Chronic pain medical treatment guidelines



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Implantable spinal cord stimulators
See Spinal Cord Stimulators (SCS)
Injection with anaesthetics and/or steroids [DWC]
See Epidural steroid injections (ESI’s), Lumbar sympathetic block, Trigger point injections, Stellate ganglion block, and Prolotherapy.
Interdisciplinary rehabilitation programs
See Chronic Pain Programs
Interferential Current Stimulation [DWC]
See Transcutaneous Electrotherapy [DWC]
Intrathecal drug delivery systems (IDDSs)
See Implantable drug-delivery systems (IDDSs).
Intrathecal drug delivery systems, medications
Recommended as indicated below. (The following recommendations were made prior to FDA approval of ziconotide.) (Hassenbusch, 2004)
Recommended 1st stage: Morphine is generally the initial IDDS medication. The maximum recommended dose for this drug is 15 mg/day with a concentration of 30 mg/mL. An alternative non-FDA approved medication is hydromorphone. The maximum recommended dose for this medication is 10 mg/day with a concentration of 30 mg/mL. Other opioids (including Fentanyl and Sufentanil) have been used for intrathecal chronic non-malignant pain but are non-FDA approved and have little research associated with their use. (Waara-Wolleat, 2006)
Recommended 2nd stage: If side effects occur, an upper limit of dosing is reached, or neuropathic pain is present, clonidine is next recommended as an addition to an opioid (maximum recommended dose of 1 mg/day and a concentration of 2 mg/mL). Bupivacaine has also been recommended as an alternative to clonidine (maximum dose of 30 mg/day and a concentration of 38 mg/mL). Clonidine, which is FDA approved for intrathecal delivery, is thought to provide analgesic effect via a non-opioid mechanism. It has been found to offer only short-term relief when used as a single agent.
Recommended 3rd stage: The recommendation has been made to add both clonidine and bupivacaine. Baclofen has been used to treat intractable spasticity from brain injury, cerebral palsy, and spinal cord injury and has resulted in improvement in muscle tone and pain relief. (Guillaume, 2005) See also Ziconotide (Prialt®). Recommended after documentation of a failure of a trial of intrathecal morphine and hydromorphone. The 2007 Polyanalgesic Consensus Conference Recommendations for the Management of Pain by Intrathecal Drug Delivery concluded that ziconotide should be updated to a first-line intrathecal drug.). This recommendation was published in a non peer reviewed journal and the conference was sponsored by Elan Pharmaceuticals. (Deer, 2007)
Intrathecal pumps
See Implantable drug-delivery systems (IDDSs).
Intravenous regional sympathetic blocks (for RSD, nerve blocks) [DWC]
Not recommended. However, if other treatments are contraindicated (e.g. when a stellate ganglion block cannot be done due to bleeding diasthesis) intravenous regional blocks may be performed. IV regional blocks, also known as Bier blocks, are not commonly done for RSD. Although there is no scientific evidence to support this treatment, it is recommended as an option in certain cases when there are no other alternatives. When the procedure is performed, it must be done in conjunction with a rehabilitation program. There is no role for intravenous regional sympathetic blocks for the diagnosis of RSD.
Ketamine [DWC]
Not recommended. There is insufficient evidence to support the use of ketamine for the treatment of chronic pain.
Ketoprofen
See NSAIDs (non-steroidal anti-inflammatory drugs)
Lamotrigine (Lamictal®)
See Anti-epilepsy drugs (AEDs) for general guidelines, as well as specific Lamotrigine listing.
Levetiracetam (Keppra®)
See Anti-epilepsy drugs (AEDs) for general guidelines, as well as specific Levetiracetam Listing listing.
Lidocaine (anesthetic)
See CRPS, medications; CRPS, sympathetic and epidural blocks; Topical analgesics.
Low-Level Laser Therapy (LLLT)
