Trauma is the leading cause of death from 1 to 44 years of age in developed countries such as the USA and Australia.^1,² It is an even greater problem in developing countries, where the majority of death and disability occurs.^3,⁴ Trauma deaths peak between the ages of 15 and 44, and therefore contribute significantly to the number of years of life lost in the population.^1,² Deaths from unintentional injury are much more common than suicide or homicide, even in the USA.¹ However, in the USA, homicide causes more deaths than suicide in the 15–24-year age group;¹ this differs from other developed countries. Suicide now causes more deaths than motor vehicle accidents (MVAs) in regions such as Australasia and the UK.^2,⁵

Morbidity due to injury affects a much larger group. For every death there are at least 15 serious non-fatal injuries, many causing long-term morbidity. The economic and social costs are great, as most victims are young and are major contributors to society through their work, family and organizational involvement.

In most developed countries there have been significant reductions in mortality and morbidity due to injury as a result of a systematic approach to trauma care. The majority of these reductions have resulted from prevention strategies, including seatbelt legislation, drink–driving legislation, improved road engineering, motor cycle and cycle helmet use, and road safety and workplace injury awareness campaigns. Changes in both trauma system configuration and individual patient management have brought about improvements in the survival rate of those who are seriously injured, although the impact has not been as great as that of injury prevention.

Civilian interest in injury morbidity and mortality was initially most evident in the USA because of the high incidence of urban violence and road trauma. Research into systems of trauma care began with epidemiological work by Trunkey and others examining trauma deaths,⁶ who developed the concept of a trimodal distribution of trauma deaths. Trunkey proposed that about 50% of deaths occurred within the first hour as a result of major blood vessel disruption or massive CNS/spinal cord injury. This could only be improved by prevention strategies. A second more important group (from the therapy perspective) accounted for about 30% of deaths and included patients with major truncal injury causing respiratory and circulatory compromise. The remaining 20% of patients were said to die much later from adult respiratory distress syndrome, multiple organ failure, sepsis and diffuse brain injury. Trunkey initially identified the second group as most likely to benefit from improvements in trauma system organization, and it is a tribute to the effectiveness of such schemes that the number of patients dying from avoidable factors within the first few hours of injury has generally declined. In some systems it is reported to be as low as 3%, but generally is probably nearer to 10–15%.^7,⁸ Improvements in trauma system provision have resulted in a redistribution of the three groups proposed by Trunkey, and it is now generally accepted that far fewer than 30% are included in the second group. In fact, more recent studies have shown that complications such as multiple organ failure (MOF) and acute respiratory distress syndrome (ARDS) have decreased to such an extent, with improved initial management, that in mature trauma systems even the third peak is now minimal, with the vast majority of deaths occurring in the first 1–2 hours from major head injury and massive organ disruption.³³

Trauma care systems have been developed to ensure a multidisciplinary approach and a continuum of care, from the roadside through hospital care to rehabilitation. Whereas initial work focused on the need for centres of expertise and trauma management, it is now accepted that the pre-hospital phase is of critical importance. Accurate triage of the patient to the closest most appropriate facility is essential. High-risk patients should be taken to a hospital capable of managing critically ill trauma patients.⁹ Table 3.1.1 lists some predictors of life-threatening injury. Using these as a triage tool without modification will result in significant over-triage: that is, many more patients with non-threatening injuries will be triaged. Over-triage is minimized if abnormal vital signs and overt major injury are used as the triage criteria. Sensitivity is still greater than 85%.¹⁰ If mechanism is used as a triage tool then documented high speed and prolonged extrication time appear to be the most significant factors.¹¹

Table 3.1.1 Major trauma victims at high risk of life-threatening injury

Vital signs	Mechanism
Glasgow Coma Score ≤13 or systolic blood pressure <90 or respiratory rate <10 or >29 Trauma score <14 Injury Penetrating injury to chest, abdomen, head, neck and groin Some significant injury to two or more body areas Severe injury to head/neck or trunk Two or more proximal long bone fractures Burns of >15% or face or airway	Evidence of high-speed impact Falls 6 m or mor Crash speed 60 kph or more 50 cm deformity of automobile Rearward displacement of front axle Passenger compartment intrusion 40 cm on patient side of car – 50 cm on opposite side of car Ejection of patient Rollover Death of same-car occupant Pedestrian hit at 30 kph or more Demographics Age <5 or >55 Known cardiac or respiratory disease (lower the threshold of severity resulting in trauma centre care)

Vital signs

Mechanism

Glasgow Coma Score ≤13 or systolic blood pressure <90 or respiratory rate <10 or >29

