mls/100gm/min. Regional flow is also closely coupled to metabolic demand, such that in normal conditions there is a linear dependence of CBF on metabolic rate for oxygen (CMRO2). About half of the CMRO2 is for baseline cellular function and the remainder represents consumption for neural activity (Popp et al. 1997). The coupling process is not fully understood but is mediated in part by a number of vasoactive metabolites such as adenosine, K+, or H+ (Phillis 1989).
Cerebral perfusion pressure (CCP) is defined as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP):
CPP = MAP - ICP
It represents the driving pressure for cerebral perfusion and estimates cerebral blood flow. In normal conditions the cerebrovascular circulation is autoregulated to maintain a constant cerebral blood flow over a wide range of CPPs. This range typically extends from a lower limit of 50mmHg to an upper limit of 150mmHg (see Fig 4.2). Within this range, only transient deviations of CBF occur before these vascular regulatory mechanisms re-establish the steady state. At each end of the autoregulation range, the relationship of CBF to CPP becomes passive and linear.
The CBF may be described in terms of the cerebral perfusion pressure and the cerebral vascular resistance ( CVR ), such that:
In the maintenance of a steady state CBF, the pivotal autoregulatory mechanism is an alteration in the CVR. This must be in the same direction and to the same degree as the CPP, either by vasodilatation or vasoconstriction of resistance vessels. In this way there in constancy of cerebral blood flow, as illustrated by the 'normal autoregulation' curve in Fig 4.2. Another very important parameter is the cerebral blood volume (CBV). According to the Monro-Kelly doctrine (see below), blood is one of the three dependent intracranial volume components that influences ICP. As such, the vascular response to changing CPP, whether it be vasoconstriction or vasodilatation, will lead directly to changes in CBV and indirectly to changes in ICP.
Traumatic brain injury frequently disrupts both the normal dependence of CBF on metabolic rate, and the normal independence of CBF on CPP, but the response is partial and heterogeneous (Orbist et al. 1984).
Of particular concern is the loss of autoregulation. In the context of trauma, a brain which has already suffered a primary mechanical injury becomes profoundly vulnerable to a further insult from systemic hypotension, because of an inability to maintain cerebral blood flow in the face of a falling cerebral perfusion pressure. In fact, hypotensive insults in severe head injuries are associated with a doubling of mortality and markedly increased morbidity (Chesnut et al. 1993). The pathology is consistent with a partial disruption to the vascular regulatory system and a resetting of the lower limit of autoregulation to a higher level (Bouma et al. 1992). There is a loss of active vasodilatation and an extension of the lower pressure-passive response, above which autoregulation commences. The end result is a variable range of cerebral hypoperfusion and ischaemia for the lower range of CPP values, normally considered adequate (see Fig 4.2, curve A). This helps explain the devastating effects of even transient episodes of hypotension (Chesnut et al. 1993), and the drive behind the common clinical goal in the head-injured patient to maintain a cerebral perfusion pressure over 70mmHg (Lang and Chesnut 1995). The theoretical response to the complete loss of autoregulation, with a pan pressure-passive response of CBF, and its effect on cerebral blood volume is also seen in Fig 4.2 (curve B).
Uncoupling of metabolism and CBF also occurs in about 50% of patients following severe head injury (Bhattacharya et al. 1989), and this may occur independently from autoregulatory dysfunction. In the first 4-8 hours post head injury, there is often a period of sustained global hypoperfusion. Figure 4.3 demonstrates the reduction in cerebral blood flow seen during this period. Values below 20ml/100gm/min are considered ischaemic (Chesnut et al. 1993), and are frequently seen. Based on nuclear medicine SPECT and Xe-enhanced CT studies, it is also evident that regional ischaemic zones exist around intracranial haematomas and contusions (Schroder et al. 1995). Evacuation of accessible haematomas however ameliorates this effect. Following the acute phase of global hypoperfusion, there is usually a phase of relative or absolute hyperaemia, with CBF either being maintained within the normal range or above it, despite a reduced metabolic rate for oxygen. The mechanism may involve increased levels of Lactate and a disruption of the normally vasoactive H+ and K+ coupling pathways (Desalles 1987).
A clinically useful parameter for assessing the adequacy of CBF is the jugular venous saturation (Sjv02). It is a measure of cerebral venous oxygen content (CvO2). Using the Fick principle the CMRO2 and CBF may be quantified.
CMRO2/CBF = (CaO2 - CvO2)
Normal arterial-venous oxygen content differences are between 50 and 75ml O2 per litre of blood. High levels of SjvO2 result in a small arterial-venous oxygen content difference and indicate an inappropriately high level of CBF for the CMR02, as is commonly seen following traumatic brain injury. Conversely, a low SjvO2 saturation indicates insufficient blood flow relative to the cerebral metabolic rate.
As discussed above, the CBF is also normally highly sensitive to the arterial PaCO2 and PaO2, with appropriate increases in hypercapnoeic and hypoxic conditions (Fig 4.1). Within the normal physiological ranges, the CBF increases 2-4% for each unit increase in PaCO2 and 2% for each percent of arterial oxygen desaturation (Fortune et al. 1992). In hypoxic conditions the reactive vasodilatation permits a higher CBF and improved oxygen delivery. However in the head-injured patient this response is both severely blunted in magnitude and is of much shorter duration, leaving the patient extremely vulnerable to even transient episodes of hypoxia. The vascular regulation seen with changes in the PaCO2 are primarily mediated by extravascular H+ concentraion, so that an increase in H+ concentration is accompanied by an increase in resistance vessel diameter (Heistad and Kontos 1983). Similarly, there is vasoconstriction and reduced CBF in hypocapnoeic conditions. The limit to this response is a PaCO2=20mmHg, at which point the effect of ischaemic driven vasodilator metabolites override the vasoconstrictor response. Temporally, the effect persists until extravascular H+ levels normalise. In normal conditions this happens within 16 hours. Following head trauma the CO2 reactivity of CBF is generally preserved, making hyperventilation an effective short term tool in the treatment of intracranial hypertension. To avoid ischaemia from hypocapnoeic vasoconstriction, the PaCO2 is generally kept above 27mmHg and if Sjvo2 is being monitored, values over 50% are usually accepted.
In response to a generalised reduction in cerebral perfusion pressures from hypotension, ischaemia is most severe in the boundary zones or 'watershed' regions of major arterial territories. Isolated arterial damage, as may occur in blunt or penetrating neck injuries or dissections, will lead to arterial territory ischaemia. Mixed forms of ischaemia are also commonly seen in the head-injured patient.
Cerebral oedema and raised intracranial pressure
The upper limit of normal adult intracranial pressures is 10-15mmHg. In uninjured brains, pressures well above this are usually well tolerated. However, following severe head injuries, cerebral oedema and intracranial hypertension are poorly tolerated and are major causes of morbidity and mortality (Popp et al. 1997). For this reason an understanding of the pathophysiology involved is essential.
The intracranial compartment is a closed space housed by the bony calvarium and base of skull. The pressure inside is determined by the total volume of its three intracranial components; blood, brain and CSF. This is the Monro-Kellie Doctrine. An increase in the volume of any one of these components will cause an increase in the intracranial pressure (ICP), once compensatory mechanisms are overcome and displaceable volume is depleted.
The buffering capacity for pressure changes is limited, and is largely mediated by redistribution of CSF. CSF normally contributes to about 10% of the intracranial volume (Popp et al. 1997). When pressures rise intracranially and CSF pathways are preserved, there is displacement of CSF to the extracranial spinal compartment and distension of the spinal dura. There is also an increase in CSF absorption. This is because the driving pressure, determined by the difference between ICP and venous pressure, is increased.
The extent to which an increase in volume results in increased pressure is called the 'compliance', and this value is pressure-dependent. As intracranial volume increases the compliance rapidly decreases.
The pressure-volume index (PVI) is another useful parameter and is measured as the change of volume required to increase ICP by a factor of 10. It is essentially independent of ICP. The relationship is as follows:
PVI = change in Volume / log(Pfinal/Pinitial)
A normal value is close to 25mls (Maset et al. 1987). Low PVIs indicate a loss of volume buffering capacity and therefore a low tolerance for any rise in intracranial pressure. It is frequently seen following traumatic brain injury, such that only small increases in volume may result in grossly elevated ICPs. Serial values are far more significant than single measurements, but values less than 18mls are generally considered pathological, and are predictive of protracted intracranial hypertension (Maset et al. 1987). The exponential manner in which ICP rises as a result of increased intracranial volume is illustrated in Fig 4.4. The effect of a low PVI, or reduced available buffering volume in decreasing compliance is also seen.
Cerebral oedema is a highly variable and potentially fatal response to head trauma. It may be focal or generalised. There are two major pathophysiological categories which may coexist: vasogenic oedema, resulting from a primary disruption to the blood-brain barrier and leading initially to extracellular accumulation of fluid, and cytotoxic oedema caused by cellular homeostatic dysfunction and resulting in intracellular accumulation.
Vasogenic oedema is a consequence of blood-brain barrier (BBB) dysfunction. The blood-brain barrier refers primarily to the high density of vascular endothelial tight junctions and the absence of fenestrations seen in the normal cerebral circulation. This permits only lipid-soluble particles to passively diffuse across the membranes. Transport systems are required for ionic particles, maintaining an intravascularly directed osmotic gradient. This inhibits the movement of water into the brain parenchyma. When the barrier is breached, the filtrate initially accumulates extracellularly, with a tendency to affect white matter preferentially. Venous or arterial pathologies may predominate.
In head-injured patients an arterial hyperaemic phase for cerebral blood flow is often seen, which usually peaks 24 hours after impact and increases the fluid flux across a disrupted BBB (Bouma et al. 1992). Intravascular pressures are also increased when the venous return is compromised. Coexisting cardiac and pulmonary pathologies such as cardiac tamponade and tension pneumothorax, are possibilities in the trauma patient. Life-threatening brain swelling may occur when there is significant cerebrovascular disruption. Treatment is directed at the correction of exacerbating factors and reversing the fluid shifts.