Not recommended. There has been interest in using low-level lasers as a conservative alternative to treat pain. Low-level lasers, also known as "cold lasers" and non-thermal lasers, refer to the use of red-beam or near-infrared lasers with a wavelength between 600 and 1000 nm and wattage from 5-500 milliwatts. (In contrast, lasers used in surgery typically use 300 Watts.) When applied to the skin, these lasers produce no sensation and do not burn the skin. Because of the low absorption by human skin, it is hypothesized that the laser light can penetrate deeply into the tissues where it has a photobiostimulative effect. One low-level laser device, the MicroLight 830 Laser, has received clearance for marketing from the U.S. Food and Drug Administration (FDA) specifically for the treatment of carpal tunnel syndrome. Other protocols have used low-level laser energy applied to acupuncture points on the fingers and hand. This technique may be referred to as "laser acupuncture." Given the equivocal or negative outcomes from a significant number of randomized clinical trials, it must be concluded that the body of evidence does not allow conclusions other than that the treatment of most pain syndromes with low level laser therapy provides at best the equivalent of a placebo effect. (Naeser, 2002) (Gur, 2002) (Basford, 1999) (Conti, 1997) (de Bie, 1998) (BlueCross BlueShield, 2005) Low Level Laser Therapy (LLLT) was introduced as an alternative non-invasive treatment for Osteoarthritis (OA) about 20 years ago, but its effectiveness is still controversial. For OA, the results are conflicting in different studies and may depend on the method of application and other features of the LLLT application. Despite some positive findings, data is lacking on how LLLT effectiveness is affected by four important factors: wavelength, treatment duration of LLLT, dosage and site of application over nerves instead of joints. There is clearly a need to investigate the effects of these factors on LLLT effectiveness for OA in randomized controlled clinical trials. (Brosseau-Cochrane, 2004) This meta-analysis concluded that there are insufficient data to draw firm conclusions about the effects of LLLT for low-back pain compared to other treatments, different lengths of treatment, different wavelengths and different dosages. (Yousefi-Nooraie-Cochrane, 2007)
Lumbar sympathetic block
Recommended as indicated below. Useful for diagnosis and treatment of pain of the pelvis and lower extremity secondary to CRPS-I and II. This block is commonly used for differential diagnosis and is the preferred treatment of sympathetic pain involving the lower extremity. For diagnostic testing, use three blocks over a 3-14 day period. For a positive response, pain relief should be 50% or greater for the duration of the local anesthetic and pain relief should be associated with functional improvement. Should be followed by intensive physical therapy. (Colorado, 2002)
Magnet Therapy
Not recommended. Biomagnetic therapy is considered investigational. The data from randomized, placebo-controlled clinical trials fails to demonstrate that biomagnetic therapy results in improved health outcomes for any type of pain. Biomagnetic therapy has been proposed for the relief of chronic painful conditions; it is proposed that magnets, worn close to the skin, create an electromagnetic field within the body that suppresses pain. The theory is that the magnetic field causes potassium channels to be stimulated, producing repolarization or hyperpolarization. Biomagnetic therapy has been investigated for various types of pain, including peripheral neuropathy, chronic low back pain, carpal tunnel syndrome, plantar heel pain and hip and knee pain due to osteoarthritis. (BlueCross BlueShield, 2005)
Manual therapy & manipulation
Recommended for chronic pain if caused by musculoskeletal conditions and manipulation is specifically recommended as an option for acute conditions. Manual Therapy is widely used in the treatment of musculoskeletal pain. The intended goal or effect of Manual Medicine is the achievement of positive symptomatic or objective measurable gains in function that facilitate progression in the patient's therapeutic exercise program and return to productive activities. Manipulation is manual therapy that moves a joint beyond the physiologic range-of-motion but not beyond the anatomic range-of-motion.
Treatment Parameters from state guidelines
a. Time to produce objective functional gains: 3-5 treatments

