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Year : 2001  |  Volume : 49  |  Issue : 1  |  Page : 11-8

Anaesthetic and intensive care aspects of spinal injury.


Department of Anaesthesiology, Postgraduate Institute of Medical Education and Research, Chandigarh- 160012, India.

Correspondence Address:
Department of Anaesthesiology, Postgraduate Institute of Medical Education and Research, Chandigarh- 160012, India.

  »  Abstract

Over the last few years, spinal injuries have been classified depending upon their causative mechanism and on the basis of three column concept of the structure of vertebral column. The concept of primary and secondary injury has laid more stress on prevention and treatment of secondary injury. Methyl prednisolone still remains the drug of choice for prevention of secondary injury. Spinal injury involves all organ systems of the body depending on the level of lesion. Immobilisation of injured spine and maintenance of adequate airway after spinal injury need immediate attention. Orotracheal intubation under general anaesthesia, with manual in-line traction, is still considered the best method. Hypotension, hypertension and hyperglycaemia should be avoided during anaesthesia. Care should be taken to avoid effects of autonomic hyper reflexia. Spinal cord functions should be monitored and, if required, induced hypotension can be used with adequate monitoring.

How to cite this article:
Grover V K, Tewari M K, Gupta S K, Kumar K V. Anaesthetic and intensive care aspects of spinal injury. Neurol India 2001;49:11


How to cite this URL:
Grover V K, Tewari M K, Gupta S K, Kumar K V. Anaesthetic and intensive care aspects of spinal injury. Neurol India [serial online] 2001 [cited 2019 Aug 23];49:11. Available from: http://www.neurologyindia.com/text.asp?2001/49/1/11/1308



'one having a dislocation in a vertebra of his neck,
while he is unconscious of his two legs and his two
arms and his urine dribbles, an ailment not to be
treated'.
Although, the current outlook is not so bleak, cervical
spine injury continues to be a catastrophic event.
There are approximately 280 spine injuries per
million population each year in USA, and about 10-30
percent result in spinal cord injury. In our institute,
190 spine injuries were treated during a period of 4
years. There were 147 males (79.1%) and 43 females
(20.3%). Fall contributed to 53% of cases, followed
by road traffic accidents. In majority of cases, cervical
region was affected, followed by dorsal and lumbar
spine.1 70% of survivors are left with significant
neurological deficits.
Mechanism and classification of spinal cord
injury
Injuries in the cervical spine are generally caused by
(i) flexion, (ii) flexion rotation, (iii) vertical
compression (axial loading), (iv) extension, (v)
extension rotation and (vi) lateral flexion.[2] The
mechanism of injury in the thoraco lumbar spine is
similar, except that there is less mobility; and injuries
are more likely to be due to compression and
rotational forces.
The three column concept of the structure of the
vertebral column helps to clarify the mechanism of
injury.[3] The posterior column is formed by the
posterior neural tract, spinous process, facetal
articular processes and their corresponding posterior
ligamentous complex. The middle column consists of
the posterior one-third of the vertebral body and
annulus fibrosus and the posterior longitudinal
ligament. The anterior column comprises the anterior
longitudinal ligament and the anterior two-thirds of
the vertebral body and annulus fibrosus. Flexion
injury causes disruption of the posterior column,
where as extension injury causes disruption of the
anterior column. Acute spinal instability exists, if two
or more columns are disrupted, and predicts the
possibility of late instability. Spinal cord injuries most
frequently involve the lower spine and the
thoracolumbar junction; the former because of its
mobility and the latter because it is the junction
between the rigid thoracic spine and the flexible
lumbar spine.
The paediatric and the elderly spine
Until ten years of age, the immature spine has
increased physiological mobility due to ligamentous
laxity, and incompletely ossified wedge shaped
vertebrae which afford some protection against spinal
column injuries, but at the same time increase the
incidence of spinal cord injury without radiographic
abnormality.[4],[5],[6] The elderly patient, on the other hand,
with the development of degenerative changes and
osteophytes and narrowing of the spinal canal, may
develop spinal cord injury even with trivial trauma
and the injury may be missed.[7]
Spinal cord injuries can be complete with loss of all
motor and sensory functions below the level of injury,
or incomplete producing the central cord syndrome,
the Brown-sequard syndrome, the anterior cord
syndrome or the posterior syndrome.
