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Abstract Number: 2133

Neuropathic Pain After Primary Total Hip and Knee Arthroplasty

Anne Lubbeke1, Gabor J. Puskas1, Domizio Suva1, Sylvette Bas2, Cem Gabay2, Axel Finckh3 and Pierre Hoffmeyer1, 1Orthopaedic Surgery, Geneva University Hospitals, Geneva, Switzerland, 2Rheumatology, Geneva University Hospitals, Geneva, Switzerland, 3Rheumatology, Geneva University Hospital, Geneva, Switzerland

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Adipokines, Joint arthroplasty, outcome measures and pain

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Session Information

Title: Osteoarthritis - Clinical Aspects II: Symptoms and Therapeutics in Osteoarthritis.

Session Type: Abstract Submissions (ACR)

Background/Purpose: A sizeable number of patients continue to suffer from pain after total joint arthroplasty (TJA). The reason for this is not well established in many cases, and the presence of persistent postsurgical pain (PPSP) of neuropathic origin has been suggested. Possible mechanisms include intraoperative nerve injury, local inflammation, and central sensitization. Little is known about neuropathic pain after joint replacement, but its prevalence has been estimated at 5%.

Leptin could play a role in peripheral pain sensitization via its pro-inflammatory cytokine-like function. Moreover, animal models have suggested a possible influence of leptin in the development of neuropathic pain. In previous studies we found that high leptin concentrations were associated with greater pain preoperatively as well as 1 year postoperative.

Our objectives were to (1) assess the prevalence of neuropathic pain 2 years after TJA, (2) describe its influence on pain, function, general health and satisfaction after surgery, and (3) identify preoperatively assessed predictors (including leptin) of PPSP of neuropathic origin.

Methods: Prospective cohort study including patients with total hip and knee arthroplasty operated upon for primary OA in a large orthopaedic center between 1 and 12/2010. Prior to surgery baseline characteristics were recorded and leptin concentrations were sampled from blood (n= 175 TJAs) and assessed using an ELISA kit. At 2 years postoperative, the following outcomes of interest were assessed via questionnaire: (1) Presence of neuropathic pain measured with Neuropathic Pain Diagnostic Questionnaire (DN4); (2) Pain, function and general health measured with WOMAC, VAS pain, SF-12; and (3) Satisfaction.

Results: 275 TJAs were included, 161 THAs and 114 TKAs. Mean age was 72 (±9) years, mean BMI 28 kg/m², 62% were women.

Neuropathic pain at 2 years postoperative was reported by 5 THA (3.1%) and 11 TKA patients (9.6%). Presence of neuropathic pain was associated with significantly higher PPSP level, lower function, worse general health and low satisfaction (see Table). Eight of the 16 patients with neuropathic pain indicated they would not undergo the operation again.

Prior to surgery patients with neuropathic pain (vs. those without) had a significantly higher BMI (32 vs. 27 kg/m²), higher ASA scores, more often OA of contra-lateral joints, greater pain (WOMAC pain 29 vs. 41), as well as significantly higher serum leptin concentrations (37 vs. 24 ng/ml, p=0.020). The latter association was seen in obese (55 vs. 44 ng/ml) and in non-obese patients (23 vs. 16 ng/ml).

Conclusion: Neuropathic pain is more frequent after knee than after hip arthroplasty. Its presence is associated with poor outcomes. Whether leptin is involved in the pathogenesis and /or a useful preoperative marker of neuropathic pain, merits further investigation.

 

Table. Patient-reported outcomes 2 years after TJA according to presence or absence of neuropathic pain

 

Neuropathic pain yes (n=16)

Neuropathic pain no (n=259)

Risk difference (95% CI )

 

<>Very satisfied/satisfied (%)

8 (50.0)

223 (86.1)

36.1 (11.2; 61.0)

Would not undergo surgery again (%)

 

8 (50.0)

 

15 (5.8)

 

44.2 (19.5; 68.9)

 

 

 

 

Scores, mean, SD

27.0 (±4.7)   

 

Mean difference (95% CI)

    Pain (VAS)

5.5 (±1.6)

1.6 (±2.0)

3.9 (2.8; 4.9)

    WOMAC pain

50.3 (±18.0)

83.6 (±18.7)

-33.3 (-42.7; -23.8)

    WOMAC function

48.7 (±21.0)

74.6 (±20.9)

-25.9 (-36.5; -15.2)

    SF-12 mcs

38.0 (±5.6)

48.0 (±10.3)

-10.0 (-15.2; -4.6)

    SF-12 pcs

33.8 (±6.1)

42.5 (±9.4)

– 8.7 (-13.6; -3.9)

 

 


Disclosure:

A. Lubbeke,
None;

G. J. Puskas,
None;

D. Suva,
None;

S. Bas,
None;

C. Gabay,
None;

A. Finckh,
None;

P. Hoffmeyer,
None.

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