Prehospital management of severe traumatic brain injury

What is the pathophysiology of severe traumatic brain injury?

Severe traumatic brain injury is defined as a head injury resulting in a Glasgow coma score of less than 9.4 Primary brain injuries that can occur at the time of impact include extradural and subdural haematomata, intracerebral contusions, and diffuse axonal injuries. Additional insults such as hypoxaemia, hypotension, or hyperpyrexia result in further cerebral damage and secondary brain injury. Modern management of head injuries focus on the identification and treatment of such potential secondary insults.

What are the priorities in prehospital management of severe traumatic brain injury?

Time from injury to definitive neurosurgical care can affect outcome for patients with severe traumatic brain injury. Patients with mass lesions have a better outcome if they receive neurosurgical treatment within four hours of injury.5 Rapid patient transfer to an appropriate secondary care facility is essential, in addition to the implementation of measures to prevent secondary brain injury. Epidemiological studies show that a third of patients with severe traumatic brain injury already have a documented secondary brain insult on hospital admission.^w1 Prehospital management of these patients focuses on provision of an adequate airway, effective oxygenation and ventilation, maintenance of an adequate cerebral perfusion pressure and avoidance of further increases in intracranial pressure. Two retrospective reviews found improved outcomes in patients with severe head injuries when these parameters were specifically targeted in the prehospital setting.^{w2 w3} Box 1 lists problems that may be encountered during extrication of the patient from a vehicle (figure⇓).

Scene from a road traffic collision demonstrating multiple difficulties encountered during extrication

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What are the options for airway management?

Airway compromise is common after severe traumatic brain injury and has an important contribution to the development of secondary brain injury. Basic airway adjuncts are used initially and high flow oxygen is administered. Controlled trials of simulated prehospital scenarios6 have shown that laryngeal mask airways have a greater success rate for establishing an airway than endotracheal intubation, particularly with inexperienced clinicians. Laryngeal mask airways are becoming increasingly popular in prehospital care for airway maintenance, particularly in situations where access to the patient is limited. The devices are easy to insert, usually provide a good seal within the oropharynx, and provide airway protection from upper airway secretions. Regurgitation and aspiration of gastric contents remains a risk, but may be reduced with the use of alternative laryngeal masks such as LMA Pro-Seal.

Endotracheal intubation is inevitably required in almost all patients with severe traumatic brain injury, although evidence for its benefit in the prehospital environment is controversial. Most studies are retrospective and study paramedics performing endotracheal intubation with minimal use of sedative agents and muscle relaxants. Several large retrospective reviews have, however, shown that this approach results in a high risk of complications, such as failed intubation and hypoxaemia.7 8 Laryngoscopy without the use of anaesthetic agents is particularly damaging in patients with traumatic brain injury because increases in intracranial pressure are not attenuated; this may explain the association between prehospital endotracheal intubation and increased mortality and poor neurological outcome in patients with severe traumatic brain injury, which was reported in two retrospective analyses of trauma registries.9 10

Data about true rapid sequence induction of anaesthesia performed by physicians are more promising. A recent retrospective analysis of prehospital rapid sequence induction procedures in the UKreported low incidences of complications, 11 and similar studies have reported intubation success rates of 94-97%, in addition to low complication rates for prehospital drug assisted intubation.^w4 These data suggest that prehospital rapid sequence induction is beneficial if done by an appropriately trained physician; this finding is in line with recommendations from the recent trauma report from the national enquiry into patient outcome and death (box 2). With few doctors present at the scene of emergency situations, only a few patients with severe traumatic brain injury are intubated before hospital transfer in the UK, although at least half of all these patients need intubation within 30 minutes of arrival at the hospital.3 A few patients, for example, those with severe facial trauma, may however require a primary surgical airway.

Which anaesthetic agents should be used to facilitate intubation?

Administering anaesthetic and neuromuscular blocking drugs to facilitate intubation leads to improved outcomes in patients with head injuries.12 Ideal agents should have minimal effects on heart rate and blood pressure and reduce intracranial pressure while maintaining cerebral perfusion. Etomidate results in a low incidence of hypotension when used to facilitate intubation in patients with head injury and is perhaps the most widely used drug despite concerns about inhibition of steroid synthesis after a single dose.13 ^w5 Ketamine has usually been avoided in patients with head injuries, but a review of randomised clinical trials concluded that with controlled normocapnic ventilation, ketamine has minimal or favourable effects on intracranial pressure in sedated patients with head injury.14 Ketamine has also been associated with maintenance of better cerebral perfusion pressure compared with other sedative agents.^w6 After intubation, adequate sedation and neuromuscular blockade must be provided for all patients during transfer to avoid rises in intracranial pressure associated with coughing.

How should patients with severe traumatic brain injury be ventilated?

Hypoxaemia is common after severe traumatic brain injury and prospective studies show an association with increased mortality rate and poorer neurological outcome.^w7 Hypoxaemia is usually multifactorial in patients with such injury and the presence of serious chest injuries—for example, haemopneumothorax or pulmonary contusions—needs to be considered. Hypercapnia is a common consequence of respiratory depression leading to cerebral vasodilatation, increased cerebral blood flow, and a rise in intracranial pressure. One argument in favour of performing rapid sequence induction before transfer to hospital is that this approach allows carbon dioxide levels to be controlled. Hyperventilation leads to cerebral vasoconstriction and ischaemia and should be avoided in patients with head injuries. A large retrospective review reported that 18% of head injured patients were hypocapnic after prehospital intubation with a worse outcome in the group that had a PaCO₂ of less than 4 KPa on admission to the emergency department.15 A well conducted prospective randomised study showed that monitoring end-tidal carbon dioxide reduced the incidence of hyperventilation by more than 50%.16 End tidal monitoring of carbon dioxide is now considered a routine standard of monitoring for all mechanically ventilated patients during transfer.17 Box 3 describes additional monitoring standards.

