Anaesthesia and pain management in cerebral palsy

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1 REVIEW ARTICLE Anaesthesia and pain management in cerebral palsy J. Nolan, 1 * G. A. Chalkiadis, 1 J. Low, 1 C. A. Olesch 2 and T. C. K. Brown 1 1 Department of Anaesthesia, and 2 Department of Child Development and Rehabilitation, Royal Children s Hospital, Flemington Road, Parkville, Victoria 3052, Australia Summary Cerebral palsy is the result of an injury to the developing brain during the antenatal, perinatal or postnatal period. Clinical manifestations relate to the area affected. Some of the conditions associated with cerebral palsy require surgical intervention. Problems during the peri-operative period may include hypothermia, nausea and vomiting and muscle spasm. Peri-operative seizure control, respiratory function and gastro-oesophageal reflux also require consideration. Intellectual disability is common and, in those affected, may range from mild to severe. These children should be handled with sensitivity as communication disorders and sensory deficits may mask mild or normal intellect. They should be accompanied by their carers at induction and in the recovery room as they usually know how best to communicate with them. Postoperative pain management and the prevention of muscle spasm is important and some of the drugs used in the management of spasm such as baclofen and botulinum toxin are discussed. Epidural analgesia is particularly valuable when major orthopaedic procedures are performed. Keywords Anaesthesia. Analgesia; postoperative. Cerebral palsy.... Correspondence to: Dr G. Chalkiadis * Present address: Department of Anaesthesia, Bristol Royal Infirmary, Bristol, UK Accepted: 7 May 1999 Cerebral palsy (CP) is a nonprogressive disorder of motion and posture. The causes are multiple, but all result in damage to the central nervous system (CNS) which may occur antenatally, perinatally or postnatally, during the period of early brain growth [1]. It is the leading cause of childhood motor disability occurring in 2 per 1000 live births in developed countries [2]. Despite improved antenatal and perinatal care, this incidence has not changed in recent years, partly due to increased survival in premature neonates and partly because neonatal asphyxia is not as common a cause as previously thought. Almost all children with CP will have at least one additional disability attributable to CNS damage [3]. Such disabilities include cognitive impairment, sensory loss (vision and hearing), seizures, communication and behavioural disturbances, as well as the chronic systemic problems resulting from their disease (gastrointestinal, respiratory and orthopaedic). Generally, the likelihood of such deficits is increased in those with a greater degree of spasticity involving a greater number of limbs [3]. An understanding of the aetiology, clinical problems and their management, including a knowledge of the drugs used in this condition, will help the anaesthetist to manage these patients better during anaesthesia and the peri-operative period. Aetiology Until about 10 years ago, the general concept for the aetiology of CP was based on an interpretation of earlier studies which over-emphasised the role of asphyxia neonatorum and perinatal complications [4]. As a result, increasing litigation against obstetricians is likely to have contributed to the escalating rates of Caesarean sections and soaring medical defence premiums. Although most cases are of unknown aetiology, there is increasing Blackwell Science Ltd

2 J. Nolan et al. Anaesthesia and pain management in cerebral palsy evidence that antenatal cerebral events may result in fetal complications that manifest themselves at delivery. These events have often been misdiagnosed as perinatal asphyxia [5]. Cerebral palsy in the premature infant is commonly due to periventricular leucomalacia as a result of periventricular haemorrhages and is manifest clinically as spastic diplegia. The aetiology in infants born at term is often unclear but may be due to insults to the immature brain during early pregnancy. Other hypotheses in the term infant include antenatal infection, thyroid disease and neuronal migration disorders. Postnatal causes include meningitis, viral encephalitis, hydrocephalus, trauma, surgical lesions and their treatment. Classification and clinical manifestations Unlike the cerebral lesion, which is by definition static, the clinical picture of CP is variable and evolves over time. It may present with an isolated neurological abnormality or with severe neurological deficit associated with cognitive impairment, sensory deficits, seizures, communication disorders, behavioural and emotional problems. The degree and type of disability depend on the extent and site of the cerebral pathology; spasticity is associated with abnormalities of the motor cortex, athetosis with defects in the basal ganglia and ataxia with defects in the cerebellum. Other systems, such as gastrointestinal and respiratory, may be secondarily involved. Attempts at classifying CP have included neuropathological, aetiological and clinical approaches, none of which has been satisfactory. The Swedish classification (Table 1) is currently the most commonly used as it addresses both the movement disorder and its distribution [4]. Spastic CP is the commonest type, accounting for 70% of cases. The spastic variety of CP commonly results in the development of contractures over time especially at the elbows, wrists, hips, knees and ankles. Spastic diplegia and spastic hemiplegia have the best prognosis for functional Table 1 Swedish classification system for CP Spastic (70%): Quadriplegia (27% of all cases of CP) Diplegia (21%) Hemiplegia (21%) Dyskinetic (10%): Dystonia (maintained twisting position of torso