Cerebral blood flow is normally maintained at a constant level over a wide range of cerebral perfusion pressures, a phenomenon known as autoregulation (Fig. 11.1). In normotensive patients, autoregulation occurs at cerebral perfusion pressures between 50 and 150 mmHg. In previously hypertensive patients, the curve is shifted to the right and autoregulation occurs at a higher blood pressure.

Fig. 11.1 Autoregulation curves.

Following significant brain injury, autoregulation is often deranged and cerebral blood flow becomes directly related to cerebral perfusion pressure (CPP).

Cerebral perfusion pressure is effectively the driving pressure across the cerebral circulation. It is calculated as shown:

Central venous pressure is sometimes included in this equation. This is because the cranium behaves as a Starling resistor – so where the CVP exceeds the ICP, the CVP becomes the effective downstream pressure and should be used to calculate CPP.

Inadequate CPP results in inadequate cerebral blood flow and the maintenance of an adequate CPP is therefore crucial. However, there is debate about what constitutes an adequate CPP and what the target values for therapy should be. Typical target values are shown in Table 11.2.

TABLE 11.2 Typical target values for cerebral perfusion (mmHg)*

* There is debate about the ideal target values. Some accept lower target values.

The skull can be conceptually considered as a rigid box containing the brain, CSF and blood. If the volume of one of these components is increased, e.g. by cerebral oedema, then the volume of the others must be reduced. Initially, CSF is displaced into the spinal canal, followed by a reduction in blood volume. Eventually, when no further compensation is possible, the ICP will rise rapidly, impairing cerebral perfusion. If the pressure is not relieved, the brain itself may become displaced, leading to so-called herniation or coning. (See Control of intracranial pressure, p. 288.)

In the presence of reduced intracranial compliance, the cerebral blood volume is an important determinant of ICP. If the cerebral circulation becomes vasodilated, cerebral blood volume increases and ICP may increase. Hypercapnia and hypoxia both cause cerebral vasodilatation and should be avoided. Brain-injured patients are normally ventilated to a PaCO₂ of 4–4.5 kPa. Hyperventilation to a lower PaCO₂ than this should be avoided, as there is a risk of significant cerebral vasoconstriction and ischaemia.

The initial assessment includes:

A Airway (with cervical spine control)

B Breathing

C Circulation

D Disability (neurological assessment).

The maintenance of a clear airway and the prevention of hypoxia and hypercapnia are paramount. Indications for intubation and ventilation are shown in Box 11.1.

(See Practical procedures: Intubation of the trachea, p. 398.)

Laryngoscopy and tracheal intubation are a major stimulus and may produce a significant elevation in blood pressure and ICP. Adequate anaesthesia and muscle relaxation must be provided in order to blunt this response and avoid potential worsening of the brain injury.

Establish intravenous access. Give volume loading, particularly if there is haemorrhage and other injuries. Blood, colloid or crystalloid is used as appropriate. If possible, establish direct arterial pressure monitoring.

Check all intubation equipment, breathing circuits, ventilators and suction, etc. Monitoring should be available for BP, ECG, SaO₂ and ETCO₂.

Note the baseline GCS score and pupil size for reference. The pupils are the principal clinical monitor of the brain following anaesthesia and paralysis.

Assume there is cervical spine injury until proved otherwise. A second person should provide in-line immobilization of the neck. (It may be useful to use a bougie / airway exchange catheter / video laryngoscope to facilitate intubation without extending the neck.)

Assume the stomach is full and perform a rapid sequence induction. Preoxygenate with 100% oxygen. Ask a trained assistant to apply cricoid pressure. Use etomidate if the BP is low, otherwise thiopentone or propofol are suitable induction agents. Suxamethonium is used to provide muscle relaxation (unless absolutely contraindicated, see p. 43).

Opioid, e.g. fentanyl 100 μg increments or remifentanil by infusion, 0.1 μg kg⁻¹ min⁻¹ can be used to help block the hypertensive response to intubation.