Trauma score <14

Injury

Penetrating injury to chest, abdomen, head, neck and groin

Some significant injury to two or more body areas

Severe injury to head/neck or trunk

Two or more proximal long bone fractures

Burns of >15% or face or airway

Evidence of high-speed impact

Falls 6 m or mor

Crash speed 60 kph or more 50 cm deformity of automobile

Rearward displacement of front axle

Passenger compartment intrusion 40 cm on patient side of car – 50 cm on opposite side of car

Ejection of patient

Rollover

Death of same-car occupant

Pedestrian hit at 30 kph or more

Demographics

Age <5 or >55

Known cardiac or respiratory disease (lower the threshold of severity resulting in trauma centre care)

Identifying weaknesses in such a system is always difficult because of the delay between cause and effect. Inappropriate management does not usually lead to immediate death: for example, a period of hypoxia may result in organ failure many hours later. Another difficulty is the relatively low incidence of death. Although this is of course to be welcomed, it does make statistical analysis more difficult when the ‘adverse event’ occurs uncommonly. Careful audit of the entire trauma process and accurate measurement of ‘input’ (i.e. injury severity) and ‘output’ (i.e. death or quality of survival) is essential if the process of trauma care is to be reviewed.

Initial management

Seamless integration with the pre-hospital personnel should ensure that the hospital is ‘on standby’ to receive the major trauma victim. The trauma team should be in attendance in the resuscitation area and the patient brought directly to a prepared bay, the layout of which is illustrated in Figure 3.1.1. The general approach is to perform a primary survey to secure the airway/cervical spine, breathing and circulation. This is followed by a brief assessment of disability (neurological) and complete exposure of the patient. Life-threatening problems are thus identified and managed immediately. This is followed by a secondary survey involving a head-to-toe examination.

Fig. 3.1.1 The layout of a typical trauma resuscitation bay.

(Reproduced with permission from Myers CT, Brown AF, Dunjey SJ, et al. Trauma teams: order from chaos. Emergency Medicine 1993; 5: 34.)

In most departments, parallel processing of the patient will occur simultaneously with management of ABCDE problems. The doctor and nurse team charged with protecting the airway immediately set about their task while the team leader obtains a brief history from the ambulance personnel and, if possible, the patient. The cervical spine is carefully controlled while the airway is being secured. The procedure doctor and the nurse team attend to intravenous access, blood tests, urinary catheter and other procedures. At this early stage of assessment and resuscitation the general philosophy should be to assume the worst and protect against all possible adverse events. Treatment is therefore designed to protect the patient against unforeseen consequences of the injury, rather than focusing on evident abnormalities. It is, however, important that this ‘better safe than sorry’ approach is not taken to extremes. Senior staff must be able to assess risk and avoid a situation where inexperienced personnel keep uninjured patients aggressively splinted for hours on end, so that the treatment itself becomes a cause of further injury.

The role of the various team members is shown in Table 3.1.2. In some facilities all these functions may have to be performed by one or two personnel, in which case a sequential rather than a parallel process will take place.

Table 3.1.2 Team roles

Airway

It should be assumed that hypoxia is present in all patients who have sustained multiple injuries. Early expert airway intervention is essential. Every patient should receive initial supplemental oxygen via a well-fitting face mask. This includes those few patients who might later be found to have chronic obstructive airways disease. Concerns regarding pre-existing dependence on hypoxic drive can be addressed once the initial trauma resuscitation has been completed.

If the airway is clear and protected, the neck should be immobilized with a semi-rigid collar, but if airway manoeuvres are necessary it is often better to use manual inline immobilization without a collar, ensuring minimal neck movement with constant vigilance. The management of an obstructed airway in a trauma patient should be undertaken by an experienced senior clinician with significant anaesthetic experience. The first priority is to clear the upper airway by direct visualization, suction, and removal of any foreign bodies. Insertion of an oropharyngeal or nasopharyngeal airway and the jaw thrust manoeuvre are usually successful in clearing an upper airway obstruction. Insertion of a nasopharyngeal airway can be hazardous in patients with a fracture of the cribriform plate. The direction of insertion (backwards not upwards) is important. Chin lift is not recommended because it may cause additional movement of the cervical spine.

Early endotracheal intubation should be undertaken if the patient is apnoeic, has an unrelieved upper airway obstruction, has persistent internal bleeding from facial injuries, has respiratory insufficiency due to chest or head injuries, or the potential for airway compromise (airway burns, facial instability, coma or seizures). Intubation may also be necessary for procedures such as CT scanning, or for the management of confused or disturbed patients.

