title: Haemodynamic and metabolic disturbances in the acute stage of subarachnoid haemorrhage demonstrated by PET.
abstract: OBJECTIVE
  To investigate the occurrence of early haemodynamic and metabolic changes in the acute stage of subarachnoid haemorrhage (SAH).
  
  
  METHODS
  Eleven SAH patients were studied. Regional cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and oxygen extraction ratio (OER) were measured with positron emission tomography (PET) 22-53 h after haemorrhage, utilizing 15O-labelled water bolus and the 15O-inhalation technique. Ten volumes of interest (VOIs) representing vascular territories were outlined in each patient according to a standardized procedure. The occurrence of irreversible ischaemia, penumbra, oligaemia, hyperperfusion and normal haemodynamics according to PET criteria was investigated. These pathophysiological categories were related to final tissue outcome as determined by follow-up computed tomography (CT).
  
  
  RESULTS
  All five tissue subtypes were represented in the vascular region VOIs; oligaemia was the predominant pathophysiological pattern. When global changes were analysed, blood flow was reduced in three, oxygen metabolism was reduced in four, and OER was increased in four of seven unsedated patients, respectively. The sedated patients all had markedly reduced CBF and CMRO2 and OER in the high or supranormal range.
  
  
  CONCLUSIONS
  Haemodynamic and metabolic disturbances proved to be common after SAH. These abnormalities probably reflect the primary brain injury caused by the initial haemorrhage. The impact of secondary insults such as acute hydrocephalus, brain oedema, vasospasm, seizures, hypotension and hypoxaemia are likely to be dependent on the degree of primary injury, which can be assessed by PET.
authors.affiliation: Department of Clinical Neurosciences, Section of Neurosurgery, Uppsala University Hospital, Uppsala, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Frykholm
authors.forename: J L R
authors.initials: JL
authors.lastname: Andersson
authors.forename: B
authors.initials: B
authors.lastname: Långström
authors.forename: L
authors.initials: L
authors.lastname: Persson
authors.forename: P
authors.initials: P
authors.lastname: Enblad
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D001921:Brain / Q000098:blood supply* / Q000502:physiology*; D002544:Cerebral Infarction / Q000209:etiology / Q000473:pathology; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption; D010104:Oxygen Radioisotopes; D012039:Regional Blood Flow; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000000981:diagnostic imaging*; D014055:Tomography, Emission-Computed
chemical_list: D010104:Oxygen Radioisotopes