and extremities) Athetosis (slow, purposeless, distal movements) Chorea (quick, jerky, proximal) Ataxic (10%): Intention tremor and head tremor (titubation) Mixed (10%): e.g. Spastic athetoid improvement. Spastic diplegia is usually associated with prematurity and implies spasticity of both lower limbs with minimal upper extremity involvement. In hemiplegia, involvement is unilateral with the upper limb usually being affected more than the lower limb. In quadriplegia, all four limbs are affected, upper limbs usually more severely. Intellectual disability and epilepsy are common in the latter group. Bulbar muscles are involved to a varying degree resulting in poor control of the mouth, tongue and pharynx. Feeding difficulties may be severe, requiring nasogastric feeding or a gastrostomy. Aspiration pneumonia is most likely in this group. The likelihood for functional improvement in patients with spastic quadriplegia is often poor. Dyskinetic CP may be associated with deafness, dysarthria and drooling. Seizures occur in about one quarter of these patients [6]. In the majority of these cases, the intelligence quotient (IQ) is low/normal. Since the introduction of exchange transfusion for blood group incompatibility and the subsequent dramatic reduction of kernicterus, the incidence of this type of CP has decreased. In ataxic CP, balance is impaired and speech disorders are common ( scanning cerebellar speech ). Intellectual disability and epilepsy are often associated findings. This group also has a poor likelihood for functional improvement. Two or more types of CP may be seen in one patient, e.g. spastic athetoid. In some cases complexity may defy classification. Anaesthetic implications for the child with cerebral palsy These children require special consideration because of their various disabilities. It must not be forgotten that they have feelings and emotions which are sensitive to the way they are handled and their understanding may be greater than seems apparent on first meeting. Patients with speech disability may use communication aids such as sign cards or computer aids and these should be available to them. Patients with dyskinetic CP are often the most intelligent but have the greatest difficulty with communication. It is important to provide these children with enough time for them to be able to communicate their needs. A questionnaire for parents and carers detailing how their child communicates and how they react to pain, hunger and other situations can be invaluable in helping staff to understand that child s behavioural manifestations. Parents and carers are best suited to allaying their fear and anxiety in addition to being their strongest advocate. As such, consideration and respect should be paid to the parents and carers and to their opinions. Parents may appear aggressive and very protective towards their child. It is important to understand that these are manifestations 2000 Blackwell Science Ltd 33

3 J. Nolan et al. Anaesthesia and pain management in cerebral palsy Anaesthesia, 2000, 55, pages of previous experience, stress, frustration, anger and perhaps guilt [7]. Pre-operative assessment Thorough pre-operative preparation is important in ensuring an uneventful peri-operative course. These children are ideal for assessment by a multidisciplinary team which may include an anaesthetist. Cognitive, communication and behavioural problems will influence the management plan as much as associated medical conditions and drug therapy. Postoperative analgesia is an essential part of the management. The importance of this is readily demonstrated in orthopaedic surgery where inadequate analgesia, anxiety and poor communication skills can lead to increased muscle tone and spasms postoperatively with consequent worsening of pain. Effective analgesia from the outset will prevent this cycle of events. The following systems may be involved and should be considered pre-operatively: Gastrointestinal Gastro-oesophageal reflux is common and may cause respiratory problems, especially in more severely affected individuals. Oesophageal dysmotility, abnormal lower oesophageal sphincter function and spinal deformity [8] contribute to reflux. Reflux can be difficult to detect; subtle suggestions include dystonic movements with posture (Sandifer syndrome). Night waking may indicate reflux or oesophageal spasm. Fundoplication, gastrostomy and oesophageal dilatation for strictures caused by oesophagitis are the second most common surgical procedures performed in these patients after orthopaedic surgery. Salivary drooling can be a debilitating problem in the child with CP. It may be related to pseudobulbar palsy with impaired swallowing [9] or tongue thrusting and is worsened by poor head control [10]. Medical treatment with anticholinergics may be indicated. Surgical intervention is sometimes undertaken with reimplantation of salivary ducts. A small group of children with CP are unable to maintain a normal nutritional state by oral feeding due to poor chewing and swallowing, with resultant failure to thrive. Nasogastric feeding or gastrostomy may be needed [8]. Pre-operative nutritional support may reduce the incidence of postoperative complications associated with malnourishment. Electrolyte imbalance from malnutrition and laxatives may require treatment. Associated anaemia is common. Respiratory Respiratory disorders are ultimately a common cause of death [11]. Problems include pulmonary aspiration from reflux [8], recurrent respiratory infections and chronic lung disease, which may be aggravated by reduced ability to cough with pooling of secretions. Poor nutritional state may depress the immune response. Respiratory pathology of some significance may go unnoticed in cases where communication is poor and exercise tolerance cannot