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