Panu Boontoterm, Boonchot Kiangkitiwan, S. Sakoolnamarka, Wiriya Homhuan, P. Fuengfoo
{"title":"Use of inhaled sevoflurane to treat post-operative intractable cerebral edema in neurosurgical intensive care unit.","authors":"Panu Boontoterm, Boonchot Kiangkitiwan, S. Sakoolnamarka, Wiriya Homhuan, P. Fuengfoo","doi":"10.54205/ccc.v30.256435","DOIUrl":null,"url":null,"abstract":"Background: Burst suppression are widely used in case of refractory increased intracranial pressure for deep state of brain inactivation. Inhaled sevoflurane via the anesthetic conserving device could be useful for the sedation of patients in the intensive care unit (ICU), but prospective studies have been small study. \n\nCase report: A 53-year-old male patient with confusion, not follow to\ncommand and status epilepticus had been hospitalized and \ndiagnosed glioblastoma multiforme at left temporal lobe. By the time \ninitial therapy had begun with dexamethasone and anti-epileptic \ndrug, the symptoms had improved. The patient was performed \ncraniotomy with tumor removal during intra-operative found \nintractable cerebral edema and changed operation to \ndecompressive craniectomy, in post-operative period after increased \ndosage of propofol and midazolam to control intracranial pressure, \npatient developed hypotension, then norepinephrine was titrated to \nmaintain mean arterial pressure more than 65 mmHg and used \ninhaled sevoflurane to decrease dose propofol for maintain \nhemodynamics then during 5 day usage inhaled sevoflurane, \nnorepinephrine could wean off and Glasgow coma scale was \nimprove. Follow up brain EEG at 1st week showed no epileptiform \ndischarge, antiepileptic drug could de-escalated and CT scan \nshowed no refractory cerebral edema or hemorrhage. Ventilator was \nweaned off and the patient was transfer to step down ward.\n\nConclusion: When managing intractable cerebral edema patient \nwith inhaled sevoflurane showed that lower opioid dose intensity, \npromote resolving from seizures or status epilepticus, decrease \ndose of vasopressor to maintain hemodynamics and no adverse \nevents supported the use of inhaled sevoflurane via the anesthetic \nconserving device in this patient who have clinical need for burst \nsuppression.","PeriodicalId":76963,"journal":{"name":"AACN clinical issues in critical care nursing","volume":"15 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"AACN clinical issues in critical care nursing","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.54205/ccc.v30.256435","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Burst suppression are widely used in case of refractory increased intracranial pressure for deep state of brain inactivation. Inhaled sevoflurane via the anesthetic conserving device could be useful for the sedation of patients in the intensive care unit (ICU), but prospective studies have been small study.
Case report: A 53-year-old male patient with confusion, not follow to
command and status epilepticus had been hospitalized and
diagnosed glioblastoma multiforme at left temporal lobe. By the time
initial therapy had begun with dexamethasone and anti-epileptic
drug, the symptoms had improved. The patient was performed
craniotomy with tumor removal during intra-operative found
intractable cerebral edema and changed operation to
decompressive craniectomy, in post-operative period after increased
dosage of propofol and midazolam to control intracranial pressure,
patient developed hypotension, then norepinephrine was titrated to
maintain mean arterial pressure more than 65 mmHg and used
inhaled sevoflurane to decrease dose propofol for maintain
hemodynamics then during 5 day usage inhaled sevoflurane,
norepinephrine could wean off and Glasgow coma scale was
improve. Follow up brain EEG at 1st week showed no epileptiform
discharge, antiepileptic drug could de-escalated and CT scan
showed no refractory cerebral edema or hemorrhage. Ventilator was
weaned off and the patient was transfer to step down ward.
Conclusion: When managing intractable cerebral edema patient
with inhaled sevoflurane showed that lower opioid dose intensity,
promote resolving from seizures or status epilepticus, decrease
dose of vasopressor to maintain hemodynamics and no adverse
events supported the use of inhaled sevoflurane via the anesthetic
conserving device in this patient who have clinical need for burst
suppression.