• Primary brain injury occurs at the time of injury. Prevention strategies include the wearing of motorcycle and cycle helmets, the use of vehicle restraint systems (e.g. seat belts and airbags) and public education.

• Secondary brain injury occurs following the primary event as a result of hypoxia, hypercarbia or hypoperfusion.

• A reduced level of consciousness may lead to airway obstruction or inadequate ventilation, resulting in poor oxygenation, carbon dioxide retention and acidosis.

• Impact brain apnoea is an immediate transient cessation of breathing following a head injury, often without significant anatomical insult. The sudden mechanical force exerted on the head can cause autonomical dysfunction, resulting in neurogenic shock characterised by a period of apnea. Hypoxia is the leading cause of mortality in these patients, and priority should be given to airway and breathing.

• Blood loss from other injuries in a patient with multisystem trauma may lead to hypovolaemia, hence a fall in mean arterial pressure (MAP) and consequently cerebral perfusion pressure (CPP).

• All patients should have an initial A‒E assessment, including assessment of:

• GCS

• pupils (size and reactivity)

• focal peripheral neurology (see below).

• Consider full cervical spine immobilisation for patients who have sustained a head injury, where appropriate

Glasgow Coma Scale

• In all communications, documentation and handovers, the individual components of the GCS should be given as well as the total GCS score.

• In some patients (for example, patients with dementia, underlying chronic neurological disorders or learning disabilities), the pre-injury baseline GCS may be less than 15. Establish this where possible and take it into account during assessment.

• Blood glucose level must be checked as part of initial assessment, as alteration in behaviour or conscious level may be attributed to this.

• History-taking must include assessment of medications (i.e. anticoagulants, antiplatelets) and other factors that either place the patient at higher risk of serious underlying injury or may suggest that the patient cannot be safely discharged at the scene.

Focal Neurological Deficit

• Focal neurological deficit covers problems restricted to a particular part of the body or a particular activity, for example difficulties with understanding, speaking, reading or writing; decreased sensation; loss of balance; general weakness; visual changes; abnormal reflexes; and problems walking.

Basal Skull fracture or Open fractures

• Signs of basal skull fracture include CSF clear fluid running from the ears or nose (late sign), bilateral peri-orbital haematoma (panda eyes), or mastoid bruising behind the ear (late sign). Signs of open head injury include a visible fracture of the skull through a scalp laceration or a penetrating foreign body to the scalp.

Airway with Cervical Spine Control

• It is well recognised that airway obstruction and aspiration are significant and often preventable causes of death in patients with severe traumatic brain injury (TBI). Basic airway manoeuvres are essential to prevent primary airway obstruction and associated brain hypoxia. 

• Once standard immobilisation has been achieved, with the head and body secured, consideration should be given to loosening or removing the collar.

• Patients with a severe head injury (GCS 8 or less) or those patients who are unable to maintain their own airway will benefit from advanced airway management and ventilation strategies to reduce secondary brain injury. Consideration should be given to whether an appropriately skilled and trained clinician is available to provide pre-hospital emergency anaesthesia at scene, or with a rendezvous en route to hospital, or whether immediate transfer should take place to hospital. The distance and journey time from an appropriate receiving unit should be considered in line with local procedures and pathways. Diverting to a trauma unit should only be for immediate airway compromise that cannot be managed in the pre-hospital setting.

Breathing and Ventilation

• Adequate ventilation is essential to the management of TBI through the avoidance of hypoxia and maintenance of ‘normocapnia’. Current evidence suggests that oxygen should initially be administered at 10–15 l/min via a non-rebreathing mask, with a target saturation of 94–98%.

• Evidence also demonstrates that those patients who remain normocapnic (4.6 and 6.0 kPa) following a TBI have significantly better outcomes. Hyperventilation reduces arterial carbon dioxide concentrations, and leads to a consequent vasoconstriction within the cerebral vasculature, worsening both cerebral hypoxia and oedema. Hypercapnia, associated with hypoventilation, increases the vasodilatation of the cerebral blood vessels, which increases intracranial volumes and therefore ICP.

Circulation

• It has been estimated that between 8 and 13% of patients with severe traumatic head injuries are hypotensive either at the scene of the injury or in the ED. In addition, a wealth of evidence demonstrates a strong correlation between hypotension and poor outcome in TBI, with some highlighting that a single episode of hypotension (SBP < 90 mmHg) is independently linked to a double increase in mortality rate.

• Haemorrhage control (especially from the highly vascular scalp) should be established early to avoid the unnecessary consumption of coagulation products, and where hypotension is identified intravenous fluid resuscitation should be commenced. Unfortunately, there still remains a lack of clear research evidence to demonstrate the most appropriate fluid for resuscitation in TBI when blood products are unavailable, and in most cases it will be dictated by local service interpretations and current formulary restrictions.