Cytotoxic or cellular oedema refers to the intracellular accumulation of fluid, and results from impaired cellular haemostasis. In this setting the blood-brain barrier is intact and there is a fluid shift from the extracellular to intracellular compartment. The pathology is multifactorial. One important process results from excessive uptake of KCL following the post-traumatic rise in extracellular K+. Hypoxia is also a significant factor, and as outlined above the metabolic derangement's produced are diverse. Events pertaining more directly to cellular oedema include; the conversion to anaerobic metabolism resulting in a breakdown of astrocyte glycogen macromolecules into multiple, osmotically active units of glucose, a loss of the full activity of the Na-K+ ATPase with accumulation of intracellular Na+ and disordered secondary active transport systems, and structural membrane damage, either directly, or as a result of oxygen-free radicals. In combination these events lead to cell swelling and predispose to its deleterious secondary effects, including depolarisation, activation of mechanosensitive Ca++ channels, and the release of excitatory neurotransmitters. A further significant factor in the generation of cytotoxic oedema is a low serum osmolality. The latter may be iatrogenic following inappropriate fluid administration, or may result from SIADH. Most vulnerable to all these changes are the astrocyte cell body and the neuronal dendrites, where swelling is preferentially focused (Popp et al. 1997).
Following a head injury each of the intracranial compartments may be expanded. Vasodilatation and extraaxial haematoma will affect the blood volume, there may be cerebral oedema or ICH to expand brain volume, and occasionally there may be obstructive hydrocephalus with dilatation of the ventricular system. These changes are partially absorbed by the available displaceable volume, and increased CSF absorption. But as the magnitude of the volume change increases and buffering capacity is overwhelmed, there is a decrease in intracranial compliance and early decompensation. The end result is a rise in intracranial pressure. At this early stage the elevated pressures can be easily normalised with hyperventilation and induced hypocapnoea, which causes vasoconstriction of intracranial feeding vessels and reduced blood volume.
As ICP increases and compliance decreases further, small volume changes lead to larger and more prolonged increases in pressure. 'Plateau' waves, also known as 'Lundberg A' waves, and other types of preterminal waveforms may be seen on the ICP monitor trace in this setting (Lundberg 1960).
Pathophysiology of neuronal injury
All degrees of neuronal injury are seen following head trauma. The outstanding feature however is the variable time course involved and the sequential pattern of cytoskeletal and metabolic derangements seen. Primary axotomy occurs at the time of impact and usually requires > 20% strain in the neurolemma (Maxwell 1997). Non-disruptively injured axons are exposed to a complex sequence of interacting events. The primary insult is to the cytoskeleton with focal disruption of neurofilaments and a loss of axoplasmic neuronal transport. Traumatic depolarisation may occur at this stage with consumption of remaining energy supplies and release of excitatory neurotransmitters. Local axonal swelling and loss of cellular transmembrane homeostasis also occurs. A critical event is the influx of Calcium with the activation of destructive phospholipases and generation of oxygen-free radicals. This leads to irreversible membrane damage and further release of damaging neuroexcitatory transmitters. Glutamate is the most widely implicated of these.
Assessment of the head injured patient is an ongoing process from the initial point of contact through to the completion of definitive management. At any time during this period the pathological sequelae of head injury may gradually or suddenly become clinically manifest. It is therefore crucial to initially obtain an accurate ‘baseline’ assessment as a reference point for gauging improvement or deterioration in the patient’s condition. This will enable prompt changes in management to optimise neurological recovery. This baseline assessment is also important as it remains the most useful indicator of the patient’s prognosis.
Assessment of the head injured patient is also a flexible process as the ability of the patient to participate in the history and examination varies from full cooperation to amnesia to combative to unconscious! It is therefore useful to develop a comprehensive, systematic approach which can be tailored to the various clinical situations that present themselves.
The information to compile a history of the trauma and the patient’s resulting symptoms often has to be obtained from a variety of sources. These may include the patient, various witnesses present at the time of the injury, and ambulance officers. The main points of the history are summarised in Table 4.9.
The time of injury is important as the starting point of the clinical ‘timeline’ and governs how long most patients with mild head injuries will be observed prior to discharge. It is often most easily obtained from the time the ambulance service was contacted on the ambulance report. The mechanism of injury is also important in helping determine the severity and pattern of pathology following head injury. Factors such as the speed of motor vehicles involved, the height of falls, the size and mass of objects striking the head should be ascertained. The use of seatbelts or helmets should also be determined if applicable. These details also serve to alert the physician to possible inconsistencies between the reported cause and severity of the patient’s injuries, which may suggest a preceding neurological event, or a desire to cover up an assault.
It is important to identify whether the patient suffered a loss of consciousness. The period of loss of consciousness is difficult to obtain as anxious bystanders vary in their ability to recall this information, so an estimate is usual. It is useful to find out the patient’s condition at the scene of the trauma, whether there was any period of airway obstruction or cyanosis, hypotension and the initial Glasgow Coma Score from the ambulance report. This can then be compared to the condition in the emergency department, again providing a temporal profile of the patient’s neurological progress.
Information about the patient’s premorbid status is sometimes available from family or friends. The patient may already have an established neurological deficit, they may be taking anticoagulants or antiplatelet medication, or may chronically abuse alcohol and have concomitant cerebral atrophy or a coagulopathy. It is also important to think about ‘which came first, the chicken or the egg’! It is not uncommon for a preceding neurological event to result in an accident or fall and subsequent head injury. Use of alcohol or recreational drugs prior to the trauma is important to ascertain as these can mask the patient’s true level of neurological function. If the patient has been intubated prior to retrieval, medications for sedation and paralysis during the transfer should be identified as these can also change the clinical picture.
It is important to find out if the patient has suffered a post-traumatic seizure prior to assessment, as the post-ictal state can be prolonged and again mask the patient’s true level of neurological function.
If the patient is able to communicate a more conventional symptom review can then proceed. Headache, nausea, vomiting, dizziness, blurred vision and photophobia are common after even mild head injury and may persist for weeks (post concussion syndrome). They may also represent ‘meningism’, the irritation of the meninges by the presence of extravasated blood such as an extradural or subdural haematoma. Clinically this may be associated with the presence of nuchal rigidity (neck stiffness).
As spinal injury is often associated with head injury it is important to ask about neck and back pain. Patients may also be able to identify specific areas of motor loss or sensory loss.
It is also useful to quantify the period of post-traumatic amnesia (PTA) in conscious patients. This is usually done by asking the patient what is the first thing they remember following the trauma, for example the ambulance officers arriving at the scene, or waking up in hospital. If the patient remains unable to recall events and exhibits poor short term memory for new information he is said to be “still in PTA”. Often patients still in PTA will perseverate questions despite the efforts of staff to dutifully answer them.
- A satisfactory history may require a number of sources such other than the patient such as witnesses and ambulance officers.
- Time of injury, mechanism, factors such as vehicle speed and used of seat belts, loss of consciousness, pre-morbid medical history, seizure activity, back and neck pain and PTA are important.
The system for examination described below can be applied, with appropriate modification, to all patients with head injuries. Those with severe injuries associated with multitrauma will require the full sequence, whilst for patients with milder injuries whose vital observations are stable, the primary survey and resuscitation may be reduced to a mental checklist. The main points of the examination are summarised in Table 4.10.
Primary survey and resuscitation
The primary tenets of Airway, Breathing and Circulation are critical in assessment of the trauma patient, and no more so than in the head injured patient. Hypoxia and hypotension are major contributors to secondary brain injury and poor patient outcomes, and therefore must be reversed as soon as possible. Management of the ‘ABC’ is usually commenced in the field by modern paramedic services. If intubation is indicated it should be performed with due concern for the haemodynamic and intracranial pressure (ICP) effects of airway manipulation (Walls 1993). It is important to remember the possibility of occult spinal injury in the unconscious patient and precautions should be adhered to from the outset. Most patients will have been transferred to hospital with a rigid cervical collar and spinal board. The collar should be checked for proper fit, and if removed to enable intubation, the neck should be maintained in neutral alignment manually (without traction) until the collar is replaced.
In the context of the head injured patient, close attention to their ventilation so as to maintain a normal PaCO2 is vital. Hypoventilation and resultant hypercapnea cause cerebral vasodilation and an increase in ICP. Hyperventilation and resultant hypocapnea cause cerebral vasoconstriction and potential hypoperfusion. In the abscence of signs of intracranial hypertension (neurological deterioration not explained by extracranial causes or evidence of transtentorial herniation) a PaCO2 range of 35-40 mmHg is recommended (Randell and Chesnut 1997).
Whilst traditionally a systolic blood pressure of <90 mmHg was considered to represent hypotension in multitrauma patients, it is now considered important to maintain a mean arterial pressure (MAP) > 90 mmHg to ensure an adequate cerebral perfusion pressure in the head injured patient (Bullock 1996). This translates to a target systolic blood pressure of > 120 mmHg.
Dysfunction of the neurological system is assessed next. Perfunctory observations such as the AVPU approach (Alert, Voice, Pain, Unresponsive) are of little value to ongoing assessment or communicating with neurosurgical colleagues, especially if the patient is subsequently intubated before a more thorough neurological examination can be performed. A Glasgow Coma Scale (Table 4.3) can be rapidly performed with practice and may alert the physician to lateralising signs early in the assessment. Pupil size and reaction can also be rapidly assessed without the aid of a torch in a properly lit resuscitation area.
The patient should be fully exposed and a ‘space blanket’ applied to ensure a thorough surface examination whilst maintaining their core temperature. Intravenous access should be secured and fluids infused as appropriate. Blood is collected for laboratory analysis (Arterial blood gases, full blood count, electrolytes, urea, creatinine, coagulation profile, serum glucose and blood alcohol level) and cross-matching. The patient is connected to appropriate equipment to monitor pulse, blood pressure, electrocardiography, and oxygen saturation. If the patient is intubated, end tidal CO2 should be monitored. An indwelling catheter (IDC) is inserted, unless there are signs of possible urethral trauma. A nasogastric tube (NGT) is inserted, unless there are signs of possible basal skull fracture (see below).
Usually the components of the primary survey and resuscitation are attended to simultaneously by a multitrauma team.
During the secondary survey, assessment is periodically interrupted to enable the acquisition of chest, lateral cervical spine and pelvic x-rays.
