Primary damage to the brain occurs at the time of injury. Secondary damage is the result of extracranial factors such as hypoxia or hypovolaemia, which lead to impaired cerebral oxygen delivery. Reperfusion of damaged brain (with the release of oxygen free radicals and lipid peroxidation) is now recognised as an additional secondary factor that can compli­cate recovery from traumatic brain injury. The problems that cause secondary damage can be minimised by systemic resuscitation. In the future, intracra­nial factors may be amenable to pharmacological interventions.

A decreased level of consciousness indicates that something is wrong with the brain or its fuel supply. It may be injury or:

• hypoxia or shock
  
• hypoglycaemia
  
• hypothermia
  
• poisoning or gross metabolic disturbance (including CO₂ narcosis)
  
• intracranial pathology (bleeding, thrombosis, em­­bolism, infection, swelling, tumour, fitting).

Biomechanics and Brain Injury

Direct trauma

may cause:

1–5 may not be associated with loss of consciousness.

Sudden acceleration/deceleration

causes shearing injury to the brain and diffuse axonal injury (DAI). This is associated with loss of consciousness but external evidence of head injury may be lacking. DAI is more common with the longer deceleration time characteristic of restrained passengers in traffic crashes. Extradural haemorrhage is more common in falls.

Cervical spine injury

is more likely to be associated with a brain injury if the mobile head hits a fixed object (deceleration/acceleration), than if a mobile object hits the fixed head (assault).

THE PATIENT WITH A DEPRESSED LEVEL OF CONSCIOUSNESS

This section deals with the management of those patients who when first seen have a Glasgow Coma Scale (GCS) score <15 (→ Table 3.1). Serious brain injury must be suspected. The principal objective of emergency management is to limit the effects of this primary insult by preventing deleterious secondary events, which could impair cerebral oxygen supply. A detailed neurological examination to determine the extent of the primary injury must be deferred until treatable secondary events have been controlled.

Table 3.1 The Glasgow Coma Scale (GCS)

Immediate Assessment and Management

The ABC approach is vital:

• Clear and maintain the airway and give high-concentration oxygen. Have suction available.
  
• Ensure that the cervical spine is protected.
  
• Obtain anaesthetic assistance as soon as possible. Emergency induction of anaesthesia, intubation and ventilation are likely to be required.

• Obtain intravenous (IV) access.
  
• Monitor and record pulse, BP, SaO₂, respiratory rate and ECG.
  
• Assess neurological status by AVPU criteria:

• Check blood glucose with a reagent strip.
  
• Treat reversible conditions (and reassess after therapy):

• Ask witnesses/paramedics if the level of consciousness has changed since the impact. Did the patient briefly recover and speak and then deteriorate? Obtain a brief history (AMPLE → p. 12). Try to establish the mechanism of the injury.
  
• Obtain radiographs of the cervical spine. Measure the blood gases.

Further Assessment and Management

• Carry out a detailed secondary survey
  
• Seek surgical/neurosurgical advice
  
• Consider catheterising the bladder.

The secondary survey searches for other injuries and establishes the neurological status. It must include examination of the following:

• The scalp
  
• The auditory canals and tympanic membranes (caution → p. 44)
  
• The pupils and limbs
  
• The face
  
• The neck.

Neurological Assessment

There are three groups of observations:

Box 3.1 Indications for CT of the Brain in Adults with Head Injuries

Children aged < 16 years → Box 3.8

(Incorporating the UK National Institute for Health and Clinical Excellence’s [NICE’s] head injury guideline, 2007)

1 The threshold for CT examination should be lowered if there are other life-threatening injuries, particularly if these will require surgery under general anaesthetic

2 The CT brain scan should extend down to the second cervical vertebra with 3-mm cuts from the level of the foramen magnum to C2. If the lower cervical spine has not been well visualised on plain radiographs, this should also be scanned

3 Patients who return to the ED after discharge with persistent complaints that could be attributed to their head injury should be discussed with a senior clinician and considered for CT

Immediate CT scan (= imaging performed and results analysed within 1 h of the request)

• GCS <13 when first assessed in the ED
  
• GCS <15 when assessed in the ED 2 h after injury
  
• Suspected open or depressed skull fracture
  
• Sign of fracture of skull base (→ p. 43)
  
• Focal neurological signs
  
• Post-traumatic seizure
  
• More than one episode of vomiting
  
• Coagulopathy with a history of loss of consciousness or amnesia (history of bleeding or clotting disorder or current anticoagulant treatment)

Delayed CT scan (= imaging performed and results analysed within 8 h of the time of injury)

• Dangerous mechanism of injury with a history of loss of consciousness or amnesia (pedestrian or cyclist hit by motor vehicle; occupant ejected from motor vehicle; fall from a height of >1 m or five stairs; lower heights are applicable for infants and young children)
  
• Amnesia >30 min for events before the impact
  
• Age 65 years with a history of loss of consciousness or amnesia

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All of the above observations should be repeated at appropriate intervals and plotted on a chart.

Other Injuries

About 50% of patients with major brain injury have serious injuries elsewhere. The more injuries there are, the greater the risk of missing some of them.

