MANAGEMENT OF THE HEAD INJURED PATIENT

Head injury can be subdivided into primary and secondary head injury. Primary injury refers to the initial injury, whilst secondary injury refers to factors which exacerbate the primary injury after the injury has occurred. The principles of management of severe head injury are aimed at preventing, or at least minimising, secondary injury.

NEUROPHYSIOLOGY RELEVANT TO SEVERE HEAD INJURY

A key factor in minimising secondary injury is avoiding cerebral ischaemia, by both maintaining

adequate cerebral blood flow (CBF) and avoidance of conditions that increase oxygen consumption by cerebral tissues.

 Hypoxia, hypotension, raised intracranial pressure (ICP) and anaemia all lead to a reduction in the delivery of oxygenated blood to cerebral tissues. Hyperthermia and epilepsy both increase cerebral metabolic rate, and therefore cerebral oxygen consumption. In addition, both hypoglycaemia and hyperglycaemia are associated with a worse outcome.2

INITIAL ASSESSMENT AND MANAGEMENT OF THE HEAD INJURED PATIENT  

Assessment

 A systematic approach to evaluation and initial management, such as that proposed by Advanced Trauma Life Support, should be adopted for these patients.

Airway patency should be assessed and the cervical spine immobilised. The airway should be secured, by tracheal intubation, in patients who do not have a patent airway or who are significantly obtunded (GCS ≤ 8). The chest should be examined and any life-threatening injuries (e.g. tension pneumothorax, open pneumothorax, massive haemothorax, flail chest, cardiac tamponade) promptly treated.3

 The circulatory state should be assessed using clinical parameters such as blood pressure and heart rate.

Any sites of external haemorrhage should be directly compressed. Patients with suspected or confirmed on-going haemorrhage will require operative intervention.

An assessment of the patient’s Glasgow Coma Score (GCS) and pupillary reflexes should be made. In addition, the presence of any lateralising neurological signs, and, in the case of spinal cord injury, a documentation of the level of altered sensation, should also be noted.  

The patient should be completely exposed to assess for other injuries, whilst taking care to prevent hypothermia. All aspects of the primary survey should be completed and identified life-threatening conditions treated, before commencing the secondary survey.

 Specific Neurological Assessment and Investigation

The Glasgow Coma Score is used to formally assess the conscious level of the patient. This score,

illustrated in Table 1 below, is composed of 3 components: eye-opening, verbal and motor response.

The best response in each component is used to calculate the final score, which ranges from 3, at worst, to 15, at best.

Table 1: Glasgow Coma Score3

Pupillary size and response to light should be assessed and recorded. Ipsilateral pupillary dilatation, unreactive to light, may indicate life-threatening intracranial pressure. In this situation, pupillary dilatation results from compression of the oculomotor nerve against the tentorium. Alternative causes include ocular trauma and the administration of certain drugs.4

Early symptoms and signs associated with raised intracranial pressure include headache, nausea and vomiting, seizures, papilloedema and focal neurology. Late signs of raised intracranial hypertension include a decrease in conscious level, hypertension and bradycardia (Cushing’s reflex) and an abnormal respiratory pattern. Pupillary dilatation, decorticate posturing (leg extension, arm flexion) and decerebrate posturing (leg and arm hyperextension) occur prior to coning and brain death.

Eye opening   Spontaneous  4 To voice  3 To pain  2 No response  1

Motor response Obeys commands  6 Localises a painful stimulus  5 Flexion away from a painful stimulus  4 Abnormal flexion  3 Extension  2 No response  1

Verbal response Orientated  5 Confused conversation  4 Inappropriate words  3 Incomprehensible sounds  2 No response  1

Early symptoms and signs associated with raised intracranial pressure include headache, nausea and vomiting, seizures, papilloedema and focal neurology. Late signs of raised intracranial hypertension include a decrease in conscious level, hypertension and bradycardia (Cushing’s reflex) and an abnormal respiratory pattern. Pupillary dilatation, decorticate posturing (leg extension, arm flexion) and decerebrate posturing (leg and arm hyperextension) occur prior to coning and brain deathFollowing head injury, the diagnostic investigation of choice is a CT scan of the head. Indications for patients requiring an urgent CT scan are listed in Box 1.

Box 1: Guidelines for urgent CT scanning in head injury

• GCS < 13 on initial assessment • GCS < 15 on assessment 2 hours post-injury • Definite or suspected open or depressed skull fracture • Signs of basal skull fracture (e.g. Battle’s sign) • Post-traumatic seizure • Focal neurological deficit • >1 episode of vomiting • Any history of amnesia or loss of consciousness post-injury in a patient who is coagulopathic (clotting disorder, warfarin treatment)

Indications for involvement of the neurosurgical team following head injury are listed in Box 2 below.

The exact definition of “surgically significant abnormalities” is determined by the local neurosurgical unit.  