A more comprehensive neurological examination can be undertaken if the patient is stable following the primary survey and resuscitation phase. The scope of this examination will obviously depend on the patient’s ability and willingness to participate. Co-operative patients (mild head injuries) can be fully assessed for dysfunction of higher centres, cranial nerves, motor system, and the sensory system. Unconscious patients require a more truncated approach (Table 4.11). This includes interpretation of the vital signs; pulse, blood pressure and respiratory rate. Bradycardia is often an indicator of neurological involvement. Associated with hypertension (Cushing’s reflex), it is a late sign of brainstem compression, whereas associated with hypotension, it suggests spinal cord injury with loss of sympathetic vasomotor tone. Respiratory pattern depends on the level of the central nervous system affected, with cheyne-stokes breathing, hyperventilation, agonal (irregular) respiration and finally apnoea occurring as injury progressively affects lower portions of the brainstem (Plum and Posner 1980). The GCS should again be assessed, although an unconscious patient will by now be intubated for airway protection and should only be assigned a score of 1 for verbal response. Similiarly, patients with significant periorbital swelling may only score 1 for eye opening response. The patient should not be hypoxic or hypotensive, and the effects of paralytic and sedative medications should be allowed to wear off, to ensure an accurate GCS (Marion and Carlier 1994). The pupils should be checked for size and reaction to light. Unilateral dilatation and sluggish or absent reaction to light (a ‘blown pupil’) occurs when herniation of the medial temporal lobe (uncus) through the tentorial notch compresses the third cranial nerve and indicates severely raised intracranial pressure (ICP). This must be distinguished from traumatic mydriasis which is usually earlier in onset, associated with external evidence of orbital trauma, and the conscious state of the patient doesn’t fit the diagnosis of severe head injury. If both pupils are fixed and dilated the patient has central tentorial herniation due to extremely raised ICP. Meiosis associated with a Horner’s syndrome can signify a carotid artery injury. An afferent pupillary defect, as detected by paradoxical dilatation during the swinging torch test, signifies optic nerve damage which may result from a fracture affecting the optic canal. Pinpoint pupils are usually due to opiates. The resting eye position is also easily assessed. Frontal lobe lesions can cause ipsilateral conjugate gaze deviation, whereas pontine lesions can cause contralateral conjugate gaze deviation. Frequently however, patients with a reduced level of consciousness exhibit a dysconjugate gaze. The fundi should be examined to check for intraocular pathology and papilloedema. Mydriatic eye drops should be avoided to enable ongoing pupillary assessment. Motor functions (tone, movement to stimulation, reflexes) should be assessed be to identify any localising signs. These may obviously be affected if neuromuscular paralytic agents are still active. Brainstem reflexes are usually only performed if the patient’s prognosis is deemed to be so poor that withdrawal of active intervention is being considered.
The rest of the secondary survey proceeds from ‘head to toe’. Examination of the head (Table 4.12) involves checking the scalp for lacerations and haematomas. This is best done by palpation as lesions can be easily hidden by hair or blood. Lacerations should be carefully explored with a gloved finger to check for underlying fractures. Arterial haemorrhage should be controlled by artery forceps, ligation or pressure until definitive suturing can be performed. The orbital margins should be palpated for steps which may signify a fracture. The presence of a periorbital haematoma is usually due to external trauma if it extends beyond the margins of the orbit, however if it is confined to the margins of the eyelids it is most likely due to blood tracking through the orbit from an anterior base of skull fracture, a sign referred to as ‘raccoon eyes’. There may also be associated subconjunctival blood extending to the posterior limits of the sclera which has tracked through the orbit. Infraorbital paraesthesia should be excluded, if present and associated with extraocular muscle entrapment it is indicative of a ‘blowout’ fracture of the floor of the orbit. The nose is examined for clinical signs of fracture and septal haematoma. If the latter is present this should be evacuated to prevent ischaemic septal perforation. Cerebrospinal fluid (CSF) rhinorrhoea can be difficult to detect at the initial assessment, especially in the presence of epistaxis, but when found denotes an anterior base of skull fracture. The ‘target sign’ may help distinguish at the bedside if CSF is present. Later, samples can be collected to analyse for glucose or beta-2-transferrin. The ears should be examined for haemotympanum, and blood or CSF otorrhoea, which indicate a temporal base of skull fracture. It is important to check whether blood in the external auditory canal has trickled in from other facial or scalp lacerations. Battle’s sign is bruising visible over the mastoid process and is also indicative of a base of skull fracture. The face should be inspected for swelling (possible underlying fractures) and symmetry (facial nerve palsy secondary to temporal bone fracture, although this usually develops late). The patient’s bite should be assessed to check for possible mandibular fractures and loose or missing teeth. Movement of the upper dentition is attempted to detect Le Fort type maxillary fractures.
The neck is then examined. Until the presence of cervical spine injury has been excluded both clinically and radiologically (see below) the patient should remain in a properly fitted hard collar. It is important to realise that these orthoses do not prevent movement of the spine, they serve to remind the patient and clinicians to maintain a neutral spinal alignment. As such a combative head injured patient may indeed require sedation and intubation to achieve this aim. In the co-operative patient the hard collar may be loosened and gentle palpation performed to assess for tenderness. Crepitus due to subcutaneous emphysema suggests an airway injury. The carotid arteries should be palpated and auscultated, as bruits can signpost arterial dissection.
Examination of the chest, abdomen, pelvis and limbs is then performed as outlined in other chapters.
The patient is then “log rolled” to permit examination of the back. This manoeuvre requires a minimum of three people to enable synchronous rotation of the head, trunk and lower limbs whilst maintaining the total spine in neutral alignment. Vertebral palpation is carried out to detect tenderness or step deformities. A sensory level may be detected. A digital rectal examination is also performed to check sphincter tone and anal sensation.
At the completion of the secondary survey it is important to reassess the patient’s ABC to ensure resuscitation is “on track”.
A space occupying lesion, such as an expanding haematoma, or generalized cerebral swelling will eventually cause displacement of brain parenchyma from one compartment of the skull to another if allowed to progress. This ‘brainshift’ results in compression of structures and causes typical clinical syndromes (Table 4.13). The presence of these signs in a head injured patient represent severe intracranial hypertension, and must be treated with the utmost emergency if rapid, irreversible brainstem injury and death are to be avoided.
Lateral tentorial herniation results from a lateral supratentorial lesion causing movement of the uncus inferiorly through the tentorial notch. The resultant compression of the midbrain causes a decrease in the level of consciousness, compression of the oculomotor nerve at the free edge of the tentorium causes ipsilateral pupillary dilatation and loss of reaction to light, compression of the cerebral peduncle causes contralateral weakness and compression of the posterior cerebral artery can cause ischaemia leading to homonymous hemianopia (although this is usually first detected on CT scanning rather than clinically). Occasionally the opposite cerebral peduncle is compressed against the contralateral tentorial edge causing ipsilateral weakness, and thus producing a ‘false localising sign’. The indentation of the opposite peduncle can be seen macroscopically at autopsy and is called ‘Kernohan’s notch’.
Post-traumatic central tentorial herniation often follows untreated lateral tentorial herniation or is the result of massive cerebral swelling. As a result, the patient is usually already unconscious and the upward gaze palsy due to pressure on the tectum is not assessable. The pupils may initially be small (pontine pupils) before becoming fixed and midsized. Traction on the infundibulum can produce diabetes insipidus.
Tonsillar herniation (‘coning’) in the context of head injury is usually a progression of central tentorial herniation. Displacement of the cerebellar tonsils through the foramen magnum compresses the medulla and rapidly leads to respiratory arrest.
The degree of urgency in managing a patient with clinical signs of brain herniation cannot be overstated. The patient has an ischaemic brainstem and every minute until this situation is reversed counts!
The most important factor in assessing for traumatic vascular lesions is a high index of suspicion, as head injured patients obviously have a number of other reasons for their altered clinical state. The hallmark finding is a delayed onset of neurological dysfunction. The delay is often hours to days after the injury and after onset the abnormalities may fluctuate. The dysfunction is due to cerebral ischaemia and its specific effects reflect the vessel involved. Carotid lesions will exhibit anterior cerebral and middle cerebral territory symptoms and signs, including hemiparesis, hemisensory loss, and dysphasia (Stahmer et al. 1997). Vertebral lesions exhibit cerebellar and brainstem abnormalities in varying degrees, including vertigo, ataxia, nystagmus, dysathria and cranial nerve palsies.
If the patient is sufficiently alert, they may also complain of unilateral neck pain or headache, and usually there are no external signs of trauma in these regions.
Carotid lesions may be associated with an incomplete Horner’s syndrome (meiosis and partial ptosis) due to involvement of the sympathetic fibres of the internal carotid artery plexus (Stahmer et al. 1997). An audible carotid bruit may also be detected on the affected side.
Patients who have developed traumatic ateriovenous fistulae usually complain of an audible whooshing noise, which is synchronous with their pulse and most noticable when resting in bed at night. An audible bruit may be evident on auscultation of the scalp. An orbital bruit is usually indicative of a carotid-cavernous fistula. Depending on the extent of haemodynamic changes in the venous system, these can progress to the development of chemosis, pulsatile exophthalmos, ophthalmoplegia and even visual loss. The clinical findings of vascular lesions are summarized in Table 4.14.
B Plain radiographs
The skull x-ray has largely become redundant in the investigation of head trauma, having been supplanted by CT scanning. Plain skull x-rays are performed to detect skull fractures, but can be difficult to interpret with confusing vascular grooves and suture lines sometimes present.
In isolation, a non-depressed fracture rarely requires treatment, so the rationale for detecting the presence of a fracture is to determine if the patient has an increased risk of underlying intracranial pathology, which may lead to subsequent deterioration in their condition. The yield of skull x-rays in this regard is very low. A review of reported series encompassing over 22,000 patients with head injury undergoing plain skull x-rays showed 3% had fractures. Of these, 91% had no intracranial pathology (Masters et al. 1987).
However even if a fracture is detected on skull x-ray, its predictive value of the patient having a haematoma or deteriorating is no better than careful neurological examination (Feurman 1988). Thus clinical grounds alone are sufficient to determine which patients warrant discharge, observation or CT scanning (see below) and skull x-rays are therefore not usually indicated.
