Download Cerebral palsy and anaesthesia

Paediatric Anaesthesia 2002
12: 296–303
Review article
Cerebral palsy and anaesthesia
P O R A N E E W O N G P R A S A R T S U K * A N D JO H N S T E V E N S †
*Department of Anaesthesia, Great Ormond Street Hospital for Children, London and
†Department of Anaesthesia, John Radcliffe Hospital, Oxford, UK
Introduction
Cerebral palsy (CP) is ‘an umbrella term covering a
group of nonprogressive, but often changing, motor
impairment syndromes secondary to lesions or
anomalies of the brain arising in the early stages of
its development’ (1). The clinical picture may vary
considerably, ranging from mild monoplegia with
normal intellect to severe total body spasticity and
mental retardation. The common denominator is the
presence of a motor disorder arising from a brain
lesion or anomaly that is nonprogressive and
presents early in life (2).
Advances in medical care, changes in society’s
attitudes to infants, children and adults with disabilities have redirected the long-term management
of CP from passive, supportive care to a more active,
interventionist treatment. As a result, anaesthetic
involvement in the care of patients, particularly
children, with CP has increased. This review aims to
discuss recent developments in the aetiology, diagnosis and anaesthetic related management of CP.
Aetiology and risk factors
Epidemiological surveillance programmes indicate
the prevalence of CP in the developed world is
relatively static at 1–2.5 per 1000 live births among
babies of normal birth weight (3,4). With advances in
neonatal medicine and improved survival of premature infants, there is some evidence indicating an
increase in the prevalence of CP in low birth weight
children (5). However, this contrasts with a recent
survey of rates of cerebral palsy Scotland and
England, suggesting that the birthweight specific
Correspondence to: Poranee Wongprasartsuk, Nuffield Department
of Anaesthetics, Level 1, John Radcliffe Hospital, Headington,
Oxford OX3 9DU, UK (e-mail: [email protected]).
296
prevalence of CP has remained stable over a 5-year
period of surveillance (4).
The aetiology of CP is probably multifactorial, and
the contribution of specific causes still debated. A
small percentage, recently estimated at 6% (95% CI
0–15%), of cases is thought to be caused by intrapartum hypoxia, with the most common presentation in this group being spastic quadriplegia and,
rarely, dyskinesia (6,7). In term and near term
infants, approximately 50% of spastic CP is caused
by prenatal problems: cerebral maldevelopment,
prenatal stroke, prenatal infection (including toxoplasmosis, rubella, cytomegalovirus, herpes virus,
i.e. TORCH) or recognized genetic disorders in
which spasticity is a feature (8). Pure ataxic or
dyskinetic CP is probably genetic in origin (9).
Because of the retrospective nature of the diagnosis
of CP, causality in individual cases is usually
difficult to establish. For infants born at over
34 weeks gestation, a recent international consensus
statement outlines criteria for defining an acute
intrapartum hypoxic event (birth asphyxia) as causation of CP (7).
Premature infants may be different to term
infants. In preterm babies, several hypotheses have
been put forward to explain the development of CP.
It may be the result of an ischaemic insult in utero,
leading to both premature birth and damage to
cerebral white matter (10). Immature babies are
vulnerable to cerebral haemorrhage and ischaemia,
with intrapartum injury more likely (11). An alternative and perhaps more realistic explanation is that
CP is a final common endpoint of a number of
factors operating at different stages of early development, rather than any specific event (12). In
general, the recognized risk factors for the development of CP in the premature infant include: perinatal hypoxia, prenatal infection, congenital
abnormalities, trauma and genetic predisposition.
Ó 2002 Blackwell Science Ltd
C E R E B R A L P A L S Y A N D A N A ES TH E S I A
Interestingly, a protective factor against the development of CP in premature infants may be maternal
hypertension (13).
Classification of cerebral palsy
Cerebral palsy, being a collective term for a variety of
syndromes and lesions, is most easily classified
according to the predominant motor defect.
