Obesity: A Mediator of Inflammation Complicating Knee Replacement
Obesity: A Mediator of Inflammation Complicating Knee Replacement
Obese patients are not only at greater risk of knee OA that leads to joint replacement, but they fare worse after the surgery. New research suggests that this is not merely a matter of excess weight on the joint; adipose cells contribute biochemically to inflammation and pain. What are the implications for management of obese patients who need knee replacement surgery?
Many studies have documented the fact that obesity is an independent risk factor for increased post-operative pain, slower recovery and lower implant survivorship after total knee arthroplasty (TKA). The fact that 50% of the patients in the US undergoing TKA have a body mass index (BMI) greater than 30 makes this a major health issue.
Treatment of the obese patient with significant knee arthritis is a challenging problem. The patients often say that their knee pain is not allowing them to exercise, which ultimately leads them to put on more weight. Increased weight then causes more knee pain, putting them into a vicious cycle. The complexity of studying obese patients (increased comorbidities, increased tissue trauma due to girth, and increased forces through their new joint) make it difficult to prove that any single variable is responsible for this vicious cycle.
We are interested in the role that adipose tissue plays as an active endocrine organ—not focusing on the passive biomechanical issues in obesity, but trying to drill down to what is different biochemically in obese patients that may cause this detrimental effect. Our hypothesis was that obese patients enter the total knee surgery in a pro-inflammatory state.
Our ongoing study has demonstrated that obesity contributes to subclinical systemic inflammation in our TKA population. In a prospective analysis of 38 patients to date, we have found that obese patients scheduled for elective unilateral TKA have significantly higher levels of IL-6 and leptin within the serum than non-obese patients. Within the cerebrospinal fluid (CSF) there is a trend (not significant at this time) for elevation of leptin in obese TKA patients.
It is important to point out that through multiple regression analysis with step-wise selection on BMI and each cytokine, we demonstrated a negative relationship between the leptin CSF:Serum ratio and BMI (p<0.0004). Therefore, despite the increased trend seen with leptin in the CSF, we feel that its increase in the serum may be the actual cause of increased pain in these patients (not that leptin is acting centrally to produce a neuropathic pain stimulus).
The levels we see in these obese patients prior to TKA are higher than those observed in ‘normal’ obese patients, so it is possible that other inflammatory cytokines promote additional release of leptin from adipocytes. We are currently following inflammatory state in these obese TKA patients, in parallel with pain and functional recovery. If a true causal relationship can be established between elevation of leptin and pain/function, then preoperative interventions to lower serum leptin levels would be appropriate. If this is the case, then future drug developments targeting leptin may prove useful.
For the time being, we must remember that for most patients, obesity is a modifiable risk factor for poorer outcomes after TKA. Exercise, change to the diet, and bariatric surgery have all been demonstrated to lower leptin serum levels in obese patients. We strongly recommend these as appropriate measures to take prior to any major surgery.
The initial management of an obese patient at risk for joint replacement should start with proper nutritional guidance and exercise, because this has been shown to improve their level of pain and ultimate outcome once they need surgery. Physicians should consider nutritional/dietician consults and physical therapy that will help the patient prior to and after the surgery. Non-surgical options such as Tylenol, NSAIDS, and injection therapy can help alleviate some of their pain while they begin to increase their level of activity.
For morbidly obese patients, a more formal consultation with a bariatric surgery program may be appropriate. These programs often enroll patients in psychological support networks as well as regular meetings with a registered dietician.
It is important for all physicians to understand that the obese patient considering undergoing a total knee arthroplasty is not the optimal candidate. Medical comorbidities such as diabetes and heart disease should be properly evaluated and optimized before considering surgery.
Obese patients with knee arthritis need to understand several facts before they undergo TKA:
• The surgery will not change their obesity. Despite what they believe, the literature clearly demonstrates that these patients will continue to gain weight after surgery if they don't do anything different.
• It is important to set realistic expectations. These patients must be informed that the surgery will improve their pain, but will not solve all their discomfort. They will likely still feel some level of discomfort getting out of chairs or climbing stairs and during daily activities.
• Obese patients must understand that they are at an increased risk for complications. Patients with diabetes must be diligent with proper management of their blood sugar during their perioperative period to avoid an infection. They are also at an increased risk for local wound complications, as well as for thromboembolic disease. Young obese patients must also realize that their excess weight will likely decrease the lifespan of their implants and that future surgery will be needed.
Joint surgeons also need to take this last fact into account, because the greater loads that obese patients place on their implant interfaces increases the risk for earlier mechanical failure. Modern TKA techniques do everything possible to optimize the lifespan of the new joint, focusing on proper balancing and alignment at the time of surgery, and considering the need to use more fixation, not less. Cementing strategies are different than in normal-weight patients: not cementing just the “top side” surface but cementing the tibial keel and considering stemming the tibial component prophylactically in very heavy patients to reduce compressive and shear stresses on the cement interface. More constrained articular components are avoided wherever possible, to decrease the transfer of forces to the cement interface.
After the surgery, during routine annual follow-up, it remains important for physicians to address these patients/ continued (or newly acquired) obesity. However carefully and successfully the surgeon has worked to compensate for the fact of the obesity, it will play a detrimental role in the lifespan of their new knee replacement, as well as in their general health.