Nerve injuries, peripheral nerve entrapments and spinal cord compression

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Contents

Introduction

Peripheral nerves may be trapped, compressed or injured at any position along their course, although there are certain regions where they are especially vulnerable. Injury to the nerve occurs when the nerve is either relatively superficial and exposed, or lying adjacent to bone so that the jagged fractured ends of the bone may directly injure the nerve. Nerve entrapments occur particularly where the peripheral nerve passes through a tunnel formed by ligaments, bone and/or muscle.

Acute nerve injuries

Peripheral nerve anatomy

The axon projects from the cell body and is surrounded by a basement membrane and myelin sheath. The axon is covered by the endoneurium, the innermost layer of connective tissue, and a number of axons are grouped together in a bundle called a fascicle, which is invested by a further connective tissue sheath called the perineurium. The peripheral nerve consists of a group of fascicles covered by the outermost layer of connective tissue, the epineurium.

Classification of nerve injuries

There is no single classification system that can describe all the many variations of nerve injury. Most systems attempt to correlate the degree of injury with symptoms, pathology and prognosis. Seddon in 1943 introduced a classification of nerve injuries based on three main types of nerve fibre injury and whether there is continuity of the nerve (Table 54, “Classification of nerve injuries”).

Table 54. Classification of nerve injuries
Neurotmesis Axonotmesis Neurapraxia Adapted from Seddon H. Surgical Disorders of the Peripheral Nerves. 3rd ed. Oxford: Blackwells; 2005. Reproduced with permission.
Pathological
Anatomical continuity May be lost Preserved Preserved
Essential damage Complete disorganisation, Nerve fibres interrupted Selective demyelination of larger fibres, no degeneration of axons
Schwann sheaths preserved
Clinical
Motor paralysis Complete Complete Complete
Muscle atrophy Progressive Progressive Very little
Sensory paralysis Complete Complete Usually much sparing
Autonomic paralysis Complete Complete Usually much sparing
Electrical phenomena
Reaction of degeneration Present Present Absent
Nerve conduction distal to the lesion Absent Absent Preserved
Motor-unit action potentials Absent Absent Absent
Fibrillation Present Present Occasionally detectable
Recovery
Surgical repair Essential Not necessary Not necessary
Rate of recovery 1–2 mm a day after repair 1–2 mm a day Rapid, days or weeks
March of recovery According to order of innervation According to order of innervation No order
Quality Always imperfect Perfect Perfect

Neurotmesis

Neurotmesis is the most severe injury. The nerve is completely divided and complete distal Wallerian degeneration occurs. There is complete loss of motor, sensory and autonomic function.

Although the term neurotmesis implies a cutting of the nerve, the term is also used when the epineurium of the nerve is still in continuity but the axons have been destroyed and replaced by scar tissue to such a degree that spontaneous regeneration is impossible.

If the nerve has been completely divided, axonal regeneration causes a neuroma to form in the proximal stump.

Axonotmesis

Axonotmesis is characterised by complete interruption of the axons and their myelin sheaths, but with preservation of the epineurium and perineurium. Spontaneous regeneration will occur, with the intact endoneurial sheaths guiding the regenerating fibres to their distal connections. Axonotmesis is initially clinically indistinguishable from neurotmesis because there is complete and immediate loss of motor, sensory and autonomic function distal to the lesion with a similar electromyographic (EMG) picture. Regeneration occurs at a rate of 1–2 mm per day so that the time of recovery will depend on the distance between a lesion and the end organ, as well as on the age of the patient. The major types of injuries causing an axonotmesis include compression, traction, missile and ischaemia.

Neurapraxia

Neurapraxia is the most mild form of injury and is likened to a transient ‘concussion’ of the nerve, where there is a temporary loss of function that is reversible within hours to months of the injury (with an average of 6–8 weeks). If there is initially a complete loss of function, neurapraxia cannot be distinguished from the more serious type of injury but will be recognised in retrospect when recovery of function has occurred sooner than would be possible followingWallerian degeneration.

Causes of peripheral nerve injury

The type of trauma will determine the nature of the injury to the nerve (Types of trauma and the nature of nerve injury).

Management of nerve injuries

The basis of management depends on a precise assessment of the damage that has been done to the nerve (General guidelines for management of nerve injuries). The types of injuries vary considerably, from an isolated single nerve lesion to a complex nerve injury in a patient with multiple trauma.

Brachial plexus injury

The mechanisms of injury are the same as for any peripheral nerve (see Types of trauma and the nature of nerve injury).

Birth injuries

Birth injuries include Erb's palsy due to damage to the upper trunk of the brachial plexus, Klumpke's paralysis due to damage to the lower trunk of the brachial plexus (C8 and T1; resulting from the arm being held up while traction is applied to the body during a breech delivery), and paralysis of the whole arm as a result of severe birth trauma.

Adolescents and adults

In adolescents and adults the most common cause is severe traction on the brachial plexus, resulting most frequently from a motorbike or motor vehicle accident. The trauma may result in damage to any part of the plexus but severe traction may result in tearing of the arachnoid and dura with nerve root avulsion from the spinal cord.

Management

The management involves determination of the exact neurological injury, particularly the part of the brachial plexus involved (The brachial plexus passing through the cervicobrachial junction. (Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.)). A Horner's syndrome is evidence there has been avulsion of the nerve roots from the spinal cord.

The brachial plexus passing through the cervicobrachial junction. (Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.)

A magnetic resonance imaging scan may show the pseudomeningocele, characteristic of nerve root avulsion. Electrical studies provide useful baseline studies for future comparison. It is reasonable to obtain these studies 8 weeks after the injury.

There is debate concerning the indications for surgical intervention for closed brachial plexus injuries in adults. In general there is little benefit from exploration of the plexus in closed injuries although some surgeons do advocate exploration approximately 4 months after the injury if clinical and electrical evidence shows the lesion to be complete. If the injury is improving there is no indication for surgery and management includes intensive physiotherapy and mobilisation of the joints. There is no place for surgery if there is evidence of nerve root avulsion from the cord.

Peripheral nerve entrapment

Entrapment neuropathies occur particularly when nerves pass near joints. Less common forms of entrapment neuropathies may lie at a distance from a joint. Entrapment neuropathies (the more common ones are shown in bold) shows a list of the common and less frequent entrapment neuropathies.

Carpal tunnel syndrome

This is by far the most common nerve entrapment and women are affected four times more frequently than men.

Anatomy

The carpal tunnel is a fibro-osseous tunnel on the palmar surface of the wrist (The carpal tunnel, just distal to the wrist. (Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.)). The dorsal and lateral walls consist of the carpal bones, which form a crescentric trough. A tunnel is made by the fibrous flexor retinaculum, which is attached to the pisiform and hook of the hamate medially and the tuberosity of the scaphoid and crest of the trapezium laterally. The contents of the tunnel are the median nerve, flexor tendons of the flexor digitorum superficialis, flexor digitorum profundus and flexor pollicis longus.

The carpal tunnel, just distal to the wrist. (Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.)

Aetiology

The initial symptoms occur in women during pregnancy and in both sexes when they are performing unusual strenuous work with their hands, although the features of carpal tunnel syndrome may present at any stage throughout the adult years. There are a number of systemic conditions that are associated with and that may predispose to carpal tunnel syndrome:

  • pregnancy and lactation
  • contraceptive pill
  • rheumatoid arthritis
  • myxoedema
  • acromegaly.

Any local condition around the wrist joint that decreases the size of the carpal tunnel will also predispose to carpal tunnel syndrome. These include a ganglion, tenosynovitis, unreduced fractures or dislocations of the wrist or carpal bones, and any local arthritis.

Clinical features

The principal clinical features of carpal tunnel syndrome are pain, numbness and tingling.

The pain, which may be described as burning or aching, is frequently felt throughout the whole hand and not just in the lateral three digits. There is often a diffuse radiation of the pain up the forearm to the elbow and occasionally into the upper arm. The symptoms are particularly worse at night, and on awakening the patient has to shake the hand to obtain any relief.

