Indications and Specific Selection Criteria

The most common indication for SCS in the United States is for back or neck radiculopathic pain. Patients presenting with conditions such as lumbar or cervical radiculopathy, postlaminectomy syndrome, spondylolisthesis, spondylosis, or even persistent and refractory axial low back pain of uncertain etiology may respond to treatment with SCS and should be assessed. Topography of pain that is amenable to overlap by paresthesia of the spinal cord stimulating device is a requirement for successful treatment.¹⁰ Radicular patterns tend to be more easily obtained than axial patterns, and for this reason, patients with pain predominantly in the extremities may be better candidates than patients with predominantly axial symptoms. This should not exclude a trial in an otherwise good candidate who has primarily axial symptoms. Although it is technically more difficult to obtain coverage of patients with predominantly axial back or neck pain, newer, more compact electrodes with multiple arrays sometimes placed bilaterally and triangularly might be useful in providing relief to patients with axial pain, and these arrays should be considered. Long-lasting relief is a reasonable goal. A large series of patients with follow-up of 2 to 20 years demonstrated that 52% of patients continued to have a 50% reduction in pain.¹¹ The authors noted that even among patients who did not claim a 50% reduction of pain, most patients continued to use their devices.

The evidence of efficacy of SCS for back and neck pain is not lacking. A literature review was performed on studies of patients with SCS for chronic leg and back pain and included all relevant articles identified through MEDLINE search from 1966 through 1994.¹² Fifty-nine percent of patients reported in these studies had greater than 50% pain relief at a time between 1 and 45 months after surgery. These authors noted the lack of a randomized trial at that time. Subsequent to this, a prospective, randomized comparison of SCS and reoperation in patients with persistent radicular pain with or without low back pain after lumbosacral spine surgery was conducted.¹³ The primary outcome measure of this study was frequency of crossover to the alternative procedure. This study showed a statistically significant advantage of SCS over reoperation. A literature review on SCS for chronic pain of spinal origin was conducted by North and Wetzel,⁹ who concluded that SCS is a valuable treatment option, particularly for patients with chronic pain of predominantly neuropathic origin and a topographic distribution involving predominantly the extremities. Efficacy may be better for spontaneous than for evoked pain.¹⁴

Pain associated with spinal cord injury has been treated with SCS. Most authors report satisfactory responses in a smaller percentage of their patients ranging between 20% and 40%.¹⁵ Case reports supporting the use of SCS for whiplash and idiopathic acute transverse myelitis have been published.^16,17 Sindou and colleagues¹⁸ reported the predictive value of somatosensory-evoked potentials assessing neural conduction in the dorsal columns. These authors suggest that if central conduction time is abolished or significantly altered, then the success rate of SCS is dramatically less than in patients with normal preoperative central conduction times.

The usefulness of SCS for the treatment of postherpetic neuralgia has recently been described. A prospective case series involving 28 patients with either acute herpes zoster or postherpetic neuralgia were studied over 29 months. Eighty-two percent of patients with intractable pain for longer than 2 years had a median decrease in their visual analogue scale score from 9 to 1 (0 to 10 scale) as well as improvement in their pain disability index. Four patients with acute herpes zoster had prompt and dramatic improvement in their pain symptoms.¹⁹

The treatment of PVOD with SCS is the most common indication for this modality in Europe. For no other indication is the early evidence of efficacy more compelling and yet SCS for PVOD is not a common treatment in the United States. One study reported 37 patients receiving adequate pain relief after a trial in 41 patients with end-stage peripheral vascular disease.²⁰ Seventy-eight percent of patients reported substantial pain relief at a mean follow-up of 25 months. Another investigator reported the results of SCS in 20 patients with ischemic rest pain and ulcers.²¹ Eighteen of 20 patients in this study had immediate relief of pain after electrical stimulation. These authors also reported improved skin nutritional flow leading to healing of ulcers of moderate size and increased salvage of feet with limb-threatening ischemia at 2-year follow-up. They report an increase in capillary density and an increase in red blood cell velocity and peak red blood cell velocity after arterial occlusion by intravital capillary microscopy.

More recently, SCS has been investigated by the European Peripheral Vascular Disease Outcome Study.²² Patients with nonreconstructable critical leg ischemia showed increased limb survival when compared with patients receiving usual treatment without SCS as well as improved pain relief. Patients with transcutaneous oxygen pressure measurement of 10 to 30 mm Hg before SCS trial or if less than 10 mm Hg, an improvement to 20 mm Hg or more during the SCS trial received an implant. Limb amputations were 20% at 12 months in the SCS group compared with 46% in the matched no SCS group. These and other authors suggest the routine use of transcutaneous oxygen pressure both before and during the trial phase as a predictor of success.²³ A useful predictor of success in patients with diabetes with PVOD is the absence of autonomic neuropathy.²⁴ Twenty-five of 28 patients with autonomic neuropathy failed SCS treatment, whereas all 32 patients without autonomic neuropathy had successful outcomes.

