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Cervical Spine Injuries

Chapter · January 2010

DOI: 10.1007/978-1-84882-070-8_6

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6
Cervical Spine Injuries
John P. Adams, Jake Timothy, and Justin McKinlay
Key Points
1. Cervical spine injuries account for about 50%
of spinal injuries
2. 10–30% of spinal trauma results in spinal cord
injury (SCI)
3. Cervical spine injuries are often associated
with other injuries, including head injury in up
to 25%
4. 5–10% of patients with a cervical SCI will be
unconscious at presentation
5. Mortality for combined head and cervical spine
injuries exceeds 10%
6. SCI should be assumed in any patient who
present with a depressed conscious level
Introduction
The main causes of spinal cord injuries (SCI) are
road traffic accidents, falls, assaults, and sporting
accidents. There is a bimodal age distribution in
cervical spine trauma with young males and the
elderly accounting for the majority of victims. The
introduction of airbags has led to a reduction in
cervical spine injuries in motor-vehicle accidents
(although they put the individual at higher risk
if deployed and a seatbelt is not being worn).
Improved emergency care, aggressive treatment of
complications, and the development of specialist
centers has led to a decrease in mortality rate from
spinal injuries to around 2–5%. The long-term
 51
physical, psychological, and socioeconomic impli-
cations for the victim and their care-givers cannot
be underestimated.
The following should increase the level of
suspicion for SCI:
1. Unexplained hypotension or bradycardia
2. Diaphragmatic respiratory pattern
3. Priapism or reduced anal tone
4. Areflexia
5. Variable response to painful stimulation
(sensory level)
6. Ejection from a motor vehicle
Primary and Secondary Spinal-Cord
Injury
Primary injury to the cord can occur through a
variety of mechanisms including compression of
neural elements by displaced bony fragments and
disc material, penetrating injuries, extradural pathol-
ogy (e.g., hematoma) or vascular compromise. Sub-
sequent swelling of the cord, loss of autoregulation,
and neurogenic shock with systemic hypotension
will exacerbate cord ischemia. In addition, the cord
is further compromised by the triggering of a sec-
ondary biochemical cascade and the local release
of cytotoxic substances.
The major cause of secondary injury is hypop-
erfusion of the cord which can be caused by vascular
damage, microthrombi, swelling, or systemic
hypotension.
52
Initial Stabilization
Trauma victims are now routinely immobilized
on a spine board with their neck in the neutral
position in a rigid cervical collar. This approach
has undoubtedly led to a reduction in SCI during
extraction and the early-management phase. Some
concerns remain, however, about the definition
of the neutral position. There is good evidence
that a small amount of forward flexion of the neck
(equivalent to a 2  cm elevation of the occiput)
leads to a favorable increase in the spinal canal/
spinal cord ratio at the C5/6 level, a region of fre-
quent unstable cervical spine injury. What is clear
is that patients with conditions such as ankylos-
ing spondylitis should not have their neck forcibly
extended into the “neutral” position and if con-
scious, should be allowed to keep their neck in the
most comfortable position.