Numbness and tingling principally occur in the lateral three and a half fingers, in the distribution of the median nerve, although the patient frequently complains of more diffuse sensory loss throughout the fingers. This symptom is also worse at night and with activity. The patient frequently complains that the hand feels ‘clumsy’, but with no specific weakness.

There are often only minimal signs of median nerve entrapment at the wrist. The Tinel sign (tingling in the median nerve innervated thumb, index and middle finger) may be elicited by tapping over the median nerve but its absence has little diagnostic value.

If the compression has been prolonged there may be signs of median nerve dysfunction including wasting of the thenar muscle, weakness of muscles innervated by the distal median nerve, especially abductor pollicis brevis, and diminished sensation over the distribution of the median nerve in the hand. The clinical diagnosis can be confirmed by EMG examination.

Treatment

Surgery involving division of the flexor retinaculum is a simple and effective method of relieving the compression and curing the symptoms. However, conservative treatment involving the use of a wrist splint and non-steroidal anti-inflammatory agents is appropriate if the symptoms are mild or intermittent or if there is a reversible underlying precipitating condition, such as pregnancy or oral contraceptive pill.

Ulnar nerve entrapment at the elbow

Anatomy

The ulnar nerve runs behind the medial epicondyle of the humerus and enters the forearm through a fibroosseous tunnel formed by the aponeurotic attachment of the two heads of flexor carpi ulnaris, which span from the medial epicondyle of the humerus to the olecranon process of the ulnar forming the cubital tunnel (The ulnar nerve passing behind the medial epicondyle of the humerus and through the cubital tunnel. (Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.)). During flexion of the elbow the ligament tightens, and the volume of the cubital tunnel decreases, putting increasing pressure on the underlying nerve. Compression can also be due to injuries in the region producing deformity of the elbow, although the features of ulnar nerve entrapment do not usually appear for some years. This delay in the appearance of symptoms led to the term ‘tardy ulnar palsy’.

The ulnar nerve passing behind the medial epicondyle of the humerus and through the cubital tunnel. (Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.)

Aetiology

In most cases there is no particular predisposing cause. In a minority there are underlying factors that predispose to nerve entrapment, including lengthy periods of bed rest from coma or major illness, and poor positioning of the upper limbs during long operations causing prolonged pressure on the nerve. Other causes include arthritis of the elbow, ganglion cysts of the elbow joint and direct trauma.

Clinical features

The clinical features include paraesthesia and numbness in the ring and little finger of the hand and the adjacent medial border of the hand, wasting of the hypothenar eminence and interossei muscles, and weakness.

In advanced cases, entrapment of the ulnar nerve will lead to weakness of the muscles of the hypothenar eminence, the interossei, the medial two lumbricals, adductor pollicis, flexor digitorum profundus (ring and little finger) and flexor carpi ulnaris. Paralysis of the small muscles of the hand causes ‘claw hand’, this posture being produced by the unopposed action of their antagonists. As the interossei cause flexion of the fingers at the metacarpophalangeal joints and extension at the interphalangeal joints, when these muscles are paralysed the opposite posture is maintained by the long flexors and extensors causing flexion at the interphalangeal joints and hyperextension at the metacarpophalangeal joints. This is most pronounced in the ring and little fingers as the two radial lumbricals, which are innervated by the median nerve, compensate to some degree for the impaired action of the interossei on the index and middle fingers. Froment's sign is demonstrated by asking the patient to grasp a piece of cardboard between the index finger and thumb against resistance. There will be flexion of the interphalangeal joint of the thumb because the median innervated flexor pollicis longus is used rather than the weakened adductor pollicis.

Treatment

Conservative treatment may be tried if the clinical features are minor and not progressive. The patient should avoid putting pressure on the nerve at the elbow during reading, sitting or lying and should cease heavy work with the arms.

Surgery involves decompression of the nerve and is indicated if there are progressive symptoms or signs and if there is any wasting or weakness.