Although there is disagreement over the nomenclature, description of the motor defect as the main
feature of the ‘diagnostic label’ has significant
advantages, including the planning of resources to
care for children and adults with this group of disabilities (2). The motor defect may be spasticity, ataxia
or dyskinesia. Spasticity can range from mild monoplegia to severe quadriplegia and total body spasticity. Accompanying the motor defect may be varying
degrees of intellectual capacity, from normal intellect
to severe handicap. Speech may also be impaired as
part of the motor or intellectual disability.
Goals of treatment
Modern care of children with CP is an integrated
approach, combining community and hospital care.
Medical and surgical treatment is closely integrated
with physical therapies such as massage and splinting. The aims of skeletal treatment are to improve
function, mobility and communication by maintaining or improving range of motion and reducing the
severity of contracture, spasms and pain. The overall
goal is to maintain or improve independence and, in
severely disabled children, improve ease of care.
Assessments regularly monitor motor function,
independence, self-care and general care. Scoring
systems such as the Ashworth Scale (monitoring
muscle tone, Table 1) are useful tools to monitor
function. Regular gait assessment in ambulatory
patients will detect deterioration in function early
enough to allow noninvasive therapy. Currently, a
more aggressive approach to nutritional care helps
prevent malnutrition, infection and renal complications.
Medical therapy
Medical treatment for controlling spasticity, preventing contractures, may reduce the need for
Ó 2002 Blackwell Science Ltd, Paediatric Anaesthesia, 12, 296–303
2 97
Table 1
Ashworth Scale scoring system
Ashworth
Score
1
2
3
4
5
Degree of muscle tone
No increase in tone
Slight increase in tone, giving a ‘catch’ when the
affected part(s) is moved in flexion or extension
More marked increase in tone but affected part(s)
easily flexed or extended
Considerable increase in tone; passive movements
difficult
Affected part(s) rigid in flexion or extension
surgical correction, but must be introduced early.
There is variation in the aggressiveness of such
treatment in different centres. Medications act either
centrally or peripherally, and their adverse effects
are usually an extension of their actions, predictable
with knowledge of the mechanism of action.
Centrally active agents
Drugs modulating central triggers of spasticity may
be administered orally or intrathecally. Drugs used
in the treatment of spasticity are baclofen, diazepam
(and other benzodiazepines), vigabatrin and
tizanidine. All of these drugs have dose proportional
side-effects, predominantly sedative; therefore,
intrathecal administration has recently been advocated to minimize the total dose given and target the
site of action.
Baclofen, 4-chlorophenyl-GABA, is an agonist at
GABA-b receptor, acting in the spinal cord to inhibit
the release of excitatory neurotransmitters (aspartate
and glutamate), reducing muscle tone. Of the medications used in the treatment of spasticity, baclofen
is the only one currently used intrathecally with
demonstrable, though unpredictable, reduction in
spasticity. Given intrathecally, it reaches more than
10 times the CSF concentration compared to oral
administration (14). Intrathecal baclofen may be
administered as a bolus (usually as a test dose to
identify nonresponders) or via an implanted, programmable pump. The major advantage of continuous intrathecal baclofen infusion is titratability.
Some children, with underlying muscle weakness
actually rely on a degree of spasticity to walk or
stand. These children may benefit from a mild
reduction of spasticity, but it would be detrimental
to their function to ablate all spasticity. Common
298
P. WONGPRASARTSUK AND J. STEVENS
adverse effects of orally administered baclofen
include drowsiness, ataxia, dizziness and lethargy.
Problems with the intrathecal route include mechanical problems with the pump, reservoir and infection. Adverse effects of intrathecal baclofen are an
extension of effects of the oral route and also include
confusion and hypotonia (14).
Diazepam and other benzodiazepines enhance
presynaptic GABA-a mediated inhibition of neurotransmission and are given orally to treat spasticity.
Common adverse problems of benzodiazepines are
lethargy and development of tolerance.
Vigabatrin (c-vinyl GABA) is a GABA transaminase inhibitor. Originally developed for the treatment
of epilepsy, it prevents the breakdown of GABA and
can be used to treat spasticity.