Pathophysiology of spinal cord injury
Primary and secondary injury : Trauma to the spinal
cord often causes immediate and complete disruption
of the cord function, however, anatomically the cord
itself is seldom transected. These observations,
coupled with findings from experimental research,
give rise to the concept of primary and secondary
injury. The primary injury results from the original
impact of force and compression against the spinal
cord, resulting in damage to the small intramedullary
vessels, causing haemorrhage in the central gray
matter of the cord, and perhaps vasospasm. This leads
to an immediate reduction of blood flow to the gray
matter, followed by a similar reduction in the white
matter.[8] The resultant ischaemia triggers a
biochemical cascade, which signals the onset of
secondary injury, leading to eventual infarction of the
spinal cord with permanent loss of function. The
primary injury cannot be treated; it can only be
prevented, primarily with educational programmes.9
Secondary injury occurs within minutes to hours
following the primary injury,[10] and is thought to be
mediated by biochemical cascade which includes the
intracellular accumulation of calcium, activation of
phospholipase A2, release of arachidonic acid and its
metabolites of prostanoids and thromboxanes, with
eventual generation of free radicals causing lipid
peroxidation and destruction of neurons and
axons.[11],[12] The reduction in blood flow during
secondary injury has been positively correlated with
functional deficits in experimental studies.[13] The
timing and mechanism of secondary injury suggest
that pharmacological treatment may be possible in the
period immediately after the initial injury. Drugs
found to be efficacious in experimental spinal injury
models include calcium channel blockers,[14]
naloxone,[15] thyrotropin releasing hormone,[16] Nmethyl-
D-aspartate antagonist[17] and corticosteroids.
[18],[19] In rabbits, MK-801, an NMDA receptor
antagonist, in a dose of 5 mg/kg, significantly
improves motor recovery after injury and significantly
reduces oedema formation at the site of injury without
altering spinal cord blood flow or vascular
permeability at the injured site.[20] High dose steroids is
the only clinically effective treatment to date. In a
multicentre, randomised, placebo controlled trial,
methylprednisolone in a dose of 30 mg/kg
administered over a period of 15 min, followed by a
45 minute pause and a continuous infusion of 5.4
mg/kg/hour, for the next 23 hours was shown to be
effective in improving both the six week and six
month outcome in patients with complete as well as
incomplete lesions.[21] Improvement in both sensory
and motor functions has been noted. However,
consistent with the mechanism of secondary injury,
the drug must be given within eight hours of injury to
have any effect. The positive effects of steroids are
probably mediated through inhibition of lipid
peroxidation and improvement of cord blood flow. In
the same study, naloxone had no demonstrable
positive effect. Other pathophysiological changes
include loss of autoregulation[22],[23] and perhaps
impairment of CO2 reactivity.[24]
Systemic effects of spinal injury
Cardiovascular system : The initial injury is
associated with a sudden increase in blood pressure
and dysrhythmias due to intense sympathetic
activation. This is followed within minutes by
hypotension, as the stage of spinal shock sets in with
total loss of neural conduction, flaccid paralysis, and
absence of tendon and plantar reflex responses below
the level of lesion. This is characterised by decrease in
systemic vascular resistance, increase in venous
capacitance with venous pooling and hypotension.
Lesions above T5, because of the interruption of
sympathetic outflow to the heart (T1-T5) and
unopposed parasympathetic tone, are frequently
associated with severe bradycardia and hypotension.
