Introduction:
Chronic pain management of patients with CRPS involves a multimodal approach to reduce pain and foster physical therapy. The complex nature of the syndrome in conjunction with severity of pain symptoms often provides a challenge in management of pain symptoms. In the case of our patient, allodynia and opioid-induced hyperalgesia stemming from high levels of opioid added to this challenge. Through the use of a multimodal approach utilizing membrane stabilizers and transdermal alpha agonist, we accomplished markedly improved pain scores and patient satisfaction with the added benefit of drastically decreasing opioid use as part of our patient’s pain management regimen.
Case Report:
A 61 year-old male with PMHx of CRPS, bilateral lower extremity lymphedema, lumbar spinal stenosis and stage IV squamous cell neck cancer status post chemo/radiation therapy resulting in severe peripheral lower extremity polyneuropathy presented to our pain management clinic to transfer management of his chronic pain. Patient had previously underwent multiple epidural steroid injections and lumbar spinal cord stimulators in addition to medication trials of Methadone, Fentanyl patch, Dilaudid and Gabapentin with minimal pain relief. Upon initial presentation, patient’s pain medication regimen consisted of MSContin 240 mg TID and Dilaudid 16 mg PO q6h for breakthrough pain. Pain scores were reported as 10/10. Patient was noted to have an agitated and hostile demeanor, at times was verbally and physically abusive, secondary to poor control of pain symptoms. Due to concern for opioid-induced hyperalgesia, the plan was to gradually decrease opioid consumption by 5-10% at each clinic visit while maximizing adjuvant therapy, which our patient was initially reluctant to follow. Ultimately the pain regimen was reduced to MS Contin 90 mg TID. Gabapentin 1200 mg TID, Baclofen 5 mg TID and Clonidine TTS patch 0.1 mg q7 days were successfully initiated. Despite his initial hesitation, our patient now reports “feeling good” with pain scores of 7/10.
Discussion:
This case highlights the difficulty in management of CRPS in a patient with opiod- induced hyperalgesia (OIH). OIH was first described as early as the 19th century as the phenomenon of paradoxical nociceptive sensitization caused by exposure to opioids2. Various mechanisms have been proposed with implications for management, involving both central and peripheral pathways, most commonly including the central glutaminergic system, spinal dynorphins, descending facilitation, differences in neurotransmitter re-uptake and genetic factors2. The patient population in which OIH is observed also plays a role in the pathophysiology, and resultantly, limited treatment options1. Despite that our patient was initially reluctant to decrease opioid consumption, a reduction by 60% ultimately resulted in improvement in subjective pain scores, patient-reported quality of life, and activity levels. Another key component of our therapeutic plan was the implementation of a multi-modal regimen including the use of anti-epileptic, muscle relaxant and transdermal clonidine. Previous studies reported the benefit of epidural clonidine for pain management in CRPS patients3. Given the mechanism of CRPS and OIH with respect to central and peripheral modulation, Clonidine’s centrally mediated reduction in sympathetic nervous system activity resulted in drastically improved analgesia and patient satisfaction.
