Cadera/Hip/Hüfte: Debilidad y dolor tras PTC, piensa en el nervio

Ipsilateral Inflammatory Neuropathy After Hip Surgery

Ruple S. Laughlin, P. James B. Dyck, James C. Watson, Robert J. Spinner, Kimberly K. Amrami, J. Sierra, Robert T. Trousdale, Nathan P. Staff

Mayo Clinic Proceedings

Volume 89, Issue 4, Pages 454–461, April 2014

Abstract

Objective

To identify whether new ipsilateral weakness after hip surgery may be due to an inflammatory as opposed to a mechanical process.

Patients and Methods

Seven patients (8 hip surgeries) seen between July 1, 2008, and June 30, 2011, developed unexplained ipsilateral leg weakness and pain within 1 month of hip surgery, mimicking mechanical etiologies. Cutaneous sensory nerve biopsy distant from the site of surgery was performed on all the patients. Patient medical records were reviewed for the clinical, electrophysiologic, radiologic, and pathologic features of the new neuropathy.

Results

Results of all the nerve biopsies were abnormal, showing axonal damage (7 patients), inflammation (7 patients), signs of ischemic injury (7 patients), and nerve microvasculitis (6 patients). Six patients were treated with intravenous methylprednisolone. At median follow-up of 6 months, 6 patients showed improvement in function and pain.

Conclusion

In this case series, we demonstrate that inflammatory neuropathy is an important etiologic consideration in some patients with ipsilateral weakness and pain after hip surgery. In these patients, the inflammatory mechanism was ischemic injury due to microvasculitis. Identification of these patients through clinical suspicion and subsequent nerve biopsy may lead to improved outcomes with prompt initiation of immunotherapy.

Cadera / Hip / Hüfte: Más inflamación y dolor en pacientes obesos tras PTC

Association of Obesity With Inflammation and Pain After Total Hip Arthroplasty

Roja Motaghedi, James J. Bae, Stavros G. Memtsoudis, David H. Kim, Jonathan C. Beathe, Leonardo Paroli, Jacques T. YaDeau, Michael A. Gordon, Daniel B. Maalouf, Yi Lin

Clinical Orthopaedics and Related Research®

May 2014, Volume 472, Issue 5, pp 1442-1448

Abstract

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