Cardiac dysfunction can also occur. Systemic
hypovolaemia from other causes may be missed as
tachycardia is frequently absent. Spinal shock may
last from hours to weeks, and with return of reflex
activity below the level of lesion,[25] somatic or visceral
stimulation may result in massive sympatheticmediated
vasoconstriction below the level of the
lesion. This phenomenon of autonomic hyperreflexia
is more prevalent in patients with lesions above T6,
because of the inadequate compensatory vasodilatory
response.[26] Interestingly, even in patients with high
cervical cord lesions, the tachycardia response to
hypercapnia and hypoxia remains intact, possibly
mediated by vagal inhibition rather than sympathetic
activation.[27]
Respiratory system : The extent of respiratory
impairment depends on the level of the lesion. The
diaphragm is innervated by C3-C5, and lesions above
this level cause total diaphragmatic paralysis and an
inability to generate adequate tidal volume. This
accounts for a large number of the pre-hospital deaths.
Patients, with lesions below C6, have an intact
diaphragm with variable intercostal and abdominal
muscle weakness depending on the level of the lesion.
There is reduction in functional residual capacity,
forced vital capacity, maximum inspiratory pressure,
maximum expiratory pressure as well as the presence
of paradoxical respiration. Vital capacity is reduced to
about 1500 ml with acute cervical spinal cord injury,
which usually improves with time to 50 percent of
normal. The reduction in tidal volume can reach 60
percent in these patients.[28] The overall effect is severe
hypoventilation with a high incidence of hypoxia and
hypercapnia. Quadriplegic patients have a higher vital
capacity in the supine position than in the seated
position, because of diaphragmatic mechanics.28 The
inability to cough and clear secretions leads to a high
incidence of atelectasis and pneumonia in the acute
period. The initial surge of sympathetic activity with
the injury can also cause neurogenic pulmonary
oedema, the mechanism of which is unclear, but may
be mediated by both haemodynamic and permeability
factors.[29]
Other systems :
(a) Spinal shock is associated with paralytic ileus and
a neurogenic megacolon may develop. This
abdominal distension may further compromise
ventilation. The anal reflex is usually lost in cases
of spinal shock. In disturbances of the conus
medullaris and cauda equina (S3-S5), faecal
incontinence and a flaccid anal sphincter with loss
of anal reflex may be a presenting feature. Saddle
anaesthesia is often seen in such cases.
(b) Initial period of spinal shock is often
accompanied by urinary retention and outflow
incontinence. Later a reflex (neurogenic or
spastic) bladder develops. The reflex bladder is
characterized by overactivity of both the detrusor
muscle and the external sphincter, which leads to
incontinence of urine. In addition, the bladder
capacity is diminished due to detrusor
contraction. The sensation of bladder distension
may be lost if ascending tracts are involved. An
autonomous flaccid bladder develops if the level
of injury is at the conus medullaris or cauda
equina. Voluntary control over bladder function is
impaired or abolished completely. Bladder
sensation is impaired. In the chronic phase,
recurrent urinary tract infection with renal
dysfunction are major problems.
(c) Disruption of the sympathetic pathways carrying
temperature sensation and loss of vasoconstriction
below the level of injury, causes spinal
cord injured patients to be poikilothermic.
Temperature is difficult to control in
poikilothermic patients. Warming blankets,
heated humidification of gases, increase in
ambient temperature and warm intravenous fluids
may be required to conserve heat.
(d) The spinal cord injured patient can develop
contractures across joint spaces and heterotopic
bone formation may develop near or within a
major joint. Mobilisation of skeletal calcium
results in osteoporosis, placing these patients at
risk of pathological fracture.
e) The incidence of head injuries in patients with
cervical cord lesions can be as high as 50%, while
thoracolumbar spine injury may be complicated
by chest contusion, rib fractures, pelvis fracture
and other long bone fractures.
Immobilisation of spine
Management of the potentially traumatised spine
emphasises three principles -(i) protection of the cord
with preservation of intact pathways, (ii) restoration
and maintenance of spinal alignment and (iii)
establishment of stability. Immobilisation of the
cervical spine prior to radiographic assessment is the
accepted standard of care for multiple trauma patients.
The rationale behind early immobilisation is the
prevention of the occurrence of exacerbation of
neurological injury in patients with unstable spine.
Stabilising devices commonly used in the pre-hospital
and early hospital management of suspected spine
injured patients do not eliminate spine movement.