Tizanidine, a derivative of the a2 agonist clonidine, probably inhibits the central release of aspartate and is effective in reducing spasticity. Common
problems reported are dry mouth and a feeling of
muscle weakness. Uncommonly, it causes reversible
abnormalities in liver function tests, which disappear on cessation of the drug. It may also cause mild
lowering of blood pressure. Drug induced hepatitis
and hallucinations are rare, serious side-effects (15).
Intrathecal administration of this drug is under
investigation.
Peripherally acting drugs
Botulinum toxin type A (botulinum toxin) is a
widely used treatment for spasticity in CP. Administered by injection into target muscles, it produces a
functional denervation of the muscle by preventing
presynaptic release of acetylcholine from the motor
end plate. The degree of paralysis is dose dependent
and the duration of effect depends on the rate of
terminal sprouting and the generation of new motor
end plates. Onset of action is within 1–3 days and
the expected duration of effect is 3–4 months.
Because of the high affinity of botulinum toxin for
the neuromuscular junction, systemic spread is
negligible and side-effects are few providing the total
dose at any one time is closely controlled. Muscles to
be injected are usually identified using a combination of clinical examination and, where appropriate,
gait analysis. Reduction in muscle tone, improved
range of motion, improved ease of care, reduced
pain from contractures and improved muscle
growth are all reported benefits of intramuscular
botulinum toxin (16). Two recent randomized, double-blind, placebo-controlled clinical trials have
demonstrated the effectiveness of botulinum toxin
A in reducing equinus foot deformity due to spasticity (17) and, also, that botulinum toxin A, administered 5–10 days preoperatively, can reduce
postoperative pain secondary to muscle spasm (18).
Occasionally, underlying weakness is revealed by
injection and the child’s overall condition is compromised. Injections are performed under topical or
local anaesthesia, sedation or general anaesthesia.
Two commercial preparations are available for use:
BotoxTM and DysportTM. They are not equipotent.
For injections into calf muscles, the recommended
dose of DysportTM begins with a starting dose of
30 UÆkg–1 in two divided doses, up to a maximum of
1000 UÆkg–1. In contrast, the recommended dose of
BotoxTM is 4 UÆkg–1 divided in two doses. There are
no published reports of interaction with commonly
used general anaesthetic agents when botulinum
toxin is used in this way. Possible unwanted effects
include leg cramps, weakness and lethargy (15).
Overdose may cause respiratory muscle weakness.
Accidental overdose requiring respiratory support
and local paralysis leading to swallowing difficulties
have also been reported (J.S. personal communication). Clinical trials have not reported adverse effects
or drug interactions.
Dantrolene inhibits calcium uptake by skeletal
muscle sarcoplasmic reticulum and relaxes tonically
active muscle. Baclofen is sometimes given orally in
the treatment of spasticity. It has no effect on the
neural mechanism of spasticity. Common adverse
effects are muscle weakness, diarrhoea, malaise,
nausea and skin rash. Liver function tests may
become abnormal (14,15).
Anaesthesia and surgical interventions
Children with CP present for surgery for a variety of
reasons, ranging from general surgical conditions to
particular interventions because of cerebral palsy.
Common surgical procedures include dental
procedures (restorative procedures and extractions),
surgery to control gastro-oesophageal reflux (GOR),
feeding gastrostomies, tracheostomies, spinal surgery, neurosurgical procedures to control spasticity
(e.g. highly selective dorsal rhizotomy) and a variety
Ó 2002 Blackwell Science Ltd, Paediatric Anaesthesia, 12, 296–303
C E R E B R A L P A L S Y A N D A N A ES TH E S I A
of upper and lower limb orthopaedic bony and soft
tissue procedures. These procedures are offered to a
broad cross-section of patients and may be indicated
for improvement in mobilization or ease of care, in
keeping with the broad goals of managing children
with CP.
Preoperative assessment
Medical, communication, general care problems and
social issues often complicate preoperative assessment of children with cerebral palsy. Often, children
have undergone repeated procedures; hence the
impact of previous experience is considerable. As
with all preoperative assessment, the aims are to
ensure the patient’s general medical condition is
optimized, a reasonable evaluation of perioperative
risk is discussed and the anaesthetic procedure
explained. Although optimization of medical condition and explanation of anaesthetic procedure may
be relatively straightforward, evaluation of perioperative risk is much more difficult, especially in
children with severe disability.