b. Frequency: 1-5 supervised treatments per week the first 2 weeks, decreasing to 1-3 times per week for the next 6 weeks, then 1-2 times per week for the next 4 weeks, if necessary.

c. Optimum duration: Treatment beyond 3-6 visits should be documented with objective improvement in function. Palliative care should be reevaluated and documented at each treatment session. (Colorado, 2003)
Marijuana
See Cannabinoids
Medications for acute pain (analgesics)
Recommended as indicated below. Pharmacologic agents are the main treatment of acute pain.\

Acetaminophen is the initial choice for treatment of acute pain in a dose of 1,000 mg. A recent study found that in a single dose, aspirin was similar to acetaminophen (mg to mg comparison) for treatment of acute pain, although aspirin is more likely to produce GI side effects. (Edwards, 2006) (Sachs, 2005) The maximum daily dose of acetaminophen is 4,000 mg. There should be caution about daily doses of acetaminophen and liver disease if over 4,000 mg per day or in combination with other NSAIDs. (Watkins, 2006)


NSAIDs are superior to acetaminophen for some types of pain, and can provide analgesia similar to opioids in some settings, including post-operatively. (Mason, 2006) They suffer from a ceiling effect above which no additional analgesic effect can be obtained. They also suffer from side effects such as GI disturbance, renal dysfunction, increased edema, and increased blood pressure. NSAIDs, and the Cox-2 NSAIDS in particular, also are associated with thrombotic cardiovascular events.
Opioids are appropriate analgesics for somatic, neuropathic and visceral pain. Hydrocodone is considered the most potent oral opioid that does not require special documentation for prescribing in some states (not including California). (Quigley, 2006) Side effects include sedation, nausea, vomiting and constipation. There is no evidence that supports the addition of pentazocine (Talwin) or butorphanol (Stadol) to decrease side effects. (Sachs, 2005) This study found a a negative association between receipt of early opioids for acute LBP and outcomes (disability duration, medical costs, subsequent surgery), but severity was also a strong predictor (confounding variable) of all the outcomes and may explain the early opioid use. (Webster, 2007) Tramadol is not recommended as a first-line oral analgesic because of its inferior efficacy to a combination of Hydrocodone/ acetaminophen. There is also no evidence that it has a safer adverse event profile. (Turturro, 1998)
Medications for subacute & chronic pain
There are few studies of the use of medications in the subacute period (7 to 12 weeks) or chronic period of pain treatment. Relief of pain with the use of medications is generally temporary, and measures of the lasting benefit from this modality should include evaluating the effect of pain relief in relationship to improvements in function and increased activity. Before prescribing any medication for pain the following should occur: (1) determine the aim of use of the medication; (2) determine the potential benefits and adverse effects; (3) determine the patient’s preference. Only one medication should be given at a time, and interventions that are active and passive should remain unchanged at the time of the medication change. A trial should be given for each individual medication. Analgesic medications should show effects within 1 to 3 days, and the analgesic effect of antidepressants should occur within 1 week. A record of pain and function with the medication should be recorded. (Mens, 2005) The recent AHRQ review of comparative effectiveness and safety of analgesics for osteoarthritis concluded that each of the analgesics was associated with a unique set of benefits and risks, and no currently available analgesic was identified as offering a clear overall advantage compared with the others. (Chou, 2006) There are multiple medication choices in the Procedure Summary. See Anticonvulsants for chronic pain; Antidepressants for chronic pain; Antidepressants for neuropathic pain; Antidepressants for non-neuropathic pain; Anti-Inflammatories; Benzodiazepines; Boswellia Serrata Resin (Frankincense); Cannabinoids; Capsaicin; Cod liver oil; Curcumin (Turmeric); Cyclobenzaprine (Flexeril®); Duloxetine (Cymbalta®); Gabapentin (Neurontin®); Glucosamine (and Chondroitin Sulfate); Green tea; Herbal medicines; Implantable drug-delivery systems (IDDSs); Injection with anaesthetics and/or steroids; Intrathecal drug delivery systems, medications; Intravenous regional sympathetic blocks (for RSD, nerve blocks); Ketamine; Methadone; Milnacipran (Ixel®); Muscle relaxants; Nonprescription medications; NSAIDs (non-steroidal anti-inflammatory drugs); NSAIDs, GI symptoms & cardiovascular risk; Opioids (with links to multiple topics on opioids); Pycnogenol (maritime pine bark); Salicylate topicals; Topical analgesics; Uncaria Tomentosa (Cat's Claw); Venlafaxine (Effexor®); White willow bark; & Ziconotide (Prialt®).
Metaxalone (Skelaxin®)
See Muscle Relaxants
Methadone
Recommended for moderate to severe pain. The FDA reports that they have received reports of severe morbidity and mortality with this medication. This appears, in part, secondary to the long half-life of the drug (8-59 hours). Pain relief on the other hand only lasts from 4-8 hours. Vigilance is suggested in treatment initiation, conversion from another opioid to methadone, and when titrating the methadone dose. One severe side effect is respiratory depression (which persists longer than the analgesic effect). Methadone should be given with caution to patients with decreased respiratory reserve (asthma, COPD, sleep apnea, severe obesity). QT prolongation with resultant serious arrhythmia has also been noted. Use methadone carefully in patients with cardiac hypertrophy and in patients at risk for hypokalemia (including those patients on diuretics). Methadone does have the potential for abuse.
Steps for prescribing methadone:
(1) Basic rules