Soft collars serve to alert clinicians to the potential for
injury but do little to prevent spinal movement,
allowing for 96 percent of normal neck flexion and
73% of extension.[29] Hard collars allow 72-73% of
normal flexion and extension.30-31 The combination
of bilateral sand bags secured with three inch cloth
tape and a Philadelphia collar is the most effective
pre-hospital stability collar allowing for almost no
neck flexion, although 35% of extension is possible.30
It has been demonstrated that methods of
immobilisation that splint both head and torso to a
rigid board (short board technique), are far superior to
collars in reducing movements in all planes.[32]
Both hard and soft collars do not prevent movement of
cervical spine during chin lift, jaw thrust and
intubation. Manual inline traction applied by an
assistant reduces movement during the process of
intubation. Aprahamian et al studied the efficacy of
both basic and advanced airway manoeuvres on the
unstable spine.[33] Basic airway manoeuvres included
chin lift, jaw thrust, head tilt and placement of both
oral and oesophageal airways. More advanced
manoeuvres included placement of an oesophageal
obturator airway, an endotracheal tube placed with
both a straight and a curved laryngoscope blade and a
nasotracheal tube blindly placed. Both chin lift and
jaw thrust resulted in expansion of the disc space more
than 5 mm at the site of injury. The blind nasotracheal
intubation was assisted with anterior pressure to
stabilise the airway which resulted in 5 mm of
posterior subluxation at the site of injury. The other
advanced airway manoeuvres produced 3-4 mm of
disc space enlargement.
Thus, any airway manoeuvre undertaken in a patient
with an unstable spine injury has the potential to do
harm. Patients recognised to be at risk and treated
accordingly with immobilisation do not appear to
have an increased incidence of neurological injuries
following intubation. Immobilisation devices are not
uniform in their ability to limit spine movement while
the airway is being secured. Short broad devices are
the most effective pre-hospital immobilising
devices.[32],[34] Once the injury is confirmed, Gardener-
Wells tongs may be quickly and effectively applied
under local anaesthesia.
Role of anaesthesiologist
The anaesthesiologist may encounter a patient with
acute spinal cord injury either in the acute phase, the
intermediate phase, or the chronic phase.
(a) Acute phase includes resuscitation in the
emergency department, typically airway
management, administration of anaesthesia for
acute decompression of the spinal cord to
preserve or improve function and administration
of anaesthesia for surgical treatment of associated
injuries.
(b) Intermediate phase includes administration of
anaesthesia for stabilisation of spinal column and
also associated injuries.
(c) Chronic phase includes administration of
anaesthesia to chronic spinal patient for related
and unrelated surgical procedures.
The goal of treatment of spinal cord injuries
is :
(i) To protect the spinal cord from further damage. (ii)
To maintain alignment of the bony structures to allow
maximal recovery in incomplete lesions. (iii) To
achieve stability of the bony column to allow
rehabilitation.
Surgical indications for treatment during the
acute phase include :
(i) Decompression with or without fusion in a
neurologically deteriorating patient. This includes
complete as well as incomplete lesions. (ii) Reduction
and stabilisation, when conservative management fails
to achieve these objectives. (ii) Surgical treatment for
other life threatening conditions, unrelated to the cord
injury.
Anaesthetic Management
The acute phase : A high index of suspicion of spinal
cord injury should always be maintained in all
multiple-injured patients and head-injured patients
(up to 10 percent may have spinal injury), particularly
in the paediatric and the geriatric groups. Until proved
otherwise, all patients suspected of having spinal
injuries should be immediately immobilised. Collars
should be used for all patients suspected of having
cervical injuries, as they not only immobilise but also
serve as reminders of the possibility of neck injury.