Meralgia paraesthetica

Meralgia paraesthetica results from entrapment of the lateral cutaneous nerve of the thigh beneath the inguinal ligament, just medial to the anterior superior iliac spine. At this position the nerve passes between two roots of attachment of the inguinal ligament to the iliac bone and there is a sharp angulation of the nerve as it passes from the iliac fossa into the thigh.

Prolonged standing or walking and an obese pendulous anterior abdominal wall accentuates the downward pull on the inguinal ligament and may predispose to entrapment of the nerve. The syndrome is most frequently seen in middle-aged men who are overweight and in young army recruits during strenuous training.

The principal symptom is a painful dysaesthesia in the anterolateral aspect of the thigh with the patient often describing the sensation as ‘burning’, ‘pins and needles’ or ‘prickling’.

The only neurological sign is diminished sensation over the anterolateral aspect of the thigh in the distribution of the lateral cutaneous nerve.

The symptoms may be only minor and the patient may be satisfied with reassurance. The unpleasant features may resolve with conservative treatment, including weight reduction in an obese patient. Surgery may be necessary if the symptoms are debilitating and the procedure involves decompression of the nerve or, if that fails, division of the nerve.

Spinal cord compression

Compression of spinal cord is a common neurosurgical problem and requires early diagnosis and urgent treatment if the disastrous consequences of disabling paralysis and sphincter disturbance are to be avoided.

Although there are a large range of possible causes of spinal cord compression in clinical practice the majority are due to:

  • Extradural
    • Trauma
    • Metastatic tumour
    • Extradural abscess
  • Intradural, extramedullar
    • Meningioma
  • Schwannoma
  • Intramedullary
    • Glioma (astrocytoma and ependymoma)
  • Syrinx

Presenting features

The two major presenting features that are the hallmark of spinal cord compression are pain and neurological deficit. There is considerable variation in the manner in which these two major features present, and depend on the pathological basis, the site of the compression and the speed of the compression.

Pain

Pain is a common early feature of spinal cord compression and often precedes any neurological disturbance, sometimes by many months. The pain is due to involvement of local pain-sensitive structures, such as the bone of the vertebral column. Involvement of a spinal nerve root will cause pain radiating in the affected region. Thoracic cord compression with involvement of the thoracic nerve root will often be associated with pain radiating around the chest wall. This ‘girdle’ pain is an important feature associated with a lesion which may cause spinal cord compression. In addition there is also a ‘central’ pain due to spinal cord compression, which is described as an unpleasant diffuse dull ache with a ‘burning’ quality.

Flexion or extension of the neck may cause ‘electric shock’ or tingling sensations radiating down the body to the extremities. This is called Lhermitte's sign, and is typically associated with cervical cord involvement.

Neurological deficit

The neurological features of spinal cord compression consist of progressive weakness, sensory disturbance and sphincter disturbance.

The motor impairment will be manifest as a paralysis, and the level of the weakness will depend on the position of the cord compression. Thoracic cord compression will result in a progressive paraparesis of the lower limbs and if the cervical cord is involved the upper limbs will also be affected. Compression of the corticospinal pathways will result in upper motor neurone weakness with little or no wasting, increased tone, increased deep tendon reflexes and positive Babinski response. As the cord becomes more severely compressed a complete paraplegia will result. The compressing mass will also cause weakness of the nerve root segment at the involved level. In the cervical region this will result in a lower motor neurone weakness of the involved nerve roots in the upper limbs. In the lumbar region involvement of the conus medullaris may produce a mixture of lower motor neurone and upper motor neurone signs in the lower limbs. Cauda equina compression produces a lower motor neurone pattern of weakness.

Sensory disturbance

A sensory level is the hallmark of spinal cord compression. In the thoracic region the sensory level will be to all modalities of sensation over the body or trunk, although there may be some sparing of some modalities in the early stages of compression. A useful guide to remember is the T4 dermatome lies at the level of the nipple, the T 7 at the xiphisternum and T10 at the umbilicus.

