Wilkinson. Essential Neurology 2005

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Management

The first question, near or at the site of the head injury, is whether there is any indication for assessment in the hospital emergency department.

Indications for hospital assessment after head injury

•Any loss of consciousness, amnesia or fall in the Glasgow Coma Scale at any time.

•Any focal neurological symptom or sign.

•Suspicion of skull fracture or penetrating injury.

•Seizure, vomiting or persistent headache.

•Current drug or alcohol intoxication (making assessment unreliable).

•High-energy head injury (e.g. pedestrian struck by car; thrown from moving vehicle; fall downstairs; fall of 1 metre or more onto head).

•Coagulopathy (history of bleeding or clotting disorder or anticoagulated).

•Previous neurosurgery.

•Suspicion of non-accidental injury.

•Age 65 years or more.

Once in hospital, patients may require management in the

emergency department, in the trauma ward of the district general hospital, or in a neurosurgical centre (Fig. 4.3). In all these places, and during transfer from one to another, management is directed towards prevention and treatment of the four serious insults causing secondary brain injury (see Fig. 4.2).

In the emergency department the patient must be assessed, Glasgow Coma Scale observations initiated (see p. 184), and if necessary the patient must be resuscitated. Then it has to be established whether there is any indication for a CT brain scan and/or neurosurgical advice.

Indications for CT brain scan after head injury

•GCS less than 13 at any time, or 13–14 at 2 hours after injury.

•Suspected skull fracture or penetrating head injury (see box).

•Post-traumatic epileptic seizure.

•Focal neurological deficit.

•More than one episode of vomiting (except perhaps in children).

•Amnesia for more than 30 minutes of events prior to impact.

•Any loss of consciousness or amnesia if also:

—aged 65 years or older;

—coagulopathy;

—high-energy head injury.

CHAPTER 4

A Airway

Clear airway, with cervical spine control until cervical injury is confidently excluded

B Breathing

Assess ventilation and chest movement. Arterial blood gases

C Circulation

Assess likelihood of blood loss. Monitor BP and P frequently. Establish IV line

DDysfunction of CNS

Assess by Glasgow Coma Scale at frequent intervals

EExposure

Identify all injuries, head to toe, front and back

Reasons to suspect a skull fracture or penetrating head injury

•Clear fluid (CSF) running from nose

•Blood or clear fluid running from ear(s)

•Bruising around eye(s) with no eye trauma (panda eyes)

•Bruising behind ear(s) (Battle’s sign)

•New unilateral deafness

•Significant visible scalp or skull wound

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It is important to:

•continue regular competent neurological observations at intervals appropriate to the patient’s condition (half-hourly, hourly, 2-hourly, 4-hourly);

•remember the head injury may be non-accidental, especially if there is any uncertainty about its mechanism (see box);

•remember that there are pharmacological dangers. If the patient smells of alcohol, the doctor may recognize that this could be a contributory factor towards the patient’s depressed state of consciousness, but he will be unwise to attribute the whole clinical picture to alcohol if a head injury is present, especially if a skull fracture is present. Do not complicate the state of consciousness, or the assessment of it, by the use of strong, CNS depressant, analgesics; by the overuse of intravenous, CNS depressant, drugs to control an individual epileptic fit; by permitting any procedures requiring general anaesthesia, which can possibly wait for 2 or 3 days; or by the use of mydriatic drugs to look at the fundi;

•continue to anticipate, prevent, detect early, and treat energetically any of the four serious insults which may further

damage the brain and cause further brain swelling (see Fig. 4.2, p. 59).

If the patient requires admission to the neurosurgical centre great attention should be paid to the maintenance of normal intracranial pressure and perfusion of the brain. This often involves the use of intracranial pressure monitors, intermittent intravenous administration of mannitol and neurosurgery (e.g. to evacuate an extradural haematoma). The routine care of the unconscious patient (see Chapter 11, p. 187) is established.

After-care

In all but the most trivial head injuries, the patient will benefit from some after-care. This may not amount to more than simple explanation and reassurance regarding a period of amnesia, headaches, uncertainty about a skull fracture, timing of return to work, etc. Without the opportunity to discuss such matters, unnecessary apprehensions may persist in the mind of the patient and his family.