be properly assessed because of neurological impairment. Scoliosis with a resulting restrictive defect may lead to cardiopulmonary compromise. To optimise their peri-operative care, pre-operative physiotherapy, bronchodilators or antibiotics may be required. The airway should be assessed for potential difficult laryngoscopy because of dental caries, loose teeth and an increased incidence of temporomandibular joint dysfunction [12]. Children with CP have an increased incidence of malocclusion probably due to tongue thrusting [13]. Open bite (vertical overlap of the incisors) and overjet (horizontal overlap of the incisors) become more prominent with increasing age. The degree of malocclusion may be more severe in those children with greatest disability. In our experience, malocclusion does not contribute to difficulties with laryngoscopy or airway maintenance with a facemask. Formal airway assessment may well be impractical and a review of previous anaesthetic charts may be helpful in this setting. Epilepsy Epilepsy occurs in 30% of patients with CP. It is most common in spastic hemiplegia and least common in ataxic and choreoathetoid forms [3]. Tonic clonic and complex partial seizures are particularly common. Normal anticonvulsant therapy should be continued up to and including the day of surgery. Visual and hearing deficits Forty per cent of all chidren with CP have an abnormality of their vision. Impairments include myopia, visual field defects and cortical blindness. Children born prematurely may have visual impairment secondary to retinopathy of prematurity. Oculomotor problems (e.g. strabismus) are common and may lead to amblyopia. Retinopathy of prematurity and ambylopia may require surgery. Behavioural and communication problems Intellectual disability is present in approximately twothirds of patients with CP [3], with many others having learning disabilities. Normal intelligence occurs in more than 60% of children with hemiplegia but in less than 30% of those with spastic quadriplegia or mixed-type. Intellectual disability is classed as severe in 50% of those affected [14]. Attention deficit disorders are especially common in Blackwell Science Ltd

4 J. Nolan et al. Anaesthesia and pain management in cerebral palsy the higher functioning child, while those with intellectual disability very occasionally suffer from self-injurious behaviour. Depression and emotional lability are common adolescent problems [15]. Other surgical procedures Orthopaedic procedures, such as soft tissue releases, are commonly performed in these children to relieve contractures. There is a more recent trend for single event multilevel surgery involving tenotomies and/or osteotomies at different levels on one or both limbs. This is usually performed between the ages of 6 and 12 years when gait has matured, prior to their growth spurt. The actual procedures are based on the individual s gait analysis. Other commonly performed operations are dental extractions and restorations and fundoplication to prevent reflux (see Table 2). Neurosurgical procedures are performed at some centres. These include ventrolateral thalamotomy to control tremor, selective cortical ablation for seizures and selective posterior rhizotomy to reduce tone [16]. Premedication Sedatives should be considered but one has to balance the unpredictable response with the advantages that may be gained at induction by reducing anxiety and spasm. Antacids and drugs to reduce secretions may be appropriate. Local anaesthetic cream should be used at the venepuncture site as, in the unsuspecting patient, painful cannulation can result in severe distress. These patients are likely to require multiple hospital admissions which may engender extreme anxiety. It is valuable to have the child s confidence. Minimising the number of anaesthetists involved in the child s care may be beneficial. Table 2 Operative procedures performed on patients with CP at the Royal Children s Hospital, Melbourne from January to December 1997 (total number of patients ˆ 402) Procedure Orthopaedic Major orthopaedic and multilevel 113 Soft tissue release/tendon transfer 71 Minor 96 Dental restorations/extractions 43 Imaging 41 Gastrostomy/endoscopy 34 General surgery and antireflux procedures 30 Neurosurgery 11 Urology 9 Ophthalmology 8 ENT 5 Total procedures performed 461 No. of cases Commonly used drugs Common drug groups encountered in children with CP are anticonvulsants, antispasmodics, anticholinergics, antireflux agents, antacids, laxatives and antidepressants. Baclofen and botulinum toxin are given particular mention below because of anaesthetic relevance and recent interest. The most commonly used anticonvulsants are carbamazepine and sodium valproate, side-effects being uncommon in both. Other drugs used include clonazepam, clobazam, lamotrigine, phenytoin and vigabatrin. Benzodiazepines, baclofen and, less commonly, dantrolene are used to reduce muscle tone. Clonidine has been shown to reduce tone and improve spasticity in patients not responding to diazepam or baclofen [17]. Baclofen Brain damage in CP affects descending inhibitory neurones resulting in inadequate release of gammaamino butyric acid (GABA) and relative excess of excitatory transmitters, notably glutamate [18]. Excessive stimulation of alpha motor neurones results in spasticity as contraction of agonist and antagonist muscle groups occurs simultaneously. Baclofen acts as an agonist at GABAb receptors in the dorsal horn of the spinal cord (Rexeds laminae II and III). It is used to reduce pain associated with muscle spasms and may delay the development of contractures. It can be used in individuals with spasticity with poor underlying strength to allow a gradual reduction in tone while muscle strength is being increased with physiotherapy. In nonambulatory patients it can also be indicated to facilitate normal daily activities and hygiene care. Baclofen crosses the blood brain barrier poorly after oral administration. Intrathecal baclofen reduces spasticity at lower doses than are required orally and with fewer sideeffects [18]. It is given via an implanted pump and drug reservoir system with external programming. A catheter inserted percutaneously via a Tuohy needle into the subarachnoid space is connected to the pump by subcutaneous tunnelling and baclofen is instilled into the reservoir percutaneously. Pumps are usually inserted under general anaesthetic and placed in a subcutaneous pocket in the lateral abdominal wall. A decrease in spasticity is usually noted within h after the start of infusion suggesting that the site of action may be in the brain. Overdose may present suddenly or insiduously and may manifest as drowsiness, respiratory depression, rostral progression of hypotonia or loss of consciousness. Overdoses are unusual however, pump programming errors being the commonest cause. The main complications are infection (5%) and catheter problems, such as disconnections or fracturing [18] Blackwell Science Ltd 35

5 J. Nolan et al. Anaesthesia and pain management in cerebral palsy Anaesthesia, 2000, 55, pages Common side-effects include apathy, urinary hesitancy and leg weakness, which respond readily to reducing the dose. Intravenous physostigmine [18] or flumazenil [19] can reverse side-effects but serious overdoses may require pump cessation, respiratory support and removal of 30 or 40 ml of cerebro-spinal fluid (CSF) via lumbar puncture. Abrupt withdrawal from oral or intrathecal baclofen may result in seizures, hallucinations, disorientation, dyskinesias and itching, with symptoms lasting up to 72 h [18]. Oral baclofen has been implicated rarely in delayed arousal after, and bradycardia and hypotension during, general anaesthesia [20, 21]. Baclofen may potentiate central nervous system depression because of its action on supraspinal receptors [22] while benzodiazepines and barbituates potentiate the action of GABA on synaptic transmission [23]. Botulinum neurotoxin (BoNT/A) This is indicated when spasticity is interfering with function and is often used when the child is too young to be considered for surgery. BoNT/A produces reversible muscle denervation and results in a temporary reduction in muscle tone. BoNT/A was first used therapeutically in humans in 1980 for the treatment of strabismus and blepharospasm, and has since been used for dystonia and spasticity disorders [24]. It is taken up at the presynaptic nerve terminal and prevents the release of acetylcholine at the neuromuscular junction. Its effects are dose-dependent and reversible as the nerves generate new junctions by terminal sprouting. Muscle fibres within 2 3 cm of the injection site are denervated. When injected intramuscularly, the rapid binding and high affinity result in only a small amount of drug reaching the systemic circulation with resulting minimal toxicity. If systemic toxicity does occur it should be treated with respiratory support and antitoxin. Two brands of botulinum toxin are currently available, Botox and Dysport. Activity is measured in units (mouse LD 50 ), but units of the two preparations are not equivalent. One unit of Botox is equivalent to 2 4 units of Dysport [25]. The effect of BoNT/A is not immediate, delay varying from 12 h to 7 days with duration of effect varying between 2 and 6 months, and occasionally longer. Theoretical concerns over stimulation of antibodies requires injections to be spaced at least 3 months apart. Injection dose and timing has not been substantiated although a dose of Botox up to 12 unit.kg 1 body weight has been recommended [26]. The most common side-effect is mild discomfort at the injection site (33 50%) lasting 1 2 days with no serious complications [24]. Other effects have been generalised fatigue and transient weakness of the injected muscle. Generalised weakness from systemic effects is very rare [25]. The long-term effect of BoNT/A can result in atrophy of the muscle. BoNT/A may be useful in delaying surgical treatment until the patient is older and at less risk of repeat surgical procedures [27]. Lower extremity injections have typically been given in the gastrocnemius or hamstrings [24] while upper extremity injections involve muscles spanning the elbow, wrist and finger joints. BoNT/A injections are commonly performed under general anaesthesia and the procedure takes min. In a co-operative child, injection may be performed after applying local anaesthetic to the skin, thus avoiding the requirement for general anaesthesia. We have also found that it reduces pain scores and relieves postoperative muscle spasm when given pre-operatively in patients undergoing adductor release surgery for hips at risk [28]. The most likely anaesthetic interaction is the potentiation of muscle relaxants, although this has not been substantiated clinically [29]. However, botulinum toxin has been reported to unmask subclinical Eaton Lambert myasthenic syndrome [30]. Peri-operative management Many of these children may be anxious because of poor understanding or difficulty communicating. In the more severely developmentally delayed, fear may make separation from carers difficult. These primary carers can often communicate with them in a way that transient carers such as anaesthetists cannot, hence the value of having them with the child during induction and in the recovery room. Vascular access may be difficult due to spasticity, dystonia or simply refusal. Children may be inadequately hydrated due to abnormal cognitive responses to thirst in addition to prolonged pre-operative fasting. Airway maintenance at induction may be complicated by excessive secretions. Tracheal intubation should be performed if this is a concern or if there is a history of gastro-oesophageal reflux. Children with CP are often small for their age. Tracheal tube size selection should be based on their age as this usually provides the most appropriate fit. If a rapid sequence induction is considered necessary, poor co-operation may allow only a modified technique at best. The risks between securing an airway rapidly and a slower inhalational induction in an uncooperative child must be balanced. For longer operations a suction catheter in the oro- or naso-pharynx may be beneficial. Anti-emetics should be considered as there is a high incidence of postoperative nausea and vomiting, particularly when opioids are used Blackwell Science Ltd

6 J. Nolan et al. Anaesthesia and pain management in cerebral palsy Careful positioning is paramount in the child with spastic CP to avoid nerve and muscle damage. Fixed contractures may add to difficulty in positioning. Drug responses may vary from the normal response in the child with CP. There may be resistance to nondepolarising muscle relaxants [31], although this is of doubtful clinical significance. Sensitivity to suxamethonium probably does not occur [32]. Train-of-four responses in a severely affected limb may not represent the actual state of neuromuscular blockade [33] and the degree of block can be underestimated. Children with CP have been demonstrated to have reduced MAC relative to normal controls [34]. Most anaesthetic agents are anticonvulsants and therefore safe in patients with seizure disorders. Enflurane, etomidate, methohexitone and ketamine should probably be avoided in patients with epilepsy. It is likely that the involuntary movements seen with propofol are myoclonic rather than epileptiform in origin. Prolonged administration of pethidine or coexisting renal failure can result in accumulation of the metabolite, norpethidine, which is epileptogenic. Latex allergy has been reported in patients with CP [35]. It probably occurs as a result of the many operative procedures to which they are exposed. A history of such sensitivity should be sought in all patients with CP. Intra-operative hypothermia is common in those children with disordered temperature regulation secondary to hypothalamic dysfunction. This is often compounded by a lack of muscle and fat deposits in the malnourished child. Normothermia may be difficult to maintain despite the use of warming blankets, forced air warmers and warmed intravenous and irrigating fluids. Warm humidified gases may also be beneficial, in addition to reducing sputum retention resulting from dry airway secretions. Standard monitoring procedures should be followed. Regional techniques are strongly recommended for both intra-operative and postoperative analgesia. Postoperative management The immediate postoperative period can present specific problems in the recovery room for children suffering from CP. In some of these patients, emergence from anaesthesia may be delayed. This can be due to hypothermia, especially in those with disordered temperature regulation. Forced air warmers such as the Bair Hugger device (Augustine Medical Inc., Eden Prairie, USA) should be utilised to normalise core temperature in the recovery room if necessary. Delayed emergence may also be due to residual volatile anaesthetic agents. MAC is reduced relative to normal controls [34] and it is conceivable that MAC awake is also reduced. Drooling, if present pre-operatively, can present difficulties with airway maintenance and frequent suctioning may be necessary. Careful attention should be paid to protecting the airway in children with pseudobulbar palsy from excessive secretions, regurgitation and vomiting. Irritability on emergence from anaesthesia is common. Eliciting the cause and excluding obvious aetiologies such as pain or urinary retention may be difficult. Irritability can be due to a child waking in an unfamiliar environment, especially in those with intellectual disability. Parental presence in the recovery room may be comforting for the child. Other factors which contribute to postoperative irritability are visual defects, e.g. cortical blindness, and hearing problems. Coexisting pathology and management of medication that patients have been prescribed pre-operatively may present problems. Those children with CP who suffer from epilepsy may be unable to have orally administered anticonvulsants if they are nil by mouth or experiencing postoperative nausea and vomiting. Most anticonvulsants, however, have long elimination half-lives (24 36 h) and, if their levels are within the therapeutic range, a 24-h period can elapse without significantly increasing the risk of seizures. Other than benzodiazepines, phenytoin and phenobarbitone, anticonvulsants cannot be administered intravenously. Sodium valproate, carbamazepine and diazepam may be administered rectally, although absorption is variable by this route. It is more important to maintain anticonvulsant cover for children with a history of generalised convulsions than for those with partial seizures. Referral of such patients pre-operatively to the appropriate physician will allow formulation of a management plan to prevent seizures peri-operatively. Those with poor cough, recurrent respiratory infections and impaired clearance of secretions will benefit most from postoperative chest physiotherapy. Spasticity is often treated with baclofen and dantrolene. Abrupt withdrawal of baclofen may lead to seizures and hallucinations [36]. Rectal, oral or intravenous diazepam ( mg.kg 1 ), with appropriate ward monitoring, may be administered until regular oral medication can be recommenced. If the child is receiving intrathecal baclofen, this should be continued in the peri-operative period. If the pump must be removed, oral baclofen should be given for 2 or 3 days beforehand, although it is less effective by this route. Contractures can cause difficulties with positioning. If epidural analgesia is used for postoperative pain management, prolonged pressure over bony prominences may lead to troublesome skin breakdown, especially in malnourished children. Children receiving regional analgesics may also be prone to compartment syndrome by nature of 2000 Blackwell Science Ltd 37

