Head injury


Head injury leads to about 5000 hospital deaths per year. Head injuries can occur in isolation or with multiple trauma. They result either from deceleration of the head, for example in road traffic accidents, or acceleration, for example in assaults with blows to the head or face. The head may come into contact with an object, resulting in damage to the scalp and/or skull, or the body may decelerate/accelerate without direct contact to the head. Since the brain is soft and jellylike, there is an inertia between it and the skull and it oscillates and is often forced against the skull several times along the line of force; damage is caused in this way, particularly in high-speed road traffic accidents. Penetrating missile injuries are unusual in the UK but common in some countries and in war zones; they cause impact damage, as above, but also focal damage along the missile tract within the brain.

Lesions are classified as primary if they occur at the time of injury and secondary if as a result of complications. Primary lesions may be:

• intracerebral haemorrhages. These may be single or multiple and vary in size from large to petechiae;

• localized areas of contusion. These (like a bruise elsewhere on the body) are softened swollen brain with haemorrhages and occur maximally in the temporal, frontal and occipital lobes. The term contre-coup contusion is used to describe the oscillation of the brain whereby it is contused at the opposite pole from the impact;

• laceration and diffuse axonal injury. Lacerations occur either from an open direct penetration or within a closed injury and can occur anywhere on the cerebral cortical surface or even in the corpus callosum. In diffuse axonal injury (DAI) there is widespread damage to the white matter of the cerebral hemispheres and fibre tracts within the brain stem.

Secondary lesions include:

• oedema. Oedema around contusions and lacerations adds to the local mass effect and there is an increase in brain tissue water and increased permeability of blood vessels. There may be diffuse brain swelling which is thought to be most likely due to vascular engorgement, although if the brain becomes hypoxic there may be cytotoxic oedema as well;

• displacement of brain and internal herniations. The brain may be herniated under the falx or the undersurface of the temporal lobe forced into the tentorial opening leading to compression of the midbrain;

• surface haematomas. These may be subdural or extradural. The former arise from tearing of surface veins or the cerebral cortical substance and tend to spread over the cerebral hemisphere. Extradural haematomas result from either tearing of one of the meningeal vessels or from a fracture site; in either event the dura is stripped from the overlying bone for some surrounding distance and the haematoma develops in the potential space. Most frequently, extradural haematomas occur in the middle fossa, but can occur in the anterior or posterior fossae. Both sub-dural and extradural haematomas lead to secondary displacement and compression of the underlying brain. The compounding effects of poor pulmonary gaseous exchange and falling systemic blood pressure upon an already damaged and deranged brain can never be overestimated (see above).

Clinical features

Neurological deficits

Focal or generalized neurological deficits can occur either from the primary or secondary injuries. Their nature varies depending on the site and severity of brain damage. These may include limb disturbance with weakness, dyspraxia and sensory loss. Eye movement disorders may occur from damage to the III, IV and VI nerves or to the midbrain. I nerve damage can occur and is irrecoverable if total and bilateral. Ataxia of the trunk with balance and gait disturbance is common after severe injuries.

Some of the most serious deficits are cognitive and speech disorders. Speech disorders may include dysphasia and dysarthria. Cognitive disorders can be severe and distressing, yet are often not appreciated in the early phases after a head injury. They include reduction of short-term memory, learning and ability to retrieve new information and logical thought. Personality changes can also occur and often best recognized by relatives and friends.


The acute management of head-injured patients can be divided temporally and logistically into three phases:

• emergency department;

• (if required) inpatient admission and care.

The scene of the incident is attended by the Ambulance Service whose paramedics are trained in resuscitation. Any unconscious patient requires immobilization of the neck in a firm collar during retrieval back to the emergency department. The airway needs protection if the patient is still unconscious.