Particular problems with respect to patients with
CP are protean. They include a range of communication difficulties; the presence of scoliosis perhaps
restricting ventilation; GOR (some have had a
corrective procedure); contractures restricting access
for examination and positioning; decubitus ulcers
and skin infections; presence of gastrostomy or
tracheostomy and problems associated with malnutrition. Medical comorbidities, in particular epilepsy
and chest infection, need to be evaluated. A clear
history of current medication should be elicited,
particularly of antacids and anticonvulsants. Cisapride, commonly used for medical treatment of GOR
in these patients has been reported to be associated
with prolonged QT interval and life threatening
ventricular dysrhythmias. However, if liver function
is normal, in the absence of drug interactions
impairing metabolism of cisapride and using modest, accurately measured doses, ventricular dysrhythmia is unlikely to be a concern (19,20). There
is evidence that sodium valproate may increase
bleeding due to platelet dysfunction, thrombocytopaenia or aquired von Willebrand factor deficiency
type 1. These problems are probably dose dependent, usually seen at serum valproate levels
> 100 lgÆml–1. Dose reduction and rarely discontinuÓ 2002 Blackwell Science Ltd, Paediatric Anaesthesia, 12, 296–303
2 99
ation of sodium valproate will normalize these
coagulation problems. Preoperative coagulation tests
are suggested for children taking long-term sodium
valproate (21). Continuation of regular medications
such as antispasmodics and anticonvulsants in the
perioperative period is important for symptom
stability and prevention of acute withdrawal problems.
Preoperative assessment should also include
screening questions for latex allergy. Children with
CP, because of multiple surgical procedures and
exposure to latex allergens from an early age, are at
increased risk of developing latex allergy (22).
Screening questions should be explicitly asked.
These include direct enquiry about respiratory
symptoms, such as wheeze or allergic rhinitis,
cutaneous manifestations, such as rash, itch, oedema
or swelling on exposure to latex products, as well as
adverse reactions during previous anaesthesia. If
perioperative anaphylaxis occurs, latex allergy
should be considered. Allergist follow-up is vital in
establishing the cause of anaphylaxis after the acute
event.
Recent attempts have been made to elucidate
preoperative predictors of complications. Stasilkelis
et al. concluded that ambulatory function correlates
well with risk of complications following osteotomies. In this series of 79 patients followed up for at
least 1 year, a nonambulatory patient with a gastrostomy or tracheostomy was at greater risk of
complications. Recorded complications of surgery
were death (three children), fracture and decubitus
ulcer. Twenty patients were reported to have had at
least one complication (23).
Lipton et al. (24) using a retrospective medical
record review, developed a preoperative risk score
(ORS) and postoperative complication score (POCS).
The ORS was primarily a reflection of severity of
neurological involvement, with a higher ORS indicating greater operative risk. Factors taken into
account in calculating the ORS were ambulation
status, mental retardation, speech, feeding ability,
care (home or institutional), weight for age, degree
of deformity, medical and surgical history in the past
year. The POCS represented severity of postoperative complication, a higher score indicating a more
severe complication. In this study of 107 patients
undergoing spinal fusion, the authors suggest the
ORS is positively correlated with the severity of
300
P. WONGPRASARTSUK AND J. STEVENS
postoperative complications. In addition, spinal
deformity greater than 70° was associated with a
significantly higher POCS. There appeared to be no
significant differences in POCS between patients
having posterior spinal fusion alone and patients
having both anterior and posterior spinal fusion. The
scoring systems developed in this study represent an
important step forward in evaluating perioperative
risk of CP patients. However, external validation is
required on a similar group of patients with further
validation on another group of CP patients, undergoing different surgeries, to extend generalisability.
The use of a preoperative feeding gastrostomy
improves nutritional status and may decrease postoperative infection and improve wound healing. It
will also allow good perioperative fluid management, decreasing the risk of renal damage and
circulatory complications such as deep venous
thrombosis.