Initial stabilization should be based on standard
ATLS protocols with airway management (a), and
cervical spine control, breathing (b), and ventila-
tion, and circulation and hemorrhage control (c).
Airway
Tracheal intubation may be required for a number
of reasons:
1. Patient is obtunded and not protecting the
airway
2. Airway obstruction (blood, vomit, edema, ret-
ropharyngeal hematoma, etc.)
3. High-cord injury associated with respiratory
failure
4. To facilitate imaging and treatment of other
injuries
5. Severe maxillofacial injuries (where a subse-
quent early tracheostomy may be appropriate)
Suxamethonium should not be used beyond the first 48 h after injury
because of the risk of hyperkalaemia.
MRI investigations have been useful in document-
ing both the occurrence and nature of secondary
SCI occurring after the initial primary injury. In the
past, deteriorations have often been ascribed to
clinical interventions such as intubation, whereas it
now seems that most cases of secondary injury are
probably an inevitable consequence of the primary
injury. Nevertheless, all airway maneuvers will
J.P. Adams et al.
result in some degree of neck movement, both in
general and at the site of the injury. The routine use
of immobilization during airway maneuvers in
at-risk patients is accepted as the standard of care.
The most appropriate technique for tracheal
intubation in patients with cervical spine injury
continues to be debated as there are no outcome
studies that clearly show superiority of one
technique over another. Although many anesthe-
tists indicate a preference for awake fiber optic
intubation, the majority of them also confess
to limited practical skill and experience with
the technique. The acute trauma setting also
largely precludes its use. Equally, there are a large
number of series and reports that confirm that
rapid sequence induction of general anesthesia
followed by direct laryngoscopy, with manual
inline stabilization and the use of bimanual
cricoid pressure is both widely practiced, and
compares as well, in terms of neurological outcome,
as other techniques.
Cricoid pressure is not contraindicated in the presence of a suspected
cervical spine injury, but a bimanual technique should be used.
Manual in Line Stabilization (MILS)
The goal of MILS is to apply sufficient force to
the head and neck to limit the movement that
might result during intubation and airway
control. The assistant should ideally apply equal
and counter forces to those generated by the
laryngoscopist, but without the application of
traction. Compared with other techniques of
C-spine immobilization (collar, tape, sandbags),
MILS provides better intubating conditions. The
incidence of Grade 3 and 4 Cormack and Lehane
view is 22% with MILS and 64% when immobi-
lization is provided by collar, tape, and sandbags.
Although MILS is superior to other immobilizing
techniques, it still impacts on the view at direct
laryngoscopy. When applied to normal patients
with normal spines, the view at laryngoscopy
deteriorates by one grade in 36% of patients, and
by two grades in 10%.
Our recommendation is to remove the anterior portion of the cervical
collar and have a skilled assistant perform MILS.
The use of a McCoy laryngoscope and gum elastic bougie will mini-
mize the force and obviate the need to achieve a Grade 1 view.
6.  Cervical Spine Injuries 53