At the emergency department, patients can be triaged into major, moderate and mild injuries. The key element of managing a patient with a head injury is the routine ABC of trauma care to ensure airway patency, adequate breathing and circulation. Following that attention is given to the exclusion of intracranial mass lesions that cause the secondary injuries as described above. Patients who have a decreased conscious level after head trauma have a high risk of an intracranial mass lesion and most of these patients will require a CT scan to exclude. The presence of a skull fracture also greatly

Figure 21.6. Lateral skull radiograph showing linear fracture (arrow) of 45-year-old man with blow to the head.
Figure 21.7. CT scan of the same patient as in Fig. 21.6 showing extradural haematoma (large arrow). Note also severe shift of the brain (thin arrow).

increases the risk of an intracranial mass lesion and if an X-ray demonstrates a fracture then a CT must follow in most cases (Figs 21.6 and 21.7).

Small children, in particular, are vulnerable and a full GCS assessment is often difficult to achieve, and the vast majority of these should be admitted. If alcohol is detected, care must be taken in assessing the patient and any confusion or reduction of GCS must not be exclusively attributed to the alcohol, irritating though this may be to the medical and nursing staff. Patients with medical conditions that might have a bearing upon their response to a head injury should also be admitted, for example diabetes mellitus, epilepsy, respiratory and cardiac conditions and also patients who are taking anticoagulants or corticosteroids.

Observations, including the GCS, should be performed half-hourly and any decline in the GCS and the development of neurological deficits or both should alert the clinician to a complication and a cause should be immediately sought. Investigations including an urgent CT scan should be performed.

Patients who are present in coma after head injury present major problems and immediate attention must be given to the establishment and maintenance of their airway and the maintenance of normal cardiovascular status. The upper airway must be protected, if necessary by an airway or endotracheal intubation. Adequate gaseous exchange must be checked by arterial blood gas analysis, and if abnormal, reasons sought and the necessity for artificial ventilatory support considered. The cardiovascular status must be checked by measuring blood pressure, pulse volume and heart rate. The patient must be checked for other injuries by using the log-roll procedure and full frontal and posterior examination carried out. After resuscitation, a GCS score is derived and note taken of any injuries about the head, face and neck. Any suspected areas about the body must be radiographed and a lateral radiograph of the cervical spine taken before the collar is removed. CT scanning is necessary for all patients with a GCS of eight or less. Following this, the nearest neurosurgical department should be contacted; if no CT scanner is available, the neurosurgical department should be contacted as soon as possible.

If transfer to a distant neurosurgical department is deemed necessary, the patient should be stabilized with respect to his pulmonary and cardiovascular status as quickly as possible before being transported by ambulance and accompanied by an anaesthetist and surgeon.

The control of pain from injuries outwith the brain can be difficult, since opiates depress the level of consciousness and lead to pupillary constriction. Codeine, as a milder opiate, can be given but if there is severe pain, morphine may be required and its use agreed between surgeons and anaesthetists.

Epilepsy can occur early after head injury. Whilst it is important to prevent further seizures, it must be appreciated that intravenous anticonvulsants (e.g. phenytoin and diazepam) may not only make neurological assessment more difficult, but can induce apnoea as well as cardiac dysrhythmias and an anaesthetist with full resuscitation equipment must be present when the drug is administered. Epilepsy requires treatment but there is no need for routine prophylactic anticonvulsants simply because the patient has suffered a head injury.

CSF fistulae may occur through the nose or ear. In these cases prophylactic antibiotics are not currently recommended but vigilant observation and investigation of all potential pyrexia are essential. CSF rhinorrhoea requires investigation and possibly repair by a neurosurgeon, as does persisting CSF otorrhoea.


Scalp lacerations The scalp is very vascular and patients can lose quite large volumes of blood from extensive lacerations. In an emergency situation, a pressure dressing can be applied. After assessment and/or resuscitation and skull radiographs, a scalp laceration requires exploration and any rough irregular edges with possible skin damage require debridement. The wound is then sutured, preferably in two layers with absorbable sutures to the galea and sutures to the skin; if done properly, haemostasis will be achieved. Skin sutures can be removed after 5 days. If there is loss of scalp, this requires urgent surgery by a neurosurgeon or a plastic surgeon.

