Primary versus secondary brain injury

Primary brain injury is the injury that occurs at the time of the trauma. Interventions that impact on primary brain injury are obviously out of immediate control of the emergency doctor, but overall are very important and include public health measures aimed at prevention. Some measures that have reduced TBI include compulsory use of seat belts in cars and helmets for motorcycle riders and pedal cyclists.

Secondary brain injury occurs after the initial injury and is due to sequelae of the original injury, such as raised intracranial pressure, hypoxia, hypercarbia or hypotension. Its effects can therefore be either minimised or prevented with good management. Many of the management strategies in the emergency department revolve around minimising secondary brain injury.

Cerebral perfusion pressure (CPP) is the pressure that drives cerebral perfusion and is defined by the equation

Normally ICP is between 5 and 10 mmHg. Autoregulatory mechanisms will maintain constant cerebral blood flow when the cerebral perfusion varies between 50 and 150 mmHg. In some patients, such as those with severe head injury, cerebral autoregulation may be lost. Any process that reduces MAP (e.g. hypovolaemic shock) or increases ICP (post-injury oedema, expanding intracranial haematoma or mass, hypercarbia) will compromise cerebral perfusion, leading to secondary brain injury.

Headache

Headache is a common symptom of a neurosurgical emergency. It may also be a symptom of a life-threatening non-surgical emergency (e.g. meningitis) or a symptom of many other less serious disease processes (e.g. migraine) or a non-specific manifestation of a non-neurological process (e.g. any serious infection such as pneumonia, pyelonephritis).

As headache is a frequent complaint of patients presenting to the emergency department, the problem is to differentiate the patients who harbour a serious cause from those who do not. The fact that some conditions are relatively uncommon (e.g. incidence of subarachnoid haemorrhage is about 12 cases per 100,000 per year) cannot be relied upon as these patients select emergency departments, either through referral from their primary doctor or self-referral.

Boxes 15.1 and 15.2 outline some criteria for computerised tomography (CT) scanning of both trauma and non-trauma patients, respectively. Further information regarding the features of different types of headaches is given under the heading of each specific diagnosis.

Features that indicate a headache is due to raised intracranial pressure are associated nausea and vomiting and headache worse on awakening in the morning and on lying down.

Glasgow Coma Scale (GCS)

The GCS is a widely accepted scale for assessing alterations to a patient’s level of consciousness. A score is given based on 3 components—eye opening, verbal response and motor response (see Table 15.1). In adults, the score achieved correlates well with the severity of the underlying condition. It is also useful for objectively following a patient’s progress. Maximum score is 15 and minimum is 3.

Table 15.1 Glasgow Coma Score

Herniation syndromes

The cranial cavity is divided into compartments by sheets of dura mater (the falx cerebri and tentorium cerebelli). The tentorium separates the cerebrum above from the cerebellum and brainstem below. Because of the rigidity and non-expansile nature of the cranial vault, significant increases in ICP can lead to herniation syndromes where the contents of one compartment herniate across an opening in these dural structures, causing specific neurological signs. The significance of a herniation syndrome is that ICP has increased beyond the capacity of the brain to compensate and death will ensue if emergent treatment is not undertaken. Raised ICP above the tentorium leads to herniation of the uncus of the temporal lobe. This manifests as dilation of ipsilateral pupil (later bilateral), contralateral pyramidal weakness and increased tone.

Raised ICP will also lead to high blood pressure and bradycardia (Cushing response).

Management principles

The aims of treatment are to prevent any further brain injury, treat the underlying condition, minimise symptoms and optimise neurological and functional recovery. Emergency department management is concerned with the first three of these.

Classification and pathophysiology

There are different ways of classifying TBI. Each is useful in that there is some relationship to treatment and prognosis. Table 15.2 outlines a classification according to actual pathology of the injury. TBI can be classified according to severity based on GCS (GCS ≤ 8 = severe, GCS 9–13 = moderate, and GCS 14–15 = mild or minor).