At the other end of the scale, somebody recovering from a major head injury (often associated with other injuries) may need a great deal of further medical and paramedical care for months after the head injury. This may mean a considerable period in hospital or in a rehabilitation unit whilst recovery from the intellectual, psychological, neurological and orthopaedic deficits gradually occurs.

CHAPTER 4

Head injury may result from:

•stroke

•cerebral haemorrhage

•epilepsy

•cardiac dysrhythmia

•alcoholic intoxication

•non-accidental injury to children

HEAD INJURY

Initial features:

•level of consciousness

•skull fracture

•focal neurological signs

Secondary features:

•epilepsy

•intracranial haematoma

•meningitis

Duration:

•of coma

•of post-traumatic amnesia

•of stay in hospital

Persisting deficits:

•intellectual

•psychological

•focal neurological

Headache

Dizziness

Impaired concentration Impaired memory Fatigue

Anxiety

Depression

Irritability

Indecisiveness

Impaired self-confidence Lack of drive

Impaired libido

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The consequences

How severe a head injury was it, doctor?

Several factors, shown in the adjacent margin, must be borne in mind when formulating a reply to this enquiry.

With regard to the duration of coma and post-traumatic amnesia, confusion may arise. The duration of post-traumatic amnesia refers to the period after the accident until the time that the patient regains ongoing memory. The patient often describes the latter as the time he woke up after the accident. He means the time he recovered his memory, not the time he recovered consciousness. The time he says he woke up is often long after the time that observers have noted return of consciousness (eyes open and paying attention, speaking and using his limbs purposefully).

The duration of hospital stay must also be clarified. If there was associated (orthopaedic) injury, the patient may have been hospitalized long after the time for discharge purely on head injury grounds.

Post-concussion syndrome

This usually follows minor concussive head injury or less, with post-traumatic amnesic periods lasting a few minutes, rather than major head injury. It consists of a remarkably stereotyped set of symptoms, as shown alongside, unaccompanied by abnormal neurological signs.

Controversy exists as to the cause of the post-concussion syndrome. On the one hand, it is accepted that concussive head injury can produce diffuse minor brain damage. (If repeated, this may accumulate to the punch-drunk state, known as post-traumatic encephalopathy, seen in some boxers towards the end of their careers.) On the other hand, the syndrome can be seen in some patients suffering head injuries at work, where the evidence of concussion or amnesia is very minimal and where litigation and financial compensation are paramount.

The syndrome can be very disabling for months, even years, after a minor head injury. Despite our lack of understanding of its precise nature, the syndrome has to be recognized as a definite entity responsible for considerable morbidity after head injury in some patients.

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Post-traumatic epilepsy

Patients surviving head injury may have developed an epileptogenic scar in the brain, which may subsequently give rise to focal or secondarily generalized epileptic attacks. Posttraumatic epilepsy shows its presence within a year of the accident in about 50% of patients who are going to develop this late complication of their head injury. In the rest, it may not occur for several years.

There are certain features of the head injury which make posttraumatic epilepsy more likely:

•post-traumatic amnesia lasting more than 24 hours;

•focal neurological signs during the week after the head injury;

•epilepsy during the week after the head injury;

•depressed skull fracture;

•dural tear;

•intracranial haematoma.

These risk factors enable fairly accurate prediction of the risk of epilepsy in a patient after head injury, and are valuable when advising patients about prophylactic anticonvulsants and driving.

Chronic subdural haematoma

In elderly patients who have suffered trivial head injury, sometimes so trivial that it is not clearly remembered, blood may start to collect in the subdural space. This is not sudden, severe arterial bleeding, but a process that evolves over several weeks, a gradual accumulation and liquefaction of blood. The blood accumulates over the convexity of the brain, with gradual elevation of intracranial pressure, shift of midline structures and eventual tentorial herniation and coning.

The clinical picture is of subacute fluctuating drowsiness and confusion, often associated with headache, in which focal neurological signs appear late. Any elderly patient presenting in this way is a candidate for a chronic subdural haematoma, with or without a history of head injury. Chronic alcoholics and patients on anticoagulants have an increased risk of chronic subdural haematoma.

