Scott S. Reuben, MD

Professor of Anesthesiology and Pain Medicine,

Department of Anesthesiology

Baystate Medical Center and the

Tufts University School of Medicine

Springfield, MA

 

 

Preventing chronic donor site pain following surgery

 

The occurrence of chronic pain following spinal fusion surgery is not an uncommon complication. Autogenous bone grafts from the ilium are frequently harvested for the purposes of bone fusion in patients undergoing spinal stabilization surgery. Often, the pain from the donor site is more severe than that from the laminectomy incision [44-47]. Although this pain usually resolves over a period of several weeks, it may persist and represent a significant source of postoperative morbidity [44-47]. In fact, donor site pain has been reported in up to 39% of patients at 3 months, 38% at 6 months, 37% at 1 year, and 19% at 2 years after bone graft harvesting from the iliac crest [45-48].

The precise mechanism of donor site pain remains obscure. It has been postulated to be muscular or periosteal in nature secondary to stripping of the abductors from the ilium [44]. In addition, the pain may be neuropathic in origin secondary to injury to small sensory nerves at the donor site. One nerve frequently injured while harvesting bone graft from the anterior ilium is the lateral femoral cutaneous nerve, which has been reported in up to 10% of cases [45].  Injury to the ilioinguinal nerve has also been reported, especially when the bone graft is harvested from the anterior ilium [45]. The superior cluneal nerves pierce the lumbodorsal fascia and cross the posterior iliac crest 8 cm lateral to the posterior superior iliac spine [49]. Injury to these nerves may occur while harvesting bone graft from the posterior ilium and may result in transient or permanent numbness and pain over the buttock area.

Three recent studies have demonstrated a significant reduction in the incidence of chronic donor site pain with the preemptive administration of analgesics [48,50,51]. Houghton et al. [52] have shown that the local application of a low dose of morphine can effectively block the development of hyperalgesia and allodynia in a rat model of bone damage. This analgesic effect was considered to be mediated through µ-opioid receptor action in the bone. Gündes et al. [51] infused 20 mL saline, bupivacaine 50 mg, or bupivacaine 50 mg with morphine, 5 mg via a 17 gauge catheter placed at the iliac crest donor site in 45 patients undergoing spinal fusion surgery. These investigators reported the absence of chronic donor site pain at 12 weeks follow-up in the bupivacaine and morphine group compared to 5 of 15 patients (33%) in the saline group and 2 of 15 patients (13%) in the bupivacaine group.

Reuben et al. [48] subsequently evaluated the analgesic effect of low dose morphine alone administered to the site of bone graft harvesting in patients undergoing spinal fusion surgery. Sixty patients were randomized to receive either saline infiltration into the harvest site (n=20), intramuscular morphine 5 mg (n=20), or morphine 5 mg infiltrated into the harvest site (n=20). This study revealed that morphine infiltrated into the bone graft harvest site resulted in a significant reduction in pain scores and opioid use for the first 24 hours following surgery. Further, the association of chronic donor site pain was significantly lower in the local morphine group (5%) compared to the intramuscular morphine (37%) or saline infiltration (33%) groups.

Reuben et al. [50] also examined the analgesic effects of preemptive COX-2 administration on chronic donor site pain following spinal fusion surgery. It has been shown that COX-2 plays an integral role in the processes of peripheral and central sensitization, [53] and it is possible that early and sustained treatment with COX-2 inhibitors may thwart the progression of acute to chronic pain [54]. Eighty patients scheduled to undergo instrumented posterior spinal fusion were randomized to receive either celecoxib 400 mg 1 hour prior to surgery and then 200 mg every 12 hours postoperatively for the first 5 days or matching placebo at similar time intervals. Patients administered celecoxib reported lower pain scores and had less opioid use during the first 5 postoperative days. Chronic donor site pain was significantly higher in the placebo group (12/40, 30%) compared to the celecoxib group (4/40, 10%) at 1 year following surgery [50]. The development of neuropathic pain following spinal fusion surgery may in part be mediated by central COX-2 expression resulting in central neuronal plasticity. Spinal COX-2 has been implicated in the development of allodynia after nerve injury in rats [55] and peripheral prostaglandins have been implicated in the pathogenesis of neuropathic pain [56]. However, after the development of neurogenic inflammation, the responses to mechanical stimuli are not affected by spinal COX-2 inhibition [55]. Thus, spinal prostaglandin synthesis may be important for the induction and initial expression, but not for the maintenance of spinal cord hyperexcitability [57]. This may explain the lack of analgesic efficacy of NSAIDs for treatment of chronic donor site pain observed in the study by Reuben et al. [50].

These three studies [48,50,51] highlight the importance of utilizing preemptive analgesics for pain management following spinal fusion surgery.  Further studies are needed to assess the appropriate dosages, timing, and duration of various preventative analgesic techniques on reducing chronic donor site pain.

 

PREVENTING OTHER CHRONIC PAIN DISORDERS

Phantom limb pain (English)

Postthoracotomy pain syndrome (English)

Postmastectomy pain syndrome (English)

 

Part II: Algorithm for Perioperative Management of CRPS Patients

Part III: Highlights for Patients

 

References