Table 15.2 Pathological lesions seen in traumatic brain injury

Assessment and diagnosis

Assessment should be performed according to advanced trauma life support principles, which use a prioritised and systematised approach (for general principles of trauma management, see Chapter 14, ‘Initial assessment and management of major trauma’). The diagnosis of TBI per se is usually obvious from the history. However, the occasional patient presents with an altered conscious state without a definite history of trauma. In cases where the patient may have been drinking alcohol, it is sometimes misdiagnosed as alcohol or drug intoxication. This is a classic misdiagnosis that can have lethal consequences.

Where alcohol use and head injury coexist, always assume that any alteration in mental state is due to the head injury.

Clinical features

The severity of mechanism of injury, a history of loss of consciousness and the duration of loss of consciousness are important. Did the patient regain consciousness? The patient may be experiencing symptoms such as headache, nausea and vomiting. There may be amnesia concerning the events around the time of injury, or for a period before the injury (retrograde amnesia). Anterograde amnesia is the inability to remember information acquired since the injury. This often manifests as the patient asking the same questions over and over again. On examination, local head trauma (lacerations, haematomas) may be present. The GCS should be measured (Table 15.1). Focal neurological signs such as pupillary dilatation with or without hemiparesis with increased tone and reflexes indicate an uncal herniation syndrome requiring emergent management. Where there is significant increase in ICP, the Cushing reflex will lead to hypertension and bradycardia. Clues to a fractured skull base are cerebrospinal fluid (CSF) leak from nose, bilateral periorbital bruising (raccoon eyes), CSF leak from the ear, haemotympanum and bruising behind the ear (Battles sign).

Investigations

Definitive investigation is a CT scan of the head. This should be done urgently for severe and moderate head injuries. For mild head injury (GCS 14–15), the indications are listed in Box 15.1.

Skull X-rays have become superfluous. Many would say the indications for a skull X-ray necessitate a cerebral CT scan. Those who advocate a place for skull X-rays in mild head injury do so in patients who do not have indications for CT, but few patients fall into this group.

Blood tests such as white cell count (WCC) and haemoglobin are relevant though not diagnostic. Coagulation studies should be done if there is intracranial haemorrhage or if the patient is on anticoagulation.

Management

A systematic trauma approach that identifies and prioritises injuries is mandatory. As outlined above under ‘General concepts’, this will allow immediate management of life-threatening problems such as airway obstruction, lack of airway protection, hypoxia, blood loss and hypotension, thus avoiding secondary brain injury. Specific management includes the following.

Surgical intervention

Surgery is required for drainage of extradural (see Figure 15.1) and subdural haematomas. This may be required emergently if they are causing mass effect with raised intracranial pressure. Supportive therapy is required for contusions, subarachnoid haemorrhage and diffuse axonal injury. Surgery is also required for depressed skull fracture. In severe head injuries, insertion of an intracranial pressure monitor and monitoring of intra-arterial blood pressure to direct therapy (see above) is aimed at reducing raised ICP. To maintain adequate cerebral blood flow, a CPP of above 70 is ideal.

Figure 15.1 CT scan showing a left-sided extradural haematoma

Subarachnoid haemorrhage

(See also Chapter 24, ‘Neurological emergencies’.)

Over the past three decades advances in diagnostic and therapeutic techniques have seen a reduction in chance of dying and an increase in the likelihood of a functional recovery from non-traumatic subarachnoid haemorrhage (SAH). However, the morbidity and mortality are still significant.

As a result of the initial haemorrhage, 50% of SAH patients either die or are permanently disabled. Another 25–35% die of a later haemorrhage if left untreated. The size of this latter group suffering repeat haemorrhages can be minimised if there is prompt diagnosis and treatment. Despite this, diagnosis of SAH is often missed or delayed.