Airway management in patients suspected of having
cervical injuries : The goal here is to establish tracheal
intubation without causing further injury to the spinal
cord. The considerations are valid for both complete
and incomplete lesions, because manipulations can
aggravate even complete lesions resulting in
ascending deterioration. The optimal method depends
on the patient's condition, the level of co-operation,
and the skill of the anaesthetist. An adequate history
and physical examination are essential before
approaching this problem. This difficult topic can be
clarified by the following facts: (1) the patient's
condition may not allow postponement of intubation
until an X-ray is taken; (2) a negative cross-table
lateral X-ray (CTLX) does not rule out all cervical
injuries, although a combination of CTLX, the open
mouth view, and the anteroposterior view would
suffice,35 (3) collars, whether soft or rigid, do not
effectively eliminate movement of the neck during
intubation,36 (4) manual in-line traction (MILT) is
more effective in immobilising the neck during
intubation,[36] (5) MILT may cause excessive
distraction in Cl-2 fractures,[37] (6) oral intubation
under general anaesthesia with MILT has an
extremely safe record.[38],[39]
Recommendations
Elective intubation in an awake patient without
hypoxia or hypercapnia : Obtain necessary X-rays to
'clear the spine' and treat the patient as a spinal cord
injured, if clinically indicated. CT scans are necessary
in equivocal cases and MR imaging may play an
increasing role.[40] In a cooperative patient, awake
intubation is recommended, and in the absence of
head injury, fibreoptic intubation, either oral or nasal,
should be performed. Blind nasal intubation is an
acceptable alternative. Nasal intubation, however,
should not be performed in any patient suspected of
having a basal skull fracture or facial fracture
involving the sinuses.
Emergency intubation in an unconscious or
uncooperative patient : Under these circumstances
fibreoptic intubation has no place and oral intubation
should be achieved under general anaesthesia with
rapid-sequence technique using MILT. Anaesthesia
induction can be achieved with thiopentone or
propofol, but the patient's unstable cardiovascular
status (spinal shock) must be taken into consideration.
Vigorous fluid resuscitation should begin
simultaneously. Hyperkalaemia from denervation
sensitivity does not occur until 48 hours after injury.
Succinylcholine, therefore, remains the muscle
relaxant of choice in the acute setting.[41] Any concern
about a potential increase in intracranial pressure is
outweighed by the benefits of expedient establishment
of airway with prompt reversal of hypoxaemia and
hypercapnia. In difficult cases, transtracheal
ventilation, or emergency cricothyroidotomy may be
necessary.
Maintenance of Anaesthesia
The main goal here is to maintain adequate spinal cord
perfusion to prevent further damage. In the acute
stage, this consideration applies equally to complete
and incomplete lesions, since in both instances
deterioration as well as improvement can occur.
Because of loss of autoregulation, spinal cord
perfusion becomes dependent on systemic perfusion,
and systemic hypotension may cause further
secondary injury. On the other hand, hypertension
may lead to haemorrhage and oedema formation.[23]
Maintenance of normal systemic perfusion and gas
exchange are the prime objectives, since spinal cord
blood flow, as yet, cannot be monitored. No single
anaesthetic technique has been shown to be superior.
On an experimental basis, all anaesthetic drugs that
decrease metabolism appear to have a protective
effect.[42] However, results are not always
consistent,[42],[43] hence, an anaesthetic regimen that can
best fulfil the outlined objectives in any given patient
is the best technique. All drugs should be given slowly
by titration because of the cardiovascular lability.
Bradycardia is a frequent occurrence in patients with
cervical cord injuries and atropine is the drug of
choice. Inotropic agents may also be required to
maintain the circulation. Theoretically, since the
spinal cord circulation is similar to the cerebral
circulation, hyperventilation may help to decompress
the cord. The efficacy of hyperventilation, however,
has not been substantiated in experimental studies.44
Moreover, it may decrease perfusion and cause
ischaemia. Therefore, normocapnia or mild
hypocapnia is recommended.
Monitoring : In addition to the standard monitoring,
which now includes pulse oximetry and end-tidal
capnometry, in acute quadriplegic patients, direct
intra-arterial pressure monitoring and the insertion of
a pulmonary artery catheter are advised because of
cardiovascular instability and an unpredictable
response to fluid challenge and the risk of pulmonary
oedema. It is recommended that hypotension should
be treated with fluid and inotropic agents rather than
direct vasoconstrictors.[45]
Hyperglycaemia : There is growing experimental
evidence to indicate that hyperglycaemia aggravates
ischaemic injury, presumably on the basis of the
occurrence of lactic acidosis.[46] Glucose-containing
solutions therefore should not be used, and serum
glucose concentrations above 200 mg/dl should
probably be treated with insulin.