7 J. Nolan et al. Anaesthesia and pain management in cerebral palsy Anaesthesia, 2000, 55, pages the frequency of orthopaedic procedures in the lower limb, and because of reduced ability to communicate pain effectively in some instances. Meticulous pressure care, vigilant observation, splitting of plaster casts and leg elevation reduce the risk of this complication. Children with CP are prone to constipation because of reduced mobility, reduced fluid intake and undiagnosed gut motility problems. Oral, intravenous or epidural opioids may compound this problem. Attention to normal bowel habits for that child and the prescription of laxatives, supplemented by enemas, may be necessary. Pain assessment Pain assessment in children with CP may be very difficult because of conceptual problems associated with intellectual disability or poor verbal communication skills. Behavioural indicators such as facial grimacing, groaning, moaning or altered sleep patterns may be present in the nonpain state and can be inconsistent and difficult to interpret. Little published literature on pain assessment in CP patients exists. Attempts have been made to construct a pain scale based on behavioural indicators. A 22-item score was constructed by physicians based on children s response to manipulation during physical examination [37]. By constructing a scale which, for a given child, would assess behavioural changes compared with a base record, it was proposed that improvement in the ability of caregivers to diagnose and evaluate pain would result. Analysis was difficult due to the wide diversity of patient responses. Although useful as a pilot study, and as a list of behaviours for caregivers to watch for, the scale lacked clinical applicability for treating acute postoperative pain in this patient group. Diversity in pain behaviours was confirmed in a study where caregivers of 20 individuals with CP were asked to recall two instances of short, sharp pain and two of longlasting pain and describe the individual s behaviour [38]. Although specific behaviours varied from one child to another, the classes of behaviours were common to most of the children studied. Identified classes were vocal, eating/ sleeping, social/personality, facial expression, activity, body and limbs and physiological. Reliability of a checklist was good. The authors concluded that further work was necessary to assess its validity and sensitivity. Scales utilising pain behaviour in patients with severe developmental disability may lack sensitivity due to pain indifference [39]. An elevated pain threshold was noted in 31 (25.2%) of 123 patients with developmental disability based on the absence of basic pain behaviour with injuries that are typically painful. The primary caregiver is usually in tune with the child s behavioural manifestations and is an invaluable resource when assessing the child postoperatively. Pain must be differentiated from hunger, anxiety, discomfort due to positioning and other benign causes, e.g. headache, toothache, otitis media, period pain in females and gastro-oesophageal reflux. Specific postoperative pain problems in cerebral palsy The most common surgery undertaken in CP patients at the Royal Children s Hospital is lower limb orthopaedic surgery. This group of patients are prone to frequent and severe muscle spasms postoperatively. Pain from muscle spasm is severe and distressing for the child, the parents and medical personnel. Diazepam mg.kg 1 administered orally, rectally or intravenously as required is used to alleviate spasm, but often results in prolonged sedation. In children undergoing extensive lower limb orthopaedic surgery, epidural analgesia is beneficial. An excellent block will prevent muscle spasm which is almost certainly a spinal reflex initiated by pain. Children undergoing single event multilevel surgery present specific difficulties. Our initial experience was with continuous epidural infusion of 0.125% bupivacaine and fentanyl 2 mg.ml 1 at ml.kg.h 1 postoperatively. Analgesia was good, but spasm was frequent, necessitating 4-hourly administration of diazepam. Patients would often have postoperative nausea and vomiting resistant to anti-emetics, resulting in plain bupivacaine 0.125% replacing the combined bupivacaine/ fentanyl solution. Subsequently we have been using bupivacaine 0.125% with clonidine 2.5 mg.ml 1 at ml.kg.h 1 with better analgesia, less muscle spasm and less postoperative nausea and vomiting. In patients undergoing extensive single-event multilevel surgery involving the hip, knee and foot, one epidural catheter at the maximum hourly rate would require frequent bolus administration because either the cephalad or caudad dermatomes were not covered. An attempt to resolve this problem has been made by employing a two epidural technique in this special group. The same concentration and total volume of the bupivacaine/clonidine mixture is used. There are several benefits to this approach, which we feel warrant the risk of inserting two catheters. One catheter is placed at the level corresponding to the dermatomes where the cephalad incision is made (usually L 1 2 ). The second catheter is placed at L 4 5. Each catheter is inserted 4 cm into the epidural space. Postoperatively the infusions are commenced at the same rate (each at one half of the hourly rate that we would have selected if only one catheter was employed). The major advantage of this technique is titratability. The appropriate catheter can be bolused with smaller volumes to cover pain and the infusion rate of each catheter can be adjusted to provide excellent analgesia. In our experience, the incidence of Blackwell Science Ltd

