Association of obesity with inflammation and pain after total hip arthroplasty.

BACKGROUND: The prevalence of obesity is increasing, and obesity often leads to degenerative joint disease requiring total hip arthroplasty (THA). Obesity is a proinflammatory state associated with an increase in chronic, low-grade inflammatory response. As such, it may augment the postoperative inflammatory response, which has been associated with postoperative pain and complications. QUESTIONS/PURPOSES: We determined whether severity of obesity was associated with (1) severity of inflammatory response, as measured by the in vivo circulating levels of cytokines and ex vivo functional reactivity of mononuclear blood cells, and (2) severity of pain, as measured by verbal pain scores and analgesic consumption, in the first 24 hours after THA.
METHODS: We studied 60 patients (20 normal weight, 20 overweight, 20 obese) undergoing elective primary unilateral THA in this prospective cross-sectional study. Blood samples were collected for C-reactive protein and cytokine levels, including IL-1β, IL-2, IL-6, IL-8, and tumor necrosis factor α (TNF-α), from patients before and 24 hours after surgery. Cytokine response of whole blood was evaluated ex vivo with or without two standard activators, phorbol-12-myristate-13-acetate and lipopolysaccharide, using standardized blood sample from patients at 24 hours. These standard immune activators are implicated in the inflammatory response to gram-negative infection, translocation of microbial products, pathophysiology of septic shock syndrome in human, and tumor promotion. Pain response was gauged using verbal pain scores (on a 0- to 10-point scale, where 0 = no pain and 10 = worst pain) at rest and with activity at 24 hours after surgery and analgesic consumption of volume of epidural analgesic solution for the first 24 hours after surgery.
RESULTS: No correlation was found between BMI and postoperative spontaneous circulating cytokine levels. However, after activation of blood leukocytes with lipopolysaccharide, there was a significant positive correlation between the BMI and IL-1β, IL-6, and TNF-α levels (r = 0.26-0.32; p = 0.03, p = 0.03, and p = 0.01, respectively), suggesting priming of the innate immune system in obesity and potential for excessive postoperative inflammatory response. Obesity was not associated with increased pain or analgesic consumption in the first 24 hours after surgery.
CONCLUSIONS: Obesity is associated with a proinflammatory state after THA as demonstrated by enhanced cytokine reactivity. Larger studies exploring the specific impact of obesity and inflammation on surgical outcomes, including pain, are warranted. LEVEL OF EVIDENCE: Level II, therapeutic study. See the Instructions for Authors for a complete description of levels of evidence.