Evidence exists of the efficacy of SCS in severe Raynaud’s phenomenon²⁵ and Buerger’s disease.²⁶ SCS has shown remarkable effectiveness and should be considered as a treatment for patients with severe PVOD that is not amenable to surgical intervention.

Despite the lack of an identifiable objective lesion, SCS appears to be quite effective for treatment of CRPS. One report retrospectively reviewed experience with SCS and found 12 patients with CRPS who were followed up for an average of 41 months after implantation.²⁷ Eight of these patients reported excellent pain relief, and four patients reported good pain relief. Another study looked at 18 patients with CRPS.²⁸ Fourteen patients had a successful trial and subsequently had their systems internalized. Follow-up varied from 4 to 14 months. Six of 14 patients had good pain relief. Five had moderate pain relief. One had minimal and three had no pain relief. Of note is that pain relief was limited to the body parts covered by the paresthesia.

In a randomized trial comparing SCS plus physical therapy with physical therapy alone in 54 patients with CRPS, the SCS group had a mean reduction in pain of 2.4 cm (on a 1- to 10-cm scale) compared with an increase of 0.2 cm in the physical therapy alone group.² Health-related quality of life also improved in the SCS group, but, interestingly, there was no difference between the groups in functional status.

A recent report has demonstrated that response to sympathetic blockade can be predictive of a better outcome from SCS for patients with CRPS.²⁹ Thirteen of 13 patients with a positive response to sympathetic blockade had pain relief during the trial period, and 87% had greater than a 50% reduction in pain at 9 months. Only 3 of 10 patients with a negative response to sympathetic blockade had good relief and went on to permanent implantation, and only 33% had a 50% reduction in pain at 9 months.

It appears that at this time there are very good data to support the use of SCS for the treatment of CRPS if it is possible to obtain paresthesia coverage that overlaps the painful area.

The treatment of postamputation phantom or residual limb pain with SCS is still a controversial area. Contradictory reports for this and for brachial plexus avulsion injury pain exist, and it is not possible to make definitive recommendations for treating or not treating phantom limb or brachial plexus avulsion injury pain with SCS based on these data.

A large body of data supports the use of SCS for intractable angina pectoris. The complexity and implications of severe coronary artery disease as an indication for SCS requires discussion. The first published report of the use of SCS for angina was in 1987.³⁰ These investigators described 10 patients with intractable angina in whom SCS devices were implanted, which led to a decrease in the frequency and severity of angina and a major reduction in the use of antianginal medications. Other investigators followed with a report on 10 patients and added bicycle ergometry as a measure of exercise tolerance and showed an increase in work capacity, increased time to angina, decrease in recovery time, and a decrease in the magnitude of ST-segment depression associated with angina.³¹ By 1991, it was shown that reductions in angina attacks continued over 9 months, and a persistence in increase in rate-pressure product (a measure of the ability of the heart to do work).³² Between 1993 and 1994, results of a randomized, prospective study demonstrated improved exercise capacity, improved quality of life, and a decrease in ischemic episodes as measured by Holter monitor.^33–35 Complications were few and of a technical nature, and a surgical algorithm that did not involve a trial before implantation was described. It has been shown that SCS does not conceal myocardial infarction that may occur in patients with implanted devices.³⁶ A decrease in hospital admissions for patients with implanted SCS devices compared with a control group has been demonstrated.³⁷ In 80% of patients, the beneficial effect has been reported to last 1 year, and in 60%, improvement in exercise capacity and quality of life lasted as long as 5 years.^38–40 There are no data showing harmful or nontherapeutic effects of SCS for angina. The use of SCS may be beneficial even in critically ill patients. Janfaza and colleagues⁴¹ reported the 6-week survival in such a patient, whereas other investigators have reported an effect insufficient to overcome the severity of ischemic disease, albeit relief of ischemic symptoms, until death occurred.⁴²

A prospective, randomized trial of SCS versus coronary artery bypass grafting in 104 patients with severe angina, increased surgical risk, and no prognostic benefits from revascularization demonstrated long-lasting improvement in quality of life and comparable survival and symptom control in both groups.⁴³ Benefit after discontinuation of SCS has been shown for as long as 4 weeks after discontinuation.⁴⁴ No difference in anginal complaints, nitroglycerin intake, ischemia, or heart rate variability was shown. SCS has been shown to decrease hospitalization in patients with angina,⁴⁵ and there is evidence that modern SCS devices are compatible with modern pacemaking devices.^46,47

Description of Technique

In our practice, patients who meet selection criteria are instructed not to eat or drink anything after midnight the night before their implantation trial. They are instructed to continue their nonsteroidal anti-inflammatory drugs, but care is taken to discontinue other anticoagulants or platelet inhibitors for proper durations of time. The procedure is done in two stages. Both the trial phase (phase 1) and the generator implantation phase (phase 2) are done in the operating room with an anesthesiologist present. The trial phase or phase 1 involves either the placement of a percutaneous cylindrical electrode or a paddle-type electrode placed via minilaminectomy. The electrodes are either removed after a period of trial stimulation or are attached to a connecting cable during phase 1 allowing the electrode to remain under the skin entirely. In this case, the connecting cable can be removed and the electrode attached to a new sterile cable during phase 2.

