title: Effect of decompressive craniectomy on intracranial pressure and cerebrospinal compensation following traumatic brain injury.
abstract: OBJECTIVE
  Decompressive craniectomy is an advanced treatment option for intracranial pressure (ICP) control in patients with traumatic brain injury. The purpose of this study was to evaluate the effect of decompressive craniectomy on ICP and cerebrospinal compensation both within and beyond the first 24 hours of craniectomy.
  
  
  METHODS
  This study was a retrospective analysis of the physiological parameters from 27 moderately to severely head-injured patients who underwent decompressive craniectomy for progressive brain edema. Of these, 17 patients had undergone prospective digital recording of ICP with estimation of ICP waveform-derived indices. The pressure-volume compensatory reserve (RAP) index and the cerebrovascular pressure reactivity index (PRx) were used to assess those parameters. The values of parameters prior to and during the 72 hours after decompressive craniectomy were included in the analysis.
  
  
  RESULTS
  Decompressive craniectomy led to a sustained reduction in median (interquartile range) ICP values (21.2 mm Hg [18.7; 24.2 mm Hg] preoperatively compared with 15.7 mm Hg [12.3; 19.2 mm Hg] postoperatively; p = 0.01). A similar improvement was observed in RAP. A significantly lower mean arterial pressure (MAP) was needed after decompressive craniectomy to maintain optimum cerebral perfusion pressure (CPP) levels, compared with the preoperative period (99.5 mm Hg [96.2; 102.9 mm Hg] compared with 94.2 mm Hg [87.9; 98.9 mm Hg], respectively; p = 0.017). Following decompressive craniectomy, the PRx had positive values in all patients, suggesting acquired derangement in pressure reactivity.
  
  
  CONCLUSIONS
  In this study, decompressive craniectomy led to a sustained reduction in ICP and improvement in cerebral compliance. Lower MAP levels after decompressive craniectomy are likely to indicate a reduced intensity of treatment. Derangement in cerebrovascular pressure reactivity requires further studies to evaluate its significance and influence on outcome.
authors.affiliation: Academic Neurosurgery Unit, University of Cambridge/Addenbrooke's Hospital, Cambridge, United Kingdom. it227@cam.ac.uk
authors.forename: Ivan
authors.initials: I
authors.lastname: Timofeev
authors.forename: Marek
authors.initials: M
authors.lastname: Czosnyka
authors.forename: Jurgens
authors.initials: J
authors.lastname: Nortje
authors.forename: Peter
authors.initials: P
authors.lastname: Smielewski
authors.forename: Peter
authors.initials: P
authors.lastname: Kirkpatrick
authors.forename: Arun
authors.initials: A
authors.lastname: Gupta
authors.forename: Peter
authors.initials: P
authors.lastname: Hutchinson
mesh_terms: D000293:Adolescent; D000328:Adult; D001930:Brain Injuries / Q000150:complications / Q000503:physiopathology* / Q000601:surgery*; D002555:Cerebrospinal Fluid / Q000502:physiology; D003399:Craniotomy; D019299:Decompression, Surgical; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019586:Intracranial Hypertension / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D007427:Intracranial Pressure / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome