title: Admission glucose and coagulopathy occurrence in patients with traumatic brain injury.
abstract: BACKGROUND
  Coagulopathy after traumatic brain injury (TBI) is a frequent event and is associated with patients' prognosis. TBI is also associated with a stress response that includes hyperglycemia. This study investigated if coagulopathy occurrence is associated with admission blood glucose levels in patients with TBI.
  
  
  METHODS
  This study retrospectively evaluated patients with TBI who were admitted to a neurosurgical department over a 4-year period. Coagulopathy was defined as an aPTT >40 seconds and/or INR >1.2 and/or a platelet count <120*10(9) per litre.
  
  
  RESULTS
  One-hundred and forty-nine patients were included in the study. Thirty-four patients developed coagulopathy. Patients with coagulopathy had significantly lower haemoglobin levels, increased INR and increased aPTT. Patients with severe TBI had more frequent coagulopathy. Patients with severe TBI had significant higher serum glucose levels compared to patients with mild TBI. Using ROC curves it was found that a serum glucose of 151 mg dl(-1) was the threshold for the discrimination of patients that developed coagulopathy. Logistic regression analysis revealed that serum glucose greater than 151 mg dl(-1) and haemoglobin levels lower than 12.4 mg dL(-1) were significantly associated with coagulopathy occurrence.
  
  
  CONCLUSIONS
  Coagulopathy frequently occur after TBI. Patients with lower GCS score and lower haemoglobin levels and increased blood glucose levels at admission are at greater risk.
authors.affiliation: Department of Neurosurgery and.
authors.forename: George A
authors.initials: GA
authors.lastname: Alexiou
authors.forename: Georgios
authors.initials: G
authors.lastname: Lianos
authors.forename: George
authors.initials: G
authors.lastname: Fotakopoulos
authors.forename: Evaggelos
authors.initials: E
authors.lastname: Michos
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Pachatouridis
authors.forename: Spyridon
authors.initials: S
authors.lastname: Voulgaris
mesh_terms: D000293:Adolescent; D000328:Adult; D001778:Blood Coagulation Disorders / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D001786:Blood Glucose / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology*; D002648:Child; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D015994:Incidence; D015601:Injury Severity Score; D019934:International Normalized Ratio; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010314:Partial Thromboplastin Time; D010343:Patient Admission; D011379:Prognosis; D012372:ROC Curve; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin; D006454:Hemoglobins; C517652:hemoglobin A1c protein, human