A non-contrast CT scan has become the primary investigation of the head injured patient. The widespread availability of this technology has significantly improved the outcome of patients with intracranial pathology (Servadei et al. 1988). The images can also be sent via teleradiology from rural hospitals for remote neurosurgical consultation.
The advantages of CT include; it is a noninvasive procedure, it is able to be performed rapidly (especially on the latest machines), it is able to accurately localise acute intracranial haematomas, it can show the presence of anatomic shift and hydrocephalus, it can adequately assess skull and facial fractures, it can detect small amounts of pneumencephaly, and can localise metal foreign bodies (Zee et al. 1996).
Skull fractures and suture diastases are detected on specific bone windows (Figure 4.5a). Although linear fractures that run horizontally and depressed fractures at the vertex may be difficult to detect on axial slices, they should be apparent on the scout view. Coronal reconstructions can be produced if doubt still exists. Fractures that involve air sinuses or the mastoid air cells will usually exhibit fluid levels. Pneumencephaly is easily distinguishable as sharply defined areas of ‘black’ within the intracranial compartment (Figure 4.5b).
Focal extraaxial and intraaxial lesions are detected on the soft tissue windows. Extradural haematomas appear as a bi-convex areas of hyperdensity adjacent to the skull, often closely associated with a fracture (Figure 4.6). They usually do not cross suture lines. The presence of hypodense regions within a hyperdense extradural collection is said to represent active bleeding (Greenburg et al. 1985). Acute subdural haematomas classically appear as a crescentic shaped hyperdensity which follows the convexity of the cortical surface (Figure 4.7). They are often associated with underlying brain injury and thus the degree of mass effect and midline shift is often greater than that expected due to the haematoma alone (Zee and Go 1998). Subacute subdural haematomas often appear isodense with the brain parenchyma and may be difficult to detect on plain CT. Chronic subdurals appear hypodense (Figure 4.8). Occasionally lamination of the haematoma is evident if an acute bleed has occurred into a chronic subdural haematoma. The membrane of a chronic subdural haematoma may eventually show calcification.
Subdural hygromas have a similiar appearance to chronic subdural haematomas, although they may appear darker. MRI can be used to better differentiate between these entities.
Traumatic subarachnoid haemorrhage is a common finding on CT following head injury. It appears as a hyperdensity in the subarachnoid spaces (fissures, sulci, or basal cisterns) in varying amounts (Figure 4.9).
Cerebral contusions maybe haemorrhagic or non-haemorrhagic and usually occur on the surface or within the brain parenchyma. They are frequently located adjacent areas where the inner surface of the skull is irregular, for example the floor of the anterior cranial fossa and the sphenoid ridge. Non-haemorrhagic contusions appear as circumscribed areas of hypodensity on CT, with a variable degree of local mass effect. Haemorrhagic contusions have an associated hyperdense lesion within them (Figure 4.10).
Intraventricular haemorrhage appears as a hyperdensity within the ventricular system. Usually a small intraventricular haemorrhage will settle in the occipital horns whilst the patient lies supine on the CT Table. Large amounts of intraventricular clot can obstruct the CSF pathways and produce hydrocephalus.
Diffuse axonal injury is not usually evident on CT. There may be multiple small focal hypodense lesions visible in the white matter, or small hyperdense petechial haemorrhages. In more severe degrees of diffuse axonal injury, hyperdense lesions may be detected in the corpus callosum and rostral part of the dorsolateral pons (Figure 4.11).
Generalized cerebral swelling maybe indicated by widespread loss of definition of the subarachnoid and ventricular spaces. Midline shift is easily measurable on CT and herniation can also be readily detected. Vascular compression maybe evident as loss of grey/white differentiation in vascular territories. Occasionally an area of hypodensity in a large vessel such as the basilar artery may alert the viewer to the presence of a dissection and subsequent thrombosis.
Indications for emergency burrholes
Patients with a decreased level of consciousness and signs of brainstem dysfunction generally have a poor prognosis but some can make good recoveries if an extra-axial haematoma is found and evacuated rapidly via craniotomy. Exploratory burrholes are a sensitive method for detecting extra-axial haematomas with negligible morbidity (Andrews et al. 1986), but they have become largely redundant through the advent of CT scanning. There remain, however, some situations in which exploratory burrholes are indicated, if a delay in obtaining a CT on a patient with suspected herniation is anticipated. These include the need to perform an urgent laparotomy on a hypotensive multitrauma patient (Thomson et al. 1993), injuries in remote geographical locations, and delayed availability of a scanning room or staff.
The side for initial exploration is determined by 1) the side of pupillary dilatation, 2) if both pupils are dilated, the side that first dilated, 3) the side with external signs of injury, 4) the left side (dominant hemisphere in majority of people) (Greenberg 1997). The sequence for placing burrholes is ipsilateral temporal, contralateral temporal, ipsilateral frontal and parietal, contralateral frontal and parietal, ipsilateral and contralateral posterior fossa. Figure 4.12 shows the suggested sites for burrholes and a method for conversion of the scalp incisions into a ‘trauma flap’ for subsequent craniotomy.
Magnetic resonance imaging is of limited use in the initial assessment of acute head injury. The reasons for this include limited availability on an urgent basis, prolonged aquisition times for the images, and limited ability to monitor patients whilst in the scanner due to incompatability of equipment in the magnetic field. The ability of MRI to delineate bony injury is poor, and in addition, its ability to detect acute haemorrhage for the first three days is markedly less than that of CT (Snow et al. 1986).
After three days however, the superior anatomical and pathological resolution and multiplanar ability of MRI do afford it some utility. It is better at detecting the presence of small extra-axial collections and non-haemorrhagic contusions than CT. Lesions in the posterior fossa which may be obscured by bone artifact on CT are often clearly evident on MRI. Re-haemorrhage into chronic subdural collections is more apparent, and differentiation of chronic haematomas from hygromas is also superior with MRI.
MRI and magnetic resonance angiography (MRA) are also useful in detecting vascular injuries involving extracranial and intracranial vessels. MRI is particularly sensitive in detecting the mural haematomas associated with dissections (Figure 4.13).
Late follow-up MRI is also used to confirm the presence and extent of structural damage resulting from head injury, as an aid to prognostication.
Assessment of cerebral perfusion
As mentioned above, MRI and MRA are increasingly being used to screen for vascular lesions following head injury. Cerebral angiography remains, however, the gold standard for defining the nature and extent of these lesions, and their effect on cerebral perfusion. A dissection of the carotid or vertebral artery usually appears as a tapering of the intravascular dye column to either occlusion or a narrowed lumen extending a variable distance, the ‘string sign’ (Figure 4.14). Dissection of the internal carotid artery usually begins around two centimetres above the bifurcation, vertebral injuries usually involve the distal extracranial segment of the vessel (Stahmer et al. 1997). An intimal flap, double lumen, thrombus or distal embolic occlusion may also be apparent. Extracranial and intracranial traumatic aneurysm formation is also well defined by cerebral angiography. Angiographic features that help distinguish traumatic from congenital (berry) type aneurysms include; location away from branch points, irregular contour of the aneurysm, abscence of a well defined neck, delayed filling and emptying, and more peripheral cortical locations (Giannotta and Gruen 1992).
Carotid-cavernous and other traumatic arteriovenous fistulas are also best defined by cerebral angiography, and it is important that six vessel angiography is performed to identify abnormal communications involving external carotid artery branches. The appearance of early venous drainage is the hallmark of these lesions.
Cerebral vasospasm following traumatic subarachnoid haemorrhage is also detected by angiography, with reported incidences ranging from 2-41% (Giannotta and Gruen 1992).
Transcranial doppler ultrasonography (TCD) is a commonly used non-invasive technique to monitor severely head injured patients. Through serial measurement of extracranial and intracranial flow velocities in the internal carotid and middle cerebral arteries, conditions such as vasospasm, hyperaemia, hypoperfusion, impaired autoregulation and vascular (CO2) reactivity can be detected (Steiger et al. 1994).
Single photon emission computed tomography (SPECT) scanning is a less commonly utilised method of evaluating cerebral perfusion and its regional variation following head injury.
Following rapid assessment and the commencement of resuscitative measures as required, ongoing management of the head injured patient is determined by the severity of the injury. Patients are triaged according to their Glasgow Coma Scale score; mild (GCS 13-15), moderate (GCS 9-12), and severe (GCS 3-8), and varying management algorithms are employed.
The patient, however, “must be evaluated and managed on an individual basis and algorithms should be used to guide rather than to dictate management” (Fuerman et al. 1988). Multitrauma patients may require further investigation, anaesthesia and surgery for injuries to other systems, and this will influence the management paradigm. The confounding effects of alcohol intoxication must also be given due consideration and make the physician err on the side of caution (Gurney et al. 1992). Increasing usage of antiplatelet and anticoagulant medication, particularly in older patients, should also be taken into account. The availability and proximity of resources will also profoundly affect what can be achieved.
It is important to note that the patient’s condition can deteriorate very quickly and therefore close neurological observation, and early response to clinical change, is paramount.
Mild closed head injury
The patient should be admitted to the emergency department and undergo hourly neurological observations for a minimum of four hours. They should remain ‘nil by mouth’ in case surgical intervention is required. CT scanning of the head should be undertaken if any of the indications listed in Table 4.15 are present. This approach will not identify all patients who would have abnormalities on CT, but should detect those patients with clinically significant abnormalities on CT and who may require neurosurgical intervention (Borzuk 1997, Miller et al. 1997). Skull x-rays may be obtained if the hospital doesn’t have a CT scanner on site. If, however, the patient fulfils any of the indications for a CT of the head then they should be transferred to a suiTable institution as soon as possible. A cervical spine x-ray series should be obtained if cervical pain or tenderness is present, or if confusion or intoxication obscures their evaluation. Simple analgesia can be tried (with a sip of water), but intramuscular/intravenous opiates may be required if the patient is vomiting or headache remains severe. Appropriate use of opiates will not affect the level of consciousness, but they should not be used (or necessary!) if the patient is intoxicated unless other major injuries, for example fractures, are causing pain. Anti-emetics should be given if the patient is nauseous. Scalp lacerations must be explored, cleaned and sutured if present. Tetanus toxoid/immunoglobulin should be administered as indicated.
If after four hours observation, the patient is normal or has only minimal symptoms (resolving headache, nausea, or dizziness), they may be considered for discharge. This should be into the care of a reliable companion who will stay with them and has been educated about the indications for returning the patient to hospital. Provision of a ‘head injury card’ with these indications listed is also useful. The patient should also be advised to attend his local general practitioner within 48 hours, or present to the next neurosurgical clinic, for a further review.
If, however, the patient meets any of the criteria listed in Table 4.16 they should be admitted for continued observation. The main points of managing mild head injuries are summarised in Table 4.17.
Moderate closed head injury
After the history, primary survey, resuscitation and secondary survey the management of this group of patients is similar to that described above except that all patients undergo urgent CT Scanning, neurosurgical consultation and are admitted for ongoing neurological observation. Intubation of restless or combative patients should be seriously considered to enable safe and artefact-free scanning.
If the scan is normal, the patient is treated expectantly with appropriate supportive measures. Most will improve within hours. If their GCS hasn’t improved to 14-15 within 12 hours, a further scan is indicated (Stein and Ross 1992).
If the scan is abnormal and a fracture or intracranial lesion requires surgical intervention (see below) the patient should be prepared for theatre. Post-operatively they will be transferred to the neurosurgical intensive care unit.
If the scan is abnormal, it should be repeated in 12-24 hours or sooner if neurological deterioration occurs.
Consideration should also be given to insertion of an intracranial pressure monitor, especially if the patient will require prolonged anaesthesia, ventilation for chest injuries, their neurological status worsens, or serial CT examinations show progression of intracranial lesions (Fearnside and McDougall 1998).
As the patient improves the frequency of ‘neuro obs’ can be decreased. All patients should have a repeat CT scan 48-72 hours post-trauma to exclude the development of delayed intracranial pathology (Stein et al. 1993). Patients with late deteriorations in their GCS should be thoroughly assessed for medical causes (sepsis, hypoxia, electrolyte disturbances, hypoglycaemia, drug toxicity, metabolic disturbances) as well as intracranial causes (vascular injury, haematomas, swelling, seizures, hydrocephalus, meningitis/cerebral abscess).
The main points of managing moderate head injuries are summarised in Table 4.18.
Severe closed head injury
Following a brief history, the importance of the primary survey (especially the ABC) and resuscitation can not be over emphasised in this group of patients. All patients with a GCS of 8 or less require intubation for airway protection and precise control of oxygenation and ventilation. The blood pressure must be restored as rapidly as possible, preferrably to a MAP > 90 mmHg, with volume replacement and pressors if necessary (Randell and Chesnut 1997). The secondary survey is then quickly performed. Once initial assessment is complete, adequate sedation should be maintained during transfers and until the patient is stabilized in intensive care. Muscle relaxants may also be required.
If the patient has signs of raised ICP (progressive neurological deterioration unexplained by extracranial causes, or transtentorial herniation signified by a blown pupil or motor posturing) then a rapid bolus of IV mannitol should be given (1gm/kg). It should not be given as a prophylactic measure due to the possibly deleterious effect of the osmotic diuresis on volume replacement. Hyperventilation should also be avoided as prophylaxis, and is only considered appropriate as a ‘last ditch effort’ when other measures have failed to reverse the clinical signs of intracranial hypertension. In this circumstance a PaCO2 range of 30-35 mmHg should be adhered to (Randell and Chesnut 1997).
An urgent CT Scan should then be obtained. If the patient has signs of intracranial hypertension and is haemodynamically sTable, this should take priority over all other investigations including deep peritoneal lavage. If there will be a delay in obtaining the CT, consideration of urgent cranial exploration is warranted. If the patient has signs of intracranial hypertension and is haemodynamically unsTable such that emergency procedures on other systems are required, simultaneous or immediately consecutive cranial exploration for an intracranial lesion should should be performed. It is important to remember however, fluctuating pupillary signs can occur due to intermittent brainstem hypoperfusion during attempts to resuscitate patients with uncontrolled blood loss.
If the scan reveals an intracranial lesion requiring immediate surgery, the patient should be transferred to the operating theatre. If surgery is not required the patient is transferred to the intensive care unit.
For prevention of early seizures, the patient is usually loaded with an IV anticonvulsant.
All patients with severe head injuries should have an intracranial pressure monitor inserted as early as possible, usually immediately after the scan unless an urgent craniotomy is required first. If surgery for other injuries is necessary, a monitor can be inserted simultaneously. Several methods of ICP monitoring are available including placement of a pressure transducer in communication with the subdural, intraparenchymal or intraventricular compartment. Insertion of an external ventricular catheter has the added benefit of enabling drainage of CSF to be used as a therapeutic option in the treatment of intracranial hypertension.
Ongoing management in intensive care and the treatment of specific pathologies associated with head injury are discussed below. The main points of managing severe head injuries are summarised in Table 4.19.
Scalp lesions and skull fractures
Injuries to the scalp following head trauma vary enormously in severity from mild abrasions, localised haematomas, and simple lacerations to stellate lacerations, degloving injuries or avulsion of scalp tissue. Because of the rich vascular supply of the scalp, lacerations tend to bleed profusely and large amounts of blood can become congealed amongst the hair, often obscuring the position and extent of tissue damage. Careful inspection and palpation of the entire scalp is therefore required, and this may necessitate log rolling the patient to access the occipital region if the cervical spine has not yet been ‘cleared’. If a scalp laceration or degloving injury is present this should be covered with a sterile-saline soaked pad held in position with a crepe bandage, until time is available for definitive repair. Infrequently, persistent arterial bleeding may demand the application of an artery forcep or judiciously placed suture prior to this, although most scalp haemorrhage is controllable with a compression bandage.
Most scalp lacerations can be sutured in the emergengy department. Shaving of the hair is not usually required. The area should be liberally washed with an antiseptic solution and the wound edges infiltrated with local anaesthetic. The laceration may be explored with a sterile-gloved finger for evidence of a fracture or foreign material. Large arterial vessels may require ligation. Copious irrigation of the wound with antiseptic solution, followed by sterile-saline, via a syringe should then be performed. Debridement of apparently non-viable tissue should be undertaken with extreme caution as a) the rich vascularity of the scalp rescues much of this tissue and b) it is easy to end up with a defect that will require more extensive surgery to repair! The scalp can be sutured in a single ‘through and through’ layer using a monofilament suture material such as nylon. Interrupted sutures are prefered to continuous, due to a lesser risk of skin-edge necrosis. If skin staples are to be used, an absorbable suture such as polyglycolic acid should be first used to approximate the galea aponeurotica. Sutures can be removed after 7 days.
If there is significant contamination of the wound, extensive degloving, tissue loss preventing simple primary closure, or cosmetically significant wounds (such as gravel or tyre rubber ‘tattooing’), the neurosurgical or plastic surgery team should be consulted regarding management. Significant scalp injuries may require skin grafting, transposition flaps, pedicle flaps or re-implantation to repair defects.
Infrequently, scalp haematomas in elderly patients can exhibit sufficient pressure to cause ishaemia of the overlying scalp. These haematomas require evacuation through a small incision which is then sutured and a compression bandage applied. It should be noted that the pinna of the ear can be made ischaemic by head bandages being too tight. Cotton padding can be positioned behind the pinna prior to application of the bandage to prevent this.
Closed skull fractures
Undisplaced fractures of the skull convexity include linear fractures, suture diastases (separation of a suture line), and comminuted (stellate) fractures. If the overlying scalp is intact, these fractures require no operative management. They do, however, indicate the need for investigation for underlying intracranial pathology. An asymptomatic patient with a linear fracture who has an otherwise normal CT scan can be discharged into the care of a reliable companion.
Compound skull fractures
Linear skull fractures associated with a small scalp laceration usually only require careful cleaning and closure of the wound as described above. Open comminuted fractures with free bone fragments should be explored and debrided in the operating theatre. Removal of contaminated bone fragments, and often dural repair, may be required.
Depressed skull fractures
Depressed skull fractures are only considered significant if the outer Table of the depressed portion is below the level of the inner Table of the normal skull. This is usually evident on axial bone window CT scans, although occasionally coronal reconstructions of the CT data may be necessary to adequately elucidate the extent of bone depression. Indications for surgical exploration and elevation of a closed depressed fracture are cosmetic deformity (particularly involving the forehead or orbital rim), underlying brain or dural injury, underlying haematoma with mass effect, underlying air sinus fracture, or compression of an underlying venous sinus. If a venous sinus is involved, surgery can be fraught with difficulty if the sinus has been lacerated by a bone fragment.
Open depressed fractures should always be urgently explored and debrided due to the risk of infection. Hair and debris can become wedged between the bone fragments which should be completely removed. If the dura has been breached, bone and debris should also be cleared from the underlying brain and a watertight dural repair performed. The bone is usually discarded, and a delayed cranioplasty will be necessary.
Traumatic CSF leak
In isolation, base of skull fractures do not require any intervention. It is the associated injuries to traversing nerves, vessels and adjacent air sinuses that may warrant attention. If the latter are associated with a dural laceration, a fistula between the subarachnoid space and air sinuses/mastoid air cells/middle ear may be formed and a traumatic CSF leak results. This provides a route for intracranial infection unless sealed. The presence of a dural laceration is often heralded by evidence of pneumocephaly on the CT scan. In one reported series of head injuries, 7% had base of skull fractures, 2% developed CSF leaks and 0.5% contracted meningitis. The majority of leaks were apparent within 48 hours, most of the others occured within 3 months, but a few were delayed months to years before their onset (Lewin 1966).
CSF otorrhea occurs with fractures of the temporal bone, either through the mastoid air cells and an external auditory canal laceration or through the middle ear and perforation of the tympanic membrane. The vast majority of these leaks settle in a few days without the need for surgical intervention. The patient should be admitted and an earpad applied to the affected side to monitor the volume of leakage. Prophylactic antibiotics should not used because of the risk of super-infection. The external auditory canal should only be cleaned by an ear,nose and throat surgeon and follow-up auditory and vestibular testing should be arranged for 6 weeks after discharge from hospital.