Anaesthetic care
Induction of anaesthesia may be challenging due to
lack of cooperation, communication difficulties and
difficult intravenous (i.v.) access. This is particularly
so in those children who have previously been in
special care baby units or neonatal intensive care;
who may have previously used and scarred veins. If
i.v. induction of anaesthesia is planned, all commonly used agents are suitable, although propofol
appears to be more painful in these patients.
Patients may be severely affected by drooling
because of decreased ability to swallow secretions,
making gaseous induction of anaesthesia both messy
and risky. A drying premedication such as atropine
can be beneficial but may also increase the risk of
chest infection by thickening lung secretions. The
increased incidence of GOR may sway anaesthetists
to choose a rapid sequence induction, although there
is no evidence to suggest that this confers any safety.
The presence of a second ‘pair of hands’ is often
helpful to establish i.v. access.
Airway management in the presence of increased
incidence of GOR in this group of patients varies.
Many anaesthetists choose a laryngeal mask airway
when clinically appropriate in conjunction with a
nasal or oral gastric tube aspirated and left on free
drainage, others chose a tracheal tube routinely. The
authors are not aware of published comparative
studies of different airway techniques in this group
of patients. Due to clinical variation, the wide
range of surgical interventions, large variation in
severity of CP and severity of GOR, such studies
may be challenging to undertake.
Studies of muscle relaxants in children with CP
indicate a slight sensitivity to succinylcholine. In a
dose response study by Theroux et al. a slightly
lower ED50 was found compared to historical controls. Although this difference was detected, it is
unlikely to be clinically significant. This finding may
be due to different structure and composition of the
neuromuscular junction (25) or an upregulation of
acetylcholine receptors (AchR’s), perhaps secondary
to chronic anticonvulsant medication (26). Vecuronium resistance has also been demonstrated in CP.
In a comparative study, using prospective controls,
Moorthy et al. showed a significant resistance to
vecuronium. The time from administration of
0.1 mgÆkg–1 to 25% recovery of control twitch height
in children with CP was less than half the time for
normal children. The mechanism of resistance to
vecuronium is unclear because all children in this
study were severely affected by CP and taking longterm anticonvulsant medication. Postulated mechanisms include drug interaction with anticonvulsant
medication (increased hepatic clearance, AchR upregulation) and chronic immobilization (27). For volatile anaesthetics, minimum alveolar concentration
(MAC) for anaesthesia may be decreased. The MAC
of halothane has been shown to be 20% lower in
children with CP, and a further 10% lower in those
currently taking anticonvulsants (28).
Most major surgical procedures undertaken in
children with CP are amenable to combined general
anaesthesia and regional analgesia. Epidural analgesia, in particular, continued into the postoperative
period will diminish both postoperative pain and
muscle spasm. Continuous infusion of epidural
bupivacaine (0.1%) and fentanyl (2 lgÆml–1), monitored by an acute pain service, is thought to provide
better analgesia with few side-effects compared to
intermittent boluses of epidural morphine (29) or
intravenous opioid infusions. The addition of clonidine may give added control of postoperative
spasm. In the control of postoperative pain following
selective posterior rhizotomy in the lumbar region (to
improve gait or stance), epidural opioids, morphine
in particular, remain the mainstay of treatment (30).
Ó 2002 Blackwell Science Ltd, Paediatric Anaesthesia, 12, 296–303
C E R E B R A L P A L S Y A N D A N A ES TH E S I A
There are pros and cons of awake versus asleep
insertion of epidural catheters. Awake placement of
epidural catheters is not a practical or safe option in
this group of patients. There is also a high incidence
of scoliosis. Because of these problems, an experienced epiduralist should be involved in placement
of the epidural. It is important to remember that
scoliosis is also a torsional deformity, and the
epidural performed accordingly.
