Treatment depends on the pattern of the fracture. Dislocations or displaced fractures of the nasal bones need to be repositioned accurately. If a deformity is to be avoided, treatment is best carried out by facial, ENT or plastic surgeons.

Once diagnosed, the fragment needs repositioning and sometimes fixation with wires or external fixation.

Treatment should be carried out by facial surgeons.

Faciomaxillary surgeons are usually responsible for treating these fractures, which may require internal fixation, interdental wiring (Fig. 10.5) or dental treatment.

Maxillary fractures were divided into three main types by Le Fort, a French surgeon of the early 20th century who broke the faces of corpses with a cudgel to study the fracture lines. His classification is as follows (Fig. 10.6):

All maxillary fractures require urgent attention because the middle third of the face may be unstable and can fall backwards to obstruct the airway. Tracheostomy may be needed.

Because facial injuries are, by definition, head injuries, they are often seen in unconscious patients with brain damage. Always look at the maxillary antrum on the skull radiograph of patients with head injuries; if it is opaque, it is probably full of blood and there is a maxillary fracture.

When the airway is secure, the fracture can be treated by the appropriate specialists. External fixation to the skull is often required to hold the displaced fragments in their correct position.

Concussion is a transient loss of consciousness following a blow to the head. Recovery is usual. The duration of amnesia following the blow is a good guide to the severity of injury. A boxer who is knocked out in a fight has concussion.

There is damage to cerebral tissue from localized bleeding or oedema. Recovery is slower than after concussion and may be incomplete, leaving a neurological deficit.

Compression is usually caused by bleeding into the skull. As the bleeding continues, the brain is compressed and the clinical condition becomes worse. Decompression and arrest of the bleeding can be life saving.

Patients with concussion and contusion are at their worst immediately after injury and then recover. Compression causes steady deterioration instead of recovery, although there may be a lucid interval.

The level of consciousness must be recorded carefully so that any deterioration can be identified quickly. It is not enough to record that the patient is ‘awake’ or ‘unconscious’. A fully conscious patient will be alert and oriented in time and space; i.e. will know where he or she is, what time it is, and will be able to hold a normal conversation.

At the other extreme, the patient will be unrousable and not responding to painful stimuli. Between these two extremes, the level of consciousness may be graded as follows:

A more accurate assessment is possible with the Glasgow coma scale (Table 10.1).

Eye signs. Raised intracranial pressure impairs the function of the iris on the side of the lesion. The size of the pupil and its reaction to light is recorded as a sign of intracranial bleeding. A fixed dilated pupil indicates an urgent problem.

Temperature. The thermoregulatory mechanism may be damaged in brain injury and the body temperature may rise. The temperature may need to be controlled by fans or tepid sponging.

Penetration of the skull always requires exploration by a neurological surgeon to remove dead bone, foreign matter and dead brain. Scalp wounds must not be sutured in the accident department if there is a depressed fracture under the wound.

Cerebral oedema follows any major head injury and can be reduced with diuretics, such as a mannitol infusion, or by controlled hyperventilation with the patient paralysed and ventilated. This treatment is best conducted in a dedicated neurosurgical unit.

The classic story of an extradural haematoma is the patient who walks into hospital after a minor head injury and gives a clear, sensible history. The radiograph shows a small temporal fracture. The patient is discharged home, lapses into unconsciousness and is found dead the following morning. This is a constant nightmare for those who treat head injuries. Extradural haemorrhage can be caused by damage to the middle meningeal artery. As the artery bleeds, a haematoma develops and the brain is gradually compressed. The level of consciousness slowly deteroriates until the patient becomes unrousable. If the diagnosis is made soon enough, the haematoma should be evacuated through a burr hole and the artery tied.

In days gone by, it was safer to drill burr holes than risk missing an extradural bleed but with the advent of CT scanning this complication should not take the surgeon by surprise. CT scanning is now an essential part of the management of head injuries and will show areas of brain damage as well as extradural haematomas and the position of the falx (Fig. 10.10).