Chronic subdural haematomas may occur bilaterally, and may be hard to visualize on conventional CT scans if the altered blood is isodense with brain tissue. They are treated by evacuation of the blood through burrholes, with good results.

CHAPTER 4

Bilateral subdural haematomas.

HEAD INJURY

Outcome from severe head injury

•50% mortality

•Disability common in survivors

•Often young people

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Outcome from severe head injury

Mortality from severe head injury (coma lasting more than 6 hours) is of the order of 50%. Those who survive are likely to have deficits in some or all of the following areas, depending on which parts of the brain have been most damaged:

•intellectual function;

•mood, behaviour, personality;

•speech and communication;

•vision;

•motor and sensory function in the limbs;

•post-traumatic epilepsy.

Most of a patient’s recovery will have occurred within 6 months of the injury, though further slower improvement may occur in the next 12–18 months.

Patients displaying deficits in all areas constitute what the general public recognize as a brain-damaged person, often unable to live independently. Commonly, the patients are young at the time of their accident, and many years of life may lie ahead of them. In general, provision for such patients is inadequate in terms of chronic young sick units, where their ongoing care may be successfully managed in some sort of shared care system with the patient’s relatives.

Compensation and medico-legal aspects

Because road traffic accidents and accidents at work cause a large percentage of head injuries, compensation for suffering, disability, loss of earnings, restriction in recreational pursuits, etc. is very commonly sought in the months and years after the accident. This occurs after both minor and major injuries, and it is unusual for a case to be settled before 2 years have elapsed after the accident.

Though this activity is entirely reasonable, it is unsettling for the patient and his family. It tends to perpetuate the accident and its effects in their minds longer than would otherwise be the case.

CASE HISTORIES

Case 1

A 12-year-old boy has been involved in an accident whilst riding his bicycle.All the details are not clear, but the accident happened at traffic lights, the boy was not wearing a helmet, he was struck by a car and he lost consciousness transiently though he was subsequently able to talk reasonably coherently. He was not able to walk into the ambulance which brought him to the emergency department.

On examination he is orientated in person but not in time or place.There is some bruising and swelling above his left ear, though no scalp laceration.There are no focal neurological signs.There are no signs of injury to any other part of his body.

a. What management would you arrange?

Ninety minutes later, some 3 hours after the accident, the neurological observations start to show deterioration. He will only open his eyes to strong

painful stimuli and his speech is reduced to mumbled incomprehensible sounds. His limb responses are variable but he can localize painful stimuli with each hand.Vital functions and pupil reactions remain normal.

b. What is your management now?

Case 2

A dishevelled middle-aged man is brought to the emergency department by ambulance. He has been found unconscious on the pavement outside a public house. He smells strongly of alcohol. He is bleeding from a large left-sided scalp wound. He is deeply unconscious with a Glasgow Coma Scale of 8 (E2 V2 M4) but no focal neurological deficit.

a. What are the possible reasons for his state?

(For answers, see pp. 256–7.)

Examining for tremor

Look for tremor at rest:

•hands in lap

•patient distracted (‘Close your eyes and count backwards’)

Look for postural tremor:

•arms outstretched

•hands slowly brought in towards the face

Look for kinetic tremor:

•‘Touch my finger, then your chin’

If you cannot see the tremor:

•listen to the affect muscles with a stethoscope

We all have some degree of tremor on sustained posture, termed physiological tremor. This is faster than parkinsonian or cerebellar tremor, absent at rest, and most evident in the hands. Most of the predominantly postural tremors are due to an exaggeration of this phenomenon.

Postural tremors are made more obvious when circulating catecholamines are increased, for example by anxiety, and by sympathomimetic drugs like salbutamol. Conversely, they are suppressed to some extent by beta-adrenergic blockade and sometimes by alcohol. The mechanisms of these effects are not understood. They are often exploited by people who require a steady hand, such as surgeons, snooker players or musicians, who may take propranolol or alcohol on important occasions. Reliance on alcohol to treat tremor can lead to dependency and liver disease.

The most disabling postural tremor is familial essential tremor, which tends to be dominantly inherited. A more jerky, asymmetrical variant of essential tremor is seen in patients with a personal or family history of dystonia, and is referred to as dystonic tremor; it is less responsive to beta-blockers or alcohol.