Sphincter involvement

Sphincter disturbance often follows compression of the spinal cord, with the first symptom being difficulty in initiating micturition, which is followed by urinary retention, often relatively painless. Constipation and faecal incontinence will subsequently occur. The clinical signs include an enlarged, palpable bladder, diminished perianal sensation and decreased anal tone.

In summary the clinical features of spinal cord compression are:

  • Pain - local and radicular.
  • Progressive weakness of the limbs.
  • Sensory disturbance - often a sensory level.
  • Sphincter disturbance.

Management

Spinal cord compression is a neurosurgical emergency. Investigation and treatment must be undertaken as a matter of urgency once the diagnosis is suspected.

The radiological studies undertaken to confirm the diagnosis of spinal cord compression include:

  • Plain spinal X-rays
  • MRI
  • CT scan (with intrathecal contrast).

The MRI is of considerable value in diagnosing the cause and position of spinal cord compression and is by far the best investigation, as it will clearly show the pathological changes in the vertebral body, spinal canal, spinal cord and paravertebral region, thereby aiding with planning the treatment. Plain X-rays and CT scan will help show the focal bony destruction.

Treatment

The standard treatment for spinal cord compression is urgent surgery, except in some cases of compression due to malignant tumour, in which treatment with highdose glucocorticosteroids and radiotherapy may be indicated.

Common causes of spinal cord compression

Malignant spinal cord compression

By far the most common cause of spinal cord compression, this results from extradural compression by malignant tumours. The most common tumours are:

  • Carcinoma of the lung
  • Carcinoma of the breast
  • Carcinoma of the prostate
  • Carcinoma of the kidney
  • Lymphoma
  • Myeloma.

Surgical management for malignant spinal cord compression utilises either:

  • Decompressive laminectomy (posterior approach)
  • Vertebrectomy and fusion (anterior approach).

Urgent radiotherapy, combined with high-dose glucocorticosteroids may be effective in controlling the tumour causing spinal cord compression and is sometimes advisable if the patient has a known primary tumour that is radiosensitive and if there is a partial incomplete neurological lesion that is only slowly progressive.

Schwannoma (neurofibroma)

Schwannomas are the most common of the intrathecal tumours and may occur at any position. They arise invariably from the posterior nerve roots and grow slowly to compress the adjacent neural structures. Occasionally the tumour extends through the intervertebral foramen to form a ‘dumbell’ tumour, which may rarely present as a mass in the thorax, neck or posterior abdominal wall.

The presenting features are those of a slowly growing tumour causing cord compression. There is frequently some degree of a Brown-Séquard syndrome due to the lateral position of the tumour. The treatment is surgical excision.

Spinal meningioma

Spinal meningiomas occur particularly in middle-aged or elderly patients and there is a marked female predominance. The tumour grows extremely slowly and there is usually a long history of ill-defined back pain, often nocturnal, and a slowly progressive paralysis prior to diagnosis.

Intramedullary tumours

Ependymoma and astrocytoma of the spinal cord are uncommon, with the presenting features depending on the level of cord involvement. Ependymomas not infrequently arise in the filum terminale and will cause features of cauda equina compression. There is often a history of low back and leg pain, progressive weakness in the legs (often with radicular features) sensory loss over the saddle area and eventually sphincter disturbance.

Intervertebral disc prolapse

Intervertebral disc herniation is a common cause of nerve root compression, but occasionally the disc may prolapse directly posteriorly (centrally), causing compression of the spinal cord in the cervical or thoracic region and of the cauda equina in the lumbar region.

Urgent surgery is essential to relieve the compression.

Spinal abscess

Spinal abscess is an uncommon condition requiring urgent treatment. The spinal cord compression is due to both inflammatory swelling and pus, and presenting features include severe local spinal pain with rapidly progressive neurological features of spinal cord compression. There are frequently constitutional features of infections such as high fever, sweating and tachycardia. The MRI is the preferred investigation and treatment consists of urgent surgery with appropriate antibiotic medication.