Box 2: Guidelines for neurosurgical referral in head injury

Presence of new, surgically significant abnormalities on imaging • GCS ≤ 8 after initial resuscitation • Unexplained confusion lasting > 4 hours • Deterioration in GCS after admission • Progressive focal neurological signs • Seizure without full recovery • Definite or suspected penetrating injury • CSF leak

Initial Management

Airway

Indications for intubation following head injury are listed in Box 3 below.

If the cervical spine has not been cleared manual in-line stabilisation is required for intubation.

The dose and type of induction agent(s) chosen should be selected with the aims of rapidly securing the airway with minimal haemodynamic disturbance and minimal rise in ICP. With the exception of ketamine, all intravenous induction agents cause a reduction in cerebral blood flow, cerebral metabolism and intracranial pressure. In circumstances where ketamine is the only available induction agent it should be used with caution as it causes a rise in intracranial pressure. The use of intra-arterial monitoring, sited pre-induction, allows more rapid detection and treatment of hypotension.

In the uncomplicated airway a modified rapid sequence induction using a pre-determined dose of thiopentone or propofol together with an opioid (alfentanil, fentanyl) and suxamethonium can be used.

The use of an opioid obtunds the pressor response to laryngoscopy and the associated, potentially life- threatening rise in intracranial pressure. A vasopressor, such as metaraminol, should be readily available to counter any hypotension.

Although suxamethonium may itself cause a rise in intracranial pressure, this is rarely clinically

significant as is offset by the reduction in intracranial pressure caused by the induction agent. The benefits of suxamethonium in facilitating adequate intubating conditions, as well as its short duration of action are often deemed to outweigh this risk in practice.

 With the availability of sugammadex, rocuronium can be used as an alternative to suxamethonium.

Following intubation and confirmation of endotracheal placement, the tube should be well secured in a fashion that ensures venous return is not obstructed. This is most easily achieved using tape rather than a cloth tie.

Box 3: Indications for Intubation Post-Head Injury1, 1

Airway o Loss of airway reflexes o Significant bleeding into the airway • Breathing o Hypoxia - PaO2 < 13kPa (98mmHg) on oxygen o Hypercarbia - PaCO2 > 6kPa (45mmHg) o Spontaneous hyperventilation causing PaCO2 < 4kPa (30mmHg) o Irregular respirations • Disability o GCS ≤ 8 o Seizures • Other o Before transfer to neurosurgical unit AND § Bilateral fractured mandible § Deteriorating conscious level (a decrease of 1 or more points in the motor component of the GCS)

Breathing

Both hypoxia and hypo- and hypercapnia should be avoided in patients with head injuries as these worsen outcome. Hypoxia, as defined as a SaO2 < 90% or PaO2 < 8kPa (60mmHg), increases morbidity and mortality from severe traumatic brain injury. A target PaO2 > 13kPa (98mmHg) should be aimed for. In the ventilated patient this may require use of PEEP. Whilst this will increase ICP to a degree, hypoxia is more likely to have a detrimental effect on patient outcome.

 Hypercapnia, through increasing cerebral blood flow, causes a rise in ICP. Conversely, hypocapnia, although lowering ICP, also lowers cerebral perfusion and may worsen ischaemia. To achieve adequate cerebral perfusion, without significantly increasing ICP, a PaCO2 of 4.5 – 5.0kPa (34-38mmHg) is targeted. In the patient with clinical or radiological evidence of intracranial hypertension modest hyperventilation can be instituted, but maintaining PaCO2 above 4kPa (30mmHg).

In the ventilated patient, arterial blood gas analysis should be used calibrate end-tidal CO2 to PaCO2.

Where appropriate changes in ventilatory settings should be instituted to ensure the above target is achieved. Continuous capnography should be used in all ventilated patients.

Circulation

Hypotension increases morbidity and mortality in severe traumatic brain injury. A cerebral perfusion pressure of 50 – 70 mmHg should be targeted. In cases where the ICP is not measured but suspected to be raised, maintenance of a mean arterial pressure of over 80mmHg should ensure an adequate cerebral perfusion pressure in all but the most severe cases of raised intracranial pressure. Once normovolaemia has been achieved a vasopressor, such as metaraminol or noradrenaline, may be required to maintain mean arterial pressure at this level and offset the hypotensive effect of any anaesthetic agents used.

Box 4: Summary of Therapeutic Targets in Managing Severe Head Injury

• PaO2 > 13kPa (98mmHg) • PaCO2 of 4.5 – 5.0kPa (34- 38mmHg) o A lower PaCO2 , ≥ 4kPa (30mmHg), should be targeted with clinical or radiological signs of intracranial hypertension • MAP ≥ 80 mmHg (in the absence of ICP monitoring) • Glucose 4 – 8 mmol/l • Temperature < 37°C • If ICP monitoring in situ o CPP 50 – 70mmHg o ICP < 20mmHg