Pain control in patients with acute burns is important because inadequate pain control can result in chronic pain syndrome. The continuous painful stimulation of nerve endings at the injury sites results not only in peripheral sensitization but also leads to central nervous system sensitization, which in turn causes a chronic pain syndrome in burn patients that is difficult to treat.1–3 Although the pain that occurs after a burn injury should be treated aggressively using both nonpharmacological and pharmacological techniques, it is often undertreated.4
Spinal cord stimulation (SCS) has been used widely to treat neuropathic pain since it was introduced by Shealy et al5 in 1967. Accumulating evidence shows that SCS is a good to excellent method for treating the neuropathic pain associated with failed back surgery syndrome and complex regional pain syndrome.6 Although postburn pain is thought to have a neuropathic origin, to our knowledge, there have been no published reports on the use of SCS for burn-related pain. Here, we report a patient with a burn injury complaining of intractable pain, which was markedly ameliorated by SCS treatment.
We obtained written informed consent from the patient to publish this report.
A 67-year-old man suffered burns caused by boiling water to 15% of his body surface area, including his left arm, lateral abdomen, and gluteal region. Two days later, he was admitted to another hospital and underwent debridement of his second degree burns 5 times. The burned surface was treated with antibacterial drugs and covered with sterile dressings. Although the injured sites healed within 2 months with hypertrophic scar formation (Figure 1), he complained of severe persistent pain to the sites of injury that was inadequately treated with diclofenac and pentazocine during his admission. On discharge from the previous hospital, he was prescribed pregabalin 300 mg/d, loxoprofen 180 mg/d, and etizolam 1.5 mg/d, but this regimen failed to improve his persistent pain.
Five months after the injury, he presented to our pain clinic. Although his burn sites did not exhibit hyperesthesia, allodynia, or loss of sensation, he perceived a continuous burning pain, as well as intermittent tingling and stabbing pains, with an intensity of 50 to 75 on a 101-point visual analog scale (VAS). He also experienced sleep disturbance because of intractable pain. We initially administered fixed-dose tramadol/acetaminophen 37.5 mg/325 mg 4 tablets/d and duloxetine 20 mg/d instead of the pregabalin, but this failed to reduce his pain. We then started a fentanyl patch at 12.5 µg/h and gradually increased this to 50 µg/h over 4 weeks. The duloxetine dose was also increased to 40 mg/d. But the patient complained of side effects, including constipation, nausea, and dizziness, with no improvement in the VAS score. Local administration of 10% lidocaine ointment also failed to reduce the VAS score. Although an epidural block using 1% mepivacaine ameliorated his pain, its effect lasted only for a few days. Therefore, we proposed a trial of SCS 11 months after the injury.
During the trial, the patient was placed in the prone position. Two 8-electrode epidural leads (Medtronic, Minneapolis, MN) were inserted at the L2/L3 and L3/L4 interspace and then threaded to the T8 level under fluoroscopic guidance (Figure 2). One electrode was placed almost in the midline, and the other was inserted slightly to the left of the midline. Because the burn regions were large and separately injured, we did not stimulate the upper arm and targeted only the left lateral abdomen (area A) and left coxal and gluteal region (area B), where his pain was the most severe (Figure 1). During the 7-day trial, the doses of the fentanyl patch (50 µg/h) and duloxetine (40 mg/d) were not changed. The VAS scores of areas A and B before the trial SCS were 69/100 and 59/100, respectively. The maximum improvements in the VAS score were observed on the fourth postoperative day and fell to 12/100 in area A and 10/100 in area B. Seven days after the end of the SCS trial, his pain scores were 49/100 in area A and 58/100 in area B. Therefore, he underwent permanent implantation of SCS leads and a generator (the RestoreSensor SureScan® MRI; Medtronic, Minneapolis, MN). The patient reported good paresthesia in areas A and B (450 µs, 2.2 V), and the VAS scores decreased again. The dose of the fentanyl patch was decreased gradually until the eleventh postoperative day when the fentanyl was stopped.
Six months after implantation, his VAS score was 30/100 in area A and 0/100 in area B. Although residual pain persisted in the left upper arm, it was treated by local anesthetic injection or paravertebral block of the left T2. The patient was satisfied with the SCS treatment and his sleep disturbance dramatically improved.
To our knowledge, this is the first report of SCS treatment used to markedly improve burn-related pain. SCS may be effective for overcoming a sufficient amount postburn pain to make treatment more manageable with oral medications at lower doses and fewer side effects.