Perioperative hypothermia is a significant problem, especially when age, understanding and ability
to cooperate are limited during induction of anaesthesia. During the performance of some anaesthetic
procedures, children may lose heat quickly. (e.g.
placement of an epidural catheter). Further exposure
to a cool operating theatre may occur during
positioning for surgery and subsequent changes in
position, such as during a multilevel orthopaedic
soft tissue release procedure. Prolonged insufflation
of the abdomen or thorax during laparoscopic
surgery may also increase heat loss. The increased
likelihood of hypothermia is unavoidable, but can be
minimized by humidification of airway gases, use of
low fresh gas flows, warmed intravenous fluids,
avoidance of a cold operating room and using active
warming methods such as forced air warming
blankets. If active warming methods are used, it is
important to monitor core temperature because
overheating is a potential hazard.
Patient positioning may be problematic, with
contractures often not allowing support by conventional operating tables and supports. Pressure sores
and nerve damage are a very real possibility.
Children with CP are especially at risk because of
their poor nutritional status and the length of many
operations. A comfortable, malleable support such
as a vacuum bag is very helpful.
Extensive plaster casting is an important aspect of
skeletal treatment in CP. However, extensive casting
can mask considerable blood loss and, when combined with epidural analgesia, may make compartment syndromes more difficult to detect. This is
particularly so following tibial osteotomy, where
there is a significant risk of compartment syndrome.
Plaster jackets and hip spicas are associated with
mesenteric occlusion and acute gastric dilatation,
and so a nasogastric tube should be inserted routinely. Chronic low fluid intake, combined with
preoperative fasting, means that children with CP
Ó 2002 Blackwell Science Ltd, Paediatric Anaesthesia, 12, 296–303
3 01
are at risk of prerenal, renal failure. The perioperative impact of this can be lessened by careful
monitoring of urine output. Insertion of a urinary
catheter should be considered to monitor urine
output, especially for long or difficult procedures
involving significant blood loss and fluid shifts.
Specific surgical procedures
Inguinal hernia repair
Often, the first time a child with CP attends for
anaesthetic care is for hernia repair early in life. Up
to 30% of boys with birth weight < 2000 g and likely
to be at risk of CP may have an inguinal hernia (31).
It is postulated this is due to increased intraabdominal pressure associated with increased tone
in the abdominal wall. In the premature neonate, the
standard practice in most UK paediatric centres is to
repair the inguinal hernia just prior to anticipated
discharge home. There is some evidence that earlier
repair may improve comfort, handling and nutrition
and does not increase morbidity. Spinal anaesthesia,
without sedation for the ex-premature baby was, in
recent years, advocated because it may reduce the
incidence of postoperative apnoea. There is limited
evidence to support this view. A comparative study
in high-risk infants undergoing inguinal hernia
repair suggests potential benefit in reducing the
incidence of postoperative apnoea. However, it also
illustrates many of the major problems that prevent
awake spinal anaesthesia for this group of patients
from being widely adopted. In a group of 24 infants
the problems were technical failure to perform the
spinal in four infants; two or more attempts in five;
supplemental general anaesthesia in six and surgical
difficulty requiring physical restraint because of
excessive upper limb movement in 14 infants (32).
During a difficult hernia repair, spinal anaesthesia
may not last long enough, especially if bilateral
repair is required. General anaesthesia can be supplemented by ilioinguinal nerve block or infiltration
of local anaesthetic in unilateral repair. In bilateral
repairs, caudal block is beneficial.
Antireflux surgery
GOR is a common problem among children with CP,
frequently requiring surgical correction. An open
302
P. WONGPRASARTSUK AND J. STEVENS
operation is associated with considerable morbidity
and laparoscopic surgery is now probably the
approach of choice in most situations. The physiological changes associated with pneumoperitoneum
in children have been described. Early experience
with laparoscopic Nissen fundoplication suggests
children are well managed with oral and rectal
analgesia postoperatively. In addition, the need for
postoperative high dependency and intensive care
appears to be minimal (33). Although there is less
postoperative pain with this approach, epidural
analgesia may still be useful in preventing painful
postoperative spasms.
Scoliosis surgery
Scoliosis surgery is associated with an acute, sometimes prolonged deterioration in respiratory
function, even if thoracotomy is not performed.