• Patients with significant head injury, hypotension and evidence of other blunt injury should have intravenous fluids titrated to maintain a palpable radial pulse OR systolic BP of >90 mmHg. Patients with significant head injury, hypotension and evidence of penetrating injury to the torso should have intravenous fluids titrated to maintain a good volume central pulse OR systolic BP >60 mmHg. In patients with evidence of severe TBI but with no other objective signs of injury (i.e. apparent isolated head injury), the therapeutic goal should be to maintain a systolic BP of 110 mmHg.

• Patients with isolated head injury can present with cardiovascular instability due to neurogenic shock. Clinicians should be mindful of this and should have intravenous fluids titrated to maintain a palpable radial pulse OR systolic BP of >110mmHg.

• NICE Head Injury guidance recommends Tranexamic acid (TXA) is administered as soon as possible to patients of all ages with a GCS of 12 or less. TXA is received on average 62 minutes earlier if given in the pre-hospital setting, highlighting the importance of pre-hospital administration.

Disability

• The patient’s GCS should be calculated, as this can be an important prognostic indicator and is useful for monitoring injury progression over time.

• Pupils should be examined for size, reaction and whether they are equal.

• Acute cerebral herniation, often referred to as ‘coning’, represents a serious neurosurgical emergency. Clinicians should be vigilant for the following clinical signs in a patient with reduced GCS:

• Hypertension

• Bradycardia

• Unilateral or bilateral pupil dilatation, non-reactive to light.

• Patients demonstrating signs of cerebral herniation require TIME-CRITICAL transfer to a neurosurgical centre. Management of cerebral herniation in the pre-hospital setting is challenging. Clinicians should ensure that they are taking all reasonable steps to manage oxygenation, ventilation and circulation/perfusion. Osmotic diuretic fluid therapy (using hypertonic saline) should be considered as a temporising measure in accordance with locally agreed clinical guidelines, and clinicians should consider seeking senior clinical advice and support.

Exposure/Environment/Extricate

• There is a high incidence of associated injuries found in patients with TBI, and an attempt to identify these during the secondary survey should be made, while remaining aware of the severe impacts of prolonged scene delays.

• Time on scene should be kept to a minimum.

Pain and Agitation

• Agitation in TBI has a number of potential causes. One commonly overlooked cause of agitation in patients with a TBI is pain, either from the head injury itself or from associated injuries sustained at the time of the TBI. Managing pain in TBI poses a challenge for the pre-hospital clinician; a patient in pain will be agitated and more difficult to manage, and may place themselves at risk of further cerebral hypoxia.

• Clinicians might consider requesting more senior assistance for patients whose TBI is complicated by agitation associated with acute pain. Midazolam can be considered as an adjunct to help settle an agitated patient

Evacuation Considerations

• The underlying principles of effective pre-hospital management of TBI are rapid assessment; swift and appropriate management; and timely transportation to a receiving centre with sufficient expertise to manage the patient. This will be dependent upon local resources and operational plans for those sustaining significant trauma, but clinicians should consider the most appropriate mode of evacuation early in the incident, to reduce on-scene time as much as possible.

• Helicopter emergency medical services (HEMS) may be able to facilitate more rapid transfer and evacuation but the decision to wait for HEMS arrival should be a balanced decision based on journey time to receiving unit and the need for additional transfer to HEMS at both incident and hospital end.

• A pre-alert call and a detailed clinical handover using ATMIST to the receiving unit is imperative for all patients with a significant TBI.

Patients with TBI can pose a challenge for management in the pre-hospital setting, and any associated hypoxia, hypercapnia and intracranial hypertension can contribute significantly to a poorer prognosis. Although not robust, the evidence suggests that the therapeutic benefits of midazolam for these patients can include amnesia, anxiolysis and, most critically, an ability to effectively provide oxygenation and ventilation, which may help reduce the detrimental secondary brain injury they incur. However, sedating agents will reduce systemic blood pressure, leading to a decrease in CPP, in addition to further jeopardising the patient’s airway. Therefore, the decision to use midazolam to facilitate safe patient management needs to be carefully considered. Such interventions should only be undertaken after additional training and confirmation of ability to deal with the complications of midazolam use. Remember – Midazolam is a sedating agent with an unpredictable dose response relationship in a head-injured patient and may cause a patient to rapidly become deeply sedated requiring immediate enhanced care intervention. Any practitioner considering the use of midazolam in head injuries should be specifically trained in and capable of undertaking the additional interventions required or consideration should be given to calling enhanced critical care.