Patients with chronic pain may have central changes that amplify painful signals. It is necessary to have the patient awake and able to answer questions appropriately to assess the location of paresthesia during the trial phase. Patients may require laminectomy for placement of a paddle-type electrode in the thoracic or cervical region. Patients with chronic pain often have multiple comorbidities, particularly patients with PVOD or intractable angina pectoris. These factors create an anesthetic challenge and require a preoperative consultation between surgeon and anesthesiologist to define goals and needs. Our typical anesthetic involves intravenous fentanyl and midazolam for analgesia, anxiolysis, and amnesia and propofol for sedation. The propofol can be turned off, and the patient awakened for questioning regarding paresthesia topography at appropriate intervals. We also use large volumes of local anesthetic, typically 0.5% lidocaine without epinephrine. A dose of 4 mg/kg (56 ml for a 70-kg person) can be safely administered even as a single dose and more can be administered after 1 or 2 hours. Another option is intravenous remifentanil plus local anesthetic, but this requires an anesthesiologist experienced in the use of this drug because the therapeutic window is often so narrow. Despite the best efforts of experienced practitioners, the implanter should be prepared for oversedation and the need for airway control during the procedure or suboptimal ability to describe the paresthesia topography. The patient should be advised that this is a possibility and that if it occurs, the electrode can still be placed without paresthesia guidance, but success rate might be reduced. The patient should also be educated about information needs that will occur intraoperatively before getting to the operating room. A recent report describes the successful implantation of an SCS device in 19 of 19 patients undergoing laminectomy with 12.5- to 20-mg bupivacaine intrathecal spinal anesthesia.⁴⁸ In all patients with spinals and anesthesia throughout the surgical procedure, SCS paresthesia was readily appreciated by the patients.

There is no description of the absolute need for alertness and ability to communicate during surgery. It is generally accepted that, due to uncertainty about anatomic and physiologic overlap, simply placing the lead at the proper anatomic location will not reliably produce a paresthesia that will be effective in reducing pain. There are published case series in which successful implantation has been done under general anesthesia.⁴⁹

A retrospective, nonrandomized review of surgical experience concluded that patients with flat electrodes placed via laminectomy had better pain relief that was longer lasting than patients who had percutaneously placed cylindrical electrodes.⁴⁹ A prospective, randomized, controlled trial has recently shown that electrode arrays implanted via laminectomy had lower amplitude requirements and better patient ratings of paresthesia coverage.⁵⁰ The decision as to whether to place a flat electrode via minilaminectomy or a percutaneously placed cylindrical electrode is a controversial and emotionally charged issue because anesthesiologists, who place most of these devices, use a percutaneous approach and many neurosurgeons place leads via laminectomy. To further complicate matters, anesthesiologists should not place leads via laminotomy because they do not have the training, experience, or ability to manage complications and many pain specialist anesthesiologists derive substantial income from placing SCS devices. Additionally, other specialists such as physiatrists and neurologists are receiving training and are eligible for board certification in pain medicine and are implanting cylindrical leads. At this time, there is no overwhelming evidence of the advantage of placing electrodes via a laminectomy compared with percutaneously placed leads, but there is at least one compelling study.⁵⁰

For percutaneous placement of a cylindrical electrode, the procedure is as follows. Patients are placed prone on a fluoroscopy table in the operating room and prepared for a surgical procedure that can last hours. We do not place a Foley catheter. Standard surgical preparation is done after identifying important landmarks fluoroscopically and marking the skin to identify them. The skin and subcutaneous tissue are anesthetized with local anesthetic before insertion of the 15-gauge epidural needle. The epidural space is identified using a loss of resistance to air or saline technique (Fig. 129-1). For a patient with an L5 radiculopathic pain pattern, the epidural space is entered at approximately T12–L1, at which point the cylindrical electrode is advanced through the needle and positioned using fluoroscopic guidance to the desired level at approximately T9–T10, at which time trial stimulation is carried out (Figs. 129-2 and 129-3). For placement of a device for stimulation of the upper extremity, entry is made at T1–T3 with the electrode tip to arrive at C3–T4 approximately. The target site for the electrode tip for a patient with angina is approximately T4–T5. For a unilateral syndrome, the electrode should be positioned approximately 3 mm ipsilaterally off midline. The electrode can be directed and “steered” using an angled stylet. Once the target anatomic site is reached, the electrode is anchored and attached to a temporary screening cable and a trial screener. The awakened patient is then questioned about the presence or absence and location of paresthesia coverage. Parameters that are available for adjustment include amplitude and pulse width and frequency, the same as with an implanted generator.