8 J. Nolan et al. Anaesthesia and pain management in cerebral palsy muscle spasm and consequent diazepam administration is markedly reduced. Surgery for correction of scoliosis may be performed in patients with CP in whom pre-operative pulmonary function testing is impossible. Patients may have preexisting reduction in respiratory reserve and they may tolerate physiotherapy poorly. Nurse-controlled opioid infusions are necessary unless the child has the ability to use patient-controlled analgesia. Adjunct analgesia using paracetamol up to 100 mg.kg.day 1 is beneficial [40]. Patients with CP who undergo extensive surgical procedures that necessitate analgesic infusions should be monitored as for any child receiving analgesia by the same route. Our current practice is 4-hourly blood pressure measurements, hourly pulse and respiratory rate and continuous arterial oxygen saturation with continual presence of a nurse for 20 min after bolus administration by the intravenous or epidural routes. Selective dorsal rhizotomy is associated with severe pain, spasm and dysaesthesia postoperatively. Epidural and intrathecal morphine have been used [41, 42] while some centres advocate the use of intravenous infusions of morphine and midazolam [43]. Chronic pain management in cerebral palsy Children are expected to experience pain postoperatively. Recognising the presence of pain in the chronic setting, however, is difficult, especially in the patient with impaired speech development. Locating the source of pain can be even more difficult, often involving a process of elimination of common causes (Table 3). These include hip subluxation, gastro-oesophageal reflux, back pain secondary to scoliosis and facet joint arthritis, period pain in adolescent females and spasticity with capsulitis. Pain can usually be located by manipulating or palpating the affected area. Patients are often attending many different specialists because of their multiple pathologies. These specialists may inadvertently offer conflicting advice. Often a treatment plan can be made for individual patients provided all treating specialists can be gathered for a meeting. This is best organised by a physician coordinator who is responsible for ensuring that the patient is treated as a whole. Priority can then be given to certain interventions, and surgical procedures can be appropriately spaced or even coordinated to occur on the same day. Medical appointments can be arranged so as to minimise hospital outpatient visits. Most importantly, the coordinating physician will be aware of the management plan and is an invaluable resource to allay anxiety if conflicting medical advice is given. As children reach adolescence, those with normal intelligence may suffer from depression which can exacerbate chronic pain. Secondary gain may maintain painful states. Children can use pain to manipulate situations in their favour. A multidisciplinary approach to chronic pain management is useful in these children. Table 3 Aetiology of pain, symptoms and treatment in children with CP Cause of pain Symptoms Treatment Hip subluxation Pain on transfer Intra-articular steroids Pain at night relieved by repositioning Paracetamol Nonsteroidal anti-inflammatory drugs Tricyclic antidepressants Gastro-oesophageal reflux Anaemia Antacid Weight loss Ranitidine Night waking Omeprazole Anorexia Nurse upright Back pain Pain on sitting for prolonged periods Transcutaneous electrical nerve stimulation Tricyclic antidepressants Night waking Paracetamol Facet joint injections Nonsteroidal anti-inflammatory drugs Pressure care in wheelchair and bed Period pain Associated with menstruation Oral contraceptive pill Spasticity Diazepam Dantrolene Baclofen Selective dorsal rhizotomy 2000 Blackwell Science Ltd 39

9 J. Nolan et al. Anaesthesia and pain management in cerebral palsy Anaesthesia, 2000, 55, pages Conclusion Cerebral palsy may be due to antenatal, perinatal or postnatal causes. Knowledge of pathology associated with different types of CP, related clinical conditions and their drug treatment will enable the anaesthetist to predict likely problems which might impinge on anaesthesia and the peri-operative period. This paper highlights relevant aspects of anaesthesia and pain management in these children. Acknowledgments We acknowledge the contribution of Dr Dinah Reddihough and Professor H. Kerr Graham in reviewing the manuscript. References 1 Bax MCO. Terminology and classification of cerebral palsy. Developmental Medicine and Child Neurology 1964; 6: Nelson KB, Emery ES. Birth asphyxia and the neonatal brain: what do we know and when do we know it? Clinics in Perinatology 1993; 20: Eicher PS, Batshaw ML. Cerebral palsy. Pediatric Clinics of North America 1993; 40: Mutch L, Alberman E, Hagberg B, Kodama K, Perat M. Cerebral palsy epidemiology: where are we now and where are we going? Developmental Medicine and Child Neurology 1992; 34: Truwit CL, Barkovich AJ, Koch TK, Ferriero DM. Cerebral palsy: MR findings in 40 patients. American Journal of Neuroradiology 1992; 13: Pranzatelli MR. Oral pharmacotherapy for the movement disorders of cerebral palsy. Journal of Child Neurology 1996; 11 (Suppl. 