  • Weigh the risks and benefits before prescribing methadone.

  • Avoid prescribing 40 mg Methadone tablets for chronic non-malignant pain. This product is only FDA-approved for detoxification and maintenance of narcotic addiction.

  • Closely monitor patients who receive methadone, especially during treatment initiation and dose adjustments.



(2) Know the information that is vital to give the patient:

  • Don’t be tempted to take more methadone than prescribed if you are not getting pain relief. This can lead to a dangerous build-up that can cause death.

  • All changes in methadone dose should be made by your treating practitioner.

  • Methadone can make your breath slow down, or actually stop.

  • Methadone can slow down your heartbeat and you might not be able to detect this.

  • If you feel like you are having an irregular heartbeat, dizziness, light-headedness or fainting, call your doctor or clinic immediately. (FDA, 2006)

(3) Be familiar with the current SAMHSA health advisory on methadone:



  • The medication has become more accessible to unauthorized users.

  • It can accumulate in potentially harmful doses (especially during the first few days of treatment.

  • There has been a rise in Methadone-associated mortality. (SAMHSA, 2004)

(4) Be familiar with the FDA final policy statement on Methadone that explicitly discusses the topic, “Can Methadone be used for pain control?”
No separate registration is required to prescribe methadone for treatment of pain. (DEA, 2006)
(5) Read the new prescribing information for Methadone and the new patient information section. (Roxane, 2006)
Microcurrent electrical stimulation (MENS devices) [DWC]
See Transcutaneous Electrotherapy [DWC]
Milnacipran (Ixel®) [DWC]
Not Recommended. It is not FDA approved and not available in the US.
Morphine pumps
See Implantable pumps for narcotics.
Multidisciplinary pain programs
See Chronic pain programs.
Muscle relaxants
Recommend non-sedating muscle relaxants with caution as a second-line option for acute LBP and for short-term pain relief in patients with chronic LBP, but benzodiazepines are not recommended. (Mens, 2005) (Van Tulder, 1998) (van Tulder, 2006) (Schnitzer, 2004) Muscle relaxants are a broad range of medications that are generally divided into antispasmodic and antispasticity drugs. (van Tulder, 2006) Antispasmodics are used to decrease muscle spasm in conditions such as LBP. These can be benzodiazepines (See Benzodiazepines) and non-benzodiazepines. Antispasticity drugs are used to decrease spasticity in conditions such as cerebral palsy, MS, and spinal cord injuries. These latter drugs block the sarcoplasmic reticulum calcium channel. Muscle relaxants may be effective in reducing pain and muscle tension, and increasing mobility. However, in most LBP cases, they show no benefit beyond NSAIDs in pain and overall improvement. Also there is no additional benefit shown in combination with NSAIDs. Efficacy appears to diminish over time, and prolonged use of some medications in this class may lead to dependence. (Homik, 2004) Sedation is the most commonly reported adverse effect of muscle relaxant medications. These drugs should be used with caution in patients driving motor vehicles or operating heavy machinery. Metaxalone (Skelaxin®) is reported to be a relatively non-sedating muscle relaxant. Carisoprodol (Soma®) is metabolized to meprobamate, an anxiolytic. There is a school of thought that its main effect is due to generalized sedation. Withdrawal symptoms may occur with abrupt discontinuation. (Reeves, 2003) See Weaning of