FIGURE 129-1 Intraoperative identification of the epidural space using a loss of resistance to air technique in preparation for placement of a percutaneous cylindrical electrode.

FIGURE 129-2 Advancement of cylindrical electrode through an epidural needle. Note that steering the electrode is possible by rotating the stylet hub of the electrode.

FIGURE 129-3 Quadripolar electrode being advanced under fluoroscopic guidance within the epidural space. Note the angle between the two most cephalad leads enabling steering of the electrode.

Once good paresthesia overlap to pain topography is obtained, the electrode is disconnected from the cable. A 5-cm vertical incision over the site of epidural needle placement is made. The subcutaneous tissue is undermined at the level of the lumbodorsal or supraspinous fascia, the epidural needle is carefully removed along with the electrode stylet, and the lead is anchored using an anchoring device that will prevent the electrode from migrating (Fig. 129-4). The electrode is attached to a percutaneous extension lead, and a tunneling device is used to exit the skin at a site approximately 10 cm lateral to the incision. The electrode is placed within the incision with only the temporary connecting cable externalized. This allows the electrode to remain beneath the skin throughout the entire trial period. Care should be taken to avoid contact of the electrocautery device with the electrode. A defect in the electrode could result in a line of continuity between the externalized lead and the epidural space. If the patient has a successful trial, then it is necessary only to remove the extension lead, and the electrode, which has already been positioned and has not been exposed to a contaminated external environment, can remain in place. The skin and subcutaneous tissue are closed with interrupted Vicryl sutures and skin staples.

FIGURE 129-4 The cylindrical electrode is anchored within an undermined incision extending to the dorsolumbar fascia.

Placement of a paddle-type electrode or flat lead is done via a standard laminotomy procedure. The electrode is placed in the epidural space using the same anatomic targets as described for cylindrical electrode placement. A dual laminotomy is sometimes required to properly position the electrode.⁵¹ Paresthesia overlap with topography of pain should be tested with the awake patient intraoperatively. The electrode cable is anchored to fascia, and the electrode is attached to a temporary percutaneous connecting wire as described previously.

At the conclusion of the phase 1 of implantation, the procedure is the same for both percutaneous and flat electrode management. The percutaneous connecting cable is attached to a trial screener, and the patient is screened at home for 4 to 7 days. When the patient returns, he or she is questioned about success of pain reduction. A general rule of thumb is that a reduction in pain of 50% or more is necessary to proceed to phase 2, but there are many exceptions and a careful assessment by the implanting surgeon is required for proper decision making. For patients with intractable angina pectoris, a reduction in the frequency, intensity, and duration of anginal episodes should be documented.

For phase 2, the patient is taken to the operating room and under local anesthesia with monitored anesthesiology care; the electrode and cable are removed if the trial was not successful. Patients who have had a successful trial will have their incision reopened, and the generator will be implanted in the buttock. A site selected below the belt line and cephalad enough to allow comfortable sitting should be selected. Generators can be implanted in a variety of anatomic sites including the abdomen, lateral thorax, and subclavicular and subaxillary space.

After local anesthetic infiltration, a horizontal incision is made in the skin planes large enough to enable placement of the generator. The pocket is created by sharp and blunt dissection and is made at a depth no greater than 2 cm to enable easy programming transcutaneously.

A tunneling tool is used to connect the midline incision to the pocket, and the extension wire is threaded through the tunnel. The system is connected, and the incisions are approximated in two layers using 3-0 Vicryl sutures for the deeper tissues and staples for skin closure. Familiarity with all the equipment is necessary before proceeding to the operating room.

Intraoperative problems peculiar to SCS implantation include an inability to properly position the electrode in the epidural space, inability to obtain paresthesia overlap of the painful area, and unanticipated events. We have described the inability to thread a percutaneous catheter in a patient with unidentified epidural lipomatosis.⁵² The catheter was readily placed under direct vision after laminotomy. We use a dual laminotomy technique in those cases in which a proper anatomic position cannot be achieved through a single laminotomy to enable proper anatomic and physiologic positioning of a flat electrode and have estimated that unanticipated anatomic complications occur as often as 18% of the time in revision flat electrode placements.⁵¹ Finally, it is uncommon, but it is sometimes impossible to obtain satisfactory paresthesia overlap of the painful area, particularly with angina pectoris and axial low back or neck pain, despite an unimpeded ability to manipulate the electrode(s). Even distal extremity paresthesia coverage can sometimes be impossible to obtain for unproven but theorized reasons such as epidural scarring or any impediment to the flow of electricity to and into the spinal cord.