Movement During Airway Interventions The level of injury influences the effect on ventilation:
Level of
All airway maneuvers will result in some degree
injury Effect on respiration Clinical consequence
of neck movement, although the amounts are
C1–C3 Complete paralysis of all Apnea and immediate death,
small and typically within physiologic ranges.
respiratory muscles. unless mechanical ventilation
is applied. Ventilator-
dependant unless a
Role of Awake Fiber Optic Intubation diaphragm stimulator is used.

The use of a technique by practitioners not skilled C3–C5 Varied impairment of Ventilation often necessary in
the diaphragmatic the acute stages. Vast
in its use carries risk. Failed awake intubations have
contraction force. majority will wean from
been implicated in morbidity and mortality claims mechanical ventilation
by the American Society of Anesthesiologists. depending upon functional
Nevertheless, AFOI does carry theoretical advan- descent of injury level,
tages that support its use in cervical-spine-injured recovery of function in
incomplete lesions, and
patients:
improvement in respiratory
· The head and neck may be left in a neutral posi- mechanics over time.
C6–C8 Diaphragm and accessory Expiration entirely passive.
tion and collars can be left on.
cervical inspiratory Secretion retention is a
· Little spinal movement is required to achieve muscles intact. problem. Respiratory failure
laryngeal visualization. Intercostals and rarely seen unless coexistent
· Protective reflexes are left intact. abdominal muscles chest/lung injury, preexisting
· A neurological examination can be performed paralyzed. lung disease, or the need for
surgery.
post-intubation.
· Patients can be positioned awake once intu-
bated, thereby avoiding potentially injurious
positions. Lung Volumes in SCI
That AFOI requires special equipment, cannot The level of injury has a great bearing on lung
be performed on uncooperative patients, is made volumes. The FVC, FEV1 and inspiratory capacity
significantly more difficult in the presence of increase with descending SCI down to T10. It is
airway secretions and blood, and is more time- estimated that the percentage of FVC increases by
consuming than direct laryngoscopy, limits its use 9% per vertebral level as the level of injury
in the A&E setting. descends. FEV1 and FVC are maximally reduced
Aspiration is a major concern, so all obtunded immediately post-injury (up to 33% of predicted)
patients should be rapidly intubated and venti- and improve initially quite rapidly up to 5 weeks
lated with MILS and cricoid pressure and a (45% predicted), with a more gradual improve-
nasogastric or orogastric tube inserted to empty ment at 5 months (60% predicted). The reduction
the stomach. in FRC occurs at the expense of expiratory reserve
volume (ERV), with a compensatory rise in residual
volume (RV). Loss of ERV means forced exhala-
Breathing
tion, and coughing is severely impaired.
Although mechanical ventilation may not be ini-
tially necessary, subsequent deterioration is not
uncommon. Factors that influence the need for
Diaphragm Function
ventilation include the level of the injury, aspiration Although the diaphragm may still contract in
pneumonia, worsening cord edema (i.e., functional patients with mid cervical cord injuries, its func-
ascent of the injury level) and neurogenic pulmo- tion is impaired by the loss of intercostal and
nary edema. Acute respiratory distress syndrome abdominal muscle function. Normally when the
(ARDS) may occur because of associated pulmo- diaphragm contracts, it increases the thorax
nary contusions, pneumonia, and systemic sepsis. volume by three mechanisms:
54
1. As a pure piston contracting downward to increase
intrathoracic volume.
2. By flattening, it functions as a piston, but one
governed by Laplace’s law.
3. By interacting through the zone of apposition
with the lower ribcage, the abdominal contents
act as a fulcrum to expand the lower ribcage.
Following cervical cord injury, intercostal muscle
function is lost, with consequent failure of AP
expansion of the ribcage. More importantly,
without intercostals muscle contraction, as the dia-
phragm contracts the chest wall is sucked in,
reducing its efficiency and causing paradoxical
chest wall movement. Lost innervation to the lower
thoracic segments causes the diaphragm to start at
a more caudal position. This increases the radius
of curvature and, from Laplace, reduces trans-
diaphragmatic pressure on contraction. As the
diaphragm descends, due to lost abdominal muscle
tone the abdominal contents are pushed out and
cannot provide the fulcrum needed to expand the
lower chest. The lower ribcage is pulled in whilst
the abdominal content are pushed out, resulting in
the “see-saw” pattern of respiration often seen.
With increased intra-abdominal compliance, the