Cervical myelopathy

Cervical myelopathy results from cervical cord compression due to a narrow cervical vertebral canal. The constriction of the canal enclosing the cervical cord is due to a combination of congenital narrowing, and cervical spondylosis involving hypertrophy of the facet joints and osteophyte formation, hypertrophy of the ligamenta flava and bulging of the cervical disc. The myelopathy results from both the direct pressure on the spinal cord and ischaemia of the cord due to compression and obstruction of the small vessels within the cord or to compression of the feeding radicular arteries within the intervertebral foramen.

There is frequently a history of slowly progressive disability, although it is not unusual for the neurological disability to deteriorate rapidly, particularly following what might be even a minor or trivial injury.

Muscular weakness manifest by clumsiness involving the hands and fingers, impairment in fine-skilled movements and dragging or shuffling of the feet is the most common initial symptom. Sensory symptoms are frequent, and occur as diffuse numbness and paraesthesia in the hands and fingers.

The MRI will confirm the severity of the cord compression and show the exact pathological basis for the compression. An additional benefit of MRI is that it may show myelomalacia (high signal within the cord) indicating the severity of the compression and a poorer prognosis following surgery.

Surgery is indicated for clinically progressive or moderate or severe myelopathy. The operation may involve either a posterior decompression laminectomy or, if the compression is predominantly anterior to the cord, an anterior approach with excision of the compressive lesion and fusion is preferred.

Spinal injuries

Trauma to the spinal column occurs at an incidence of approximately 2–5 per 100 000 population. Adolescents and young adults are the most commonly affected, with most serious spinal cord injuries being a consequence of road traffic accidents and water sports (especially diving into shallow water), skiing and horse riding accidents.

MECHANISM OF INJURY

Although severe disruption of the vertebral column usually causes serious neurological damage it is not always possible to correlate the degree of bone damage with spinal cord injury. Minor vertebral column disruption does not usually cause neurological deficit, but occasionally may be associated with severe neurological injury. The mechanism of the injury will determine the type of vertebral injury and neurological damage

Trauma may damage the spinal cord by direct compression by bone, ligament or disc, haematoma, interruption of the vascular supply and/or traction.

CERVICAL SPINE

Flexion and flexion-rotation injuries are the most common type of injury to the cervical spine, with the C5/6 level being the most common site. There is often extensive posterior ligamentous damage and these injuries are usually unstable. Compression injuries also most frequently occur at the C5/6 level. The wedge fracture injuries are often stable because the posterior bony elements and longitudinal ligaments are often intact. However, those with a significant retropulsed fragment are likely to have disruption of the associated ligaments and are considered unstable. When combined with a rotation force in flexion, a ‘tear drop’ fracture may occur, with separation of a small anterior-inferior fragment from the vertebral body, and these should also be considered unstable.

Hyperextension injuries are most common in the older age group and in patients with degenerative spinal canal stenosis. The bone injury is often not demonstrated and the major damage is to the anterior longitudinal ligament secondary to hyperextension.

THORACOLUMBAR SPINE

Flexion-rotation injuries most commonly occur at the T12/L1 level and result in anterior dislocation of T12 on the L1 vertebral body.

Compression injuries are common with the vertebral body being decreased in height. These injuries are usually stable and neurological damage is uncommon.

Open injuries may result from stab or gunshot wounds that result in damage to the spinal cord.

Neurological impairment

There is a state of diminished excitability of the spinal cord immediately after a severe spinal cord injury, which is referred to as ‘spinal shock’. There is an areflexic flaccid paralysis. The duration of spinal shock varies, with minimal reflex activity appearing within a period of 3–4 days or being delayed up to some weeks.

COMPLETE LESIONS

The most severe consequence of spinal trauma is a complete transverse myelopathy in which all neurological function is absent below the level of the lesion, causing either a paraplegia or quadriplegia (depending on the level), impairment of autonomic function including bowel or bladder function, and sensory loss.

