Review Anaesthesia for Correction of Scoliosis in Children P. R. J. GIBSON*

Anaesth Intensive Care 2004; 32: 548-559
Anaesthesia for Correction of Scoliosis in Children
Department of Anaesthesia, Children’s Hospital at Westmead and Westmead Hospital, Sydney, New South Wales
Surgical correction of spinal deformities in children presents a challenge to the anaesthetist because of the extensive
nature of the surgery, the co-morbidities of the patients and the constraints on anaesthetic techniques of intraoperative
neurophysiological monitoring of the spinal cord. Adolescent idiopathic scoliosis is the most common deformity.
Patients with scoliosis secondary to neuromuscular conditions are at greatest risk of perioperative problems,
particularly excessive blood loss and respiratory failure. The risk of spinal cord damage can be decreased by the
use of intraoperative spinal cord monitoring, particularly monitoring of the lower limb compound muscle action
potential evoked by transcranial electrical stimulation. Specific anaesthetic techniques are required for this
monitoring to be reliable. Because of concerns about spinal cord perfusion there is now less reliance on induced
hypotension and haemodilution to reduce blood loss, with emphasis on proper patient positioning, controlled haemodynamics and antifibrinolytic therapy. Effective postoperative pain management requires a multimodal approach.
Key Words: Scoliosis, spine, anaesthesia, monitoring, complications
Spinal deformities have been known since ancient
times. The Greek physician Galen introduced the
terms scoliosis, kyphosis and lordosis1. Scoliosis refers
to lateral curvature of the spine though is often
used generically to refer to all spinal deformities in
children. Kyphosis refers to posterior curvature and
lordosis to anterior curvature2. Many curves are
mixed and scoliosis etymologically refers to the torsion or twisting of the spinal column which underlies
many deformities.
Hippocrates noted that spinal deformities compromised respiratory function3. He developed traction as
a treatment, albeit ineffectually. An orthosis to be
used as a brace was developed in the 16th century
by Pare. Modern bracing techniques, particularly the
Milwaukee brace developed by Blount, are effective
at preventing progression of curvature in some cases
and still have a place in management.
Hibbs performed the first spinal fusion for scoliosis
in 19111, but operative treatment had poor results
until the development of an internal fixation system,
*M.B.B.S., F.A.N.Z.C.A., Staff Specialist Anaesthetist, The Children
Hospital at Westmead and Westmead, Hospital.
Address for reprints: Dr Peter Gibson, Department of Anaesthesia, The
Children’s Hospital at Westmead, Westmead, N.S.W. 2145.
Accepted for publication on March 24, 2004.
the Harrington Rod in 19622. Prolonged casting to
allow the fusion mass to become solid was still
required. Modern internal fixation systems allow
early mobilization without casting.
Anaesthesia for correction of scoliosis is a challenge because of the frequent co-morbidities of the
patients presenting for surgery, the extensive nature
of the surgery and the constraints put on the available
anaesthetic techniques because of intraoperative
spinal cord monitoring. The postoperative period
may be complicated by problems common to any
major surgery such as continued blood loss, ileus,
ventilatory failure and the syndrome of inappropriate
anti-diuretic hormone secretion (SIADH), but also
by unique complications such as superior mesenteric
artery (SMA) syndrome4. Postoperative pain can be
severe and its management requires a multimodal
This review will describe the pathophysiology of
scoliosis, the techniques of surgical correction and
spinal cord monitoring and the implications of these
for anaesthetic management. The protocol for perioperative anaesthetic management of these patients
developed at The Children’s Hospital at Westmead
(CHW) will be described.
Classification of Scoliosis
The aetiology of most cases of scoliosis is idioAnaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
Classification and description of aetiology of scoliosis
Mesenchymal diseases
About 70% of cases.
A strong genetic component.
Three distinct periods of onset, infantile
(0-3 yrs), juvenile (4 yrs-puberty) and
adolescent (puberty to skeletal
Infantile curves more common in boys.
Most resolve spontaneously.
Juvenile curves evenly distributed
between the sexes.
Adolescent curves the most common
idiopathic curves.
Severe curves occur predominantly in
girls. 25% have mitral valve prolapse.
Associated with congenital vertebral
anomalies e.g. spina bifida,
hemivertebra or congenital rib fusions.
Associated with other defects,
particularly renal and cardiac defects.
MRI is indicated preoperatively as there
is a high incidence of underlying cord
abnormalities including tethering.
Neuropathic curves associated with
upper or lower motor neurone diseases
e.g. cerebral palsy, spinal muscular
Myopathic curves with myopathies e.g.
Von Recklinghausen’s Disease
Dwarfisms, Marfan’s, Rheumatoid
arthritis, Osteogenesis imperfecta,
Scheuermann’s, disease (juvenile
Vertebral fracture, irradiation.
pathic but scoliosis can be associated with a variety of
conditions. A system of classification of scoliosis with
its disease associations is shown in Table 12,3.
Idiopathic scoliosis is a complicated deformity
involving the thoracic and/or lumbar spine, with
lateral curvature, vertebral rotation and rib cage
deformity. It may be associated with kyphosis and lordosis. As the curvature increases, rotation progresses
and the chest cavity becomes narrowed resulting in a
restrictive lung defect. This is rarely significant for
curves of <65 degrees. With severe curves, restriction
increases, V/Q mismatching occurs and respiratory
failure and pulmonary hypertension may result. This
severe respiratory compromise probably only occurs
in curves >100 degrees. After skeletal maturity,
curves <30 degrees do not progress but more severe
curves may continue to progress another 10-15
degrees. Surgical correction does not reverse the
restrictive lung deficit but will halt its progression2,3.
In scoliosis associated with neuromuscular disease,
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
the underlying disease often further compromises
respiratory function because of inability to cough,
reduced protection against aspiration because of
bulbar palsy and reduced ventilatory capacity.
Neuromuscular scoliosis tends to involve most of the
thoracolumbar spine in a long C shaped curve that
includes an oblique pelvis5.
The most popular and reproducible method to
measure the curve is that described by Cobb3. A line
is drawn parallel to the superior border of the highest
vertebral body that points most to the concavity of
the curve and similarly from the inferior border of
the lowest vertebral body. Perpendiculars from
these lines are drawn and the angle of intersection
measured. The greater the angle measured the more
severe the curve (Figure 1).
Indications for Surgery
The indications for surgery in idiopathic scoliosis
are usually given as progression in a curve over 40
degrees with nonoperative treatment, a 40-45 degree
curve in a patient not skeletally mature, and curves
over 50 degrees in a mature adolescent2. Juvenile
scoliosis may progress to severe curves with resulting
severe restrictive lung defects. Follow up of untreated
adolescent idiopathic scoliosis over 50 years failed to
show major disability related to the scoliosis. Only
patients with apical thoracic curves of over 100
degrees are at risk of death from cor pulmonale and
respiratory failure6. A large multi-centre follow-up
of patients with idiopathic scoliosis who have had
surgery found decreased back pain, improved selfimage, and increased levels of activity as compared
with preoperative status. Overall, patients were highly
satisfied with the results of surgery7. The indications for surgery in congenital scoliosis depend on
the underlying anomaly and the prediction for
For scoliosis secondary to neuromuscular disease,
surgery may be indicated to improve wheelchair posture and aid nursing care as well as to prevent progression of restrictive lung defect in patients with
already compromised respiratory function. The inevitable decline in respiratory function in patients
with progressive weakness due to diseases such
Duchenne muscular dystrophy, (DMD) or spinal
muscular atrophy, may be slowed but is not halted8,9.