Autonomic hyperreflexia : This phenomenon only
occurs after recovery from spinal shock. About 75-85
percent of patients with lesions above T6 will exhibit
some manifestations of this phenomenon. Both deep
general anaesthesia and regional anaesthesia have
been used successfully to block this response.26 At
least on a theoretical basis, the latter approach is
preferable, if the surgical procedure is amenable to
regional anaesthesia.
Most patients with acute cord injuries have such
unstable cardiovascular and respiratory status that
their tracheas should not be extubated at the end of the
surgical procedure. Instead they should be transferred
directly to an intensive care unit for further care. In
patients with low lumbar lesions without respiratory
impairment, extubation can be accomplished in the
operating room.
In the intermediate/chronic phase induction, patients
are more stable and may or may not have recovered
from the stage of spinal shock. In patients with
incomplete lesions or intact neurological function but
with bony injuries, presenting for stabilisation
procedures, awake fibreoptic intubation is again the
technique of choice. For patients with complete
lesions, general anaesthesia should be used for
induction. Succinylcholine should not be used in this
phase because of the risk of hyperkalaemia.
Spinal cord monitoring
In patients who have suffered vertebral column
injuries without neurological deficit, spinal cord
monitoring has become almost mandatory at least
from legal point of view. In all intact patients with
cervical injuries, awake intubation is preferred and
general anaesthesia is not administered until the
patient is in final position for surgery and normal
movement of all four limbs has been documented.
lntraoperatively somatosensory evoked potential
(SSEP) monitoring should be done routinely.
Although the interpretation of SSEP remains
imprecise, still its use is gaining popularity. The major
limitation at present is that it monitors only dorsal
column function and, theoretically, motor paralysis
can occur despite unchanged SSEP signaIs.[47] In
patients with incomplete lesions and abnormal
preoperative SSEP interpretation of intraoperative
findings is impossible. SSEP signal is susceptible to
anaesthetic influence and inhaled anaesthetics in high
doses can abolish these responses. Nitrous oxide, is no
less depressant than an equipotent dose of an inhaled
anaesthetic. The recommended anaesthetic regimen
for intraoperative monitoring of SSEP is continuous
intravenous infusion of a narcotic (fentanyl or
sufentanil) supplemented with low-dose inhaled
anaesthetic (isoflurane or halothane) or with nitrous
oxide. The combination of nitrous oxide and an
inhaled anaesthetic should be avoided. In cases where
an epidural electrode can be placed, the choice of
anaesthetic becomes a minor matter, since epidural
recordings are more resistant to anaesthetic influence
than cortical recordings. Recent advances have made
it possible to record motor-evoked potentials using
either electrical or magnetic stimulation of the motor
cortex.[48],[49] This complements SSEP and allows
simultaneous monitoring of both anterior and
posterior column functions. Unfortunately, motorevoked
potentials are even more sensitive to
anaesthetic influence and, despite early enthusiasm,[48]
its clinical application remains in doubt. Alternatively
'the wake-up test' may be used. This technique is
however, limited by the technical difficulty involved,
as well as its nature of being a one-time evaluation.
Induced hypotension is frequently used during fusion
procedures on the spine to reduce blood loss and
improve operating conditions, and is appropriate in
patients with stable complete lesions. However, in
patients with incomplete lesions or intact but
marginally perfused spinal cords the reduction in
blood flow may cause ischaemia in the spinal cord,
and therefore may be relatively contraindicated. This
underscores the importance of monitoring intraoperative
neurological functions, as manipulation of
blood pressure can sometimes reverse neurological
deterioration during these procedures.[50] In addition,
intracranial pressure in patients with head injury may
increase with induced hypotension, and should be
monitored if this technique is to be employed. It
should also be noted that the ability of this technique
to reduce blood loss has been substantiated by some
investigators
 

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