Complications and Troubleshooting

Possible problems and complications of spinal cord stimulating devices have been well described. North and colleagues¹¹ had no major morbidity or mortality in their series of 320 patients undergoing implantation over 20 years. Their incidence of surgical wound infections, all superficial, was 5%, and they all cleared promptly with the removal of hardware and a short course of antibiotics, permitting a second implantation. They had a 7% failure rate manifested by fracture of the electrode or insulation failure; 5% of their systems failed because of a defect in the radiofrequency receiver.

There are case reports of cord compression due to hematoma, and these have mostly followed laminectomy rather than percutaneous implantation. Transient and reversible neurologic deficit have also rarely been reported. Radicular muscle twitches have rarely been reported, and there is one death reported due to pulmonary embolism. Prolonged and exaggerated postoperative pain has been reported, and the reason for this complication is not clear. Erosion through the skin of implanted materials has occurred, particularly in cachectic ill patients. The complication rates have continued to decrease with refinement of equipment and surgical technique and should be expected to continue to decrease. Late failure has also been reported.

There is a steady decrease in the success of pain relief over many years after implantation. Early failure may represent a defect in our ability to carefully screen these patients before implantation.

Patients should have a near-normal prothrombin time before proceeding with implantation. Patients with thrombocytopenia should be transfused with platelets before implantation. These patients should be carefully monitored for symptoms of acute epidural hematoma, and if these symptoms occur, they should be treated as a neurosurgical emergency.

All patients in our practice received a single preoperative dose of prophylactic antibiotic. The most common infectious agents were Staphylococcus aureus and Staphylococcus epidermidis. Pocket seromas are a self-limiting complication and usually will resolve within 2 months. Patients should be reassured, and only very occasionally is it necessary to aspirate these fluid collections. If there are signs of infection, the fluid can be aspirated and sent for Gram stain and culture and sensitivity.

A visible collection of fluid found subcutaneously under the back wound may represent a cerebrospinal fluid hygroma, especially if a known subarachnoid puncture occurred during electrode placement. These are self-limiting complications that have no clinical consequence. If there is a cerebrospinal fluid leak through the incision, the surgical wound should be taken down and resutured. For persistent postdural puncture headaches, a blood patch can be done. This should be done under fluoroscopic guidance to ensure no damage to the implanted electrode. Infected hygromas necessitate removal of the entire system.

Patients will present after successful implantation with complaints about their systems. Complaints can include a lack of stimulation, intermittent stimulation, a change in stimulation pattern, undesirable sensations, or inadequate pain relief. The most common solution is a simple reprogramming. A decrease in postoperative swelling or slight lead migration may account for many of the above problems, and careful, thoughtful reprogramming can solve most of these difficulties. A lack of stimulation can indicate a dead battery, which will be evident with reprogramming but can also represent an open circuit. Measuring individual electrode impedances, palpation, and radiography can all help make this assessment. Fluid within a connector can cause intermittent stimulation as well as simply a loose connection. Palpation and impedance measurement can help identify the source of the problem. Burning at the pocket or lead-extension junction can indicate electrical leakage. A change in stimulation pattern can indicate lead migration. Insufficient relief can indicate disease progression or patient expectations that may have been too high.

If the source of the problem can be identified easily, then a directed surgical solution can be planned. For example, a patient with burning at the lead-connecting cable junction and lack of stimulation with abnormal impedances can have the lead-connecting cable junction site explored and repaired. Unfortunately, there are times when the precise site of malfunction is not clear and a surgical plan is necessary. The lead-connecting cable junction is a common malfunction site, and a good surgical plan would be to explore this junction first. If no abnormality such as fluid within the boot is evident, then the lead can be disconnected from the cable and the lead tested with alligator clips intraoperatively. If the lead is the source of the problem, it can be replaced. If it is not, then the system should be reconnected and retested in the operating room. If the system is still not functioning properly, then the generator-connecting cable incision can be opened and the connecting cable lead can be tested with alligator clips. The connecting cable can be replaced if indicated and if the lead-connecting cable complex is working but the generator connecting cable-lead complex is not, the generator should be replaced. The entire system should be explored if necessary, and the system should be functional by the time the patient leaves the operating room, even if the entire system needs to be replaced. There are three pieces of equipment that can potentially malfunction, and each piece can be isolated and tested. The intact and repaired system should be tested before leaving the operating room.

Generator life span is variable and depends on programming parameters and patient preferences for use. A patient who uses the device 24 hours per day at a voltage of 9 V with a high frequency may deplete an implanted battery in less than a year, whereas a patient with low voltage and frequency who uses the device 4 hours per day may obtain a decade of life from his or her battery. The former patient should probably be implanted with a radiofrequency transducer rather than a battery. Some implanters favor transducers for all their patients, citing no need for battery replacement as a valid reason. Many if not most patients will prefer the convenience of not needing a rubber donut on their skin with a portable power supply.