Recently, some surgeons have adopted a thoracoscopic approach to anterior release in an attempt to
reduce pulmonary morbidity. Such surgery in severe
CP should not be undertaken lightly, and only in a
facility with full intensive care provision. Postoperative nasal continuous positive airway pressure
(CPAP) may help to prevent respiratory complications. The occasional patient will need long-term
ventilation, perhaps even tracheostomy during the
weaning process. Preoperative respiratory function
tests are unreliable in this scenario and not predictive of outcome.
Ethical considerations
In a child severely affected by cerebral palsy,
decisions about invasive procedures and the use of
increasingly scarce intensive care facilities are difficult to make. Once invasive therapy has been
embarked upon, it is difficult to judge when the
next step is a step too far. Each procedure needs to
be considered on its merits; the likelihood of survival and morbidity, as well as the likelihood of
improving quality of care and life. It is important for
surgeons to be realistic about the likely achievements of the procedure and for anaesthetists to be
realistic about the likelihood of anaesthesia related
morbidity. Only then can parents (guardians)
approach giving truly informed consent for many
of these procedures.
A particularly contentious subject area of consent
is for anaesthesia administered to facilitate magnetic
resonance imaging (MRI). MRI has become a compulsory investigation in the pursuit of litigation
claims related to CP and causation. Many law firms
will not consider a case before an MRI has been
performed and reported on by a recognized expert.
Although the anaesthetic risk is small, it exists. This
is a difficult ethical dilemma as the anaesthetic is not
administered for a therapeutic reason and the test
(MRI) may lead to failure of the compensation claim.
Conclusions
In summary, cerebral palsy is currently managed by
combined physiotherapy, medical and surgical
approaches. The aim of such coordinated care is to
significantly improve quality of life and quality of
care. Anaesthetic involvement may be in the operating room, in intensive care or providing technical
support for insertion of spinal infusing devices in
medical therapy. Modern medical advances have
enabled more aggressive and invasive care. The
challenge for all those caring for patients with CP is
to consider the ethics of embarking upon highly
invasive care, with marginal benefit to the patient.
References
1 Mutch I, Alberman E, Hagberg B et al. Cerebral palsy epidemiology: where are we now and where are we going? Dev Med
Child Neurol 1992; 34: 547–555.
2 Badawi N, Watson L, Petterson B et al. What constitutes
cerebral palsy? Dev Med Child Neurol 1998; 40: 520–527.
3 Paneth N, Stark RI. Cerebral palsy and mental retardation in
relation to indicators of perinatal asphyxia. Am J Obstet Gynecol
1983; 147: 960–966.
4 Pharoah POD, Cooke T, Johnson MA et al. Epidemiology of
cerebral palsy in England and Scotland 1984–9. Arch Dis Child
Fetal Neonatal Ed 1998; 79: F21–F25.
5 Dite GS, Bell R, Reddihough DS et al. Antenatal and perinatal
antecedents of moderate and severe spastic cerebral palsy.
Aust NZ J Obstet Gynaecol 1998; 38: 377–383.
6 Nelson KB, Grether JK. Potentially asphyxiating conditions
and spastic cerebral palsy in infants of normal birthweight. Am
J Obstet Gynecol 1998; 179: 507–513.
7 MacLennan A, International Cerebral Palsy Task Force. A
template for defining a causal relation between acute intrapartum events and cerebral palsy: international concensus
statement. BMJ 1999; 319: 1054–1059.
8 Nelson KB, Grether JK. Maternal infection and cerebral palsy
in infants of normal birthweight. JAMA 1997; 278: 207–213.
9 Steinlin M. Non-progressive congenital ataxias. Brain Dev 1998;
20: 199–205.
Ó 2002 Blackwell Science Ltd, Paediatric Anaesthesia, 12, 296–303
C E R E B R A L P A L S Y A N D A N A ES TH E S I A
10 Pharoah POD, Cooke T, Cooke RW et al. Birthweight specific
trends in cerebral palsy. Arch Dis Child 1990; 65: 602–606.
11 Leviton A, Paneth N. White matter damage in preterm
newborns: an epidemiologic perspective. Early Hum Dev
1990; 24: 1–22.