Intubate the patient and pass an orogastric tube to drain stomach contents.

Ventilate to normocapnia or moderate hypocapnia (PaCO₂ 4–4.5 kPa). Significant hypocapnia is associated with cerebral vasoconstriction and reduced cerebral perfusion. This may potentially cause cerebral ischaemia and worsen brain injury.

Monitor the SaO₂ and ETCO₂. Measure direct arterial blood pressure and blood gases as soon as possible. Maintain adequate cerebral perfusion pressure with fluids and vasoactive drugs (see below).

Maintain sedation with benzodiazepines, propofol and opioids. During the early resuscitation and stabilization phase continue paralysis with a cardiovascularly stable non-depolarizing muscle relaxant.

It is vital to maintain adequate cerebral perfusion pressure in brain-injured patients:

Give colloid or normal saline to restore circulating volume. Avoid hyponatraemic fluids as these worsen outcome.

Give blood if Hb low and correct any coagulopathy.

Consider inotropes / vasopressors early to maintain blood pressure.

Boluses of hypertonic saline (3–7.5%) may be valuable to maintain perfusion / circulating volume and limit cerebral oedema formation. Follow local protocols or seek advice.

Exclude other sites of bleeding.

(See Intensive care management below.)

Neurological assessment requires serial documentation of conscious level, pupillary signs, lateralizing limb signs (suggesting space-occupying lesion), tone and posture. Fundal haemorrhages, papilloedema, CSF rhinorrhea / otorrhoea and bleeding from the ear should be documented.

The simplest assessment of conscious level utilizes a four-point scale:

A Alert

V Responds to Vocal stimuli

P Responds to Painful stimuli

U Unresponsive.

This score is insufficiently sensitive for neurological assessment of the brain-injured patient and is only used during A&E resuscitation to give a broad indication of conscious level. Response to pain only represents a significant decrease in conscious level equivalent to a GCS score of 8 or less.

The Glasgow Coma Scale (GCS), shown in Table 11.3, is a more comprehensive neurological assessment, which is universally used to describe conscious level and has prognostic value. It should be performed as soon as the patient is stabilized. It is repeated throughout the resuscitation process to identify any deterioration in the patient’s condition, which may suggest expanding intracerebral haematoma or brain swelling.

TABLE 11.3 Glasgow Coma Scale (GCS)

Maximum score 15. Minimum score 3. (A modified GCS is used for children under 5 years)

Pupillary size and response to light (direct and consensual) should be documented regularly. Any asymmetry greater than 1 mm or a change in response to light must be assumed to be due to the effects of an intracranial space-occupying lesion causing compression of the ipsilateral third nerve. Urgent CT scan of the brain is required. Bilateral, dilated and unresponsive pupils in the context of a brain injury and in the absence of mydriatic agents is a grave sign.

Having completed a primary survey and stabilized the patient, the patient should be reassessed before moving on to secondary survey. Traumatic brain injury may be an isolated injury, but this should never be assumed. The care of the brain injury must proceed alongside the continuing re-evaluation and resuscitation of the other injuries according to ATLS protocols. In particular, remember:

cervical spine injury (immobilize, X-ray lateral cervical spine, CT spine)

cardiothoracic trauma (CXR, CT ± drains)

abdominal injuries (diagnostic peritoneal lavage, US, CT, laparotomy)

pelvic fractures (X-ray, early external fixation)

splint limb injuries (assess neurovascular integrity).

In the multiply-injured patient with a brain injury priorities must be decided. The following are important considerations:

Many brain injuries do not require neurosurgical intervention.

Any brain injury will be worsened by significant hypoxia or hypotension.

Any injury that compromises the airway, breathing or circulation takes priority. In particular, life-threatening bleeding from the chest or abdomen requires immediate surgical intervention and should not be delayed by CT head scan or neurosurgery. In exceptional cases, blind burr holes or craniotomy can be performed simultaneously with other surgery, and a CT scan performed before transfer to ICU.