The following course of action is recommended for the emergency intubation of the major trauma victim:

• Skilled personnel (anaesthetist or emergency physician with appropriate anaesthetic experience)

• A fully equipped resuscitation area (suction, oxygen, drugs, monitoring equipment)

Any operator undertaking emergency intubation of major trauma victims (MTVs) should be prepared for a difficult intubation. When there is a high risk of difficult intubation and there is sufficient time, other techniques may be used, such as fibreoptic intubation. These are not appropriate as first-line emergency techniques. If the cords cannot be visualized and the ETT inserted within 30 seconds (try holding your breath for 30 seconds), then bag/mask ventilation should be resumed. If ventilation is possible then there is no urgency; if ventilation is not possible, a second attempt at ETT insertion should be made. If this is unsuccessful then a surgical airway using a cricothyroidotomy should be created. A laryngeal mask airway may also be useful as a temporary measure. The intubating laryngeal mask has also proved useful. Gum-elastic bougie and fibreoptic techniques may be helpful for difficult airways.

Cricothyroidotomy is the surgical airway of choice in an emergency because it is a relatively easy technique compared to tracheostomy, can be performed in a matter of seconds, has a low complication rate in adults, and requires only a scalpel, forceps and ETT. A cricothyroidotomy using a large-bore needle may be used as a temporary measure, especially in children, but will not allow adequate ventilation in adults, as it results in CO₂ accumulation. A number of proprietary kits are available. It must be emphasized that a needle cricothyroidotomy does not protect the airway from aspiration.

Ventilation

Once the airway is secure the patient should be ventilated to optimize oxygenation and maintain normocapnia. There is evidence that severe hypocarbia (<32 mmHg) may be harmful to the cerebral circulation by causing cerebral vasoconstriction.^12,¹³ Conversely, hypercarbia will produce cerebral vasodilatation with a resultant increase in intracranial pressure (ICP). Although modest hypocarbia was advocated until relatively recently, it has been found that this does not confer any significant benefit. The objective should be to maintain normocarbia. Arterial blood gases should be monitored closely, but capnography should only be used as a guide as there are frequently gross discrepancies. Ventilatory rates should be approximately 10–14 breaths per minute, with a tidal volume of 10 mL/kg (lean mass).

Paralysing agents

Suxamethonium (1.5 mg/kg) is the drug of choice for intubation because of its fast onset, short duration and relative guarantee of complete relaxation. Because it is a depolarizing muscle relaxant it has the disadvantage of transiently increasing ICP and intraocular pressure. It will also cause release of potassium from damaged tissues (e.g. burns/crush injury), but this is not an issue in the first 24–48 hours of injury. Experimentally, it has been shown that the rise in ICP caused by suxamethonium is short-lived and not as significant as that caused by prolonged attempts at intubation and gagging. The rise in ICP can be lessened if adequate sedation (e.g. midazolam) is used.

The use of a non-depolarizing agent for intubation has never gained favour, mainly because of the slow onset. Newer agents such as rocuronium have a much faster onset (60 seconds), but are still not as good. For ongoing paralysis non-depolarizing agents such as cisatracurium are used.

Sedation

Sedation may be necessary in the MTV for the following reasons:

• Preparation for endotracheal intubation

• In the agitated patient

• In association with analgesics for pain relief.

A major risk with these agents is that in patients with hypovolaemia the loss of sympathetic drive and relaxation of vascular smooth muscle may result in sudden hypotension. Of the commonly used sedative drugs, thiopentone is the most likely to cause hypotension; however, if titrated (50 mg aliquots), it may be used successfully. It is effective in reducing ICP rises associated with intubation, and has a very short duration of action. Midazolam may cause hypotension even with small doses (0.5 mg), but it is also useful in reducing ICP. Fentanyl is not as effective in sedating the patient and reducing ICP, but may be used in relatively high doses (100–500 μg) without causing hypotension. Etomidate (0.2–0.3 mg/kg) is used in the USA and Asian centres such as Hong Kong because of the rapid onset, short duration and minimal haemodynamic effects. Ketamine should not be used in the head-injured patient because of its potential to cause a rise in ICP. It is very effective in producing a dissociative state in patients without neurotrauma, which may allow fracture manipulation and other procedures. Pain or discomfort (such as a distended bladder) may be expressed as agitation in the obtunded patient, and giving sedatives alone will increase the problem. It is therefore important to assess the cause of agitation/anxiety before treatment is given.

Circulation

Shock is a clinical syndrome in which the perfusion of vital organs is inadequate to maintain function. Blood loss is the major cause of shock in the MTV. Other less common causes of shock also need to be considered:

• Tension pneumothorax. This will cause rapid and severe disruption to the circulation.

• Cardiogenic shock. This may be pre-existing (e.g. AMI causing accident, drugs causing reduced cardiac compensation and hypovolaemia) or secondary to injury, i.e. myocardial contusion, valvular/septal injury or pericardial tamponade.

• Neurogenic shock. This results from loss of sympathetic tone. It may be caused by central brainstem injury and vasomotor instability, or spinal cord injury and interruption of descending sympathetic tracts. It is characterized by bradycardia, but this may also occur in profound hypovolaemic states (see below).

• Anaphylactic shock and septic shock may coexist with hypovolaemic shock.

Clinical presentation

The initial stages of hypovolaemia are difficult to detect. Although four stages of blood loss have been described, the distinction made on blood pressure and pulse is usually not clear cut. The cardiovascular response to simple haemorrhage is modified by the presence of tissue injury. Although most major trauma victims have a combination of both, it should be appreciated that those who present with pure blood loss (for example after a stab wound) will often have maintained their blood pressure but may have a bradycardia despite blood loss due to a vagal response. Tissue injury will result in a tachycardia. Hence a normal blood pressure and pulse may be found in patients who have lost a significant amount of blood through a mixture of tissue injury and major blood vessel disruption. Of course, once a very large amount of blood has been lost (30–40% of blood volume), the blood pressure and pulse will become abnormal. An intravenous infusion of even a relatively small amount of fluid to such a patient may bring the recordings back to normal despite persisting hypovolaemia. The picture is further complicated in older patients, and particularly in those who are receiving vasoactive drugs. The absolute values are less important than the trends.

Monitoring

All patients who have sustained an injury that could be associated with significant blood loss, however remote the possibility, must be carefully monitored. In the initial phase, measurement of the clinical parameters will give some information about vital organ perfusion. However, more invasive monitoring will be required if hypovolaemia is severe or sustained. Central venous pressure can be useful to detect changes in venous capacitance, and the response of the CVP to a fluid challenge may be a useful test. Blood pressure is most accurately measured by an indwelling arterial catheter. The acid–base status should be checked frequently.

Management

Venous access

It is essential to gain good venous access at the earliest phase in resuscitation. This is usually via two large-bore (>16 G) peripheral cannulae. In the absence of accessible arm veins, central venous access may be indicated. The recommended site (subclavian, jugular or femoral) depends on a number of factors. The subclavian vein is reliable in terms of patency, but the ease of access to the femoral vein is offset by its potential futility in major truncal haemorrhage. The internal jugular veins can be difficult to access in the immobilized trauma patient. Cut-downs of the saphenous veins and cubital fossa may also be used.

Fluids

Patients with class I and II haemorrhage, where there is no hypotension, can usually be managed without blood transfusion, unless there is ongoing blood loss. Initial treatment is with crystalloid. The Cochrane Collaboration has reviewed the choice of fluid in the trauma patient and favours the use of crystalloids over colloids.¹⁴^–¹⁶ Given that there have been reported adverse events associated with colloid infusion, there is growing consensus that crystalloids should be the fluid of first choice. Hypertonic crystalloid has also been suggested, but the available data are inconclusive and more research is required.¹⁷

For class III and IV haemorrhage, where there is hypotension and tachycardia, blood transfusion should commence immediately, initially using O-negative blood and changing to group-specific or cross-matched blood as it becomes available. There is no evidence that whole blood is superior to packed cells and replacement of clotting factors, unless the blood is fresh (less than 1–2 days old). The availability of fresh blood is extremely limited.

Filters

Micropore blood filters slow the transfusion and do not appear to reduce complications from blood transfusion in the MTV.

Hypothermia

This is common in MTVs because of exposure and the use of cold intravenous fluids. Crystalloid infusions are usually administered at room temperature, although some centres prewarm fluids in blanket cupboards and microwave ovens. It is important to monitor this, as temperatures can fluctuate wildly. Blood is stored at 4°C and it is important to warm it; however, traditional blood warmers are cumbersome and slow to set up unless this can be done in anticipation. The use of the more expensive rapid infusion blood warmers is justified in trauma reception centres. There is growing consensus that a mild degree of hypothermia is probably not harmful and may well be cerebroprotective. Rapid active rewarming may cause worse outcomes in the context of isolated severe head injury.¹⁸ However, hypothermia < 32°C will interfere with coagulation, reduce myocardial contractility and predispose to arrhythmias.