How should circulatory complications be managed?

Patients with severe traumatic brain injury who are hypotensive have a doubled risk of mortality compared with normotensive patients.3 Hypotension results in reduced cerebral perfusion and neuronal ischaemia and is often multifactorial in origin in trauma patients. It is best to assume that hypotension is due to hypovolaemia until proven otherwise. Cerebral perfusion pressure (CPP) is calculated by subtracting intracranial pressure from the mean arterial pressure. Maintaining a CPP of 60-70 mm Hg is an essential foundation of hospital management of severe traumatic brain injury. However, measuring an accurate mean arterial pressure is difficult in the prehospital environment so most guidelines use the systolic value as a target during the resuscitation phase.

The Brain Trauma Foundation recommends a minimum systolic pressure of 90 mm Hg in adults with severe head injuries.4 This target is based on prospectively collected large datasets showing that a systolic blood pressure of less than 90 mm Hg is an independent risk factor for mortality after severe traumatic brain injury.19 No studies have been done to assess the effects of aiming for values higher than 90 mm Hg, although this approach is probably desirable in patients with isolated severe traumatic brain injury. In patients with multiple injuries and hypovolaemia a conflict exists between “permissive hypotension” resuscitative strategies to minimise blood loss and the need to maintain an adequate cerebral perfusion pressure to prevent secondary brain injury. The ideal resuscitation fluid is unknown for patients with severe traumatic brain injury. A well conducted large multicentre randomised controlled trial found a relative risk of death of 1.8 in patients with such injuries in intensive care who were resuscitated with albumin compared with 0.9% saline.20 This finding has led guidelines to recommend use of small boluses of isotonic crystalloid to correct hypotension in patients with severe traumatic brain injury.18 Hypertonic crystalloid solutions may have a future clinical role in this subgroup. A meta-analysis of randomised, double-blinded controlled trials,21 found improved survival rates in patients with head injury who were resuscitated with hypertonic saline and dextran solutions compared with those who received standard care. Currently the use of hypertonic solutions is not widespread in prehospital care in the UK.

What treatments can be used to reduce intracranial pressure?

Intracranial pressure is often raised in patients with severe traumatic brain injury and specific treatment should be given to lower it if clinical signs are present (for example, pupillary dilatation) and if transfer time allows. Hypoxaemia, hypotension, hypercapnia, and inadequate sedation (in an intubated patient) should all be addressed before specific treatment. Little data is available about strategies to reduce intracranial pressure in the prehospital environment. A recent Cochrane review reported a relative risk of death of 0.8 when mannitol was used to reduce intracranial pressure compared with standard care in hospital, but it concluded that there was insufficient data to support prehospital administration of the drug.22 Hypertonic saline can be used as an alternative to mannitol; studies directly comparing the drugs’ capacity to lower intracranial pressure have yielded conflicting results. A large randomised prehospital trial of hypertonic saline in traumatic brain injury is about to begin recruiting.

What is the role of corticosteroids in patients with severe traumatic brain injury?

Owing to the findings of a large randomised controlled trial published in 2004, which showed a significant increase in the risk of death in patients randomised to receive corticosteroids, routine use of corticosteroids is no longer recommended for patients with head injury.23

How should patients with severe traumatic brain injury be immobilised?

The presence of a head injury is the strongest independent risk factor for injury of the cervical spine. In patients with severe traumatic brain injury, an assumption of spinal injury should be made and full spinal immobilisation should be implemented as early as practically possible in the field. Early assessment of the cervical spine should be done after transfer to hospital to avoid the risk of intracranial hypertension associated with hard cervical collars.^w8 In sedated and paralysed patients the use of sandbags and tape may achieve better immobilisation than rigid cervical collar.

Is hypothermia beneficial?

There is little doubt that hyperpyrexia is detrimental to outcome after severe traumatic brain injury, but the role of induced hypothermia in severe head injury is unclear. Early randomised controlled trials showed benefits in outcome for hypothermia as a treatment for refractory intracranial hypertension in patients with severe traumatic brain injury, but subsequent meta analyses have not confirmed this benefit.24 One randomised trial^w9 showed improved neurological outcome at six months in younger patients (younger than age 45 years) who arrived at hospital with a low body temperature, which was then maintained, suggesting that patients with severe traumatic brain injury who are cold should not be actively rewarmed. This observation must be considered in relation to the fact that hypothermia is a key factor in the development of traumatic coagulopathy in patients with multiple injuries.

Should patients with traumatic brain injury be transferred directly to a neurosurgical centre?

A recent retrospective analysis showed a reduction in mortality in patients with head injuries managed in neurosurgical centres and concluded that all patients with severe traumatic brain injury should be managed in such centres (box 4).25 Although this review was large, it only included data from about two thirds of institutions in the UK and may have been subjected to a triage bias because patients with very severe injuries are not usually accepted for treatment in neurosurgical centres. Currently, in the UK, neurointensive care beds are insufficient to manage all patients with severe traumatic brain injury and so a substantial proportion will still be treated in non-specialist centres. The presence of other injuries to the patient, mode of transport and proximity to institutions should all be considered when deciding which secondary care facility is appropriate.

Conclusion

Severe traumatic brain injury is common and often results in a poor neurological outcome. Outcomes can be improved if patients receive definitive treatment for their head injury as soon as possible after injury, preferably in a neurosurgical centre. Hypoxaemia and hypotension are common in these patients and together result in a mortality rate of more than 75%.3 Careful identification and treatment of these factors can reduce the development of secondary brain injury.