For patients with DMD, surgery is indicated once the
curve reaches 20 degrees. Curves in DMD rapidly
progress once the patient is confined to a wheelchair
and stabilization should be offered before the decline
in cardiorespiratory function make the risks of
surgery prohibitive10. Despite a significant perioperative complication rate in this group, most patients and
F IGURE 1: Measurement of Cobb angle. (See fine lines and
measured angles in lower thoracic region in particular.)
their families report an improved quality of life
following surgery and would undergo the procedure
Surgical Technique
Surgical techniques for correction of scoliosis have
evolved over the last 40 years after the development
of the Harrington rod instrumentation. The technique chosen depends on the aetiology and severity of
the curve and the skeletal maturity of the patient.
Modern correction techniques aim to prevent progression of the curve and to correct the threedimensional deformity taking into account the rigidity
of the spine and the risk of neurological injury1,2.
A posterior approach is most commonly utilized.
Combined anterior and posterior approaches are
utilized in more severe and rigid curves or where
there is a need to prevent anterior growth. The combined approaches may be staged over one to two
weeks, or done as one operation. Staged operations
result in less morbidity and mortality in patients at
high risk12. For some congenital curves, or curves confined to the lumbar spine, an anterior approach only
is used.
Systems used for the posterior approach are extensions of the Cotrel-Dubousset design13. These involve
multi-level fixation with pedicle screws or laminar
hooks, two contoured rods to correct deformity in
all planes and allow distraction and compression on
each rod and cross bracing to provide stability2. For
smaller children, or patients with bones unable to
support the laminar hooks, including most of the
patients with neuromuscular curves, Luque rods and
sub-laminar wires are used for fixation5. Fusion alone
with cast bracing is used occasionally in small children
with congenital deformities.
The surgery is extensive. For posterior fusion the
skin and supraspinous ligament are incised and the
para-spinal muscles reflected. The spinous processes
and interspinal ligaments are removed and the facet
joints destroyed. After instrumentation and correction of deformity, bone graft is applied to the
entire fusion area. The instrumentation is designed
to provide stability allowing early postoperative
mobilization before bony fusion is complete.
An anterior approach involves retroperitoneal dissection through a large thoraco-abdominal or flank
incision. Single lung ventilation may aid surgical
access. After exposure of the vertebral bodies, the
intervertebral discs are removed on the convex side,
shortening that side and increasing flexibility, allowing correction with less chance of neurological injury.
Bone grafts are placed and instrumentation with
vertebral screws and rods may be utilized if there is to
be no posterior correction.
Preoperative Assessment and Preparation
The preoperative evaluation is a multidisciplinary
process where staff from all disciplines involved both
assess the patient for surgery and anaesthesia and
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
explain the complex nature of the surgery and perioperative care. Anaesthesia procedures such as
invasive cardiovascular monitoring, urinary catheterization, neurophysiological monitoring, postoperative
analgesic regimes and the wake-up test are explained.
Patients and families may benefit from talking to
patients who have been through the procedure.
Unless contraindicated, patients at CHW are premedicated with oral midazolam 0.5 mg/kg to a
maximum of 15 mg.
The focus in the medical assessment is on cardiorespiratory function. For most patients with idiopathic scoliosis a good exercise tolerance is the best
guide to cardiorespiratory status. These patients have
a 25% incidence of mitral valve prolapse14, but this is
rarely of haemodynamic significance and appropriate
antibiotic cover is given to all patients. Spirometry
is routinely performed and most often shows a
moderate restrictive defect. Postoperative ventilation
is rarely required unless the defect is severe, such
as an FVC <30% predicted3. A full blood count is
assessed and either crossmatch or group and screen
done depending on patient size and preoperative
The cost effectiveness of autologous predonation
in adults has been questioned15. In adolescent idiopathic scoliosis, preoperative autologous donation
reduces allogenic blood exposure and seems cost
effective. In scoliosis patients most at risk of needing
perioperative transfusion, smaller children and children with scoliosis secondary to neuromuscular
disease, predonation does not reduce the need for
allogenic blood16,17. Preoperative anaemia may be a
problem unless iron and erythropoietin therapy is
also used18. The small number of suitable patients,
and problems due to timing of donations with
surgery, limits the use of autologous predonation in
our unit.
Patients with scoliosis secondary to neuromuscular
disease have a higher incidence of complications and
assessment of cardiorespiratory status is more difficult. They may be unable to perform spirometry and
relatively immobile. Anaesthesia for patients with
cerebral palsy has recently been reviewed19.
Cardiomyopathy complicates many progressive
muscle diseases such as DMD and myotonic dystrophy and should be assessed by ECG and transthoracic echocardiography (echo) or radionuclide
imaging if echo is technically difficult. The value of
normal resting values to predict intraoperative events
has recently been questioned20. Acute intraoperative
heart failure has occurred in a DMD patient with
a normal preoperative echo and stress echocardiography has been recommended. Intraoperative monAnaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
itoring with transoesophageal echo (TOE) may be
Determining the point at which the risks of surgical
complications outweigh the benefits of scoliosis
surgery is difficult, particularly in patients whose life
expectancy is limited by the progressive nature of the
disease. Ramirez et al examined complications in 30
patients with DMD who underwent posterior spinal
fusion. No patients were symptomatic of cardiomyopathy preoperatively and only two had FVC
<40% predicted. Four patients died in the first postoperative year and three more in the second year of
follow-up. Eight patients suffered major complications resulting in significant morbidity. Fifteen of the
twenty-one patients and families who could be surveyed over several years postoperatively said surgery
had improved their quality of life11. Morris, in a recent
editorial quoting extensive experience in anaesthesia
and DMD, considered a left ventricular ejection fraction of less than 50% and a forced vital capacity
(FVC) of less than 25% of predicted contraindicated
elective surgery21.
Rawlins et al looked at complications in 32 patients
undergoing spinal fusion with FVC <40% predicted22. There were no perioperative deaths. Six
patients had major pulmonary complications and
three patients required tracheostomy. They concluded that reduced FVC alone should not contraindicate surgery, but emphasized the need for intense multidisciplinary approach to the perioperative
care of these patients. Most of the patients in this
review had a congenital cause for their scoliosis and
only one had DMD. Wazeka et al looked at twentyone patients with spinal deformities with an average
FVC of 32%23. The deformities had a variety of
aetiologies, including four due to myopathy. Four
patients were on assisted home ventilation preoperatively, including two of the myopathy patients. They
also had no perioperative deaths. The four patients
on assisted ventilation preoperatively continued it
postoperatively and two additional patients required
assisted ventilation postoperatively for up to three
months. The authors concluded that major spinal
surgery is feasible in these patients with severe
restrictive lung disease and again emphasized the
need for a multidisciplinary approach, including
particular attention to nutritional status.