Coagulation factors

There is little evidence for the use of clotting factors if the total haemorrhagic loss is less than 5 L. In the clinical situation, where there is evidence of ongoing blood loss after the replacement of five to six units, clotting factors should be replaced, as a blood loss of twice this volume would be anticipated. Coagulopathy is frequently present on arrival and may be secondary to mediators released as a result of direct tissue injury. Worsening coagulopathy is usually dilutional, but pre-existing problems such as liver disease and warfarinization should be looked for. Platelets should also be given if more than 10 units of blood are transfused. Although controversial, it is reasonable to give four units of fresh frozen or freeze-dried plasma for every six units of blood transfused. The use of cryoprecipitate is also recommended if fibrinogen levels are low. Haematologists have traditionally asked for evidence of coagulopathy before issuing clotting factors; however, in a rapidly deteriorating MTV requiring massive transfusion there is little logic in waiting for a coagulation result that reflects the situation 30–60 minutes previously. The place of Factor rVIIa in massive haemorrhage following trauma is still uncertain. At this stage there is little evidence of improved outcomes, although preliminary trials suggest a reduction in blood loss.¹⁹ It should be seen as a potential rescue therapy after reversible factors such as surgical bleeding, hypothermia, acidosis and clotting factor replacement have been rectified.²⁰

MAST suit

Once popular, these devices are now very rarely used. A number of complications have been reported and, importantly, no therapeutic benefit has been demonstrated.²¹ There may be some value in applying the MAST suit to patients who have an unstable pelvic fracture associated with massive internal bleeding, but the advent of external fixators and specific pelvic binders that can be applied either pre-hospital or in the resuscitation area of the ED has largely removed this last indication.

Hypotensive resuscitation

In the last decade, increasing attention has been paid to the potential harm in overaggressive resuscitation of patients prior to definitive treatment of the cause of the bleeding. A number of studies have shown that in major trauma victims with penetrating injuries to the trunk, vigorous fluid resuscitation prior to operation actually results in a worse outcome.^22,²³ This concurs with vascular surgical protocols, where it is acknowledged that outcomes are improved by limiting fluid resuscitation prior to the repair of leaking aneurysms. Logically, if the blood pressure is higher, more blood loss will occur. Therefore, more dilution of clotting factors, increased usage of blood products for replacement, hypothermia, coagulopathy, ARDS, sepsis etc. will result. Conversely, if there is no perfusing pressure to vital organs then irreversible injury to those organs may occur.

The essential point in this debate is that the most important determinant of outcome in MTVs is the time to definitive surgery. There is certainly no point in delaying surgery ‘to normalize the intravascular volume’. The relevance of penetrating injury studies to blunt trauma is unclear. However, where there is a cause of bleeding that can be ligated, this should be done as soon as possible. This principle applies to bony injury (using fixation) as well as spleen, liver and other sources of bleeding. If there is no surgically remediable bleeding point, the physiological status should be returned to normal as soon as possible to prevent long-term complications from prolonged ischaemia to bowel and other organs.

Next steps

By this stage the trauma patient will have been received into a well-organized resuscitation area and the first life-saving procedures will have been initiated by an integrated and skilled team of doctors and nurses. Any immediately life-threatening conditions can be expected to have been identified and dealt with. Constant vigilance and reassessment are essential. Other occult injuries may be present in those patients identified with serious injuries.

While the trauma team leader continues to review the situation in the light of a constantly changing clinical scenario, and hopefully the provision of more biomechanical data from the site of the incident, he or she should also be beginning to consider the next steps. The first of these is the calling in of other experts. Whereas it will have been clear that an airway doctor will be an essential part of the initial resuscitation team, it may be some minutes before it is known which other skills are required. Usually orthopaedic surgeons and neurosurgeons are near the top of the list. General surgery is not required as often as is commonly supposed,²⁴ although general surgeons are often useful in coordinating ongoing care. Whichever specialty is required, the patient’s emergency problems demand experience, therefore, ‘if in doubt, refer’.

Radiographs are required at this stage. The initial films should be limited to those that will have a direct bearing on immediate management, including a chest AP view and a pelvis AP view.

Lateral X-ray of the cervical spine is no longer mandatory at this stage of assessment. Cervical immobilization is routine, and it is not possible to exclude cervical injury with a lateral cervical spine X-ray. Therefore, a cervical X-ray does not alter initial management. Its utility at this stage would be to confirm an irretrievable injury, i.e. craniocervical dislocation.

