title: Effects of mannitol bolus administration on intracranial pressure, cerebral extracellular metabolites, and tissue oxygenation in severely head-injured patients.
abstract: BACKGROUND
  Osmotic agents are widely used to lower elevated intracranial pressure (ICP). However, little data are available regarding cerebral oxygenation and metabolism in the traumatized brains studied under clinical conditions. The present prospective, open-labeled clinical study was designed to investigate whether administration of mannitol, with the aim of reducing moderate intracranial hypertension, improves cerebral metabolism and oxygenation in patients after severe traumatic brain injury (TBI).
  
  
  METHODS
  Multimodal cerebral monitoring (MCM), consisting of intraparenchymal ICP, tissue oxygenation (ptiO2), and micro dialysis measurements was initiated in six male TBI patients (mean age 45 years; Glasgow Coma Scale score <9). A total of 14 mannitol boli (20%, 0.5g/kg, 20 minutes infusion time) were administered to treat ICP exceeding 20 mm Hg (2.7 kPa). Temporal alterations determined by MCM after mannitol infusions were recorded for 120 minutes. Microdialysates were assayed immediately for extracellular glucose, lactate, pyruvate, and glutamate concentrations.
  
  
  RESULTS
  Elevated ICP was successfully treated in all cases. This effect was maximal 40 minutes after start of infusion (25 +/- 6 mm Hg [3.3 +/- 0.8 kPa] to 17 +/- 3 mm Hg [2.3 +/- 0.4 kPa], p < 0.05) and lasted up to 100 minutes. Cerebral ptiO2 remained unaffected (21 +/- 5 mm Hg [2.8 +/- 0.7 kPa] to 23 +/- 6 mm Hg [3.1 +/- 0.8 kPa], n.s.). Microdialysate concentrations of all analytes rose unspecifically by 10% to 40% from baseline, reaching maximum concentrations 40 to 60 minutes after start of the infusion.
  
  
  CONCLUSIONS
  Mannitol efficiently reduces increased ICP. At an ICP of up to 30 mm Hg [4 kPa] it does not affect cerebral oxygenation. Unspecific increases of extracellular fluid metabolites can be explained by transient osmotic dehydration. Additional mechanisms, such as increased cerebral perfusion and blood volume, might explain an accelerated return to baseline.
authors.affiliation: Department of Neurosurgery, University of Heidelberg, Heidelberg, Germany. oliver.sakowitz@med.uni-heidelberg.de
authors.forename: Oliver W
authors.initials: OW
authors.lastname: Sakowitz
authors.forename: John F
authors.initials: JF
authors.lastname: Stover
authors.forename: Asita S
authors.initials: AS
authors.lastname: Sarrafzadeh
authors.forename: Andreas W
authors.initials: AW
authors.lastname: Unterberg
authors.forename: Karl L
authors.initials: KL
authors.lastname: Kiening
mesh_terms: D000328:Adult; D006259:Craniocerebral Trauma / Q000150:complications / Q000378:metabolism; D004234:Diuretics, Osmotic / Q000008:administration & dosage / Q000627:therapeutic use*; D015600:Glasgow Coma Scale; D006801:Humans; D007267:Injections; D019586:Intracranial Hypertension / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D007427:Intracranial Pressure / Q000187:drug effects*; D008297:Male; D008353:Mannitol / Q000008:administration & dosage / Q000627:therapeutic use*; D017551:Microdialysis; D008875:Middle Aged; D009994:Osmolar Concentration; D010100:Oxygen / Q000378:metabolism*; D011446:Prospective Studies; D018709:Statistics, Nonparametric; D016896:Treatment Outcome
chemical_list: D004234:Diuretics, Osmotic; D008353:Mannitol; D010100:Oxygen