Although these investigations are reliable, ligation of the middle meningeal artery can be life saving and the correct site for the burr hole should be memorized by everyone who may be exposed to the treatment of patients with an extradural haematoma. The middle meningeal artery crosses the pterion, which lies two fingers above the zygoma and three fingers behind the orbit (also see Fig. 10.11). The artery can be found either by exposing the fracture and nibbling away the edges of the skull, or by making a burr hole at the pterion itself.

Acute subdural haematomas usually accumulate slowly and cause more gradual loss of consciousness than an extradural haematoma. The cause is the gradual enlargement of a blood clot beneath the dura. As the clot liquefies, serum is drawn into its centre and it gradually increases in size. A chronic subdural haematoma is not a clinical emergency but any patient whose level of consciousness deteriorates in the weeks following a head injury should have a CT scan.

The fact that a patient appears alert and oriented does not exclude brain damage. It is by no means uncommon to find that patients who have been unconscious for only a few minutes are unable to recall events for several days after their accident.

The period of post-traumatic amnesia is a reliable guide to the severity of the head injury:

Cerebrospinal fluid (CSF) can leak from nose or ears if the fracture enters the subdural space. The leak usually ceases spontaneously but if it is profuse or persists for more than 2 weeks the defect in the dura may need to be patched with fascia.

The long-term results of brain damage include continued neurological deficits, personality change, epilepsy, and serious physical disabilities requiring long-term care and rehabilitation.

A neurosurgeon should be consulted in the following circumstances:

Crush fractures are the result of vertical compression as well as flexion. They are stable but cause severe pain in the neck.

Treatment. Symptomatic relief with a four-post collar or cast and analgesia for approximately 6 weeks is all that is required (Fig. 10.14).

Violent flexion of the neck can tear the supraspinous ligament or avulse a spinous process. The fact that the radiographs may show little bony injury is deceptive. The posterior part of the cervical spine may be grossly unstable and neurological damage can occur if the flexion force is repeated.

Treatment. A supporting collar to hold the cervical spine in extension while the soft tissues heal is adequate.

Forward flexion with rotation may cause one or both of the posterior facet joints to ‘jump’ over the edge of the facet below and dislocate (Fig. 10.15). The dislocation cannot occur without associated soft tissue injury but neurological damage is unusual after a simple facet dislocation.

Treatment. A simple dislocation can be treated either by traction or careful manipulative reduction, but this should only be done by an experienced surgeon with special knowledge of spinal disorders.

Fracture dislocations in which the vertebral bodies and the facet joints are disrupted often lead to paraplegia and are usually caused by a fall onto the head, e.g. falling off a horse.

Treatment. The fracture must be reduced and held stable, either by traction or fixation, until it has united. Radiographs taken in flexion and extension are useful in determining the progress of bone union. These views should not be attempted within 6 weeks of injury in case the cervical cord is damaged.

Traction applied with a halter is a useful temporary measure but the pressure on the jaw is uncomfortable for long periods and prevents the patient eating. Skull traction, like skeletal traction in general, is much more acceptable to the patient and is applied through tongs attached to the skull.

Hyperextension must be avoided and traction should be applied in the line of the dislocated segment, not the normal line of the neck.

External fixation can be applied to the neck with a halo screwed to the outer cortex of the skull and supported on metal rods attached to a rigid ‘vest’ (‘vest’ is American for waistcoat) (Fig. 10.16). ‘Halo-vest’ traction is used for unstable fractures, but those which are less unstable may be treated in a firm four-post collar.

Internal fixation may be required to fix the unstable levels of the cervical spine. The operation must be carefully planned so that the exposure does not make the cervical spine completely unstable. If, for example, a hyperextension injury has occurred, the tissues in the front of the cervical spine will be damaged and exploring the spine from behind will weaken the posterior structures as well, leaving little to hold the vertebrae together and the head with no visible means of support.

Cast immobilization of the neck is also possible but is now largely historical (Fig. 10.17). A Minerva cast was used, named after the incident when the demigod Vulcan (himself reputed to have a club foot) split Jupiter’s skull to relieve his headache. Minerva sprang out, fully armed, wearing a heavy metal helmet and singing triumphantly.