CSF rhinorrhea results from base of skull fractures entering the paranasal air sinuses or the middle ear with passage of CSF through the eustachian tube. This form of traumatic CSF leak is less likely to heal of its own accord. The patient should be admitted and a nasal bolster applied to monitor the volume of leakage. Again, prophylactic antibiotics should not used because of the risk of super-infection. A lumbar drain may be inserted to divert CSF at a rate of 5-10 millilitres/ hour, although this is controversial as it may promote entry of bacteria through the fistula and increase the risk of infection. Non-surgical management is usually attempted for 1-2 weeks. but if the leak is persisting the exact location of the fistula is usually sought with CT cisternography or radioisotopic studies, and surgical repair undertaken. Depending on the site of the leak, a transsphenoidal or intracranial approach may be utilised to repair the dural defect.
Base of skull fractures involving the cribriform plate often cause anosmia due to shearing of the traversing olfactory fibres. Management is expectant, with a poor prognosis for improvement. The patient will also complain of a reduction in the taste of food.
The optic nerves can be damaged by fractures involving the apex of the orbit and optic canal. Surgical decompression does not improve the recovery rate and therefore management is again expectant, unless deterioration occurs after the initial insult.
The abducens nerve can be injured by clival fractures. Management is expectant.
The facial nerve can be injured in temporal bone fractures (especially with the less common transverse pattern of fracture), leading to a partial or complete lower motor neurone facial palsy. Most lesions recover with time and expectant management is most commonly employed. The use of steroids and decompressive surgery remain controversial. Facial nerve grafting can be utilised to treat permanent lesions.
The vestibulocochlear nerve can also be damaged by transverse temporal bone fractures. Management is expectant.
Focal intracranial lesions
The classical presentation of head injured patients with an extradural haemtoma (EDH) involves an initial period of loss of consciousness due to the initial impact, followed by a ‘lucid interval’ before they again lapse into unconsciousness as the haematoma expands. Only a minority of cases actually present this way however, and the pattern described is certainly not pathognomonic for extradural collections. The patient may remain conscious or unconscious depending on the severity of any underlying brain injury and the size of the EDH. Extradural haematomas are very uncommon in older patients due to greater adherence of the dura to the inner Table of the skull with increasing age.
The treatment for extradural haematomas is urgent craniotomy, evacuation of the blood clot and control of the source of haemorrhage (usually a branch of the middle meningeal artery or vein, less commonly a dural venous sinus). Burrholes are insufficient for this purpose. In remote areas or when urgent burrhole exploration is undertaken, the hole in the skull can be enlarged with bone nibblers to enable some decompression of the solid clot prior to transfer for definitive neurosurgical care. Haematomas that are 5 millimetres or less in thickness may be managed non-operatively. but given their propensity to enlarge in a delayed fashion, close observation in a neurosurgical unit and serial CT scanning is advisable.
Acute Subdural Haematoma
Acute subdural haematomas (ASDH) are more common in older patients due to cerebral atrophy increasing the risk of tearing cortical bridging veins, and are the most common haematoma associated with falls. There is also a greater likelihood of significant underlying brain injury associated with ASDH, which tends to obscure the relative contribution of the haematoma to the patient’s clinical condition, as well as adversely affect outcome.
Subdural haematomas that are 5 millimetres or less in thickness can usually be managed without surgical evacuation, but again, close observation in a neurosurgical unit and serial CT scanning to ensure resolution and not expansion is required. The management of haematomas greater than 5 millimetres in thickness depends on the clinical state of the patient. A small ASDH in a patient with no neurological deficit may be followed with serial CT scans until it liquefies and then drained via a burrhole. However, small haematomas can be deceptively voluminous if spread out widely over the convexity. In patients with severe underlying brain injury even small volume clots can add significantly to raised intracranial pressure problems and should be evacuated via urgent craniotomy. Generally all ASDH greater than 10 millimetres in thickness or associated with greater than 5 millimetres of midline shift should be urgently evacuated via a craniotomy and the source of bleeding controlled. An ICP monitor should also be inserted during the procedure, as many patients will have elevations in intracranial pressure following surgery.
Chronic subdural haematoma
Chronic subdural haematomas (CSDH) tend to occur in older patients and are often the result of very minor head trauma weeks to months prior to presentation. Symptoms vary from headaches or confusion, to hemiparesis.
Treatment is drainage via burrhole with or without placement of a subdural drain. Craniotomy and removal of the haematoma membranes is unnecessary and adds to the morbidity in a generally elderly patient population.
Subdural hygromas are traumatic subdural collections of CSF due to laceration of the arachnoid. Symptomatic lesions are treated with burrhole drainage.
The management of traumatic intracerebral haematomas is guided by the size of the haematoma and the clinical condition of the patient. Patients with small haematomas may be followed with close neurological observation and serial CT scanning. Haematomas causing significant mass effect and midline shift or contributing to elevations in ICP should be evacuated via craniotomy. This also applies to large cerebral contusions.
Raised Intracranial Pressure
The indications for insertion of an intracranial monitoring device in head injured patients have been discussed above. The ICP is considered elevated if the patient’s pressure is consistently above 20 mmHg, and therapeutic measures should be instituted to try and prevent secondary brain injury from reduced cerebral perfusion pressure. These therapeutic measures tend to be categorised as general measures, first line treatments and second line treatments.
General measures for the maintainence of a normal ICP following head trauma obviously include surgical evacuation of any extra- or intra-axial haematomas with significant mass effect. The greater the elevation in a patient’s ICP due to generalised cerebral swelling, the smaller a haematoma has to be to contribute significantly to reducing cerebral compliance. Elevation of the head of the bed by 15-30 degrees is recommended to displace CSF into the thecal sac and facilitate cerebral venous outflow. This manoeuvre is controversial, however, due to the possibility of a paradoxical increase in ICP in the presence of decreased cerebral compliance (Durwand et al. 1983). On balance, it appears useful but the effect on ICP should be carefully observed in each patient. It is important to avoid compression of venous outflow through the neck by ensuring tracheostomy tapes and cervical collars are not too tight and that the neck remains in reasonably neutral alignment.
Ventilation should be controlled to maintain a normocapnic range of 35-40 mmHg. It should be remembered that positive airway pressure from mechanical ventilation is transmitted to the intracranial cavity through the mediastinal structures and therefore can influence ICP, but generally a positive end expiratory pressure (PEEP) of 5-15 cmH2O is tolerable (Frank 1993). A normotensive blood pressure should be maintained. Hypotension will reduce the CPP, which will cause reflex vasodilation, increased CBF, increased cerebral blood volume and increased ICP if autoregulation remains intact, or will cause reduced CBF and ischaemia if autoregulation has been lost. Hypertension can exacerbate cerebral oedema if autoregulation is impaired or the blood brain barrier is disrupted in the injured brain. The patient should also be kept normothermic, as fever has a detrimental effect on ICP by increasing cerebral blood flow and cerebral blood volume.
Adequate sedation is important for patients on ventilators to prevent coughing and ‘Fighting the ventilator’ by breathing against its breaths, both of which increase intrathoracic pressure and reduce cerebral venous outflow. Short acting benzodiazepines such as midazolam are often used for this purpose. Pain is also an important factor in stimulating CBF, CBV and ICP. Multiple injuries, surgical sites and airway irritation from the endotracheal tube will all contribute to the patients’ discomfort and adequate analgesia is therefore also very important. Narcotics such as morphine are commonly used.
Firstline treatments of raised ICP include heavy sedation to reduce cerebral metabolism and therefore reduce required CBF and CBV. Hypotension is a potential complication with increased sedation. Drainage of CSF via an external ventricular drain is an effective way of reducing intracranial volume and improving compliance. Drainage should be intermittent rather than continuous to enable close monitoring of sudden rises in ICP. Generally, opening the drain for 5 minutes, up to 4 times per hour is sufficient. Intermittent boluses of an osmotic diuretic such as mannitol can be utilized to draw water from the interstitial space into the intravascular space. Mannitol is also believed to assist oxygen delivery by improving the rheological characteristics of the blood. A typical regimen is100 ml of 20% mannitol solution repeated 6 hourly. Careful attention must be paid to electrolyte and fluid balance during this treatment and the therapy is discontinued when the serum osmolality is above 310 mosmol/L. Loop diuretics are also useful as an adjuvant to osmotic therapy, particularly in controlling the associated increase in intravascular volume. Frusemide is generally used. Non-depolarizing neuromuscular paralysing agents can be used to facilitate mechanical ventilation by improving chest wall compliance and lowering mean airway pressures. Again these tend to be used intermittently, to avoid the complications of prolonged neuromuscular paralysis (Frank 1993).
Second line treatments are utilised when the above measures fail to consistently maintain an ICP of less than 20 mmHg. Precipitous rises in ICP or patients with difficult to control ICP should be investigated with further CT scanning to exclude a surgically correcTable lesion. Second line treatments include barbiturate coma. High dose barbiturates lower the ICP by reducing the cerebral metabolic rate and therefore the CBF. The complications can be significant however, particularly hypotension and increased susceptibility to infection. Generally, following a loading dose, an infusion of barbiturate such as thiopentone or pentobarbital is titrated to ‘burst suppression’, which involves continuous EEG monitoring to confirm suppression of cerebral electrical activity.
Hypothermia is also an effective means of reducing cerebral metabolism and ICP (Metz et al. 1996). Patients are usually cooled to a core temperature of 34-36 degrees celcius via a ‘cooling blanket’, but it is important they are sufficiently sedated.
An increasingly utilized treatment for raised ICP is cerebral perfusion pressure management (Rosner et al. 1995). This involves maintaining the MAP above the threshold required to ensure the CPP is greater than 70 mmHg (CPP=MAP-ICP) with careful intravascular volume control and vasopressors as necessary.
Hyperventilation to reduce the PaCO2 to a range of 25-35 mmHg is now considered a ‘last ditch effort’ to control ICP, and can only be utilized for short periods before physiological tolerance develops.
Other methods used for control of severe intracranial hypertension include decompressive craniectomy with or without partial lobectomy. Indomethacin has also been shown to be an effective agent in reducing ICP (Harrigan et al. 1997), and can be administered rectally. Lignocaine boluses can also be used to control BP and ICP surges during procedures in the intensive care unit which may cause airway irritation. The modalities available to treat raised ICP are summarized in Table 4.20.