Imaging

As soon as the patient with a depressed level of consciousness is stabilised, a CT scan of the brain should be obtained (→ Boxes 3.1 for adults and 3.8 for children). Most patients will be intubated and ventilated before scanning. If a patient who is aged over 65 presents ‘out of hours’ and the only positive CT indicator from Box 3.1 is amnesia of events for more than 30 min before the injury or a dangerous mechanism of injury, then it is acceptable to admit them for overnight observation with CT the next morning.

For safety, logistical and resource reasons, MRI is not currently indicated as a primary investigation in patients with head injuries. Moreover, it is contraindicated in both head and cervical investigations unless there is absolute certainty that the patient is not harbouring an incompatible device, implant or metallic foreign body.

Skull radiographs do not contribute to initial management. Therapy is concerned with brain injury rather than bone injury and this is detected initially by the neurological signs.

The indications for imaging of the cervical spine in patients with head injuries are summarised in Box 3.2. In most circumstances, plain radiographs are the initial investigation of choice – three views in adults, two in children under 10 years.

Box 3.2 Indications for Imaging of the Cervical Spine in Adults and Children with Head Injuries

(Incorporating NICE’s head injury guideline, 2007)

Assessment of the injured neck → p. 55.

Immediate plain radiographs:

• Cannot actively rotate neck to 45° (left and right)
  
• Not safe to move neck (→ p. 54)
  
• Focal neurological signs (including paraesthesia in the extremities)
  
• Neck pain or midline tenderness with:
  
  
  
  • dangerous mechanism of injury (fall >1 m or five stairs; axial load to head: diving injury, ejection from a motor vehicle, high-speed motor vehicle collision or roll-over, bicycle collision, crash involving motorised recreational vehicles; use lower threshold for falls for infants and children <5 years)
    
  • aged >65 years
  
  
• Definitive diagnosis required urgently, e.g. before surgery

Immediate CT scan:

• GCS <13 on initial assessment
  
• Has been intubated
  
• Plain films technically inadequate, suspicious or definitely abnormal
  
• Continued clinical suspicion despite normal plain films
  
• Patient is being scanned for multi-region trauma

Note that CT is now recommended more often than previously but the risks from irradiation to children <10 years limits CT in this group to those with severe head injury (GCS <8) and where there is a strong clinical suspicion of injury despite normal plain films.

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Management of Specific Problems

Airway and Breathing

Inadequate respiration leads to hypoxia, hypercapnia and acidosis. This results in cerebral vasodilatation and a rise in intracranial pressure (ICP). Although simple manoeuvres to clear and maintain the airway may be initially successful, intubation and ventilation are required for most patients with impaired respiration (→ Box 3.3).

Box 3.3 Indications for Immediate Intubation and Ventilation After Head Injuries

Aiming for PaO₂ >100 mmHg (13 kPa) and PaCO₂ of 35–38 mmHg (4.5–5.0 kPa)

• Coma or deteriorating conscious level
  
• Apparent loss of protective airway reflexes
  
• Ventilatory insufficiency as judged by oximetry/blood gas measurement:
  
  
  
  • PaO₂ <75 mmHg (10 kPa) on air or <100 mmHg (13 kPa) on oxygen
    
  • PaCO₂ >45 mmHg (6 kPa)
  
  
• Spontaneous hyperventilation causing a PaCO₂ <30 mmHg (4 kPa)
  
• Irregular respiration
  
• Multiple fits
  
• Significant facial injuries
  
• Bleeding into the airway
  
• Extreme agitation

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Intubation should not be attempted without sedation, analgesia and muscle paralysis (even in apparently ‘flat’ head-injured patients) because this would cause a sudden rise in intracranial pressure.

Even patients with no apparent respiratory disturbance may benefit from controlled ventilation. (→ Box 3.4). Hyperventilation to a PaCO₂ <40 mmHg (5.3 kPa) causes cerebral vasoconstriction and a consequent fall in intracranial pressure (ICP). Excessive hyperventilation can, however, be dangerous. Only the undamaged brain responds to changes in blood gas tension, and vasoconstriction in normal areas may result in redistribution of blood flow to the injured tissue. This increases the penumbra around the damaged area. Brain ischaemia leads to lactic acidosis and reflex vasodilatation.

Box 3.4 Reasons for Intubating and Ventilating Patients with Brain Injuries

1 To clear, maintain and protect the airway

2 To maintain adequate gas exchange

3 To reduce ICP and PaCO₂

4 To facilitate CT

5 To allow safe patient transport

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Circulation

In a healthy person, changes in arterial BP between 80 and 200 mmHg do not influence cerebral blood flow. Brain injury impairs this autoregulatory function and hence cerebral blood supply in damaged areas is less well protected from changes in the systemic circulation.

Hypotension is only very rarely caused by brain injury. Trauma to the trunk and neck must be considered together with the biomechanics of the impact.

Cushing’s response (bradycardia and hypertension) is a late sign and indicates rising ICP.