With modern perioperative care it seems that low
values for FVC alone should not contraindicate
surgery. In patients with progressive weakness however such as DMD the guidelines of Morris mentioned above would seem wise21.
It is now thought that DMD and other dystrophinopathies are not associated with malignant
hyperthermia24. Suxamethonium is contraindicated in
patients with a dystrophinopathy as it may cause
rhabdomyolysis and hyperkalaemic cardiac arrest.
Volatile agents may also cause rhabdomyolysis in
these patients though this is often subclinical25,26.
While some units with vast experience report no
problems with the use of volatile agents in patients
with dystrophinopathies, minimizing the risk of
rhabdomyolysis by avoiding volatile agents seems
Complications During Surgery and their Implications
for Anaesthesia
Scoliosis has complications common to other
extensive operations including problems of temperature maintenance and compression neuropathies
from positioning. The problems of perioperative
hypothermia have been extensively reviewed27. Active
warming measures should be commenced before induction of anaesthesia and continued throughout.
Positioning prone on the four-post frame commonly
used for posterior fusions is a team responsibility.
Care should be taken not to extend the arms more
than 90 degrees in abduction or forward flexion, and
to avoid compression of the axilla, the ulnar nerves at
the elbow and the lateral cutaneous nerves in the
upper thigh. Correct positioning on the frame should
allow free movement of the abdomen, ensuring adequate ventilation, and avoid elevated venous pressure, which contributes to bleeding3. The eyes should
be protected and checked frequently throughout
surgery to make sure there is no external pressure.
Other complications, including major neurological injury, blood loss, coagulopathy, venous air embolism28
and postoperative visual loss29 are reviewed below.
Neurological Injury
The risk of spinal cord injury from surgery to correct spinal deformities varies from 0.3-0.6% according to data from surveys of the Scoliosis Research
Society. Scoliosis correction for congenital kyphosis,
neurofibromatosis, skeletal dysplasias and postinfectious scoliosis carry higher neurologic risk30,31.
Neurological injury can be due to:
1) direct contusion of the cord by implant or instrument.
2) reduction of spinal cord blood flow by stretching
or compression of vessels or direct interruption of
radicular blood flow.
3) distraction injury of the spinal cord
4) epidural haematoma.
Risk factors may be additive. Ischaemic injury is
the most common and the areas of the cord most vulnerable to ischaemic injury are the motor pathways
supplied by the anterior spinal artery. Intraoperative
spinal cord monitoring has been developed to
decrease the risk of neurological injury. With early
detection by monitoring it is hoped intervention may
prevent irreversible damage. Despite this, occasional
patients may be neurologically normal immediately
postoperatively, yet develop paralysis over the next 48
hours due to spinal cord ischaemia32.
Methods of spinal cord monitoring
Wake-up test
The wake-up test allows intraoperative emergence sufficient to test lower limb motor, but not sensory, function for early detection of spinal cord injury
after correction of deformity33. Although confirmation of function is reassuring, loss of function may
already be irreversible. The single window of observation does not allow correlation of loss of function
with surgical events. If positive, the surgeon is obliged
to remove all the implants. Patient cooperation is
needed and gross patient movement may result in
accidental extubation or loss of IV access, while inspiratory efforts may promote venous air embolism34.
Clonus test
Clonus can normally be elicited in patients with
intact spinal reflexes and lack of central inhibition. It
is possible to elicit clonus in a neurologically normal
patient just awakening from general anesthesia,
because anaesthesia has reduced cortical inhibition.
This has been utilized in the clonus test. Eliciting
clonus of the ankles is attempted just prior to wakeup. If clonus is present spinal cord integrity is
assumed, if absent the full wake-up test is performed.
Although it does not require patient cooperation
there is only a small window when clonus can be
elicited and the absence of clonus does not reliably
predict injury35.
Continuous Intraoperative neurophysiologic
Intraoperative neurophysiologic monitoring involves stimulating one part of the nervous system and
measuring a response (an evoked potential) in a distant part across the area of the spinal cord at risk. The
two modalities that have been developed are somatosensory evoked potentials (SSEPs) and motor
evoked potentials (MEPs). SSEP monitoring involves
stimulation of a peripheral nerve, usually the posterior tibial nerve, and detecting a spinal response
with epidural electrodes or a cortical response with
scalp electrodes. MEP monitoring involves stimulating the motor cortex by electrical impulses transcranially and detecting the resulting signal at spinal
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
level with epidural electrodes or from muscles as a
compound muscle action potential (CMAP). These
modalities of monitoring are now the accepted
standard of care for spinal corrective surgery36.
Transcranial magnetic stimulation of MEP’s has been
described but is now rarely used.
SSEP monitoring
The SSEP response is small compared to background noise, so signal averaging techniques are used
with a 2-3 minute delay in processing information.
There may also be a delay between onset of ischaemia
and changes in potentials37. Only the dorsal sensory
pathways are monitored, not the most vulnerable
anterior motor pathways. In an international survey
of 60,000 cases, 342 neurological deficits were reported with SSEP monitoring in place and 28% were
not detected by the monitoring38. It has been estimated that the use of SSEP monitoring by teams
experienced in its use has reduced the rate of paraplegia following scoliosis surgery by 50%39. However,
continued reports of false negative SSEP monitoring
led Winter (1997) to conclude that “SSEP monitoring
alone does not appear adequate ... the best available
motor monitor is the wake up test but hopefully
a good electronic monitor will become generally
MEP monitoring
In response to false negatives with SSEP monitoring, motor evoked potential monitoring was
developed37. MEPs monitor the more vulnerable
anterior cord. Stimulation of the motor cortex results
in direct stimulation of pyramidal cells and conduction down spinal pathways resulting in a “D” wave
that can be recorded from the spinal cord via epidural
electrodes. Stimulation also results in polysynaptic
transmission recorded as subsequent “I” waves.
Summation of these waves results in firing of the
anterior horn cell and peripheral transmission via
motor nerves to the muscle. Muscle depolarization results in the CMAP40. CMAPs may also be
generated by surgical manoeuvres that result in irritation of nerve roots or cord concussion. Transcranial stimulation with recording of potentials from
peripheral nerves has also been used. These recordings result predominantly from conduction via the
dorsal columns. They are not true MEPs and have the
same false negative problems as SSEPs monitoring35.
Anaesthetic agents and Spinal cord monitoring
The impact of anaesthetic agents on spinal cord
monitoring increases with the number of synapses
in the pathway to be monitored. Volatile anaesthetic
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
agents and propofol depress SSEPs and MEPs in a
dose-dependent manner in parallel to their effects on
the EEG, probably due to inhibitory effects on polysynaptic pathways. Ketamine and etomidate may
enhance recordings40. Epidural recordings of MEPs
and SSEPs are more robust than both cortical SSEPs
and CMAPs because they rely less on polysynaptic
transmission. Nitrous oxide profoundly depresses
SSEPs and MEPs unless epidural recordings are
used41. Opioids, including intrathecal opioids, have
little effect on either modality except in large bolus
doses. Muscle relaxants reduce background noise
enhancing SSEP recordings. Profound degrees of
muscle relaxation abolish CMAPs but not epidural
MEPs. Recordings of CMAPs are possible with minor
degrees of relaxation corresponding to train of four
(TOF) counts of 2-342.