diaphragm is pulled down by the weight of the
abdominal content, especially when upright, dra-
matically reducing the zone of apposition.
Lung compliance is also reduced, mainly due to
a loss of gas containing alveoli secondary to
atelectasis. Reduced lung volume compounds the
problem by reducing surfactant production.
Muscles of Expiration
Loss of abdominal muscle activity results in a
decrease in maximal expiratory force and a
reduced ability to cough, clear secretions, and
protect the airway. Atelectasis increases the load
placed on already compromised muscles of inspi-
ration and V/Q mismatch occurs. Alveolar hypov-
entilation is inevitable and respiratory failure very
common.
Principles of Respiratory Care
Spontaneously breathing patients with SCI require
close observation and aggressive management
including:
J.P. Adams et al.
· Close monitoring of respiratory muscle strength
and ability to cough and clear secretions.
· Intensive chest physiotherapy, including early use
of BIPAP and cough assist devices (mechanical
insufflators–exsufflator devices which alternate
positive and negative airway pressures to generate
a cough).
· Nurse in the supine position. Some of the physi-
ological changes caused by SCI can be lessened
by maintaining patients in a supine position.
When supine, the weight of abdominal contents
pushes the diaphragm higher into the chest,
increasing apposition with the ribcage, reducing
diaphragm radius of curvature and helping to
restore the fulcrum effect lost with higher
abdominal compliance. Supine values of FVC
and FEV1 are larger compared with values when
seated, down to an injury level of T1. Binding the
abdomen when patients are sat upright helps
diaphragm function.
· Humidified oxygen and mucolytic therapy, for
example, nebulized N-acetylcysteine, oral car-
bocisteine, and nebulized dornase alfa
· Adequate hydration and nutrition
· Prevention of pressure sores, by frequent turning,
and prophylaxis for venous thromboembolism
(VTE).
Ventilation and Weaning
Where there is an associated lung injury for example,
pulmonary contusions or an underlying lobar infec-
tion then traditional lung protective ventilation
should be employed to prevent ventilator associated
lung injury. Weaning from mechanical ventilation
can take weeks or months, and it is essential that
patients are prevented from becoming tired during
the weaning process. Normally, it should only be
embarked upon once active pulmonary pathology
has resolved (i.e. once FiO2 is less than 30%), and
little progress is often made until flaccid intercostal
muscles develop some spasticity. Weaning strategies
include conventional SIMV weaning, pressure
support weaning and “T-piece” or “Sprint” weaning.
Tracheostomies are usually essential in weaning
patients, but thought should be given to facilitating
speech – using fenestrated tubes, having periods
where cuffs are left down to allow air to pass upward
through the vocal cords, or using a one- way speaking
valve (for example, a Passy-Muir valve).
6.  Cervical Spine Injuries
Circulation
Hypotension is common after SCI and must be
treated aggressively. Causes include hypovolemia,
neurogenic shock, and the effects of sedation and
positive pressure ventilation.
The terms spinal shock and neurogenic shock
are often confused.
Spinal shock refers to the acute phase following
spinal cord disruption where descending autonomic
pathways are interrupted, resulting in loss of all
somatic and reflex activity below the level of the
injury. It is seen in about 50% of cases and symp-
toms include flaccid paralysis, priapism, and loss of
bowel and bladder function. It usually starts to
resolve within the first 48 h. In the weeks after SCI,
flaccid paralysis is replaced with spastic paralysis
and a gradual improvement in respiratory function
is often seen.
Neurogenic shock is characterized by hypotension
(disrupted sympathetic outflow), bradycardia (unop-
posed vagal tone) and hypothermia. It is more com-
monly seen with injuries above T6 and needs to be
distinguished from spinal shock and hypovolaemic
shock, the latter being more often associated with
tachycardia. Neurogenic shock needs careful treat-
ment with fluid resuscitation, vagolytic agents (e.g.,
atropine 0.3–0.6  mg) and pressor agents such as
noradrenaline (norepinephrine) or phenylephrine
(Neo-Synephrine) on an intensive care unit with
invasive hemodynamic monitoring.
Spinal cord blood flow is around 50 mL/100g/ min
and is under autoregulatory control between mean
arterial pressures of 60-150  mmHg. It is also
dependent on intrathecal pressure and in certain
situations (e.g., thoracic aneurysm surgery) spinal
cord perfusion can be improved by draining CSF.
Autoregulation can be disrupted in traumatic SCI;
hypotension and hypoxia must be avoided as they
may result in further ischemic damage to the cord.