Neurogenic pulmonary oedema is occasionally seen. It is thought to be caused by vasoconstriction resulting from sympathetic overactivity (an alpha effect). It should be treated aggressively with standard drugs and always necessitates ventilation (→ p. 208).

Raised Intracranial Pressure

Hyperglycaemia increases brain swelling and must be avoided. IV mannitol 1 g/kg is used as a short-term agent to reduce brain swelling before clot evacuation; IV furosemide 0.5 mg/kg is an alternative. Mannitol actually causes a transient ICP rise and leaks into the extracellular space, exerting an osmotic effect. Furosemide does not have these deleterious effects and causes a reduction in cerebrospinal fluid production. Neither drug should be used for the long-term management of cerebral oedema.

Fits

Both ICP and metabolic demand for oxygen rise dramatically during a fit and this may increase the extent of the brain damage. Intravenous lorazepam or diazepam is usually effective, but be aware of the possibility of respiratory arrest.

Suspected Alcohol Intoxication

Drunkenness increases the risk of sustaining a head injury and of that injury causing brain damage. Nevertheless, changes in conscious level must not be attributed to alcohol or other drugs except after exclusion of all other possible causes – and in retrospect. The plasma osmolality may be a useful investigation in this circumstance (→ p. 221) if direct measurement of plasma alcohol is unavailable.

Urine Output

Catheterisation of the bladder is mandatory in an unresponsive, brain-injured patient. A full bladder leads to increasing restlessness. In addition, the urine output is a good indicator of adequate tissue perfusion – it should be at least 1 mL/kg per h.

Pain

Analgesia may be needed if the patient is not deeply unconscious and has other painful injuries. Initially, it can be achieved by fracture splintage. Once baseline observations are established, give small doses of opiates intravenously.

Bleeding from the Scalp

Examination of the scalp must be meticulous; the hair must be shaved off to a distance of at least 1 cm around the wound edges. Lacerations should be palpated with a gloved finger to detect fracture lines and foreign bodies. Severe bleeding can be controlled with a single layer of deep sutures, using 2/0 silk on a hand-held needle. A pressure dressing should then be applied. The application of Raney clips to the wound edges can be a useful holding measure.

Deterioration

Early, rapid, neurological deterioration is very rarely caused by a remedial intracranial lesion but more often is due to:

• severe primary brain injury
  
• hypoxaemia
  
• hypovolaemia.

Guidelines for Neurosurgical Consultation

Regional neuroscience centres should collaborate with their linked EDs and ambulance service to provide clear written guidance on consultation and referral practices. In particular, the definition of ‘surgically significant’ must be agreed by both par­ties. There is increasing evidence that all seriously brain-injured patients will benefit from care at a neuroscience centre, whether or not neurosurgical intervention is required, but clearly it is imperative that all those requiring surgery should be transferred as soon as possible. Seek neurosurgical/neurointensive care advice in any of the following instances:

• Positive intracranial findings on CT scan including cerebral oedema
  
• Penetrating injury
  
• Depressed skull fracture
  
• Basal skull fracture
  
• Skull fracture with any depression of consciousness, repeated fits, severe headache, persistent vomiting or acute focal neurology
  
• CSF leak
  
• GCS <13 after resuscitation
  
• Unexplained confusion persisting after >4 h
  
• Deterioration of GCS (especially motor score)
  
• Progressive focal neurological signs.

Transfer from an ED to a neuroscience centre should be well planned, well resourced, speedy and documented. In all circumstances complete initial resuscitation and patient stabilisation, and establish comprehensive monitoring, before transfer, to avoid complications during the journey. If the patient is persistently hypotensive despite resuscitation, do not transport until the cause has been identified and the patient stabilised.

A doctor with appropriate training should accompany the patient. Child or infant transfer requires relevant paediatric critical care expertise. A communication system capable of being used en route is essential; it must not interfere with on-board equipment function.

THE AMBULANT PATIENT WITH A HEAD INJURY

These patients will mostly have a GCS score of 15. This score does not necessarily imply normal mental functioning because the GCS score is not sensitive to changes in alertness or higher intellectual function. Some ambulant patients may be confused (GCS score = 14).

The diagnosis of a minor head injury can be made only in retrospect. The following points should help to distinguish between those with no signifi­cant brain injury and those at risk of serious complications.

History

The history of the incident is important because it often influences management. When the history is unknown or unreliable the patient must be considered for admission to hospital.

• Establish the speed of impact and the nature of the object struck by the head. The part of the head involved and the area of contact are also important (e.g. occiput hitting a carpeted floor is less serious than temple hitting the corner of a radiator).
  
• Establish the pattern of subsequent behaviour and ask about any period of unconsciousness, confusion, amnesia or fitting. Ask about the occurrence of headache and vomiting. Changes to hearing and vision, including diplopia, must also be noted.

Post-traumatic Amnesia

The duration of post-traumatic amnesia (PTA) correlates fairly well with the degree of primary brain injury. Under 1 h usually denotes mild injury, whereas over 24 h is associated with severe injury. PTA is often underestimated. It should be measured up to the time when memory of consecutive events returns. This usually corresponds with the duration of spatial disorientation and is much longer than the period during which the patient did not speak.