Systemic Lidocaine to Control Neuropathic Pain at End-of-Life

By Don H. Bivins, MD

Medical Director, Good Samaritan Hospice
Associate Professor of Neurosciences,  Virginia College of Osteopathic Medicine

Nociceptive pain is common in patients presenting to palliative care or hospice programs. This pain may be somatic or visceral, depending on the original lesion. For example, cancer of the lung may create visceral pain as it stretches the bronchial tissue and the pleural reflections, and then presses against adjacent structures. This nociceptive pain usually responds to opiates.

Neuropathic pain (NpP) is distinctive from nociceptive pain: permanent injury has occurred to neural structures, and those injured nerves now generate their own pain signals spontaneously. Neuropathic pain was once thought to be refractory to opiates, though multiple studies demonstrate that opiates indeed have benefit.(1, 2, 3)

As visceral or somatic tumors grow, neural structures are compressed. Typically, lung cancer may invade the brachial plexus, the thoracic spinal nerve roots, or the phrenic and vagus nerves. Colorectal cancer can invade the lumbosacral plexus; lymphoma or melanoma can irritate superficial nerves. The initial nerve injury leads to de novo gene expression and local inflammation. These two phenomena damage the local nerve, leading to changes in the ion channels and neurotransmitter receptors at the site of injury. Inflammation is harmful to the neural structures; unless the body’s restorative mechanisms control the ensuing damage. If restoration is unsuccessful, the ongoing damage to injured nerves results in the spontaneous generation of pain impulses, even if no painful stimulus occurs. Patients use specific descriptors for their NpP, such as burning, tingling, stabbing, electric-like, or jabbing. Numbness may be present at the site of intense pain. If a painful stimulus occurs at the injury site, exquisite pain results, far beyond what most people can tolerate.

It is well known that opiates have numerous adverse effects, especially if used in doses high enough to control NpP. Finding alternatives for the management of NpP is prudent. Sodium channel abnormalities often contribute to NpP. Medicines which block sodium channels prove efficacious in reducing spontaneous pain impulses. Lidocaine is a potent blocker of sodium channels (which explains its utility as a local anesthetic). When given intravenously, lidocaine can reduce NpP dramatically, and the benefit can last up to 3 weeks. It can be used as frequently as every 3 – 4 days, if necessary. A typical starting dose is 3 mg/kg, with a maximum of 5 mg/kg. The dose is administered as a rapid drip over 25-30 minutes. Giving the dose more slowly provides less benefit.

A meta-analysis by Kalso et al in 1998 confirmed the effectiveness of intravenous lidocaine in the treatment of NpP.(4) Five different disorders with NpP were studied with placebo controls, and the lidocaine provided substantial relief when administered in the dose ranges described above. EKG abnormalities or cardiac palpitations are rare with infusions. Common side effects are perioral numbness, lightheadedness, and somnolence. Lidocaine infusions are seldom effective for lesions of the spinal cord or brain. Otherwise, lidocaine infusions should be considered when treating NpP due to any disorder resulting in neural injury.

References

1. Gilron I, Bailey TM, Tu D, et al, “Morphine, gabapentin, or their combination for neuropathic pain”; NEJM 2005; 352:1324-34.
2. Judad A, Carroll D, Glynn C, et al, “Morphine sensitivity of chronic pain: a double-blind randomized crossover study using patient-controlled analgesia”; Lancet 1992; 1:1367-71.
3. Practice Parameter: treatment of postherpetic neuralgia. An evidence-based report of the Quality Standards Subcommittee of the American Academy of Neurology; Neurology 2004; 63:959-65.
4. Kalso E, Tramer MR, McQuay HJ, et al, “Systemic local-anaethestic-type drugs in chronic pain: a systematic review”; European Journal of Pain 1998 Mar; (2)1:3-14.