Summary

SCS is the most useful new tool in the armamentarium combating chronic pain to emerge in more than a decade. Its use is supported not only by overwhelming case series but by well-controlled clinical trials. The precise niche for SCS in the management of angina pectoris, PVOD, and even chronic low back and neck pain is still developing in the paradigm of care for patients with chronic pain. Future vectors of care and usefulness include discovering the role of different drugs when used in combination with SCS. Subeffective doses of gabapentin and pregabalin when combined with subeffective levels of SCS have been shown to be effective in reducing neuropathic pain.⁵³ Patients with neuropathic pain effectively treated with SCS have been shown in a double-blind, randomized study to respond to carbamazepine but not to sustained-release morphine when their SCS devices were turned off and they were “switched” to a painful state.⁵⁴

Other areas under investigation include an automated, patient-interactive SCS adjustment device, which has been shown to provide better paresthesia overlap of painful regions, better analgesia, and longer battery life.⁵⁵ Better methods of obtaining axial paresthesia coverage, electrode placement under the arch of C1 and C2 for use in atypical facial pain, nerve root SCS cannulation, chemical augmentation with intrathecally administered drugs, sacral root stimulation for urinary incontinence, and improvements in systems and equipment all may add to the success of SCS as a therapeutic, nondestructive, reversible, and minimally invasive analgesic tool.⁵⁶

Introduction and General Selection Criteria

Intraspinal administration of opioids has been shown to be useful in patients who have not responded to other therapies or who have excessive side effects with other routes of administration. It is most useful and has proven efficacy when used for patients with cancer pain who develop unmanageable side effects to the high doses of opioids sometimes necessary to control pain or intractable pain states.^57–63 Success in treating nonmalignant chronic pain with intraspinal opioids has not been confirmed to the same extent but is commonly employed.^64,65 As with SCS, patient selection is likely to be the key predictor of success, but identifiable preimplantation variables have not yet been definitively identified. Negative predictors of success have been suggested to include major psychopathology, active mood disorders, dementia, severe anxiety, addictive disease, and severe social or economic stressors.

Patients whose pain does not respond to opioids may benefit from the addition of other drugs to their intraspinal regimen. Drugs reportedly used include local anesthetics, clonidine, baclofen, and opioids.^3,66 Local anesthetics, clonidine, and baclofen are typically used in combination with opioids and, except for clonidine, may not be useful as analgesics when administered alone. A recent review investigated clinical practices via an Internet-based survey and described drugs and combinations of drugs used by practitioners.⁶⁷ Drugs and combinations are shown in Fig. 129-5.

FIGURE 129-5 Drugs used by high (more than 15 patients being managed) and low (fewer than 15 patients being managed) managers of patients with analgesic infusion systems.

(From Hassenbusch SJ, Portenoy RK. Current practices in intraspinal therapy—a survey of clinical trends and decision making. J Pain Symptom Manage. 2000;20:S4-S11.)

The general indications for implantation of an analgesic infusion system are the same as for SCS. A trial with a single intraspinal injection or continuous infusion should be conducted before implantation.

Drug Selection and Systems

The use of neuraxial morphine through a continuous infusion pump as an effective treatment for pain of malignant origin has been well documented.^57–63 Morphine, hydromorphone, bupivacaine, baclofen, clonidine, sufentanil, ketamine, ropivacaine, fentanyl, meperidine, tetracaine, and experimental agents are used in academic pain centers in the United States.³ The use of spinally administered drugs in the noncancer pain group is more complex. The indication for this therapy is very simply opioid-responsive pain in patients unable to tolerate alternate routes of administration or in whom alternate routes of administration are ineffective. The complexity arises when considering the impact of social, psychological, physical, financial, and emotional factors. Further complicating the issue is the impact of ongoing litigation, disability, and substance abuse, which are so prevalent in our society.

In a blinded, placebo-controlled study conducted in Australia, less than one third of patients using oral opioids for nonmalignant pain were found to have opioid-responsive pain on intrathecal testing.⁶⁸ Furthermore, these patients were significantly more distressed by testing with a battery of psychometric tools including the Beck Depression Inventory, Pain Self-Efficacy Questionnaire, and other measures of catastrophe and disability. These data are consistent with a recent report showing that 40% of patients treated with opioids in two major academic pain centers exhibited aberrant behaviors that could be construed as drug seeking or had urine toxicology results inconsistent with reported use of drugs.⁶⁹ These studies underscore the complexities and difficulties inherent in treating patients with noncancer chronic pain.

Other problems in attempting to define efficacy in this group include the fact that there are only case series reporting the efficacy of intraspinal opioids in patients with nonmalignant pain and not the same overwhelming evidence of efficacy as exists for SCS. There are no studies with a control group comparison. There are few accurate descriptions of the incidence of continued use of supplemental oral opioids in patients receiving neuraxial opioids. Patients have not been stratified into etiologies of pain. Measurement of outcomes is largely unsatisfactory in all published studies. An expert panel recently produced an evidence-based review of the literature on intrathecal drug delivery, and their conclusion was that further study is warranted.⁷⁰

It has been suggested that there are not enough data at this time to warrant the use of intraspinal opioids for nonmalignant pain. The likely real truth is that there are criteria that can be applied to select patients with specific painful conditions who are likely to respond to intraspinal opioid therapy. Patients with chronic pain are a heterogeneous, not a homogeneous, group. These conditions and criteria need to be defined.