Burn injuries result in one of the most intense types of sensory nociception. Furthermore, acute uncontrolled burn pain increases the incidence of mental health disorders and decreases patient compliance with rehabilitation therapy.4 Although the pain experienced during acute postburn injury has been well documented, many patients experience ongoing pain long after the early phases. Choinière et al7 reported that 35% of 104 patients experienced pain 1 year or more after burn injuries, 82% of patients complained of paresthesias in the healed burns, and 67% of patients with chronic pain stated that the pain interfered with their social lives. Dauber et al2 reported that 52% of 336 patients complained of ongoing burn-related pain at the time of a survey completed an average of 11 years after their injuries.
Although the mechanism of chronic neuropathic pain after burn injuries remains obscure, several preclinical studies suggest that central sensitization mechanisms are involved in its development. Dendritic spine dysgenesis was observed in ipsilateral wide dynamic range neurons in burn-injured rats.8 Furthermore, Chang et al9 demonstrated that unilateral burn injury pain can spread to the contralateral limb via dorsal horn neuronal hyperexcitability and microglial activation on both sides of the spinal cord in a rodent burn injury model. In a human study, Hamed et al10 showed that the density of nociceptive nerve fibers was increased in the skin of patients with chronic pain after burns, and this was thought to be associated with central plasticity. Taken together, these reports suggest that persistent chronic pain after a burn injury is related to changes in the dorsal horn, as well as in cutaneous innervation.
Opioids are a therapeutic option for analgesia in selected cases. However, long-term opioid use can induce tolerance, independence, and hyperalgesia, resulting in escalation of the opioid dose with a resultant increase in opioid side effects.4,11 In our patient, the fentanyl patch dose was increased to 50 µg/h and caused several side effects. Thus, we felt that pain management using higher opioid doses was inappropriate in our patient. Moreover, as observed in this case, postburn patients may develop psychological disorders, including depression, anxiety, posttraumatic stress disorder, and sleep disturbance that can worsen their pain.12 Our patient complained of severe sleep disturbance that could not be managed with hypnotics. At present, the ideal treatment for postburn pain remains unclear; consequently, a new strategy for the treatment of postburn pain is required.
Since its introduction in the late 1960s, SCS has often been used for the treatment of chronic pain. SCS is recommended for patients suffering from refractory chronic neuropathic pain conditions, such as failed back surgery syndrome and complex regional pain syndrome.6 A systematic review and meta-analysis showed that SCS provides good analgesia, decreases the dose of analgesics, and improves quality of life. In addition, SCS was shown to be cost-effective for long-term pain management.13,14
Although the analgesic mechanism of SCS has not been fully elucidated, presynaptic inhibition of nociceptive inputs by Aβ fiber stimulation, a reduction in sympathetic nervous system activity, and activation of the descending inhibitory pathway are thought to be involved.15 Moreover, an animal study demonstrated that SCS could reverse and prevent central sensitization after nerve injury. Guan et al16 showed that SCS attenuated wide dynamic range neuronal hyperexcitability in the neuropathic condition and counteracted the activity-dependent increase in neuronal excitability in rats. As mentioned above, central sensitization is involved in chronic pain after burn injuries, and its inhibition is thought to be a potential therapeutic target to alleviate pain. Therefore, we hypothesized that SCS treatment could suppress the burn-related pain in the present case.
The success of SCS treatment depends on the presence of paresthesias in the affected area. Burn patients can have injured skin in several areas, which means that multiple separate nerves are involved in the burn pain. Furthermore, in patients with widely injured areas, SCS will not be able to produce paresthesias in all affected areas. This is one of the reasons why SCS has not been applied for the treatment of burned patients. In the present case, the injured left upper arm, which is supplied by the second thoracic nerve, could not be covered by dual lead SCS. Our treatment focused on the left lateral abdomen and gluteal region, which caused the most severe pain. As a result, the patient could stop using fentanyl patches.
In summary, we reported the successful SCS treatment of postburn pain. If the painful region is relatively small and can be covered with dual lead SCS, SCS is an option for the management of postburn pain.
Name: Takeshi Kubota, MD.
Contribution: This author was the attending physician of the patient, and surgeon of SCS implantation.
Name: Yuuhei Ishikawa, MD.
Contribution: This author provided technical assistance of SCS implantation.
Name: Rie Ishikawa, MD.
Contribution: This author provided technical assistance of SCS implantation.
This manuscript was handled by: Raymond C. Roy, MD.
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