A technique using relaxant, moderate to high dose
opioid, and sub MAC volatile agent or propofol infusion is usually used for SSEP monitoring. Nitrous
oxide may be used if epidural rather than cortical
evoked potentials are monitored. Once baseline
SSEPs are recorded it is important to avoid boluses of
depressive agents to avoid false positive results37,39,40.
The effects of general anaesthetic agents and
muscle relaxants frustrated early attempts at MEP
monitoring particularly of CMAPs. Using multi-burst
transcranial stimulation and epidural recording of
spinal signals, which are relatively robust in the face
of standard anaesthetic regimes, overcame some of
the problems43. Epidural electrodes create some difficulties. They reduce the epidural space, clutter the
surgical field and require extension of the surgical
field cranially and caudally. Accidental dislodgement
results in loss of presurgical baseline. Epidural
recordings are less sensitive to the effects of
ischaemia and change later than CMAPs44. CMAPs
may also be generated by nerve root irritation or cord
concussion. If only epidural recordings are used these
additional warning signs are lost.
A protocol for reliable MEP monitoring
By blocking arousal stimuli, high dose opioid, as a
component of anaesthesia allows marked reductions
in both volatile concentrations and propofol doses
used45,46. Remifentanil may also have a small hypnotic
effect47. Reducing the concentration of volatile agent
or propofol dose needed for anaesthesia allows reliable recording of CMAPs and eliminates the need
for epidural recordings. There is no logical reason
to prefer propofol to volatile agents as the sedative
component of anaesthesia as has been advocated40
because the effects of both on CMAPs are dosedependent and the dose of both required in a
balanced anaesthesia regime is greatly reduced by
remifentanil. The great advantage of volatile agents is
that end-tidal concentrations can be readily measured
and rapidly titrated to a level that results in satisfactory recordings usually in the 0.4-0.7 MAC range.
Sevoflurane or desflurane may be preferable volatile
agents because they are the most rapidly titratable.
Volatile agents and propofol may also be titrated to
bispectral index (BIS) though this is awaiting validation in children. The addition of nitrous oxide (N2O)
offers no advantages when using remifentanil and it
profoundly depresses CMAPs so should be avoided.
The CHW anaesthetic protocol consists of high
dose remifentanil and 0.4-0.7 MAC end-tidal sevoflurane without N2O or muscle relaxants. Others have
developed similar protocols utilizing propofol48.
Etomidate and ketamine as supplements to N2O/opioid anaesthesia also seem compatible with reliable
High dose opioid anaesthesia leads to the development of acute tolerance and possibly to postoperative
hyperalgesia50, an effect abolished by low dose ketamine51. Ketamine also fortuitously may enhance the
generation of CMAPs with transcranial stimulation,
so we usually include low dose intraoperative ketamine (initial dose of 0.15 mg/kg followed by 2 µg/kg/
min) in our protocol.
CMAP monitoring results in patient movement
because the stimulus causes muscle contraction.
Reducing the stimulus intensity can reduce the vigour
of the muscle contraction and movement. Some units
use partial neuromuscular blockade as described
above, though we have not found it necessary.
Avoidance of muscle relaxants also makes awareness
less likely52. Complications of CMAP monitoring are
few but have included tongue lacerations or kinking
of the endotracheal tube from biting (bite blocks are
recommended), and the production of seizures in
patients with poorly controlled epilepsy53. Contraindications to CMAP monitoring use include metallic
cranial implants such as components of shunts,
aneurysm clips, or cochlear implants.
We rely on CMAP monitoring alone. From our
unreported series of over 300 patients at CHW and
Westmead Hospital (WH) there have been no false
negatives reported and two false positives (patients
who had persistent abnormal traces intraoperatively,
who had no postoperative deficit). In all neurologically normal patients and almost all patients with
neuromuscular curves CMAPS have been recordable.
(Dr Jim Lagopoulos PhD, neurophysiologist CHW,
personal communication). Patients in whom we
have been unable to obtain initial recordings have
been paraplegic or had spinal muscular atrophy.
Combined SSEP and CMAP monitoring to cover
sensory and motor areas has been recommended35.
This requires epidural lead placement, as it is not possible to simultaneously measure cortical SSEPs and
stimulate transcranially for CMAP monitoring. The
gain from this combined monitoring would appear
to be theoretical and has not been demonstrated
Managing neurological abnormalities detected by
Once a neurological abnormality is recognized, it is
important to correct any contributing factors as soon
as possible. Anaesthetic contribution to the loss of
traces should be ruled out, the blood pressure normalized or even increased above normal values and
anaemia corrected to maximize oxygen delivery to the
spinal cord. If the loss of function can be attributed to
a single event such as placing a sublaminar wire or
hook this should be removed. If distraction has been
applied it should be released. Doubts about the
validity of monitoring may be by settled by a wake up
We perform the wake-up test as follows. An assistant at the patient’s feet watches for movement. The
anaesthetist should be prepared to restrain the
patient to prevent gross movement and accidental
extubation. The volatile agent is turned off and the
remifentanil infusion decreased to 0.1 ug/kg/min.
When the end tidal volatile concentration falls to
0.2 MAC or below the patient is asked to squeeze
hands and then wriggle toes. When this occurs the
volatile agent is reintroduced and a small dose of hypnotic agent may be given, bearing in mind that this
will interfere with spinal cord monitoring for some
time. Using our current monitoring we perform about
one wake-up test per year.
Methylprednisolone 30 mg/kg should be administered followed by infusion of 5.4 mg/kg/hr for any persistent deficits in line with accepted spinal cord injury
protocols54,30. The same measures should be applied if
deficits appear in the postoperative period. Reversal
of paraplegia has been reported with restoration of
normal blood pressure, correction of anaemia and
release of distraction31.
From all of the above it is clear that successful intraoperative neurophysiological monitoring requires
close cooperation between the surgeon, anaesthetist
and neurophysiologist conducting the monitoring.
The cost of monitoring at CHW includes an initial
equipment set-up cost of A$60,000, a cost/case of
A$200 in disposable electrodes and the hourly cost of
the neurophysiologist.
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
Blood loss and Coagulopathy
Scoliosis correction may be associated with major
blood loss (>50% of blood volume) and the development of coagulopathy. Blood loss is related to length
of procedure and number of segments fused. About a
third of the blood loss occurs in the postoperative
period. The 24 hour blood loss has been calculated at
about 200 ml/segment fused17. The coagulopathy is
both dilutional and consumptive55, and also related to
the length of procedure and number of segments
fused. Patients with neuromuscular disease may be
particularly at risk because of a number of factors.
They often have longer procedures with more segments fused. They have osteopenic bone which bleeds
more and requires sublaminar wiring, rather than
laminar hooks, prolonging the procedure. They may
also have subclinical coagulation abnormalities56.
Large bore intravenous access with an efficient
fluid warmer and an intra-arterial line for monitoring
arterial pressure and blood sampling is necessary for
all patients. Careful monitoring of blood loss is important. Central venous access is indicated in patients
who may need inotropic support, those having combined procedures and those in whom peripheral
access is difficult. CVP may not accurately reflect cardiac filling in the prone position57. Transoesophageal
echocardiography (TOE) may be more useful for
patients with cardiac defects to more accurately
assess filling58.