Seizures within the first 48 hours of a head injury are common and do not necessarily foreshadow the occurrence of later seizures. Approximately 2% of persons suffering head injury will go on to develop post-traumatic epilepsy. Of those surviving a severe head injury, the risk of epilepsy is 10-15% (Hauser 1990). Seizures in the early period following head injury are believed to contribute to secondary brain damage by increasing metabolic demands, raising the ICP, and via excess release of neurotransmitters (Schierhout and Roberts 1998).
It appears that the presence of extravasated blood in the brain parenchyma contributes to the pathogenesis of post-traumatic epilepsy. The iron in haemoglobin is a potent epileptogenic agent, and the ability of the brain’s chelating agents to neutralize its effect may be overcome if sufficient blood is present following trauma.
To try and prevent the development of post-traumatic epilepsy, and reduce the negative impact of early seizures, prophylactic anticonvulsants have been widely used in treating head injured patients. However clinical trials have shown that whilst anticonvulsant usage reduces the incidence of seizures in the first week post-injury by 73%, there is no reduction in the incidence of late seizures (Temkin et al. 1990). It is also unclear whether preventing early seizures actually improves outcome (Schierhout and Roberts 1998).
Therefore at present it would appear reasonable to use prophylactic anticonvulsants in cases of severe head injury for the first week after injury and then cease. Phenytoin is most commonly used as it can be administered intravenously. A skin rash occurs in approximately 4% of patients and necessitates a change of anticonvulsant. Monitoring of serum concentrations and liver function tests is required, as well as periodic full blood counts.
Patients who develop late seizure activity (post-traumatic epilepsy) require education about the implications of epilepsy such as inability to drive for a prescribed seizure free period, and risks of swimming alone or climbing ladders etc.
Traumatic subarachnoid haemorrhage
Traumatic subarachnoid haemorrhage (tSAH) is the most common pathological finding following head injury. In patients with severe head injuries, the incidence of tSAH on CT is up to 39% (Eisenberg et al. 1990). The presence of tSAH has also been shown to be independently associated with a significant worsening of prognosis. Patients with severe head injuries and evidence of tSAH have a twofold increase in mortality (Eiseberg 1990), and a twofold increase in unfavourable outcome at six months (European Study Group 1994), compared to those patients without tSAH.
There is increasing evidence that the prognostic significance of tSAH is partly related to its association with vasospasm. Other trauma admission CT findings associated with the development of vasospasm include subdural and intraventricular haemorrhage (Martin 1995). Vasospasm is one of the many causes of cerebral ischaemia, a major contributor to secondary brain injury. Angiographic studies from the pre-CT era, and more recently, transcranial doppler studies report the incidence of post-traumatic vasospasm to be 20-40%. The timecourse of vasospasm associated with tSAH is similiar to the vasospasm witnessed following aneurysmal SAH, with an onset around day 2 and peak around days 10-14 post injury.
Head injured patients without vasospasm appear to be twice as likely to have a favourable outcome, compared to those with vasospasm (Martin et al. 1995). This has led to increasing vigilance for post-traumatic vasospasm with serial transcranial doppler examinations and routine angiography of patients with tSAH. Confirmed vasospasm is treated in a similiar manner to that related to aneurysmal SAH. Several trials appear to show an improved outcome using the calcium channel blocker nimodipine prophylactically in head injured patients with tSAH (Kakarieka 1997).
The main hurdle in treating traumatic vascular lesions associated with head injury is recognising the problem when it occurs. Delayed diagnosis transpires in the majority of cases. This has been compounded by the advent of CT scanning replacing angiography as the mainstay of head injury investigation.
In cases of thrombosis or dissection of neck or intracranial vessels, the aim of treatment is to prevent completed stroke. The type of therapy utilised depends on the pattern of clinical presentation, the neurological status of the patient and the duration of their deficits. Patients with a sTable clinical state are usually treated medically with anticoagulation followed by antiplatelet therapy and followup angiography to assess for resolution or progression of the lesion. Patients with a fluctuating or evolving neurological deficit may require mild hypertensive therapy or interventional radiological procedures such as intra-arterial thrombolysis or stenting. Occasionally surgical procedures such as endarterectomy, ligation, vascular reconstruction or extracranial- intracranial bypass may be warranted.
Traumatic intracranial aneurysms often present with delayed subarachnoid haemorrhage and thus conservative treatment has a high mortality rate. Various endovascular and open surgical techniques can be utilised to repair these lesions.
Carotid-cavernous fistulae require treatment if they cause progressive proptosis, ophthalmoplegia or visual loss. Usually transarterial or transvenous embolisation is successful in closing the arteriovenous communication. Dural arteriovenous fistulae are most frequently asymptomatic, however they can be responsible for progressive headaches, neurological deficits and subarachnoid haemorrhage and may require endovascular treatment in such circumstances.
Intensive care of head injured patients
The intensive care unit is where ongoing resuscitation, critical monitoring and maintenance of physiological homeostasis, and recognition and treatment of the sequelae of severe head injury occurs. The prime aim is to prevent secondary brain injury and rescue salvageable brain tissue .This role includes optimum ventilation and prevention of chest infections in the unconscious patient. Blood pressure control, maintenance of an adequate intravascular volume and haemaglobin, and prevention of coagulopathies are also vital. Fluid and electrolytes must be carefully monitored, as imbalances can result from the development of SIADH, Cerebral Salt Wasting Syndrome and, less commonly, Diabetes Insipidus following head trauma.
The monitoring of intracranial pressure and medical treatment of raised ICP (see above) is also a key task of the intensive care unit. An increasingly used technique is continuous monitoring of jugular venous oxygen saturation in an effort to match cerebral blood flow with cerebral oxygen consumption (Cruz 1998).
Other important facets of the management of head injured patients include provision of adequate nutrition, prophylaxis against deep venous thrombosis, skin care to prevent pressure areas, and the early management of increasing tone to prevent contractures.
Continuing research into the pathophysiology of brain trauma has shown that primary brain injury is not an immediate, irreversible process, but that the initial event sets in train a neurochemical cascade which eventually causes the ‘primary injury’. This window of opportunity has led to inceased efforts to find therapies to attenuate or reverse this pathological cascade and thus salvage neuronal tissue. Compounds such as calcium channel blockers, calpain inhibitors, excitatory amino acid antagonists, free radical and lipid peroxidation inhibitors, inflammation cytokine inhibitors and neurotrophic factors are currently being evaluated (McIntosh et al. 1997).
Penetrating head injury
Penetrating head injuries can be subclassified as missile and non-missile injuries. Missile injuries include those caused by bullets and shrapnel, and their incidence is increasing in civilian settings. Non-missile injuries can be caused by a variety of implements including knives, screwdrivers, arrows, spears, axes, rocks and pens.
The primary injury caused by a missile involves the scalp, skull and brain. There are two main biomechanical effects that produce damage to the brain tissue. Firstly, the passage of the missile causes a direct crush injury that creates a permanent cavity along its pathway through the parenchyma. Secondly, a pressure wave caused by the projectile leads to a rapid expansion and contraction of the tissues around the pathway, referred to as temporary cavitation. This results in a stretch injury which may damage tissue and blood vessels distant to the missile’s pathway.
Secondary injury follows, including oedema and raised intracranial pressure which can exacerbate ischaemic damage. Respiration can also be affected, with variable periods of apnea occuring immediately after the injury contibuting to hypoxic injury. This is believed to be due to distortion of the brainstem at the time of impact. Coagulation disorders are also common, including disseminated intravascular coagulopathy, due to the release of brain tissue thromboplastin.
Late complications of missile injuries include CSF leaks, infection and abscess formation, traumatic aneurysm formation, seizures and migration of retained bullet fragments.
The initial assessment and resuscitation of the patient with a penetrating head injury due to a gunshot wound is similiar to that of the patient with a closed head injury, but with special consideration of the following points. The scalp should be shaved to assist detection of entry and exit wounds and control of bleeding points. Tetanus immunisation status should be checked and tetanus toxoid +/- immunoglobulin given as required. Prophylactic antibiotics to cover gram positive and gram negative organisms should be commenced. Due to the increased incidence of post-traumatic seizures following missile injuries, prophylactic anticonvulsants are usually recommended, at least in the short-term. The CT scout view and bone windows are the most useful in determining the location of retained missile fragments. Strong consideration of angiography is warranted if the missile has passed anywhere near a major intracranial artery. The timing of angiography is often delayed due to the urgent need for operative intervention.
Prognosis following penetrating head injury due to a missile is predominantly determined by the level of consciousness on admission: 94% of patients with a GCS < 8 die (Benzel et al. 1991). Other factors indicating a worse prognosis include the pathway of the bullet traversing both hemispheres, multiple lobes or a ventricle, and if the injury was sustained in a suicide attempt.
Because of the relatively poor prognosis in many of these injuries, the indications for surgery are controversial. A useful published protocol suggests surgery be performed on (a) patients with a GCS 9-15, (b) patients with a GCS 6-8 in whom the missile hasn’t traversed both hemispheres, multiple lobes on the dominant side or through a ventricle, and (c) patients with a GCS 3-5 with a large extra-axial haematoma (Graham et al. 1990). The aims of surgery are to debride necrotic scalp, bone fragments and necrotic brain tissue; remove haematomas and control bleeding; remove accessible bullet fragments; repair violated air sinuses and achieve a watertight dural closure.
The main difference with this form of injury is that the penetrating object is often left protruding from the cranium. In this situation the implement should be stabilised insitu until removal in theatre can be accomplished. Again, consideration of angiography should be cardinal.
- Penetrating head injuries can be subclassified as missile and non-missile injuries
Prognosis of head injury
The outcome from a head injury is often described with the aid of an outcome scale. The simplest and most widely used is the Glasgow Outcome Scale (Table 4.21) (Jennett and Bond 1975). The clinical state of the patient is often assessed, using this scale, at 3 months or 6 months, although given the propensity of these patients to continue improving for 1-2 years, later assessments may be more accurate.