Ideally, the resuscitation room should have an integrated X-ray facility, but if this is not available portable films should be obtained. It is not appropriate to transfer a multiply injured unstable patient to a separate X-ray facility.

Other forms of imaging have become popular in localizing the source of haemorrhagic shock. The increasing availability of FAST (focused abdominal sonogram in trauma) has superseded diagnostic peritoneal lavage (DPL) as the bedside adjunct for detecting intraperitoneal haemorrhage. Subsequent chapters deal with individual trauma problems, but it is essential that throughout the patient’s stay in hospital a single clinician has overriding responsibility for his or her care. In the resuscitation area this is the ‘team leader’, who may be from any discipline. Handover to the clinician responsible for ongoing care must be comprehensive, timed, and well documented.

Trauma audit

Trauma kills people in a variety of ways, hence no one department in a hospital will see a large number of deaths. Many trauma victims die before they reach hospital, some in the ED, and others scattered through the inpatient specialties and in intensive care. Hence from any one clinician’s perspective, trauma is not an outstanding problem. However, when looked at from a public health perspective it is clearly a major issue, not least because some of the deaths are avoidable. Identifying these, and the much more difficult-to-define group of patients who survive but whose outcome is not as good as expected, is a major problem.

The most important variables to measure are the extent of the anatomical injury, the degree of physiological derangement that results, age, and the previous wellbeing of the patient. All these have a direct effect on outcome, and must therefore be measured before any comment can be made about the process of care. Outcome itself must also of course be measured. This is relatively easy in terms of mortality: the general accepted definition is death within 31 days of the incident. However, disability is a much more difficult issue, and currently there are no universally accepted measurement tools. The functional independence measure used in MTOS,²⁵ the Glasgow Outcome Scale,²⁶ GOSE²⁷ and the SF36²⁸ (Short Form – 36 Questions) are the best available tools. As 90% of MTVs survive their injury in a mature trauma system, it is important to measure disability and quality of life following major trauma when comparing outcomes.²⁹

Trauma audit was first formalized by Champion at the Washington Hospital Centre in the 1970s. The TRISS ³⁰ system is now widely used, but there have been many proposals for its modification.

Most current trauma systems are now audited using some variation of the TRISS methodology. This combines measurement of anatomical injury using the Abbreviated Injury Scale and the Injury Severity Score, together with the Revised Trauma Score to measure physiological derangement, with an adjustment made for age. A probability of survival can be calculated by reference to large databanks with known outcomes that contain a range of these scores. Perhaps more importantly, the comparative performance of hospitals, or the change in a single hospital’s performance over time, can be determined by bringing together the probability of survival of a number of patients and comparing them with the actual survival. Anonymous league tables can then be developed with the objective of identifying features of the best hospitals associated with high survival rates (and vice versa).

Trauma in developing countries

On an international scale, trauma has become a major issue. According to the World Health Organization, by 2020 road trauma will rank third on the list of lives lost to death and disability.¹ That is, after cardiovascular disease and mental illness, road trauma causes the greatest loss of life when using the scale of DALYs (Disability-Adjusted Life Years).^3,⁴

Globally, national governments are beginning to recognize the burgeoning human and economic cost of trauma, particularly road trauma. The public health achievements of the developed countries (seatbelts, helmets, alcohol and speed restrictions) are being implemented,^3,^4,³¹ and similarly, governments of developing countries are looking to implement trauma systems.^31,³²

Research in developing countries reinforces the benefits of trauma systems previously described in countries with established EMS systems. For example, evidence indicates that people with life-threatening but potentially treatable injuries are up to six times more likely to die in a country with no organized trauma system than in one with an organized, resourced trauma system.³² Trauma system development requires trauma outcome measurement. As such, developing countries are likely to adopt trauma registries over the next several decades, in an attempt to track the burden of trauma and the impact of system-wide interventions.

As developing countries embark upon trauma system development, it is becoming increasingly important to access standardized trauma care education through intensive short-courses. Advanced Trauma Life Support (ATLS) has been widely used. Other courses (such as Primary Trauma Care (PTC)) have also become popular in the developing world. Such courses are often less expensive and more flexible than ATLS.

Controversies

• The number of MTVs necessary for a hospital to maintain high-quality trauma care.

• The degree to which potential MTVs should be over-triaged to ensure that patients with major trauma are received at major trauma centres. There may be a greater risk in bypassing hospitals to take patients to a trauma centre, depending on distance and injury type. There is also the issue of deskilling of personnel from non-trauma centres, and what effect this has on overall system outcomes.