The cast was modelled on the helmet and was applied to the head rather like a balaclava helmet extending down onto the chest, but it was heavy and restricted movement of both chest and jaw. A four-post collar is both more effective and more comfortable.

Fractures of the odontoid process, or dens, are difficult to diagnose and are often missed in accident departments. The fracture causes a feeling of unsteadiness in the neck and pain at the base of the skull. These symptoms should suggest the diagnosis.

There are three types of fracture (Fig. 10.19). Type II fractures, in the middle of the dens, have a roughly 50% incidence of non-union and may need atlantoaxial fusion to stabilize the neck.

Judicial hanging fractures the spine by distraction and hyperextension. Similar forces can be applied in falls or by patients slipping under seat-belts. The fracture usually occurs through the pedicles of C2 and is a traumatic spondylolisthesis of C2 on C3 (Fig. 10.20).

Treatment. The fracture should be managed by holding the head steady, with the minimum of traction. Too much traction can cause neurological damage: that is how hanging kills.

Hyperextension in the degenerate cervical spine of the elderly may kink the posterior longitudinal ligament and this can compress the anterior spinal artery (Fig. 10.21), leading to central cord damage. The result is weakness and sensory symptoms in the upper limbs with sparing of the lower limbs, sometimes accompanied by poor bladder control.

Treatment. Immobilization in a collar is all that can be offered.

These lesions may cause permanent damage to the spinal cord.

Treatment. Urgent decompression and stabilization is required in cases where CT scans confirm the diagnosis.

The ring of the atlas can be disrupted by a vertical compressive force, often caused by something landing on the head or the patient falling directly onto the vertex.

Treatment. The fracture should be immobilized in a halo-vest for approximately 6 weeks, followed by a collar for another 2 weeks.

Vertical compression can disrupt the vertebral bodies, and causes severe pain. The fracture must be distinguished from a wedge compression or crush fracture.

Treatment. If there is no neurological damage, a halo-vest for 6 weeks and then a collar is sufficient – as for a fracture of the atlas. If there is neurological damage, the halo-vest is still needed but the paraplegia must also be treated and rehabilitation begun as soon as possible.

There may be no symptoms until 6 or even 12 h after the injury, but patients involved in road traffic accidents are sometimes brought to hospital immediately after the accident before the symptoms have developed. The radiograph is usually normal and the patient may be discharged from the casualty department with a normal X-ray before the onset of symptoms. This may be difficult to explain to sceptical lawyers if the accident becomes the subject of litigation, as many do.

The leading symptoms are pain and stiffness in the neck, accompanied by aching across the shoulders and down the arms, and sometimes dysphagia. Neurological symptoms such as tingling or numbness are sometimes present but usually transient.

The prognosis is notoriously unpredictable. Ninety per cent of patients are free of symptoms within 2 years, but in a very small proportion the symptoms can last for many years. Some patients may be unable to turn the head enough to reverse a car, which may have a serious impact on everyday life and ability to work.

Unfortunately, many patients seeking compensation for their injuries without demonstrable pathology complain of identical symptoms.

A soft supporting collar and analgesics have been advocated in the first few days after injury but the collar should be discarded as soon as possible and physiotherapy begun to restore neck movement. If this is not done, the cervical spine may remain stiff and painful.

Compression, or crush, fractures occur at the thoracolumbar junction where the thoracic kyphosis ends and the lumbar lordosis begins. They are caused by a vertical force just in front of the midline of the spine which compresses the anterior lip of the affected vertebra (Fig. 10.25 and Fig. 10.26).

The injury is commonest in elderly patients with porotic bone who slip and land on their bottom, but it can also occur in younger patients who fall from a height and land on their heels, an injury which also causes a crush fracture of the calcaneum. Pilots who eject from jet aircraft also suffer from this fracture because the upward force of the rockets in the ejector seat is enough to crush the vertebra.