In two-thirds of patients with SAH the source of bleeding is a rupture of a cerebral aneurysm. The commonest site is the anterior communicating artery.

In about 20% of patients no identifiable cause is found and a small number have an arteriovenous malformation (AVM). A family history of aneurysmal haemorrhage increases the patient’s risk of the same.

Investigations

Diagnosis of the bleed is usually by cerebral CT scan (see Figure 15.2). The ability of a cerebral CT to pick up a SAH degrades over time. If scanned with a third-generation CT scanner within the first 24 hours, 98% will be visible;³ however, by 1 week post-bleed only 50% are visible.

Figure 15.2 Non-contrast cerebral CT scan showing extensive subarachnoid haemorrhage

Because the consequences of missed diagnosis of SAH are very serious, a lumbar puncture (LP) should be performed in patients with a negative CT so that those with a false-negative CT can be picked up.

The LP should be examined for the presence of blood (either macroscopic or microscopic). If red blood cells are present, it is difficult to differentiate a traumatic tap from a subarachnoid haemorrhage. The CSF should be examined for breakdown products of red blood cells (oxyhaemoglobin and bilirubin) by CSF spectrophotometry. Oxyhaemoglobin takes 2 or more hours to develop, but bilirubin takes 12 hours to develop. A traumatic tap can give rise to oxyhaemoglobin only, but the presence of both bilirubin and oxyhaemoglobin peaks on spectrophotometry is suggestive of SAH.

Xanthochromia is the yellow appearance to the naked eye of the supernatant of the centrifuged CSF specimen. The yellow colour is due to the presence of bilirubin. Inspection of the CSF for xanthochromia is less reliable than measuring the bilirubin peak with CSF spectrophotometry. Therefore, CSF spectrophotometry should always be done when LP is performed to rule out SAH.

Because it does take 12 hours for red blood cells in CSF to break down to bilirubin, it is theoretically possible that performing an LP too soon after the occurrence of the haemorrhage may lead to false-negative LP.

Once a SAH is detected, further imaging is required to demonstrate the source of the bleed. This is done with either 4-vessel cerebral angiography or CT angiogram (Circle of Willis). The latter is a less invasive alternative that can identify aneurysms and AV malformations. It has a sensitivity of approximately 96% for aneurysms greater than 3 mm diameter.³ It has not replaced conventional cerebral angiography but is useful in investigating patients with high clinical suspicion of SAH but who have equivocal or negative CT and LP.

Other investigations in SAH include full blood count, prothrombin time (PT)/activated partial prothrombin time (APTT), electrolytes, urea, creatinine (EUC), liver function tests (LFTs), blood group and screen and chest X-ray.

Spontaneous intracerebral haemorrhage

Spontaneous intracerebral haemorrhage is usually related to poorly controlled hypertension. Patients who are anticoagulated with warfarin are also at risk of intracerebral haemorrhage.

Patients usually present with sudden onset headache and neurological impairment. Focal neurological signs are usually related to the location of the bleed. In larger bleeds (see Figure 15.3), especially where there is mass effect, there is usually reduced level of consciousness or coma. Herniation syndromes may be seen, especially with posterior intracranial fossa bleeds.

Figure 15.3 Non-contrast cerebral CT scan with large intracerebral bleed with blood extending into ventricles

Most intracerebral bleeds are treated medically with attention to the priorities of airway, breathing and circulation as well as correction of any coagulopathy (e.g. reversal of anticoagulation).

Indications for surgery include:

Subdural haematoma

Subdural haematoma occasionally presents without definite history of trauma; however, it is usually traumatic in origin. Subdural haematomas arise from injury to the bridging veins in the subdural space (between the dura mater which follows the contour of the bony skull and the pia mater which follows the contour of the cortex of the brain). Where there is cortical atrophy this space is prominent and more at risk of subdural haematoma from an injury.