• The degree to which MTVs should be managed by protocol rather than clinical judgement. Clinicians are increasingly being asked to follow protocols in these critical situations. This prevents some adverse outcomes but may cause over-investigation and treatment.

• The role of hypotensive resuscitation in blunt trauma has not been defined. Where victims have prolonged delays to theatre, or the bleeding is not surgically correctable, then hypotensive resuscitation may cause more complications.

• The role of controlled hypothermia in head-injured patients.

References

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28 Garratt AM, Ruta DA, Abdulher MI. The SF36 Health Survey Questionnaire: an outcome measure suitable for routine use within the NHS. British Medical Journal. 1993;306:1440-1444.

29 Willis CD, Gabbe BJ, Cameron PA. Measuring quality in trauma care. Injury. 2007;38:527-537.

30 Boyd CR, Tolson MA, Copes WS. Evaluating trauma care. The TRISS method. Journal of Trauma. 1987;27:370-378.

31 Fitzgerald M, Dewan Y, O’Reilly G. India and the management of road crashes – towards a national trauma system. Indian Journal of Surgery. 2006;68:237-243.

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Introduction

Neurotrauma is a common feature in the presentation of multisystem trauma, particularly when associated with motor vehicle accidents and falls. Over 50% of trauma deaths are associated with head injury. The implications for the health system are enormous, with an annual rate of admission to hospital wards associated with head trauma approaching 300 per 100 000 population,¹ and twice this in the elderly.² The long-term sequelae of moderate and severe neurotrauma are a major health resource drain, and the morbidities associated with mild brain injury are becoming clearer.

Advances in preventative strategies, trauma systems, resuscitative therapies and rehabilitation management have improved outcomes. However, neurotrauma remains a serious health issue, predominantly affecting the productive youth of society.

Pathogenesis

Primary brain injury occurs as a result of the forces and disruptive mechanics of the original incident: this can only be avoided through preventative measures, such as the use of bicycle helmets.

Secondary brain injury is due to a complex interaction of factors and typically occurs within 2–24 hours of injury.³ A principal mechanism of secondary injury is cerebral hypoxia due to impaired oxygenation or impaired cerebral blood flow. Cerebral blood flow is dependent on cerebral perfusion pressure (CPP), mean arterial systemic blood pressure (MAP) and intracranial pressure (ICP).

Intracranial pressure may be raised as a result of the mass effect of the haemorrhage, or by generalized cerebral oedema. Cerebral vasospasm further reduces cerebral blood flow in patients in whom significant subarachnoid haemorrhage has occurred.

Cellular dysfunction is a result of both primary and secondary mechanisms and involves sodium, calcium, magnesium and potassium shifts across the cell membrane, the development of oxygen free radicals, lipid peroxidation and glutamate hyperactivity. Excessive release of excitatory neurotransmitters and magnesium depletion also occur.⁴

Classification of primary injury in neurotrauma

Primary injuries are classified as:

• Skull fracture

• Concussion

• Contusion

• Intracranial haematoma

• Diffuse axonal injury

• Penetrating injury.

Skull fracture

The significance of skull fracture is not related to the specific bony injury but rather the associated neurotrauma. Fractures in the region of the middle meningeal artery in particular may be associated with acute extradural haemorrhage. Fractures involving the skull base and cribriform plate may be associated with CSF leak and the risk of secondary infection. Depressed skull fractures may compress underlying structures, cause secondary brain injury and require surgical elevation. Injury to underlying structures may result in secondary epilepsy.

Concussion

Concussion is a transient alteration in cerebral function, usually associated with loss of consciousness and often followed by rapid and complete recovery. The proposed mechanism is a disturbance in the function of the reticular activating system. Post-concussive syndromes, including headache and mild cognitive disturbance, are not uncommon.^5,⁶ Symptoms, particularly headache, are usually short-lived but may persist. ‘Second-impact syndrome’ describes a greater risk of significant reinjury following an initial injury causing a simple concussion. It is likely to be due to diffuse cerebral swelling.⁷ In animal models concussion may be associated with modest short-term increases in intracranial pressure and disturbances in cerebral cellular function.⁸

Contusion

Cerebral contusion is bruising of the brain substance associated with head trauma. The most common mechanism is blunt trauma. Forces involved are less than those required to cause major shearing injuries, and often occur in the absence of skull fracture. Morbidity is related to the size and site of the contusion, and coexistent injury. Larger contusions may be associated with haematoma formation, secondary oedema or seizure activity. The most common sites for contusions are the frontal and temporal lobes.⁹

