_in cerebral palsy脑性瘫痪患儿麻醉课件

Anesthesia in Cerebral Palsy R i 鄭玠峰、林鉉智 Directed by R3 林子富 VS 范守仁 Part 1 Case Presentation 蔡 3-year 55: 32-41 Cerebral Palsy Non-progressive disorder of motion and posture. CP is a result of an injury to the developing brain during the antenatal, perinatal, or postnatal period. Clinical manifestation relate to the area affected. CP is the leading cause of childhood motor disability in developed country. Such disabilities include cognitive impairment, sensory loss, seizures, communication and behavioral disturbances. Etiology of Cerebral Palsy Premature： Periventricular hemorrhage Periventricular leucomalacia In spastic diplegia type Term baby： Antenatal infection Thyroid disease Neuronal migration disorder Postnatal causes： Meningitis, viral encephalitis, hydrocephalus, trauma, etc. Classification for Cerebral Palsy Spastic type：(70%) Diplegia、Hemiplegia、Quadriplegia Dyskinetic type： (21%) Dystonia、Athetosis、Chorea Ataxic type： (10%) Intention tremor and head tremor Mixed type： (10%) Pre-operative assessment Gastrointestinal Problems Gastro-esophageal reflux： Esophageal dysmobility、LES abnormal、 Spinal deformity Salivary drooling： Impaired swallowing or tongue thrust and poor head control Drooling Tx：Anticholinergics MalnutritionFailure to thrive： Poor chewing and swallowing pre-operative nutrition support is needed. Electrolyte imbalance 73: 275- 7 nAn increase number of junctional and extrajunctional acetylcholine receptors nImmobilization with muscle atrophy nConcomitant administration of phenytoin and phenobarbital nDrug interactions: nincreased metabolism of the muscle relaxant via hepatic enzyme ndecreased sensitivity of muscle receptors to the MR nincreased numbers of receptors nincreased muscle end-plate cholineasterase activity Children with CP and severe mental retardation may require lower concentration of inhalational anaesthetics than healthy children. nFrei FJ, Haemmerle MH, Brunner R, Kern C. Minimum alveolar concentration for halothane in children with cerebral palsy and severe mental retardation. Anaesthesia 1997; 52: 1056-60 nElevated pain threshold, decreased central pain perception nLower motor neuron more sensitive to inhalational anaesthetics nChildren with CP had significantly lower MAC values whether they took anticonvulsant drugs or not. Post-operative management Emergence from anaesthesia may be delayed nHypothermia nResidual volatile anaesthetic agents Postoperative chest Physiotherapy nDrooling nPoor cough nRecurrent respiratory infections nImpaired clearance of secretions Irritability on emergence from anaesthesia is common nPain nUrinary retention nUnfamiliar environment Maintain anticonvulsant / baclofen nLong half-lives nIV or rectal route nPre-operative referral Children with CP are prone to constipation nReduced mobility nReduced fluid intake nUndiagnosed gut mobility problems Reference: nJ. Nolan, G.A. Chalkiads, J. Low, C.A. Olesch and T.C.K. Brown. Anaesthesia and pain management in cerebral palsy. Anaesthesia, 2000; 55: 32-41 nMoorthy SS, Krishna G, Dierdorf SF. Resistance to vecuronium in patients with cerebral palsy. Anesthesia and Analgesia 1991; 73: 275-7 nFrei FJ, Haemmerle MH, Brunner R, Kern C. Minimum alveolar concentration for halothane in children with cerebral palsy and severe mental retardation. Anaesthesia 1997; 52: 1056-60 nDelfico AJ, Dormans JP, Craythorne CB, Templeton JJ. Intraoperative