12 Murphy DJ, Hope PL, Johnson A. Neonatal risk factors for
cerebral palsy in very preterm babies: case control study. BMJ
1997; 314: 404–408.
13 Gray PH, O’Callaghan MJ, Mohay HA et al. Maternal hypertension and neurodevelopmental outcome in very preterm
infants. Arch Dis Child Fetal Neonatal Ed 1998; 79: F93.
14 Albright LA. Cerebral palsy: approaches to drug treatment.
Pract Therapeut 1995; 4: 17–27.
15 Collier J, ed. The management of spasticity. Drug Therapeut
Bull 2000; 38: 44–46.
16 Gordon N. The role of botulinus toxin type A in treatment –
with special reference to children. Brain Dev 1999; 21: 147–151.
17 Koman LA, Mooney JF, Smith BP et al. BOTOX study group.
Botulinum toxin type A neuromuscular blockade in the
treatment of lower extremity spasticity in cerebral palsy: a
randomised double-blind, placebo-controlled trial. J Pediatr
Orthop 2000; 20: 108–115.
18 Barwood S, Baillieu C, Brereton K et al. Analgesic effects of
botulinum toxin A. a randomized, placebo-controlled clinical
trial. Dev Med Child Neurol 2000; 42: 116–121.
19 Khoshoo V, Edell D, Clarke R. Effect of cisapride on the QT
interval in infants with gastroesophageal reflux. Pediatrics 2000;
105: E24.
20 Levine A, Fogelman R, Sirota L et al. QT interval in children
and infants receiving cisapride. Pediatrics 1998; 101: E9.
21 Acharya S, Bussel JB. Hematologic toxicity of sodium valproate. J Pediatr Hematol Oncol 2000; 22: 62–65.
22 Landwehr LP, Boguniewicz M. Current perspectives on latex
allergy. J Pediatr 1996; 128: 305–312.
Ó 2002 Blackwell Science Ltd, Paediatric Anaesthesia, 12, 296–303
3 03
23 Stasilkelis PJ, Lee DD, Sullivan CM. Complications of osteotomies in severe cerebral palsy. J Pediatr Orthop 1999; 19:
207–210.
24 Lipton GE, Miller F, Dabney KW et al. Factors predicting
postoperative complications following spinal fusions in children with cerebral palsy. J Spinal Disord 1999; 12: 197–205.
25 Theroux MC, Brandon BW, Zagonev M et al. Dose response of
succinyl choline at the adductor pollicus of children with
cerebral palsy during propofol and nitrous oxide anesthesia.
Anesth Analg 1994; 79: 761–765.
26 Antognini JF, Gronert GA. Succinylcholine sensitivity in
cerebral palsy. Anesth Analg 1995; 80: 1248–1253.
27 Moorthy SS, Krishna G, Dierdorf S. Resistance to vecuronium
in patients with cerebral palsy. Anesth Analg 1991; 73: 275–277.
28 Frei FJ, Haemmerle MH, Brunner R et al. Minimum alveolar
concentration for halothane in children with cerebral palsy and
severe mental retardation. Anaesthesia 1997; 52: 1056–1060.
29 Brenn BR, Brislin RP, Rose JB. Epidural analgesia in children
with cerebral palsy. Can J Anaesth 1998; 45: 1156–1161.
30 Albright LA. Neurosurgical treatment of spasticity: selective
posterior rhizotomy and intrathecal baclofen. Steroetact Funct
Neurosurg 1992; 58: 3–13.
31 Reimers JI, Latocha JE. Incidence of inguinal hernia in children
with congenital cerebral palsy. Dev Med Child Neurol 1990; 32:
1058–1060.
32 Somri M, Gaitini L, Vaida S et al. Postoperative outcome in
high-risk infants undergoing herniorrhaphy: comparison
between spinal and general anaesthesia. Anaesthesia 1998; 53:
762–766.
33 Rowney DA, Aldridge LM. Laparoscopic fundoplication in
children: anaesthetic experience of 51 cases. Paed Anaesth 2000;
10: 291–296.
Accepted 26 July 2000