Treatment. The deformity can usually be accepted but if more than 50% of the anterior vertebral height is lost, distraction and internal fixation may be needed (Fig. 10.27). Even in slight deformities, back pain may persist for 2 or more years after injury and sometimes indefinitely.

If there is less than 50% loss of vertebral height, the patient can be mobilized rapidly within the limits of pain.

A crush fracture is caused by axial compression of the anterior margin of the vertebra but a burst fracture is the result of a pure axial force. The sides of the vertebra are pushed outwards and disc material may be forced into the vertebral body or the spinal canal (Fig. 10.28). CT scans are invaluable (Fig. 10.29 and Fig. 10.30).

Burst fractures may be stable or unstable, depending on the pattern of the fracture. They are often associated with neurological damage from backward displacement of the vertebral body or its fragments.

Treatment. Unstable fractures can be treated by bed rest for 6 weeks, brace immobilization or operative fixation. Stable fractures can be mobilized more rapidly, as soon as pain permits.

Rapid deceleration in a road traffic accident throws the victim forwards against the seat-belt and may cause a flexion–distraction injury. The vertebral body may be split, and displacement can be severe.

Combined flexion, compression and rotational forces occur in many injuries, including the fall of masonry onto the flexed spine and falls from a height (Fig. 10.31). The vertebral body is split, or the pedicles fractured and the facet joints may be dislocated. Paraplegia is usual.

Treatment. Fracture dislocations may be treated conservatively or operatively. If the patient is paraplegic, early spinal fusion allows the patient to begin rehabilitation at the earliest possible moment. The onset of paraplegia is a terrible experience for the patient and early rehabilitation helps to give a sense of purpose.

If the patient is not paraplegic, the aim of treatment should be stabilization of the spine to prevent neurological damage. Stabilization can be achieved by immobilization in bed for an extended period of time or by operative fixation to support the spine until union has occurred.

The transverse processes have powerful muscles attached to them and can be avulsed by violent twisting or flexing movements or by violent muscle spasm such as an epileptic fit. An avulsed transverse process is not a serious injury but the pain and muscle spasm last for 6–8 weeks.

Compression or crush fractures at the thoracolumbar junction are described on page 159.

Twisting and rotational forces disrupt vertebrae in the lumbar spine (Fig. 10.32), as they do in the thoracic spine (p. 156), and cause neurological damage. Because the spinal cord does not extend below the first lumbar vertebra, only the lower motor neurone and sensory nerves are involved and the neurological problem is very different from the cord injuries of the cervical and thoracic spines.

Treatment. As in other situations, treatment may be conservative or operative but conservative treatment is the rule because the cauda equina is involved in this region and nerve roots are more robust than the spinal cord. Cauda equina lesions have a much better prognosis than cord lesions.

The large mass of cancellous bone and muscle makes non-union of such fractures unusual but fixation may be required to stabilize an unstable fracture (Fig. 10.33). Details of management depend upon the anatomy and the CT scan.

One of the difficulties in determining the final result is ‘root escape’. The nerve roots are tougher than the spinal cord and it is possible for the cord to be crushed or severed while the roots that cross the fracture remain intact. Surviving roots may not work normally at first because of oedema, axonotmesis or neurapraxia, but recovery from these conditions is possible. The lower the lesion, the more roots are likely to escape damage.

The prognosis depends on the neurological findings 48 h after injury. Patients with complete cord loss at 48 h do not recover but those with some cord function may continue to improve for up to 2 years after injury.

The completely denervated bladder distends without the patient being aware of it and retention with overflow develops. If this is not recognized, back pressure on the kidneys and renal failure may follow. Urinary infection is a serious problem and every care must be taken to prevent it by catheterization with strict sterile technique and careful management.

If the bladder retains some autonomic activity, there may be reflex spasm of the detrusor muscle and unexpected emptying of the bladder. As with the completely denervated bladder, the automatic bladder must be catheterized with full sterile precautions.

In the later stages of rehabilitation, the voiding reflex can sometimes be put to good use if it can be initiated by a simple manoeuvre such as pressure on the lower abdomen.