Many strategies to reduce blood loss have been
described. Simple measures such as infiltration of
skin with dilute local anaesthetics containing
1:500,000 adrenaline and ensuring free abdominal
movement reducing venous pressure are important3.
Controlled hypotension has been widely advocated3,34, and does reduce blood loss, at least intraoperatively, but may also be associated with increased
risk of neurological deficit because of reduced spinal
cord perfusion, particularly if this is compromised
by distraction30,31. Recommendations are now more
conservative, with control of mean arterial pressure
limited to 70 mmHg30, a figure easily achieved with
a regime of high dose remifentanil and sub-MAC
volatile agent without the need to resort to other
measures to induce hypotension described in
standard texts3,34.
Antifibrinolytics have been shown to reduce blood
loss during scoliosis surgery, particularly in patients
with neuromuscular disease59-62. The serine protease
inhibitor aprotinin is the most studied and the most
effective, halving blood loss in high-risk patients.
There is a risk of hypersensitivity reactions, particularly with re-exposure within six months63, so
aprotinin should not be reused during staged proceAnaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
dures. We confine aprotinin use to high risk patients
and use a dose of 15000 KIU/kg loading dose over 20
minutes and 7500 KIU/kg/hr for the duration of the
Reduction in exposure to allogeneic blood transfusion can be achieved by preoperative autologous
donation, acute normovolaemic haemodilution and
intra-operative cell salvage64. Preoperative autologous
donation has been discussed. We do not use acute
normovolaemic haemodilution because of the possible exacerbation of any spinal cord ischaemia by
anaemia, although other units use it routinely. We do
use cell salvage, particularly in patients at high risk. In
small patients, allogeneic transfusion is often needed
before there is enough processed blood from cell
salvage to return to the patient.
Air embolism
Air embolism should be considered in the differential diagnosis of sudden cardiovascular collapse in
patients operated on in the prone position. Initial
management should follow standard lines of preventing further air entrainment, ventilation with 100%
oxygen, fluid boluses, and attempts to aspirate air
from the heart. In a report of two cases of fatal air
embolism, central catheters were not able to aspirate
air28. Paradoxical air embolism has also been reported65. Cardiac arrest in the prone position is difficult to manage, but successful resuscitation has been
reported using posterior thoracotomy for both internal cardiac massage and defibrillation66. External cardiac massage in the prone position has also been used
successfully67, but it is hard to see how effective compressions could be obtained on the four-poster frame
commonly utilized for scoliosis surgery. If the spine is
stable the wound should be covered and the patient
turned onto a bed for resuscitation, if unstable then
consideration given to left posterior thoracotomy and
internal massage. Consideration should be given to
the placing of external defibrillator pads in patients at
particular risk of cardiac arrest such as those with
DMD66. Fat embolism has also been reported as a
rare complication of scoliosis surgery68.
Visual loss
The reports of visual loss in patients having prone
spinal surgery have been in adults. The most common
cause is thought to be ischaemia of the optic nerve.
Optic nerve and retinal perfusion pressure depends
on maintaining the difference between arterial pressure and intra-ocular pressure or CVP. The risk
factors for postoperative visual loss are the same as
those for vascular disease plus intra-operative hypotension, anaemia and prolonged surgery29,69. Prone
positioning is known to cause a rise in intraocular
pressure related to the length of surgery70. Slight head
up positioning may reduce somewhat the rises in
intraocular pressure and the facial oedema that
occurs with prolonged prone positioning. The eyes
must be checked regularly throughout surgery to
ensure there is no external pressure being applied,
particulary as patient movement may change the
initial head position.
Postoperative Management
Pain Control
Effective pain control and active rehabilitation
following scoliosis correction requires a multimodal
regimen of pain management71. Spinal and systemic
opioids, local anaesthetic techniques and NSAIDs are
the major components.
Intrathecal morphine has been shown to be associated with reduced intraoperative bleeding and
better postoperative analgesia than systemic morphine alone in scoliosis surgery72. At CHW we use
spinal morphine 5 µg/kg, to a maximum of 300 µg,
administered intrathecally preoperatively by the
anaesthetist or, if this is difficult, intraoperatively by
the surgeon. If these routes are not feasible the drug
may be administered caudally in a dose of 50 µg /kg to
a maximum of 3 mg. Intrathecal morphine does not
interfere with CMAP monitoring and seems to
decrease the amount of intraoperative remifentanil
required. It results in smooth emergence from high
dose remifentanil anaesthesia. Patient controlled
analgesia (PCA) with morphine is added to this regimen, initially with a small bolus dose of 10 µg/kg.
After 12-24 hrs the bolus dose can be increased and a
background infusion commenced if necessary. For
patients incapable of using a PCA, nurse controlled
analgesia (NCA) can be initiated.
Opioids used alone can result in excessive sedation,
nausea, vomiting and ileus and do not alleviate pain
on movement. For posterior spinal surgery, surgically
placed epidural catheters can be utilized73,74. We
prefer to use PCA systemic morphine, as described
above, rather than continuing epidural or spinal
opioids. For anterior corrections, a catheter can be
placed in the paravertebral space, underneath the reconstituted parietal pleura, and used for a continuous
infusion of local anaesthetics. In some patients we
have found these infusions have provided very effective analgesia. In others, the blocks appear patchy,
presumably because of interruptions to the epidural
or paravertebral space by surgery.
The use of NSAIDs in scoliosis surgery is controversial. NSAIDs provide effective pain relief and
reduce opioid requirements75. A study in rats using
high dose indomethacin showed interference with
bone fusion76. The clinical relevance of this study has
been questioned, due to the extremely high doses
of indomethacin used. Nevertheless, a retrospective
study of 288 patients undergoing instrumented
lumbar spinal fusion showed a significantly higher
number of failed fusions in the group given ketorolac
for analgesia. The rate of failure seemed doserelated77. Ketorolac was given to those patients whose
pain was not well controlled by opioids and perhaps
pain was an indicator of failed fusion. A later
prospective study of 35 adolescent patients showed
the expected improvements in analgesia in the
ketorolac group with no difference in failed fusion at
two year follow up78. Failed fusion in adolescent idiopathic scoliosis surgery is extremely rare and a large
prospective study would be required to demonstrate
any effect of NSAIDs.
The COX-2 specific NSAIDs show similar analgesic efficacy and opioid sparing to conventional
NSAIDs in adult spinal fusion patients79 and a
parenteral preparation, parecoxib is available80. In an
animal model, the COX-2 specific NSAID, celecoxib,
did not affect the rate of bony fusion81, but celecoxib
and rofecoxib resulted in non-union of fractures in
another animal model and it seems COX-2 is needed
for fracture healing82. The significance of these findings for short-term perioperative use is unknown. The
COX-2 specific NSAIDS do not affect platelet function. As bleeding into drains can continue for some
time following spinal corrective surgery the COX-2
specific agents would seem a logical choice of NSAID
in these patients, though studies in children are lacking and they are yet to be licensed for use in children.
The pharmacology of these agents of relevance to
anaesthesia has recently been reviewed83.