INCOMPLETE LESIONS

There are numerous variations of neurological deficit manifest in incomplete lesions but with some specific syndromes:

  • Anterior cervical cord syndrome - due to compression of the anterior aspect of the cord resulting in damage to the corticospinal and spinothalamic tracts with motor paralysis below the level of the lesion and loss of pain, temperature and touch sensation but relative preservation of light touch, proprioception and position sense, which are carried by the posterior columns.
  • Central cord syndrome - due to hyperextension of the cervical spine with damage located centrally causing the most severe injury to the more centrally located cervical tracts, which supply the upper limbs. There is a disproportionate weakness in the upper limbs compared with the extremities. Sensory loss is usually minimal.
  • Brown-Séquard syndrome - from hemisection of the cord resulting in ipsilateral paralysis below the level of the lesion with loss of pain, temperature and touch on the opposite side.

Management of spinal injuries

As little can be done to repair the damage caused by the initial injury, major efforts are directed towards prevention of further spinal cord injury and complications resulting from the neurological damage. The general principles of management are:

  • Prevention of further injury to the spinal cord
  • Reduction and stabilisation of bony injuries
  • Prevention of complications resulting from spinal cord injury
  • Rehabilitation.

The initial first-aid management of patients with injuries to the spinal column and spinal cord require the utmost caution in turning and lifting the patient. The spine must be handled with great care to avoid inflicting additional damage. Sufficient help should be available before moving the patient to provide horizontal stability and longitudinal traction. Spinal flexion must be avoided. A temporary collar should be applied if the injury is to the cervical spine. Hypotension and hypoventilation immediately follow an acute traumatic spinal cord injury and this may not only be life-threatening but also may increase the extent of neurological impairment. Respiratory insufficiency may require oxygen therapy and ventilatory assistance. Loss of sympathetic tone may result in peripheral vasodilatation with vascular pooling and hypotension. Treatment will include the use of intravascular volume expanders, alpha-adrenergic stimulators and intravenous atropine. Careful attention should be paid to the body temperature as the spinal patient is poikilothermic and will assume the temperature of the environment. A nasogastric tube should be passed to avoid problems associated with vomiting due to gastric stasis and paralytic ileus and a urinary catheter is necessary. Prophylaxis for deep vein thrombosis and subsequent pulmonary embolus should be commenced as soon as possible.

Radiological investigations will include plain X-rays, computer tomography and MRI.

High-dose dexamethasone is usually administered as soon as possible for patients with spinal cord compression but there is no conclusive proof of its effectiveness.

Spinal reduction and stabilisation

Skeletal traction for restoration and/or maintenance of normal alignment of the spinal column is an effective treatment with a variety of cervical traction devices available. The traction must be commenced under X-ray or fluoroscopic control and great care should be taken to avoid distraction at the fracture site, as traction on the underlying cord will worsen the neurological injury. Reduction of facet dislocations may involve either manipulation under fluoroscopic control with the patient under general anaesthesia or may require open surgery. This management must only be undertaken in specialised neurosurgical or spinal injury departments. Following reduction the position is usually maintained with either skeletal traction or halo immobilisation.

Injuries of the thoracolumbar spine can usually be managed conservatively by postural reduction in bed.

There has been considerable controversy over surgical intervention with spinal cord injuries. The damage to the spinal cord occurs principally at the time of the injury and there has been no evidence to show improved neurological function from acute operative decompression of the spine. The following are the general indications for surgical intervention:

  • Progression of neurological deficit is an absolute indication
  • Patients with a partial neurological injury who fail to improve, with radiological evidence of persisting compression of the spinal cord
  • An open injury from a gunshot or stab wound
  • Stabilisation of the spine if there is gross instability or if it has not been possible to reduce locked facets by closed reduction.

Further management

Following reduction and immobilisation of fractures, the principles of continuing care involve avoidance of potential complications in patients who are paraplegic or quadriplegic and early rehabilitation, which commences as soon as the injury has stabilised.

Further reading

Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.

Kline DG, Judice DJ. Operative management of selected brachial plexus lesions. J Neurosurg. 1983;58:631–649.

Pang D,Wessel HB. Thoracic outlet syndrome. Neurosurgery. 1988;22:105–121.
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