Intracranial haematoma

Diffuse axonal injury

Diffuse axonal injury (DAI) is the predominant mechanism of injury in neurotrauma, occurring in up to 50% of patients.¹¹ Shearing and rotational forces on the axonal network may result in major structural and functional disturbance at a microscopic level. Disturbance to important communicative pathways sometimes results in significant long-term morbidity, despite non-specific or minimal changes on CT scanning. The exact pathogenesis of diffuse axonal injury is incompletely understood. Specific injury in the regions of the corpus callosum and midbrain has been proposed; however, DAI is believed to be the mechanism for persistent neurological deficits seen in head-traumatized individuals with normal CT scans.¹²

Penetrating injury

Penetrating neurotrauma is characterized by high levels of morbidity and mortality. This is especially true of gunshot wounds. Exposure of cerebral tissue through large compound wounds, or through basilar skull structures, is associated with a dismal outlook. Penetrating injury in the periorbital and pernasal regions is associated with high risk of infection.

Epidemiology

Neurotrauma is commonest in the young and the old: under 5 and over 80 years of age. In young children the majority of injuries are, fortunately, mild (although a significant proportion are the result of non-accidental injury). It is the leading cause of trauma deaths in under 25s.¹³

Common causes include motor vehicle accidents (including vehicle versus pedestrian and bicycle collisions), falls, assault and firearms. In young males, alcohol is often involved.

Prevention

Primary prevention of neurotrauma depends on the cause. Most preventative strategies are directed at vehicular traffic, and include speed-calming measures, in-car safety devices, and bicycle helmets. Improving roadside lighting and enhancing pedestrian visibility contribute to reduction of injury in this group.

Prevention of secondary injury involves maintenance of cerebral perfusion and oxygenation, and is addressed under clinical management.

Clinical features

Definition

Neurotrauma may be classified according to severity as minimal, mild, moderate or severe (Table 3.2.1).¹⁴ Such a classification allows for directed investigation and management, but there is clearly a continuum of injury within the spectrum of neurotrauma.

Table 3.2.1 Neurotrauma severity

Minimal
No loss of consciousness, and Glasgow Coma Score (GCS) 15, and Normal alertness and memory, and No neurological deficit, and No palpable depressed fracture or other sign of skull fracture

Mild
Brief (<5 minutes) loss of consciousness, or Amnesia for event, or GCS 14, or Impaired alertness or memory No palpable depressed fracture or other sign of skull fracture

Moderate or potentially severe
Prolonged (>5 minutes) loss of consciousness, or Persistent GCS <14, or Focal neurological deficit, or Post-traumatic seizure, or Intracranial lesion on CT scan, or Palpable depressed skull fracture

History

A detailed history of the mechanics of the trauma is essential. This should be followed by consideration of time courses, pre-hospital care, pre-sedative and pre-relaxant neuromuscular function, and episodes and duration of hypotension or other decompensation. A history of previous health problems, allergies, medications and social setting is desirable.

Primary survey

As with all trauma patients, the initial assessment and therapy must be directed at maintenance of airway, ventilation and circulatory adequacy along standard ATLS principles. Early assessment of neurological disturbance is important: the use of the formal Glasgow Coma Score (GCS) can be difficult in the primary survey, and this assessment may be reliably undertaken with the AVPU scale (Alert: GCS 14–15; response to Verbal stimuli: GCS 9–13; response to Painful stimuli: GCS 6–8; or Unresponsive: GCS 3–5). Simultaneous protection of the cervical spine by immobilization is fundamental. This management should commence in the pre-hospital setting and the level of care be maintained.

Inline stabilization of the cervical spine during rapid-sequence induction and orotracheal intubation is the preferred method for gaining definitive airway control in the head-injured patient.

The greatest risks to the patient with a moderate to severe head injury are hypoxic injury and deficient cerebral perfusion due to systemic hypotension.

Secondary survey

A full secondary survey, including log-roll, should follow.

Clinical assessment of the neurological status of head-injured patients commences with formal documentation of the GCS (Table 3.2.2). The maximum score is 15 and the minimum 3. The GCS has been incorporated into other assessment scales in trauma (Trauma Score, Revised Trauma Score) and in TRISS estimation of probability of survival.

Table 3.2.2 Glasgow coma score

Best motor response
Obeys command	6
Localizes to pain	5
Withdraw to pain	4
Abnormal flexion to pain	3
Abnormal extension to pain	2
Nil	1
Best verbal response
Oriented	5
Confused	4
Uses inappropriate words	3
Incomprehensible sounds	2
Nil	1
Eye opening
Spontaneously	4
To verbal command	3
To pain	2
Nil	1