Ketamine, as an opioid-sparing component of a
postoperative analgesic regimen, has met with mixed
results in clinical studies despite theoretical considerations and animal studies suggesting it should be
effective84. A recent study showed that low doses in
recovery were highly effective in treating morphine
resistant pain85. Other studies showed it to be ineffective when routinely added to PCA regimes for
abdominal surgery86,87. We reserve ketamine’s use
postoperatively for patients with continued pain or
opioid use resulting in excessive sedation with our
usual protocol. It may be added to a PCA in a dose
ratio of 1:1 with morphine 88 or separately as a
continuous infusion.
Other Postoperative Complications
The Superior Mesenteric Artery Syndrome is
thought to arise because of compression of the third
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
part of the duodenum between the superior mesenteric artery and the aorta, the relationship between
these structures having been distorted by correction
of scoliosis. It has been reported after cast bracing
and Harrington rod instrumentation, but is thought
to be less common after modern instrumentation
techniques. Symptoms consist of nausea and intermittent bilious vomiting occurring up to twelve days
after surgery. Abdominal pain and distension may
occur in 50% of cases. It usually settles with
conservative management4.
Problems with fluid management
Careful fluid management is required postoperatively with hourly urine measures and replacement of
ongoing losses. Ileus is inevitable but can be minimized by avoiding nitrous oxide and utilizing a multimodal analgesic regimen. We do not now routinely
place nasogastric tubes. The postoperative period is
associated with high levels of ADH, which may contribute to oliguria89. Hypotonic fluid administration
in the face of high ADH levels will lead to hyponatraemia and hypo-osmolality90. Assessment of the
patient’s volume status should precede fluid administration to correct oliguria if the problems associated
with perioperative fluid excess are to be avoided91.
Respiratory complications
Atelectasis and deterioration in respiratory function is common following surgery and an intense
postoperative analgesic regimen should be utilized
to provide frequent physiotherapy and early mobilization. Chylothorax has been reported rarely after
anterior surgery along with other more usual postthoracotomy complications of air-leak, haemothorax
and persistent chest pain92. Deterioration in bulbar
function has been reported following surgery in
patients with myotonic dystrophy93.
Anaesthesia for scoliosis surgery has evolved over
the last decade. New drugs and techniques allow continuous intraoperative monitoring of motor pathways,
permitting safer correction. Modern perioperative
care has enabled surgery in patients previously considered unsuitable. Because of concerns about spinal
cord ischaemia there is now less emphasis on induced
hypotension to reduce blood loss and allogeneic
transfusion requirements with increased emphasis on
antifibrinolytic therapy and cell salvage. The postoperative course of patients has been improved by
multi-modal postoperative pain therapy. The success
of this surgery requires a dedicated team approach.
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
The author wishes to thank Dr John Cummine,
Spinal Surgeon, The Children’s Hospital at Westmead for his advice on surgical aspects, Dr Jim
Lagopoulos PhD, Neurophysiologist, for his advice
on monitoring and Dr Neil Street, Anaesthetist, for
reviewing the manuscript and sharing his extensive
experience in spinal surgery.
1. Ogilvie JW. Historical Aspects of Scoliosis. In: Winter RB,
Bradford DS, Lonstein JE, Ogilvie JW, eds. Moe’s Textbook of
Scoliosis and other Spinal deformities 3rd Edition. WB
Saunders Company. Philadelphia, USA, 1995; 1-4.
2. Winter RB, Lonstein JR. Juvenile and Adolescent Scoliosis. In:
Herkowitz H, Garfin SR, Balderstone RA, Eismont FJ, Bell
GR, Wiesal SW, eds. Rothman-Simeone, The Spine 4th
Edition. WB Saunders Company, Philadelphia, USA, 1999;
3. Salem MR, Klowden AJ. Anesthesia for Orthopedic Surgery.
In: Gregory GA, ed. Pediatric Anesthesia. Churchill Livingstone, New York, USA, 2002; 617-661.
4. Shapiro G, Green DW, Fatica NS, Boachie-Adjei O. Medical
complications in scoliosis surgery. Curr Opin Pediatr 2001; 13:
5. Newton PO, Wenger DR, Mubarek SJ. Neuromuscular
scoliosis. In: Herkowitz H, Garfin SR, Balderstone RA,
Eismont FJ, Bell GR, Wiesal SW, eds. Rothman-Simeone, The
Spine 4th Edition. WB Saunders Company, Philadelphia, USA,
1999; 373-403.
6. Weinstein SL, Dolan LA, Spratt KF, Peterson KK, Spoonamore
MJ, Ponseti IV. Health and function of patients with untreated
idiopathic scoliosis. A 50 year natural history study. JAMA
2003; 289:559-567.
7. Merola A, Haher T, Brkaric M, et al. A multicenter study of the
outcomes of the surgical treatment of adolescent idiopathic
scoliosis using the Scoliosis Research Society (SRS) outcome
instrument. Spine 2002; 27:2046-2051.
8. Chng SY, Wong YQ, Hui JH, Wong HK, Ong HT, Goh DY.
Pulmonary function and scoliosis in children with spinal muscular atrophy types II and III. J. Paediatr Child Health 2003;
9. Miller RG, Chalmers AC, Dao H, Filler-Katz A, Holman D,
Bost F. The effect of spine fusion on respiratory function in
Duchenne muscular dystrophy. Neurology 1991:41:38-40.
10. Galasko CSB, Delaney C, Morris P. Spine stabilisation in
Duchenne Muscular Dystrophy. J Bone Joint Surg Br 1992;
11. Ramirez N, Richards BS, Warren PD, Williams GR. Complications after posterior spinal fusion in Duchenne’s muscular
dystrophy. J Pediatr Orthop 1997; 17:109-114.
12. Tsirikos AI, Chang W, Dabney KW, Miller F. Comparison of
one stage versus two stage anteroposterior spinal fusion in
pediatric patients with cerebral palsy and neuromuscular
scoliosis. Spine 2003; 28:1300-1305.
13. Cotrel Y, Dubousset A, New segmental posterior instrumentation of the spine. Orthop Trans 1985; 9:118.
14. Hirschfeld SS, Rudner C, Nash CL, Nussbaum E, Brower EM.
Incidence of mitral valve prolapse in adolescent scoliosis and
thoracic kyphosis. Pediatrics 1982; 70:451-454.
15. Etchason J, Petz L, Keeler E, et al. The cost effectiveness
of preoperative autologous blood donations. NEJM 1995;
16. Ridgeway S, Tai C, Alton P, Barnardo P, Harrison DJ. Predonated autologous blood transfusion in scoliosis surgery.
J Bone Joint Surg Br 2003; 85:1032-1036.
17. Murray DJ, Forbes RB, Titone MB, Weinstein SL. Transfusion
management in pediatric and adolescent scoliosis surgery:
Efficacy of autologous blood. Spine 1997; 22:2735-2740.
18. Goodnough LT, Shander A, Spence R. Bloodless medicine:
clinical care without allogeneic blood transfusion. Transfusion
2003; 43:668-676.
19. Wongprasartsuk P, Stevens J. Cerebral palsy and anaesthesia.
Paediatr Anaesth 2002; 12:296-303.
