title: Thoracic epidural analgesia inhibits the neuro-hormonal but not the acute inflammatory stress response after radical retropubic prostatectomy.
abstract: BACKGROUND
  Epidural anaesthesia and analgesia has been shown to suppress the neuro-hormonal stress response, but its role in the inflammatory response is unclear. The primary aim was to assess whether the choice of analgesic technique influences these processes in patients undergoing radical retropubic prostatectomy.
  
  
  METHODS
  Twenty-six patients were randomized to Group P (systemic opioid-based analgesia) or Group E (thoracic epidural-based analgesia) perioperatively. Induction and maintenance of anaesthesia followed a standardized protocol. The following measurements were made perioperatively: plasma cortisol, glucose, insulin, C-reactive proteins, leucocyte count, plasma cytokines [interleukin (IL)-6, tumour necrosis factor (TNF)-α], and pokeweed mitogen-stimulated cytokines [interferon (IFN)-γ, IL-2, IL-12p70, IL-10, IL-4, and IL-17]. Other parameters recorded were pain, morphine consumption, and perioperative complications.
  
  
  RESULTS
  Plasma concentration of cortisol and glucose were significantly higher in Group P compared with Group E at the end of surgery, the mean difference was 232 nmol litre(-1) [95% confidence interval (CI) 84-381] (P=0.004) and 1.6 mmol litre(-1) (95% CI 0.6-2.5) (P=0.003), respectively. No significant differences were seen in IL-6 and TNF-α at 24 h (P=0.953 and 0.368, respectively) and at 72 h (P=0.931 and 0.691, respectively). IL-17 was higher in Group P compared with Group E, both at 24 h (P=0.001) and 72 h (P=0.018) after operation. Pain intensity was significantly greater in Group P compared with Group E (P<0.05) up to 24 h.
  
  
  CONCLUSIONS
  In this small prospective randomized study, thoracic epidural analgesia reduced the early postoperative stress response but not the acute inflammatory response after radical retrobupic prostatectomy, suggesting that other pathways are involved during the acute phase reaction.
authors.affiliation: Department of Anesthesiology and Intensive Care, University Hospital, Örebro SE-701 85, Sweden. federica.fant@orebroll.se
authors.forename: F
authors.initials: F
authors.lastname: Fant
authors.forename: E
authors.initials: E
authors.lastname: Tina
authors.forename: D
authors.initials: D
authors.lastname: Sandblom
authors.forename: S-O
authors.initials: SO
authors.lastname: Andersson
authors.forename: A
authors.initials: A
authors.lastname: Magnuson
authors.forename: E
authors.initials: E
authors.lastname: Hultgren-Hörnkvist
authors.forename: K
authors.initials: K
authors.lastname: Axelsson
authors.forename: A
authors.initials: A
authors.lastname: Gupta
mesh_terms: D000368:Aged; D015360:Analgesia, Epidural / Q000379:methods*; D016058:Analgesia, Patient-Controlled / Q000379:methods; D000701:Analgesics, Opioid / Q000008:administration & dosage; D001786:Blood Glucose / Q000378:metabolism; D016207:Cytokines / Q000097:blood; D005283:Fentanyl / Q000008:administration & dosage; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008875:Middle Aged; D009490:Neurosecretory Systems / Q000503:physiopathology*; D010149:Postoperative Pain / Q000517:prevention & control; D011182:Postoperative Care / Q000379:methods; D011446:Prospective Studies; D011468:Prostatectomy / Q000009:adverse effects*; D016037:Single-Blind Method; D013312:Stress, Physiological; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000209:etiology / Q000517:prevention & control*
chemical_list: D000701:Analgesics, Opioid; D001786:Blood Glucose; D016207:Cytokines; D005283:Fentanyl; D006854:Hydrocortisone