Similarly, severe hypertension and hyperemia may
worsen cord edema and lead to further secondary
injury.
Keep MAP ~80–90 mmHg
Like the brain, the spinal cord is susceptible to secondary insults after
the primary injury. Hypoxia and hypotension must be avoided as they
may lead to further ischemic damage and a worse neurological
outcome.
55
Neurogenic pulmonary edema may be associated
with SCI. The intense autonomic discharge after
injury leads to marked vasoconstriction and an
increase in afterload, with blood being shunted from
the systemic to the pulmonary circulations. There is
disruption of the pulmonary capillary endothelium,
which leads to alveolar hemorrhage and pulmonary
edema. Myocardial stunning may also occur and the
patient may appear moribund. Treatment consists of
ventilation with PEEP, careful fluid resuscitation
(guided by invasive hemodynamic monitoring), and
titration of inotropes and vasopressors. This has
been discussed in detail in Chap.9.
Neurology
A thorough neurological assessment should docu-
ment the precise level of sensory and motor deficit
(including any evidence of sacral sparing), and
record details about tendon reflexes and sphincter
tone. Despite optimal treatment, the injury level may
rise in the hours or days after the initial event, so
repeated neurological examination is mandatory.
Definitions:
· Complete injury: loss of all sensory and motor
function below the lesion, including loss of
control of bowel and bladder function.
· Incomplete injury: Some ascending or descend-
ing tracts are spared. Examples include:
· Brown-Séquard syndrome: cord hemisection with
ipsilateral hemiplegia and contralateral pain and
temperature-sensory deficits.
· Central cord syndrome: usually follows a hyper-
extension injury with a greater loss of motor
function in the arms than in the legs, and a vari-
able amount of sensory loss below the level of
the injury.
· Sacral sparing: this is a significant prognostic
sign as it is often associated with better outcomes
and recovery after SCI.
Autonomic hyper-reflexia: In the chronic phase
after SCI, many patients with lesions above T6 will
exhibit exaggerated responses to triggers such as
bladder or bowel distension. This is characterized by
hypertension, bradycardia, and vasodilatation
above the level of the lesion. If left untreated,
complications including stroke, pulmonary
edema, and myocardial infarction can occur.
56
The stimulus must be removed promptly (e.g.,
bladder catheterization or bowel evacuation) and
occasionally the condition will warrant drug treat-
ment with a rapidly acting vasodilator (e.g., sub-
lingual nifedipine or GTN).
Radiology
Traditionally, all patients with suspected cervical
spine trauma will have the three standard plain
X-rays consisting of lateral, anterior–posterior
and open-mouth odontoid peg views. In the intu-
bated patient the latter will be replaced by a sub-
mental projection. When stable, the patient will
also have thin CT cuts of the occipito–atlanto-axial
region and the C7/T1 region. Modern radiological
techniques allow for very rapid helical CT scans
of the cervical spine which, increasingly is removing
the need for the three plain views.
The combination of good-quality plain films and focused CT slices
excludes over 99% of significant cervical spine trauma in adults.
If pathology is discovered, the patient will probably
require an MRI scan to plan further treatment
and further imaging of the whole spine to look
for additional damage. Other imaging modalities
Figure 6.1.  The diagnosis of acute injury can be difficult in the presence of the degenerative spine. Flexion-extension views demonstrate
stability. This X-ray shows what looks like an acute slip at C4/5 but the flexion-extension views demonstrate that this is old and stable.
J.P. Adams et al.
such as flexion–extension fluoroscopy should not
be done without expert advice, and only when
other imaging has been negative (see Fig. 6.1).
Other Injuries
Patients with cervical spine trauma are likely to
have other injuries and a thorough assessment is
required. High spinal injuries may mask intra-
abdominal injury, and further imaging or a diag-
nostic peritoneal lavage should be performed if
this is suspected.
Types of Cervical Spine Fractures
Injuries to the C1–2 complex are associated with
a lower incidence of serious neurological injury
than injuries lower down (C3–7), possibly as a
result of increased space for the cord at the higher
level. Atlanto–occipital disruption, however, is
associated with a higher risk of immediate fatal-
ity due to disruption of brainstem function.
Those who survive will need stabilization by
either nonsurgical or surgical techniques (see
Fig. 6.2).
Cervical spine fractures are often described by
their mechanism of injury:
6.  Cervical Spine Injuries 57

· Hyperflexion: Excessive neck flexion in the

Saggital plane (e.g., diving in to shallow water,
trampoline accidents) resulting in disruption of
the posterior ligament, for example, flexion-burst
fracture (Fig. 6.3a), unilateral facet (Fig. 6.3b), or
bilateral facet dislocation (Fig. 6.3c).
· Hyperextension: Excessive neck extension in
the Saggital plane (e.g., hitting the dash board
in a motor vehicle accident resulting in a Hang-
man’s fractures – Fig. 6.4)
· Axial compression: Excessive force applied
directly downward through the skull may result
in compression fractures (e.g., Jefferson frac-
ture – burst fracture of C1 – Fig. 6.5)
Stability: The stability of the cervical spine has
three determinants:
1. Biomechanical factors, which take into account
the disc, vertebral body, ligaments, and facet joints.
There are different biomechanical concepts,
a widely recognized example being the three
concept model of Denis.
2. Radiological factors, which are determined by
abnormal radiological features and abnormal
movements on dynamic films.
3. Clinical factors, which takes the clinical fea-
Figure 6.2.  Posterior occipito-cervical fixation with bone graft to
tures in conjunction with the radiological
treat an unstable fracture in the upper cervical spine. findings.

Figure 6.3.  (a) Flexion injury after diving in to a shallow pool. Lateral view shows a burst fracture of C6 (red arrow). (b) Unifacetal fractures
are potentially unstable and the management varies substantially. They are characterized by < 50% of vertebral body slip. (c) Bifacetal fracture
of C5/6 where > 50% of the vertebral body has slipped forward. This is a highly unstable fracture that requires urgent stabilization.
58 J.P. Adams et al.

The Importance of Clearing the

Cervical Spine on the ICU
Unconscious patients in the Intensive Care Unit
will often have their spine immobilized for pro-
longed periods of time, mainly because of con-
cerns about adequacy of plain films and the
inability to assess the patient’s neurology. There is
understandable concern about displacing poten-
tially unstable spinal injuries with subsequent neu-
rological deficit.
However, the complications of prolonged immo-
bilization are often understated and underestimated
(see Table  6.1). As previously stated, good-quality
plain films combined with focused CT slices will
detect over 99% of serious cervical spine injuries.
Imaging should be interpreted by a senior radiolo-
gist and after appropriate documentation by the
orthopedic or neurosurgical specialist, the collar
should be removed. The patient should then be
closely monitored for any subsequent spinal pain,
weakness, or paresthesia.

Figure 6.4.  Hangman’s fracture (hyperextension injury) showing

anterior dislocation of C2 body with C2 pars interarticularis
fractures (red arrow).
Fluid Balance
Careful attention is required to avoid excessive
volume loading and tissue edema, particularly
where there is an associated lung injury. Spinal
shock will result in bladder distension, but in the
longer term intermittent catheterization may be fea-
sible as reflex emptying of the bladder develops.

The Role of Steroids

Steroids are not universally used in the treatment of acute SCI, and
administration is dictated by local policy.