Reliably predicting the outcome of a head injured patient, particularly those classified with severe injuries, has long been an objective of researchers and clinicians, with a view to withdrawing prolonged and expensive treatment from patients who ultimately will not benefit. A number of factors have been shown to correlate with poor outcome, including low post-resuscitation GCS, older age of the patient, pupillary abnormalities, the presence of hypoxia and/or hypotension prior to definitive treatment, traumatic subarachnoid haemorrhage, and inability to control intracranial pressure (Eisenberg et al. 1991, Vollmer et al. 1991, Kakarieka 1997). However the ability to select patients, in the early phases of assessment and treatment, who will definitely have poor outcomes remains an inexact science at present.
The mortality rate from head trauma climbs as the patients’ post-resuscitation GCS (an indicator of severity of the primary injury) falls. The Traumatic Coma Data Bank results showed patients with an inital GCS of 3 had a 78% mortality rate, whilst those with a GCS of 8 had an 11% mortality rate. Overall results for patients with severe head injuries (GCS 3-8) were good recovery 26.5%, moderate disability 16.4%, severe disability 15.6%, vegetative 5.2%, and dead 36.3% (Eisenberg et al. 1991).
Elderly patients who sustain a head injury have higher rates of morbidity and mortality as compared to younger patients with similar injuries. The progressive increase in morbidity and mortality with age becomes most apparent beyond the age of 55 (Vollmer 1991). This adverse effect of age on outcome appears to be related to intrinsic changes in the ability of the brain to recover from pathological insults as a result of the ageing process. It is independent of extrinsic factors such as mechanism of injury, non-neurological complications following injury, or premorbid systemic illness (Vollmer et al. 1991).
- •The Glasgow Outcome Scale is the most commonly used scale to describe outcome from a head injury.
Approximately 75% of all head injuries are mild head injuries (Kraus and Nourjah 1988), and up to 50% of these patients will suffer some form of post-concussion syndrome (Mandel 1989). Post-concussion Syndrome refers to a constellation of symptoms and signs which may occur in varying degrees following mild head injury.
The sequelae of mild head injury are listed in Table 4.22. These include headaches, cranial nerve symptoms, psychosomatic complaints and cognitive impairment. Rare sequelae of mild head injury include subdural and extradural haematomas, seizures, transient global amnesia, tremor and dystonia (Evans 1992). The most common symptoms are headaches, dizziness, irritability, decreased concentration, memory problems and sensitivity to noise.
The mainstay in treating post-concussion syndrome is reassurring the patient and family that the symptoms are not unexpected, and educating them about the condition. Symptom control with specific therapies may be required.
The majority of patients have significantly improved by 3 months, and 85 -90% will have a full recovery by 1 year (Borzuk 1997). If symptoms persist beyond one year, the patient is described as having Persistent Post-concussion Syndrome (Rutherford et al. 1978). Risk factors for persistent post-concussion syndrome include age > 40, female gender, lower educational, intellectual and socioeconomic level, alcohol abuse, prior head injury, multitrauma, serious other illness, and ongoing litigation (Evans 1992, Edna and Cappelen 1987). Controversy continues about what percentage of these patients are malingerers.
Brain death criteria
The mortality rate of severe head injury remains approximately 36%. Not infrequently these patients reach the point of non-survival whilst having their respiratory function supported artificially in an intensive care unit. It may then be necessary to establish that brain death has occurred so that continuation of futile treatment may be ceased. If the patient is a candidate for organ donation and consent is obtained to harvest tissues, it is usually a legal requirement that certification of brain death has been performed by at least 2 medical practitioners in accordance with local laws. Brain death is established by determining the presence of irreversible coma and irreversible loss of brainstem reflexes and respiratory centre function OR by the demonstration of the cessation of intracranial blood flow (ANZICS 1998).
The clinical criteria for confirming the presence of brain death are i) an appropriate period of observation is required, ii) certain preconditions must be satisfied before clinical testing of brainstem function is undertaken, and iii) clinical testing verifies the abscence of brainstem function. A minimum total period of observation of six hours is recommended to show irreversibility beyond all doubt. During this period the patient should be documented to have a GCS of three, non-reactive pupils, absent gag and cough reflexes and no spontaneous respiratory efforts. Preconditions that must be satisfied prior to clinical testing include; a diagnosis consistent with progression to brain death, exclusion of coma due to drugs or poisoning, exclusion of metabolic causes of coma, exclusion of hypothermia (core temperature > 35 degrees) and intact neuromuscular conduction (ANZICS 1998). Suggested clinical testing of brainstem function should include; response to painful stimuli in cranial nerve distribution, pupillary response to light, corneal reflexes, gag reflex, cough reflex, oculovestibular reflexes, and respiratory function in presence of an adequate stimulus (ANZICS 1998). This last clinical test is usually performed following preoxygenation. The ventilator is then stopped whilst oxygen is administered to the airway and the arterial PCO2 is allowed to rise above 60 mmHg. This represents an adequate stimulus to spontaneous ventilation, during which the patient must remain apnoeic. All of the above reflexes must be absent to certify brain death.
If the above clinical criteria cannot be met, three or four vessel cerebral angiography may be used to demonstrate absent intracranial blood flow (both anterior and posterior circulation) following the minimum period of observation of 6 hours (Greenberg et al. 1997).
A Sport related head injury
Concussion is an alteration in mental status produced by trauma that may or may not involve a loss of consciousness. It is characterized by confusion and amnesia, which may commence immediately after the injury or develop several minutes later (Greenberg et al. 1997).
Minor head injuries resulting in concussion are extremely common in contact and impact sports. Most rugby or football fans will have witnessed a player who, following a knock to the head, gets to his feet dazed and takes a while to register where he is, or runs in the wrong direction, or appears inco-ordinate and fumbles a pass. Initial symptoms are those of mild head injury; headache, nausea and vomiting, dizziness and confusion. Persisting symptoms represent the post-concussive syndrome and can last for days to weeks; persistent headache, poor concentration, memory problems, irritability, photophobia, tinnitus, anxiety, depression, and sleep disturbance.
The American Academy of Neurology has graded concussion into 3 levels and produced recommendations to guide physicians as to when to allow athletes suffering each grade of concussion to return to competition (Greenberg et al. 1997). Grade 1 concussion is defined as transient confusion, no loss of consciousness, and symptoms/mental status abnormalities resolve in less than 15 minutes. Grade 2 concussion involves transient confusion, no loss of consciousness, and symptoms/mental status abnormalities lasting more than 15 minutes. Grade 3 concussion refers to any loss of consciousness, either brief or prolonged.
When an athlete suffers a concussion, they should be immediately removed from the competiton and assessed at frequent intervals. If they have returned to normal by 15 minutes (grade 1), the athlete may return to play. If a grade 2 injury or further grade 1 injury is sustained, they should be removed from the contest and not resume sport until they have been asymptomatic for a full week. If a grade 3 or a second grade 2 injury is sustained, the athlete should remain out of competition until asymptomatic for 2 weeks. A second grade 3 injury should see the competitor resting at least 1 asymptomatic month. Those suffering a grade 2 or 3 injury should be assessed by a neurologist or neurosurgeon prior to resumption of their sport. Persisting symptoms warrant investigation with CT or MRI scanning, and any abnormality detected terminates the athletes season (Greenberg et al. 1997).
Second impact syndrome
Second impact syndrome refers to the precipitous events which may follow a second head injury that is sustained before symptoms associated with a previous head injury have had time to resolve (Cantu 1998).
The most common situation in which closely repeated head injuries are likely is sport. Reported cases of second impact syndrome follow a general pattern; an athlete suffers an initial head injury, the severity of which may vary from grade 1 concussion to the presence of cerebral contusions, and following this has post-concussive symptoms such as headache, nausea, vomiting, visual disturbances or cognitive problems. Before the symptoms have settled they return to participation in the sport and suffer a further head injury. The second injury may again be very mild. The athlete then often appears dazed for a few seconds to minutes before suddenly collapsing, becoming deeply comatosed, dilating both pupils and exhibiting respiratory failure (Cantu 1998). Many of those affected die either before or despite intensive medical care. At autopsy the usual findings are massive cerebral oedema and transtentorial or tonsillar herniation. Loss of autoregulation and resultant cerebral vascular engorgement are believed to be the pathophysiological mechanism behind the extreme cerebral swelling and rapidly ensuing brainstem failure.
Prevention is the best cure for this dangerous condition. It is important that all cases of concussion are identified and athletes must not be allowed to practice or compete until at least 1 week after all post-concussive symptoms have resolved, no matter how long this takes (Cantu 1998). It is also suggested that athletes with persistent symptoms should have a CT scan of the head (Saunders and Harbaugh 1984). Education of athletes, coaches and parents about the risk of second impact syndrome is also critical, so that pressure to perform is not unduly exerted on those who are perceived to have suffered only a minor ‘knock to the head’.
Chronic traumatic encephalopathy
Chronic Traumatic Encephalopathy (CTE) refers to a spectrum of neurologic injury caused by repetitive head trauma. It is most frequently observed in professional boxers and there is a clear relationship between the number of bouts fought and the development of CTE (Ryan 1998).
Repetitive blows to the head cause an accumulation of neuropathological changes. These include compromise of the blood brain barrier, loss of neuronal reserve and cerebral atrophy, diffuse axonal injury, loss of pigments and neurons in the substantia nigra, repeated contusions and gliosis, loss of purkinje cells in the cerebellum, an increased incidence of cavum septum pellucidum with larger fenestrations, development of neurofibrillary tangles and amyloid deposition (Mendez 1995). A recent study has suggested individuals who carry the Apo E e4 allele in their genotype are at increased risk of developing dementia pugilistica (the severest form of CTE), through the association of this allele and an increase in amyloid deposition following acute head injury (Jordan et al. 1995).
The clinical manifestations of CTE range from mild motor, cognitive, and psychiatric abnormalities through to dementia pugilistica. The majority of affected boxers exhibit the mild, non-progressive end of the spectrum. This is characterized by dysarthria, tremor, mild inco-ordination, decreased attention and emotional lability. A small minority of boxers progress to dementia pugilistica. This syndrome includes advanced parkinsonism, cerebellar dysfunction, slow mentation, amnesia, disinhibition, decreased insight and occasionally overt psychosis (Mendez 1995).
Measures suggested to diminish the risk of progressive CTE include preventing commencement of the sport at a young age, limiting the number of bouts fought, discouraging amateurs from turning professional and stricter medical supervision of the sport (Mendez 1995). There is also an increasing call from medical societies to ban the sport altogether.