Clinical features

The clinical presentation is by virtue of the enlarging size of the lesion, mass effect (local or general) or surrounding oedema (see Figure 15.4). Symptoms vary greatly from just headaches, with features suggestive of raised ICP, to patients with coma and herniation syndromes at the severe end of the spectrum.

Figure 15.4 Cerebral CT scan with contrast showing left frontal enhancing space-occupying lesion with surrounding oedema resulting in marked mass effect (shift of midline to right, compression of ventricles). Patient had presented with status epilepticus and dilatation of left pupil due to herniation syndrome

The patient may present with seizures (focal or generalised). Persistent depression of GCS post ictally or development of status epilepticus should raise clinical suspicion and necessitate urgent cerebral CT.

Investigations

Definitive diagnosis is usually by CT scan. Box 15.2 outlines the indications for CT in nontrauma patients in the emergency department.

Management

Treatment of these conditions is guided by the same principles outlined at the beginning of this chapter. Raised ICP from tumours is often responsive to treatment with bed rest and dexamethasone. Further seizures can be prevented with phenytoin (15 mg/kg slow IV infusion).

Blocked ventriculoperitoneal (VP) shunt

Patients with VP shunt not infrequently present to the emergency department with shunt problems. The commonest of these are shunt obstruction and shunt infection. It is important to recognise these complications when they occur as, untreated, they can lead to significant morbidity or mortality.

Clinical features

Investigations

In patients who cannot be cleared clinically, radiological assessment should be done.

At a minimum, three views should be taken of the cervical spine. These are lateral, anteroposterior (AP) and odontoid peg (open-mouth) views. The sensitivities of each of these views for detecting a cervical spine injury are 85–90%, 1–2% and 5%, respectively. The lateral view must show down to the cervicothoracic junction (C7 and at least upper part of body of T1). If it does not, a swimmer’s view can be obtained to better show the cervicothoracic area. This view needs to show both the alignment and some detail of the C7/T1 area. For patients who have large shoulders and upper torsos, or who cannot physically be placed in the swimmer’s position (one shoulder abducted), a CT scan may be required to image the cervicothoracic junction.

Other films may be useful in certain situations. Oblique views of the cervical spine can be used to evaluate the facet joints on each side. They can also be used as an alternative to swimmer’s view in imaging the cervicothoracic junction. Flexion and extension views are indicated to detect instability in an otherwise normal cervical spine with symptoms. Recent literature has questioned the value of flexion and extension views in detecting injuries not already seen on plain films.

Accurate interpretation of plain cervical spine films can be difficult and less experienced doctors should check their interpretation with an emergency physician. Box 15.3 outlines a system for reviewing cervical spine X-rays. Abnormalities may be non-specific and simply draw attention to the need for further imaging. (See also the ‘plain X-ray views’ section under ‘Trauma’ in ‘Emergencies in the neck’ in Chapter 4, ‘Diagnostic imaging in emergency patients’)

Determination of stability of vertebral column injury

The ability of the vertebral column to protect the spinal cord from abnormal movement and, therefore, injury should be evaluated. Ideally, this should be done by a spinal surgeon.

The vertebral column can be considered to consist of three structural components: the anterior, middle and posterior columns. The anterior column consists of bone and ligaments from the anterior half of the vertebral bodies forward. The posterior column is made up of the neural arch (laminae and pedicles), spinous processes and posterior ligamentous complex. The remainder, the middle column, is from the posterior longitudinal ligament and posterior half of the vertebral body. If at least two out of three of these columns are disrupted, the injury is considered unstable.

Treatment

In the patient with multiple injuries, vertebral column and spinal cord injuries should be managed as part of a prioritised management plan that addresses other serious injuries in context (see Chapter 14 for general principles of trauma management). The consequences of injury to the spinal cord in a patient with an unstable vertebral column injury are of major life-changing significance for the patient. Precautions to prevent further injury to the cord should therefore be instituted from the beginning.