With the advancements in health care management and technology, surgical volume has increased dramatically over the last few decades. An estimated, 313 million procedures were performed worldwide in 2012.¹ This was an increase from 226 million operations performed in 2004.² In the United States, 28 million inpatient surgical procedures and 48 million ambulatory surgeries were reported in 2006 and 2010, respectively.³,⁴ Postoperative pain is normal and expected for a temporary period after surgical procedures. However, poorly controlled and persistent postoperative pain can have serious consequences. According to the U.S. Institute of Medicine, 80% of patients undergoing surgery report postoperative pain with 88% of this group reporting moderate, severe, or extreme pain levels.⁵ These numbers are expected to grow with the increasing surgical volume.

Poorly managed acute postoperative pain leads to the development of chronic pain, delayed recovery from surgery, prolonged opioid use, increased morbidity, impaired function, decreased quality of life, and increase health care economic burden.⁶ The incidence of chronic postsurgical pain (CPSP) varies by type of surgery. In a 2-year Spanish prospective study of 2929 patients undergoing hernia repair, vaginal hysterectomy, abdominal hysterectomy, and thoracotomy, this ranged from 37.6% for thoracotomy to 11.8% for vaginal hysterectomy at 4 months postoperatively.⁷ In a French prospective study of 2397 of patients undergoing cholecystectomy, inguinal herniorrhaphy, saphenectomy, sternotomy, thoracotomy, knee arthroscopy, breast cancer surgery, or elective cesarean section, patients reported the highest mean pain scores after knee arthroscopy and thoracotomy, and the lowest after herniorrhaphy and cesarean section.⁸

Orthopedic surgeries are commonly performed procedures both in the inpatient and ambulatory settings. These procedures can range from elective knee and shoulder arthroscopies, joint replacement surgeries to urgent fracture repair and removal of primary bone and soft tissue benign or malignant tumors. Upper and lower extremity surgeries provide the unique advantage of performing peripheral nerve blocks to provide postoperative analgesia in the acute setting. Given that poor management of acute postoperative pain is associated with progression to chronic persistent pain, every effort should be made to adequately control acute pain. In addition to surgery type, other risk factors for CPSP include younger age, female gender, high body mass index (≥25), preexisting psychological conditions such as anxiety or depression. Furthermore, intraoperative surgical technique, the extent of nerve injury and tissue ischemia, and postoperative complications increases the risk of CPSP.⁹

CPSP syndromes are difficult to treat. Thus, prevention and early intervention are key to successfully keeping the rates of progression from acute pain to chronic pain to a minimum. Peripheral nerve blocks, either single-shot or continuous techniques with a catheter; central neuraxial blockade such as epidural or spinal anesthesia; neuromodulation with peripheral nerve stimulation (PNS) or spinal cord stimulation are all potential preventative and/or
therapeutic modalities to optimally manage pain in the acute postoperative setting to minimize progression chronic persistent pain.

Understanding the mechanism of action of PNS is important in the implementation and the development of new treatment modalities using PNS. This is a topic of ongoing research, with likely both centrally and peripherally mediated effects. PNS is a method of orthodromic stimulation of nonnociceptive AB fibers. One theory suggests that the effect of PNS may be carried out via the gate control theory similar to dorsal column stimulation.¹⁰ The PNS activates the A-beta fibers at the location of the peripheral leads.¹⁰ This leads to excitation of inhibitory dorsal horn interneurons, which in turn inhibit the transmission of nociceptive, small-diameter A-delta and C nerve fibers.¹⁰

Additional theories attempted to explain the pain relief provided by PNS. They include the following:

A second paradigm focuses on the local effects at the site of peripheral stimulation.¹⁰ Chemical mediators, such as neurotransmitters and endorphins, may play a key role in transmission of pain signals by increasing local blood flow.¹⁰ Animal models have demonstrated that nerve injury leads to localized inflammatory changes such as edema, ischemia, and increased vascular permeability.¹⁰ Studies have suggested that PNS may reduce the levels of these biochemical mediators thus producing their analgesic effect.¹⁰ This theory is supported by a study that demonstrated increased latency of afferent signals via A and C nerve fibers when stimulated by electrical stimulation.¹⁰ This effect was most significant on small-diameter fibers primarily carrying nociceptive signals.¹⁰

A number of studies have looked at different models to understand how PNS is effective in reducing pain. Cat models have shown that repeated direct stimulation of the sciatic and tibial nerves decreases C fiber response within the spinal cord.¹² Additionally, using a rat model, investigators found that electrical field stimulation to the dorsal root ganglion plays a key role in modulating chronic pain pathways.¹² In rats, exposure of the dorsal root ganglion to electric field stimulation for 90s at 60 Hz causes a measured decrease in somatic excitability and action potential though modulation of calcium influx.¹² Calcium influx is modulated through pathways including the calcium-sensitive potassium channels, kinases, and phosphatases.¹²

Currently, it is unknown what the optimum frequency, duration, and modulation pattern is most effective to produce analgesia in PNS. The different settings of commercially available devices are titrated to patient affect in the clinical setting.