20. Schmidt GN, Burmeister MA, Lilje C, Wappler F, Bischoff P.
Acute heart failure during spinal surgery in a boy with
Duchenne muscular dystrophy. BJ Anaesth 2003; 90:800-804.
21. Morris P. Duchenne muscular dystrophy: a challenge for the
anaesthetist. Paediatr Anaesth 1997; 7: 1-4.
22. Rawlins BA, Winter RB, Lonstein JE et al. Reconstructive
spine surgery in pediatric patients with major loss in vital
capacity. J Pediatr Orthop 1996; 16:284-292.
23. Wazeka AN, DiMaio MF, Boachie-Adjei O, Oheneba MD.
Outcome of pediatric patients with severe restrictive lung
disease following reconstructive spine surgery. Spine 2004;
24. Finsterer J. Current Concepts in Malignant Hyperthermia.
Journal of Clinical Neuromuscular Disease 2002; 4:64-74.
25. Farrell PT. Anaesthesia-induced rhabdomyolysis causing
cardiac arrest: case report and review of anaesthesia and the
dystrophinopathies. Anaesth Intens Care 1994; 22:597-601.
26. Kleopa KA, Rosenberg H, Heiman-Patterson T. Malignant
hyperthermia-like episode in Becker muscular dystrophy.
Anesthesiology 2000; 93:1535-1537.
27. Sessler DI. Mild perioperative hypothermia. N Engl J Med
1997; 336:1730-1737.
28. Winter RJ, Sutherland RW. Two cases of fatal air embolism in
children undergoing scoliosis surgery. Acta Anaesthesiol Scand
1997; 41:1073-1076.
29. Myers M, Hamilton SR, Bogosian A, Smith CH, Wagner TA.
Visual loss as a complication of spine surgery: A review of 37
cases. Spine 1997; 22:1325-1329.
30. Mooney J, Bernstein R, Hennrikus W, MacEwen GD. Neurologic risk management in scoliosis surgery. J Pediatr Orthoped
2002; 22:683-689.
31. Winter R. Neurologic safety in spinal deformity surgery. Spine
1997; 22:1527-1533.
32. Bridwell K, Lenke L, Baldus C, Blanke K. Major intraoperative
neurological deficits in pediatric and adult spinal deformity
patients: Incidence and etiology at one institution. Spine 1998;
33. Vauzelle C, Stagnara P, Jouvinroux P. Functional monitoring of
spinal cord activity during spinal surgery. Clin Orthop 1973;
34. Cohen DE, Steven JM. Anesthesia for orthopedic surgery. In:
Motoyama EK, Davis PJ eds. Smith’s Anesthesia for Infants
and Children 5th Edition. CV Mosby, St Louis USA, 1990; 611626.
35. Owen J. The application of intraoperative monitoring during
surgery for spinal deformity. Spine 1999; 24:2649-2780.
36. Padberg A, Wilson-Holden T, Lenke LG, Bridwell KH.
Somatosensory and motor-evoked potential monitoring without a wake-up test during idiopathic scoliosis surgery: An
accepted standard of care. Spine 1998; 23:1392-1400.
37. Cronin AJ. Spinal Cord Monitoring. Current Opinion In
Orthopaedics 2002; 13:188-192.
38. Dawson EG, Sherman JE, Kanim LEA,Nuwer MR. Spinal
cord monitoring: Results of the Scoliosis Research Society and
the European Spinal Deformity Society survey. Spine 1991;
16(suppl): S361-S364.
39. Nuwer MR. Spinal cord monitoring with somatosensory techniques. J Clin Neurophysiol 1998; 15:183-193.
40. Sloan TB, Heyer EJ. Anesthesia for intraoperative neurophysiologic monitoring of the spinal cord. J Clin Neurophysiol
2002; 19:440-443.
41. Zentner J, Thees C, Pechstein U, Scheufler K, Wurker J,
Nadstawek J. Influence of nitrous oxide on motor-evoked
potentials. Spine 1997; 22:1002-1006.
42. Lang E, Beutler AS, Chesnut M, et al. Myogenic motor-evoked
potential monitoring using partial neuromuscular blockade in
surgery of the spine. Spine 1996; 21:1676-1686.
43. Stephen JP, Sullivan MR, Hicks RG. Cotrel-Dubousset instrumentation in children using simultaneous motor and somatosensory evoked potential monitoring. Spine 1996; 21:24502457.
44. deHaan P, Kalkman C, Ubags LH. A comparison of the sensitivity of epidural and myogenic transcranial motor-evoked
responses in the detection of acute spinal cord ischemia in the
rabbit. Anesth Analg 1996; 83:1022-1027.
45. Lang E, Kappila A, Shlugman D, Hoke JF, Sebel PS, Glass
PSA. Reduction of isoflurane minimum alveolar concentration
by remifentanil. Anesthesiology 1996; 85:721-728.
46. Guignard B, Menigaux C, Dupont X, Fletcher D, Chauvin M.
The effect of remifentanil on the bispectral index change and
hemodynamic responses after orotracheal intubation. Anesth
Analg 2000; 90:161-167.
47. Koitabashi T, Johansen JW, Sebel PS. Remifentanil dose/
electroencephalogram bispectral response during combined
propofol/regional anesthesia, Anesth Analg 2002; 94:15301533.
48. Langeloo D, Lelivelt A, Journee L. Transcranial electrical
motor evoked potential monitoring during surgery for
spinal deformity: A study of 145 patients. Spine 2003; 28:10431050.
49. Ubags LH, Kalkman CJ, Breen HD, Porsius M, Drummond
JC. The use of ketamine or etomidate to supplement sufentanil/N2O anesthesia does not disrupt monitoring of myogenic
transcranial motor evoked responses. J Neurosurg Anesthesiol
1997; 9:228-233.
50. Guignard B, Bossard AE, Coste C et al. Acute opioid
tolerance: Intraoperative remifentanil increases postoperative
pain and morphine requirement. Anesthesiology 2000; 93:409417.
51. Guignard B, Coste C, Costes H et al. Supplementing desflurane-remifentanil anesthesia with small-dose ketamine reduces
perioperative opioid analgesic requirements. Anesth Analg
2002; 95:103-108.
52. Sandin RH, Enlund G, Samuelsson P, Lennmarken C. Awareness during anaesthesia: a prospective case study. Lancet 2000;
53. Legatt A. Current practice of motor evoked potential monitoring: results of a survey. J Clin Neurophysiol 2002; 19:454-460.
54. Spine and Spine Cord Trauma. Advanced Trauma Life Support
for Doctors American College of Surgeons Committee on
Trauma Instructor Course Manual 1997, p. 277.
55. Horlocker TT, Nuttall GA, Dekutoski MB, Bryant SC. The
accuracy of coagulation tests during spinal fusion and instrumentation. Anesth Analg 2001; 93:33-38.
56. Edler A, Murray DJ, Forbes RB. Blood loss during posterior
spinal fusion surgery in patients with neuromuscular disease: is
there an increased risk? Paediatr Anaesth 2003; 13:818-822.
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
57. Soliman DE, Maslow AD, Bokesch PM et al. Transoesophageal
echocardiography during scoliosis repair: comparison with
CVP monitoring. Can J Anaesth 1998; 45:925-932.