The literature addressing the efficacy of intraspinal opioids for the relief of pain has continued to expand since 1980 when Bromage and colleagues⁷¹ showed clearly that narcotics administered epidurally were capable of providing profound postoperative analgesia. Although postoperative and other short-term catheters for acute pain can be placed epidurally, catheters placed for cancer or long-term chronic pain conditions should be placed intrathecally. Catheter migration from the epidural to intrathecal space has been reported and can result in massive overdose and diffusion conditions across the dura/arachnoid membrane and can be affected by conditions such as carcinomatous meningitis or other inflammatory conditions, which can result in severe pain from a decrease in drug reaching the intrathecal space. For these reasons, catheters for implanted devices will typically be placed in the subarachnoid space.

Advantages of implanted systems include a decreased incidence of infection compared with percutaneous systems, increased patient comfort, and greater patient convenience. One model of care is to use an implanted system in patients with a life expectancy of greater than 3 months and to use an externalized percutaneous system in other patients.

The gold standard infusate for opioids administered via an implanted intraspinal device is morphine. Drug selection is a complex issue requiring knowledge and experience. Clinical guidelines for drug selection are shown in Fig. 129-6, and physiologic guidelines are outlined in Table 129-1.⁷² Morphine can be maximally concentrated to approximately 50 mg/ml and is commercially available at a concentration of 25 mg/ml. Hydromorphone is commonly used in spinally administered opioid infusion devices and is available in a concentration of 10 mg/ml. Clinicians can mix either morphine or hydromorphone (or another opioid) with bupivacaine in an attempt to manage severe neuropathic or somatic incident pain. Unfortunately, the maximal concentration of available bupivacaine is 40 mg/ml, limited by solubility, which may necessitate refilling the devices as often as monthly. The limiting factor is the size of the pump reservoir, which is only 18 ml in available programmable devices. Patients receiving bupivacaine infusion in their implanted devices often need to have refills on a monthly basis, whereas patients receiving opioid alone will usually require refills only every 90 days. Stability data for morphine in implanted pumps ensure stability for only 90 days.

FIGURE 129-6 Clinical guidelines for drug selection for intraspinal infusion.

(From Hassenbusch SJ, Portenoy RK, Cousins M, et al. Polyanalgesic consensus conference 2003: an update on the management of pain by intraspinal drug delivery—report of an expert panel. J Pain Symptom Manage. 2004;27:546-563.)

Clonidine has been approved by the U.S. Food and Drug Administration for intraspinal delivery and is useful in managing refractory neuropathic pain, as are the local anesthetics. The limitation again with clonidine is a concentration factor requiring frequent refills of implantable devices when this agent is used. Clonidine is commercially available in a 100-μg/ml concentration, and patients will frequently require this amount and more on a daily basis. Compounding pharmacies can often provide much more potent concentrations limited only by solubility. There is evidence of synergy when the combination of clonidine and opioid is used as well as when opioid and bupivacaine are used together. Some practitioners use triple analgesic intraspinal therapy, particularly in patients with cancer, and combinations of morphine, bupivacaine, and clonidine are employed.

Baclofen is an extremely useful agent in the treatment of refractory spasticity. Sufentanil, fentanyl, ketamine, and meperidine are also reportedly used in implanted devices, but, again, there are no safety or efficacy data for these agents in these devices.

Both programmable and continuous flow rate devices are available for implantation in the United States. Programmable devices offer the advantage of the ability to change doses by adjusting flow rates. Continuous infusion devices require refilling with a different drug concentration to alter doses. Continuous infusion devices are not substantially less expensive than programmable devices, although they are available with larger reservoirs for drug and may enable longer refill intervals.

Trial, Implantation, and Complications

Before permanent implantation, it is generally accepted that a trial for responsiveness and tolerability is mandatory. Trials can be done by continuous infusion or bolus injection, with patients as inpatients or outpatients, and with drug administered epidurally or intrathecally for as short a period of time as 1 day, a single intrathecal bolus, or as long as 60 days. A recent comparison of a single intrathecal bolus of morphine versus as long as 4 days of continuous epidural infusion of morphine showed no difference in outcome.⁷³ Whatever the method or rationale for a trial, it is imperative that the trial be adequate to satisfy the physician’s assessment of potential efficacy and tolerability. An arbitrary reduction in pain that has been selected by most practitioners is a 50% reduction in pain. This degree of reduction is necessary to define a trial sufficient to demonstrate the efficacy of an opioid.