Burr holes It must be realized that only liquid haema-tomas can effectively be removed though burr holes, and therefore this form of surgery is only suitable for a fluid chronic subdural haematoma. However, burr holes are the starting point for a craniectomy or craniotomy (see below). A burr hole is performed by making a linear 4 cm long incision down to the pericranium, which is then scraped to each side. A Hudson brace with a perforator is then used to drill as far as the dura. The perforator is changed for a conical or spherical burr which enlarges the hole to about 15 mm. The exposed dura is then incised in a cruciate fashion to expose the brain.

Craniectomy and craniotomy Ideally, it is better to perform a craniotomy, although for the less experienced surgeon, a craniectomy can be life-saving for the patient. For a craniotomy, four burr holes are drilled at the corners of a square with sides at least 6-8 cm in length. Three of the four burr holes are connected with a saw and the 4 th side is broken to keep the pericranium and/or temporalis muscle intact, thereby rendering the bone flap osteoplastic such that the bone will survive.

A craniectomy is performed by drilling a burr hole and then, with a bone rongeur, nibbling bone away to give sufficient exposure (the minimum being at least 5 cm in diameter); adequate exposure is vital and bone defects can always be repaired at a later date. An extradural haematoma is immediately encountered if the burr hole is in the right place; this will be solid and requires suction removal. The dura should be opened if a subdural haematoma is also suspected. The cause of the haematoma needs to be sought; if it is from the skull fracture this requires smearing with bone wax, but if it is from a tear of a branch of the middle meningeal artery, diathermy is required. The exposed dura must then be hitched, by interrupted sutures, over the bone edge to the pericranium to prevent further stripping of the dura and further extradural haematoma formation. A suction drain must be inserted and left for at least 24 h postoperatively.

Depressed skull fracture Compound depressed skull fractures require a CT scan and need to be fully explored by a neurosurgeon, since bone fragments or other solid objects may be driven into the brain and lead to subsequent brain abscess. Simple depressed fractures require elevation only if they are significant and in a cosmetically important area. In the child under 3 years of age, considerable remodelling of the skull is possible and only severe depressions require elevation.

Missile injuries Penetrating missile injuries demand particular expertise in their management, ideally by a neurosurgeon.


Any patient who suffers a head injury requires rehabilitation, although in the case of minor injuries the patient may require advice rather than major rehabilitation. A head injury with a PTA of <1h may take 1-2 months, but often less, for full recovery. Whilst it is important to get the patient back to his former life style, it is also important to ensure he is fully recovered before so doing. Headaches are a frequent problem and are variable in intensity and duration but usually subside after a few months; if they continue, a CT scan is required to check for chronic lesions such as a subdural haematoma or hydrocephalus.

Patients with longer PTAs and those with neurological deficits need longer to recover and may have continuing cognitive problems that require assessment by a clinical neu-ropsychologist. Those with severe problems require the services of a fully trained rehabilitation team, which will include a neurosurgeon, rehabilitation expert, physiotherapist, occupational therapist, speech therapist and neuropsychologist or, in the case of children of school age, an educational psychologist. The CNS is slow to repair and reorganize and 2 years is usual time span for maximal recovery to take place. Relatives are particularly important since they often have to bear the heavy burden of a difficult patient in the home environment and they need support; they can also often make useful contributions in rehabilitation.

Post-traumatic epilepsy requires treatment. Patients at greatest risk for this complication have penetrating brain injuries with the dura being breached, long PTAs, intracranial haematomas, and early post-traumatic epilepsy. In the UK, such patients should not drive a motor vehicle until they have reported themselves to the Chief Medical Officer and to the Driving and Vehicle Licensing Authority (DVLA), who may suspend them from driving for between 6 and 12 months, or longer if they have epilepsy or neurological deficits.

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