Table 6.1  Complications of prolonged spinal immobilization

Figure 6.5.  Jefferson fracture (axial compression fracture) of the
bony ring of C1 (unstable). This open mouth view shows bilateral
offset of the C1 lateral masses on C2 (white arrows).
In the acute setting stability may be difficult to
confirm, especially in the unconscious patient, and
therefore patients should be treated as unstable
until they can be properly assessed.
•  P ressure sores: common (especially after 48 h ) and potentially
devastating
•  Venous obstruction, increased ICP
•  Potential airway and central venous access difficulties
•  Restricted physiotherapy: increased risk of VAP and VTE
•  Problems with enteral nutrition, reflux and aspiration
•  Oral hygiene (bacteraemia, sepsis)
•  Cross-infection (at least five people required for log-roll)
6.  Cervical Spine Injuries
Following the NASCIS II (1990) and NASCIS III
(1997) studies, high-dose methylprednisolone was
routinely used in acute SCI. However, in both
studies the drug only had an impact when given
early (<8 h after injury) and was associated with
an increase in infectious complications. Serious
concerns subsequently arose about the methodol-
ogy of both studies, and the current consensus in
the United Kingdom is that corticosteroids are not
recommended after traumatic SCI. Elsewhere they
continue to be used in selected patient groups and
their use is dictated by local policy.
Thromboprophylaxis
· Patients with SCI are at high risk for throm-
boembolic complications.
· All patients should be fitted with graded com-
pression stockings or intermittent pneumatic
calf-compression devices.
· Low molecular weight heparin (LMWH) should
be started within 72 h of injury, unless there is
a specific contraindication.
· Warfarin can replace LMWH once the acute
phase of injury is over, provided there are no
plans for additional surgery (aim for INR ~ 2.0).
· Where anticoagulation has failed or is contrain-
dicated, a vena cava filter should be considered.
· Prophylaxis should continue at least until dis-
charge from rehabilitation.
Infection
Infective complications are common in patients
with SCI, with sepsis being the leading cause of
death in this patient group. Chest and urinary-
tract infections are the most common infections,
although occult peritonitis should always be con-
sidered as the usual characteristic signs and
symptoms may be absent.
Pressure Sores
It is vital that all efforts are made to prevent pressure
sores. This includes pressure-relieving mattresses,
regular turning, rotating beds, and ensuring the
patient spends as little time as possible on spinal
59
boards or transfer trolleys. Patients who develop
pressure sores will require early referral to the
tissue viability team and possible input from the
plastic surgeons.
Occipital pressure sores are commonly seen,
especially in patients with poorly fitting hard collars
and scalp lacerations. Some spinal units advocate
shaving off the hair in ventilated SCI patients.
Temperature Regulation
Impaired temperature regulation and vasodilata-
tion leads to a drop in core temperature. Preven-
tion of heat loss and the usual rewarming methods
should be employed.
Surgical Management
Surgical intervention aims to realign the spine,
provide mechanical stability, decompress neural
tissue, and prevent further SCI. The options are:
· Mechanical traction: halo jacket or cranial tongs
· Operative intervention: reduction of the fracture
and fixation
In patients with cord compression but stable neu-
rology, there remains debate about the optimal
timing of surgery. However, emergency surgery is
required in patients with rapidly deteriorating
neurology.
Patients who require surgical intervention are
at high risk of needing mechanical ventilation post-
operatively. Preoperative optimization of the chest
(e.g., aggressive physiotherapy, prophylactic BIPAP,
and use of a cough assist device) is advised. Post-
operatively, patients should be monitored in a
High-Dependency environment and non-invasive
ventilation used to maintain alveolar recruitment
and hopefully avoid the need for invasive ventilation.
Longer-Term Management
Patients with cervical spine injuries may require
prolonged intensive care and early involvement
from the Regional Spinal Team is recommended.
Ideally the patient should be managed in a unit
with dedicated physiotherapy input and a proto-
colized weaning program. Attention during acute
60
treatment and rehabilitation must be directed to all
facets of care including prevention of complica-
tions, pain management, nutrition, occupational
therapy, and psychosocial needs.
Acknowledgments  Images kindly supplied by Dr.Dominic
Barron and Mr. Jake Timothy, Leeds Teaching Hospitals.
Further Reading
Baxendale BR, Yeoman PM (1997) Spinal injury. In:
Goldhill D, Withington PS (eds) Textbook of inten-
sive care. Chapman & Hall, London, pp 639–651
Bracken MB, Shepard MJ, Collins WF et  al (1990) A
randomized, controlled trial of methylprednisolone
or naloxone in the treatment of acute spinal-cord
injury. Results of the second national acute spinal
cord injury study. N Engl J Med 322(20):1405–1411
Bracken MB, Shepard MJ, Holford TR et al (1997) Admin-
istration of methylprednisolone for 24 or 48 hours
or tirilazad mesylate for 48 hours in the treatment of
View publication stats
J.P. Adams et al.
acute spinal cord injury. Results of the third national
acute spinal cord injury randomized controlled
trial. national acute spinal cord injury study. JAMA
277(20):1597–1604
Crosby ET (2006) Airway management in adults after cervi-
cal spine trauma. Anesthesiology 104:1293–1318
Denis F (1983) The three column spine and its signifi-
cance in the classification of acute thoracolumbar
spine injuries. Spine 8:817–831
Fraser M (2005) Management of acute spinal injury.
In: Galley H (ed) Critical Care Focus 11, Trauma.
Blackwell Publishing, UK, pp 36–51
Heath K, Erskine R (2000) The anaesthetic manage-
ment of spinal injuries and surgery to the cervical
spine. In: Matta B, Menon D, Turner J (eds) Textbook
of neuroanaesthesia and critical care. Greenwich
Medical Media, London, pp 241–252
Stevens RD (2004) Spinal cord injury. In: Bhardwaj A,
Mirski M, Ulatowski J (eds) Handbook of neurocritical
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