The implantation procedure is done in the operating room with an anesthesiologist present to monitor the patient. Before moving the patient to the operating room, the patient is examined, and, while the patient is standing, the skin is marked at the site where the pump pocket will be placed. This should be below the costal margin and above the belt line if possible.

The patient is then carefully positioned laterally on the operating table so that the pump pocket side of the abdomen is up, and the patient is prepped such that the surgical team will have access to both the abdomen and the back where the catheter is to be inserted. Patients are administered antibiotic prophylaxis, usually with cefazolin, and sedation. The patient should preferably be awake enough to report pain should the placement needle touch a nerve root or spinal cord.

The procedure is well described by an experienced group of implanters attempting to reach a consensus on the best technique, with special attention to a low technical complication rate.⁷⁴ Complications addressed included catheter dislodgment and migration, fracture, kink or occlusion, cut or puncture, disconnect, and leak.

Other complications related to drug infusion devices have been described by Krames.⁷⁵ Surgical complications include bleeding, infection, pump pocket seroma, cerebrospinal fluid leak, cerebrospinal fluid hygroma, postdural puncture headache, and improper pocket placement. Catheter tip fibroma formation has been reported and is discussed further. Catheter tip epidermoid tumors can occur if epidermal cell are delivered into the subarachnoid space when accessing via the epidural needle. A small skin incision with a scalpel blade is necessary before inserting the epidural needle to prevent this complication.

The prevalence of catheter tip inflammatory masses or fibromas is a topic of controversy and importance. Although initially thought to be a rare occurrence, the prevalence may be as high as 1%. Spinal cord compression and permanent neurologic injury has been reported. The formation of these tumors is thought to be a direct response to opioid infusion and has been reported with both morphine and hydromorphone at the full range of doses. The occurrences are not limited to just high-dose infusions. There have been no reports of inflammatory catheter tip masses with infusions of baclofen alone or bupivacaine alone, but there is a report of occurrence with a bupivacaine/morphine infusion. The policy at Dartmouth Hitchcock Medical Center is to obtain an annual screening computed tomography scan to identify the catheter tip and fine-cut magnetic resonance imaging at the catheter tip level to assess for the presence of a mass. There are reports in the literature of spontaneous regression of masses when infusions are stopped, but if neurologic injury has occurred, consensus exists that they should be excised.

Catheter tip fibromas and epidermoid tumors may require excision and explantation of the catheter. Patients with increased pain or new neurologic deficits occurring some time after implantation should undergo magnetic resonance imaging to identify these treatable complications.

Mechanical problems include catheter kinking, catheter obstruction, catheter dislodgment, catheter disconnection, pump failure, and pump battery depletion. The first indication of a mechanical problem is an increase in the patient’s pain. This has to be distinguished from development of tolerance or progression of disease. Pharmacologic complications include opioid-induced nausea and vomiting, urinary retention, pruritus, or inadequate analgesia. Nausea and vomiting, urinary retention, and pruritus should have been identified during the trial, but occasionally they will occur when increasing doses in an attempt to treat tolerance or control pain. These symptoms can be pharmacologically managed most of the time. If they cannot be managed, then a change to a different opioid can be attempted. Tolerance can also be managed by the addition of another agent such as a local anesthetic or clonidine.

It is imperative to follow careful technique when refilling these devices. The recommended technique for a programmable device is to expose the pump and surrounding areas completely and to cleanse with Betadine three times. A sterile fenestrated drape is then placed over the pump access site. Sterile gloves are used by the practitioner. The pump is palpated, and the desired access port is carefully identified. Templates can be used to aid in identifying these sites. A 22-gauge Huber (noncoring) needle is used to access the center port. Once accessed, the pump should be gently aspirated and the remaining fluid removed. The amount of fluid aspirated from the pump should reflect the amount described on interrogation of the pump by the programming computer in a programmable device. Five milliliters of refill solution should then be gently injected into the pump. Five milliliters should then be aspirated out, confirming the intrapump needle position.

The volume of solution representing the capacity of the pump should then be injected. The pump can then be reprogrammed to reflect the full reservoir volume. It is imperative that all these steps be followed when refilling the device. It is possible for even the most experienced practitioner to instill fluid subcutaneously. Occasionally, a thick fibrous capsule can form around implanted pumps, particularly pumps without the Dacron pouch, and passing the Huber needle through the fibrous capsule can feel the same as passing the needle through the rubber access port.

For a more thorough and recent review of neuraxial medication delivery including a literature review, indications, comparison of techniques, comparison of different types of pumps, and a synopsis of troubleshooting, the reader is referred to Prager.⁷⁶

Summary

Spinal cord stimulation and the use of intraspinal infusion systems for cancer and chronic pain are efficacious, cost effective, and integral tools in the armamentarium of anyone treating cancer or chronic pain. Patient selection, improvement in systems, increased safety, and the development of new drugs are targets for future work.