58. Vischoff D, Fortier L, Villeneuve E, Boutin C, Labelle H.
Anaesthetic management of an adolescent for scoliosis surgery
with a Fontan circulation. Paediatr Anaesth 2001; 11:607-610.
59. Florintino-Pineda I, Blakemore LC,Thompson GH, PoeKochert C, Adler P, Tripi P. The effect of EACA on perioperative blood loss in patients with idiopathic scoliosis undergoing
posterior spinal fusion: a preliminary prospective study. Spine
2001; 26:1147-1151.
60. Neilipovitz DT, Murto K, Hall L, Barrowman NJ, Splinter WM.
A randomized trial of tranexamic acid to reduce blood transfusion for scoliosis surgery. Anesth Analg 2001; 93:82-87.
61. Colovic V, Walker RWM, Patel D, Rushman S. Reduction of
blood loss using aprotinin in spinal surgery in children for nonidiopathic scoliosis. Paediatr Anaesth 2002; 12:835.
62. Cole JW, Murray DJ, Snider RJ, Bassett GS, Bridwell KH,
Lenke LG. Aprotinin Reduces Blood Loss During Spinal
Surgery in Children. Spine 2003; 28:2482-2485.
63. Kovesi T, Roysten D. Pharmacological approaches to reducing
allogenic blood exposure. Vox Sang 2003; 84:2-10.
64. Spahn DR, Casutt M. Eliminating blood transfusions: new
aspects and perspectives. Anesthesiology 2000; 93:242-255.
65. Dang CP, Péréon Y, Champin P, Delecrin J, Passuti N. Paradoxical air embolism from patent foramen ovale in scoliosis
surgery. Spine 2002; 27:E291-E295.
66. Reid JM, Appleton PJ. A case of ventricular fibrillation in the
prone position during back stabilisation surgery in a boy with
Duchenne’s muscular dystrophy. Anaesthesia 1999; 54:364367.
67. Tobias JD, Mencio GA, Atwood R, Gurwitz GS. Intraoperative
cardiopulmonary resuscitation in the prone position. J Pediatr
Surg 1994; 29:1537-1538.
68. Gittman JE, Buchanan TA, Fischer BJ et al. Fatal fat embolism
after spinal fusion for scoliosis. JAMA 1983; 249:779-781.
69. Roth S; Barach P. Postoperative visual loss: still no answers-yet.
Anesthesiology 2001; 95:575-577.
70. Cheng MA, Todorov A, Tempelhoff R, McHugh T, Crowder
CM, Lauryssen C. The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology 2001;
71. Kehlet H, Dahl JB. The value of “multimodal” or “balanced
analgesia” in postoperative pain treatment. Anesth Analg 1993:
72. Gaff O, Aubineau J, Berniere J, Desjeux L, Murat I. Analgesic
effect of low dose intrathecal morphine after spinal fusion in
children. Anesthesiology 2001; 94:447-452.
73. Shaw B, Watson TC, Merzel DI, Gerardi J, Birek A. The safety
of continuous epidural infusion for postoperative analgesia in
pediatric spine surgery. J Pediatr Orthop 1996; 16:374-377.
74. Tobias JD, Gaines RW, Lowry KJ, Little D, Bildner C. A dual
epidural catheter technique to provide analgesia following posterior spinal fusion for scoliosis in children and adolescents.
Paediatr Anaesth 2001; 11:199-203.
75. Aubrun F, Langeron O, Heitz, D, Coriat P, Riou B. Randomised, placebo-controlled study of the postoperative analgesic effects of ketoprofen after spinal fusion surgery. Acta
Anaesthesiol Scand 2000; 44:934-939.
Anaesthesia and Intensive Care, Vol. 32, No. 4, August 2004
76. Dimar JR, Ante WA, Zhang YP, Glassman S. The effects
of nonsteroidal anti-inflammatory drugs on posterior spinal
fusions in the rat. Spine 1996; 21:1870-1876.
77. Glassman SD, Rose SM, Dimar JR, Puno RM, Campbell MJ,
Johnson JR. The effect of postoperative nonsteroidal antiinflammatory drug administration on spinal fusion. Spine 1998;
78. Munro HM, Walton SM, Malviya S et al. Low-dose ketorolac
improves analgesia and reduces morphine requirements following posterior spinal fusion in adolescents. Can J Anaesth
2002; 49:461-466.
79. Reuben S, Connelly N. Postoperative analgesic effects of celecoxib or rofecoxib after spinal fusion surgery. Anesth Analg
2000; 91:1221-1225.
80. Malan TP, Marsh G, Hakki SI et al. Parecoxib sodium, a
parenteral cyclooxygenase 2 selective inhibitor, improves
morphine analgesia and is opioid-sparing following total hip
arthroplasty. Anesthesiology 2003; 98:950-956.
81. Long JVM, Lewis S, Kuklo T, Zhu Y, Riew KD. The effect of
cyclooxygenase-2 inhibitors on spinal fusion. J Bone Joint Surg
Am 2002; 84:1763-1768.
82. Simon A, Manigrasso M, O’Connor J. Cyclo-oxygenase 2 function is essential for bone fracture healing. J Bone Miner Res
2002; 17:963-976.
83. Gajraj NM. Cyclooxygenase-2 inhibitors. Anesth Analg 2003.
84. Hirota K. Lambert DG. Ketamine: its mechanism(s) of action
and unusual clinical uses. Br J Anaesth 1996; 77:441-444.
85. Weinbroum A. A single small dose of postoperative ketamine
provides rapid and sustained improvement in morphine analgesia in the presence of morphine-resistant pain. Anesth Analg
2003; 96:789-795.
86. Reeves M, Lindholm D, Myles P, Fletcher H, Hunt JO. Adding
ketamine to morphine for patient controlled analgesia after
major abdominal surgery: a double blinded, randomized
controlled trial. Anesth Analg 2001; 93:116-120.
87. Dix P, Martindale S, Stoddart P. Double blind randomized
placebo-controlled trial of the effect of ketamine on postoperative morphine consumption in children following appendicectomy. Paediatr Anaesth 2003; 13:422-426.
88. Sveticic G, Gentilini A, Eichenberger U, Luginbuhl M,
Curatolo M. Combinations of morphine with ketamine for
patient controlled analgesia: a new optimization method.
Anesthesiology 2003; 98:1195-1205.
89. Cregg N, Mannion D, Casey W. Oliguria during corrective
spinal surgery for idiopathic scoliosis: the role of antidiuretic
hormone. Paediatr Anaesth 1999; 9:505-514.
90. Brazel PW, McPhee IB. Inappropriate secretion of antidiuretic
hormone in postoperative scoliosis patients: the role of fluid
management. Spine 1996; 21:724-727.
91. Holte NE, Sharrock NE, Kehlet H. Pathophysiology and
clinical implications of perioperative fluid excess. Br J Anaesth
2002; 89;622-632.
92. Grossfeld S, Winter RB, Lonstein JE, Denis F, Leonard A,
Johnson L. Complications of anterior spinal surgery in
children. J Pediatr Orthop 1997; 17:89-95.
93. Colovic V, Walker RWM. Myotonia dystrophica and spinal
surgery. Paediatr Anaesth 2002; 12:351-355.