1): S Ong LC, Afifah I, Sofiah A, Lye MS. Parenting stress among mothers of Malaysian children with cerebral palsy: predictors of child- and parent-related stress. Annals of Tropical Paediatrics 1998; 18: Brett EM, Scrutton D. Cerebral palsy, perinatal injury to the spinal cord and brachial plexus birth injury. In: Brett EM, ed. Paediatric Neurology Textbook. New York: Churchill Livingstone, 1997; Reddihough D, Johnson H, Staples M, Hudson I, Exarchos H. Use of benzhexol hydrochloride to control drooling of children with cerebral palsy. Developmental Medicine and Child Neurology 1990; 32: Sochaniwskyj AE, Koheil RM, Bablich K, Milner M, Kenny DJ. Oral motor functioning, frequency of swallowing and drooling in normal children and in children with cerebral palsy. Archives of Physical Medicine and Rehabilitation 1986; 67: Evans PM, Evans SJ, Alberman E. Cerebral palsy: why we must plan for survival. Archives of Disease in Childhood 1990; 65: Pelegano JP, Nowysz S, Goepferd S. Temperomandibular joint contracture in spastic quadriplegia: effect on oral motor skills. Developmental Medicine and Child Neurology 1994; 36: Franklin DL, Luther F, Curzon ME. The prevalence of malocclusion in children with cerebral palsy. European Journal of Orthodontics 1996; 18: Robinson RO. The frequency of other handicaps in children with cerebral palsy. Developmental Medicine and Child Neurology 1973; 15: Hurley AD, Sorner R. Psychiatric aspects of cerebral palsy. Psychiatric Mental Retardation Review 1987; 6: DeLuca PA. The musculoskeletal management of children with cerebral palsy. Pediatric Clinics of North America 1996; 43: Dall JT, Harmon RL, Quinn CM. Use of clonidine for treatment of spasticity arising from various forms of brain injury: a case series. Brain Injury 1996; 10: Albright AL. Intrathecal baclofen in cerebral palsy movement disorders. Journal of Child Neurology 1996; 11 (Suppl. 1): S Saissy JM, Vitris M, Demazière J, Seck M, Marcoux L, Gaye M. Flumazenil counteracts intrathecal baclofeninduced central nervous system depression in tetanus. Anesthesiology 1992; 76: Gomar C, Carrero EJ. Delayed arousal after general anesthesia associated with baclofen. Anesthesiology 1994; 81: Sill JC, Schumacher K, Southorn A, Reuter J, Yaksh TL. Bradycardia and hypotension associated with baclofen used during general anesthesia. Anesthesiology 1986; 64: Blaxter TJ, Carlen PL. Pre- and postsynaptic effects of baclofen in the rat hippocampal slice. Brain Research 1985; 341: Cheng S, Brunner EA. Inducing anesthesia with a GABA analog, THIP. Anesthesiology 1985; 63: Forssberg H, Tedroff KB. Botulinum toxin treatment in cerebral palsy: intervention with poor evaluation? Developmental Medicine and Child Neurology 1997; 39: Albright AL. Spastic cerebral palsy. Approaches to drug treatment. Practical Therapeutics 1995; 4: Graham HKG, Aoki KR, Auti-Ramo I, et al. Recommendations for the use of botulinum toxin type A in the management of cerebral palsy. Gait and Posture in press. 27 Koman LA, Mooney JF, Smith B, Goodman A, Mulvaney T. Management of cerebral palsy with botulinum-a toxin: preliminary investigation. Journal of Pediatric Orthopedics 1993; 13: Barwood S, Ballieu C, Boyd R, et al. The analgesic effects of botulinum toxin A. A randomised, double blind, placebo controlled clinical trial. Developmental Medicine and Child Neurology in press. 29 Fiacchino F, Grandi L, Soliveri P, Carella F, Bricchi M. Sensitivity to vecuronium after botulinum toxin Blackwell Science Ltd

10 J. Nolan et al. Anaesthesia and pain management in cerebral palsy administration. Journal of Neurosurgical Anesthesiology 1997; 9: Ergbuth F, Claus D, Engelhardt A, Dressler D. Systemic effect of local botulinum toxin injections unmasks subclinical Lambert Eaton myasthenic syndrome. Journal of Neurology, Neurosurgery, and Psychiatry 1993; 56: Moorthy SS, Krishna G, Dierdorf SF. Resistance to vecuronium in patients with cerebral palsy. Anesthesia and Analgesia 1991; 73: Dierdorf SF, McNiece WL, Rao CC, et al. Effect of succinylcholine on plasma potassium in children with cerebral palsy. Anesthesiology 1985; 62: Zuckerberg AL, Yaster M. Anesthesia for orthopaedic surgery. In: Motoyama EK, Davis PJ, eds. Smith s Anesthesia for Infants and Children. St. Louis, MO: CV Mosby, 1996; Frei FJ, Haemmerle MH, Brunner R, Kern C. Minimum alveolar concentration for halothane in children with cerebral palsy and severe mental retardation. Anaesthesia 1997; 52: Delfico AJ, Dormans JP, Craythorne CB, Templeton JJ. Intraoperative anaphylaxis due to allergy to latex in children who have cerebral palsy: a report of six cases. Developmental Medicine and Child Neurology 1996; 39: Siegfried RN, Jacobson L, Chabal C. Development of an acute withdrawal syndrome following the cessation of intrathecal baclofen in a patient with spasticity. Anesthesiology 1992; 77: Giusiano B, Jimeno MT, Collignon P, Chau Y. Utilization of a neural network in the elaboration of an evaluation scale for pain in cerebral palsy. Methods of Information in Medicine 1995; 34: McGrath PJ, Rosmus C, Canfield C, Campbell MA, Hennigar A. Behaviours caregivers use to determine pain in non-verbal, cognitively impaired individuals. Developmental Medicine and Child Neurology 1998; 40: Biersdorff KK. Incidence of significantly altered pain experience among individuals with developmental disabilities. American Journal on Mental Retardation 1994; 98: Shann F. Paracetamol use in children. Australian Prescriber 1995; 18: Sparkes ML, Klein AS, Duhaime A, Mickle JP. Use of epidural morphine for control of postoperative pain in selective dorsal rhizotomy for spasticity. Pediatric Neuroscience 1989; 15: Harris MM, Kahana MD, Park TS. Intrathecal morphine for postoperative analgesia in children after selective dorsal root rhizotomy. Neurosurgery 1991; 28: Geiduschek JM, Haberkern CM, McLaughlin JF, Jacobson LE, Hays RM, Roberts TS. Pain management for children following selective dorsal rhizotomy. Canadian Journal of Anaesthesia 1994; 41: Blackwell Science Ltd 41

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