medications. Soma has been noted to be a street drug of abuse and is often combined with acetaminophen and codeine, a combination labeled as “Soma-Coma”. (Schears, 2004) Cyclobenzaprine (Flexeril®) has similar effects to tricyclic antidepressants. It has a central mechanism of action, but it is not effective in treating spasticity from cerebral palsy or spinal cord disease. See Cyclobenzaprine. Muscle relaxants are effective in acute LBP. Cyclobenzaprine is associated with a number needed to treat of 3 at 2 weeks for symptom improvement and is associated with drowsiness and dizziness. Carisoprodol is also effective but has abuse and dependency potential. Metaxalone and low-dose cyclobenzaprine have fewer adverse effects. (Kinkade, 2007)\
Naproxen
See Anti-inflammatory medications
Narcotics
See Opioids
Norepinephrine serotonin reuptake inhibitors (NSRIs)
See Duloxetine (Cymbalta®); & Milnacipran (Ixel®)
Neuromodulation devices
See Spinal cord stimulators
Neuromuscular electrical stimulation (NMES devices) [DWC]
See Transcutaneous Electrotherapy [DWC]
Neurontin®
See Gabapentin
Nonprescription medications
Recommended. Acetaminophen (safest); NSAIDs (aspirin, ibuprofen). (Bigos, 1999) There should be caution about daily doses of acetaminophen and liver disease if over 4 g/day or in combination with other NSAIDs. (Watkins, 2006) See also NSAIDs (non-steroidal anti-inflammatory drugs).
NSAIDs (non-steroidal anti-inflammatory drugs)
Recommended for acute pain, acute LBP, short-term pain relief in chronic LBP, and short-term improvement of function in chronic LBP. There is no evidence of long-term effectiveness for pain or function. There is conflicting evidence that NSAIDs are more effective that acetaminophen for acute LBP. (van Tulder, 2006) There is inconsistent evidence for the use of these medications to treat long-term neuropathic pain, but they may be useful to treat breakthrough pain in this condition. (Namaka, 2004) See NSAIDs, GI symptoms & cardiovascular risk. See also Anti-inflammatory medications and Medications for acute pain (analgesics).

Besides the above well-documented side effects of NSAIDs, there are other less well-known effects of NSAIDs, and the use of NSAIDs has been shown to possibly delay and hamper healing in all the soft tissues, including muscles, ligaments, tendons, and cartilage. (Maroon, 2006)


NSAIDs, GI symptoms & cardiovascular risk
Recommend with precautions as indicated below.
Clinicians should weight the indications for NSAIDs against both GI and cardiovascular risk factors.
Determine if the patient is at risk for gastrointestinal events: (1) age > 65 years; (2) history of peptic ulcer, GI bleeding or perforation; (3) concurrent use of ASA, corticosteroids, and/or an anticoagulant; or (4) high dose/multiple NSAID (e.g., NSAID + low-dose ASA). Recent studies tend to show that H. Pylori does not act synergistically with NSAIDS to develop gastroduodenal lesions.
Patients with no risk factor and no cardiovascular disease: Non-selective NSAIDs OK (e.g, ibuprofen, naproxen, etc.)
Patients at intermediate risk for gastrointestinal events and no cardiovascular disease: (1) A non-selective NSAID with either a PPI (Proton Pump Inhibitor, for example, 20 mg omeprazole daily) or misoprostol (200 µg four times daily) or (2) a Cox-2 selective agent. Long-term PPI use (> 1 year) has been shown to increase the risk of hip fracture (adjusted odds ratio 1.44).
Patients at high risk for gastrointestinal events with no cardiovascular disease: A Cox-2 selective agent plus a PPI if absolutely necessary. (Laine, 2006) (Scholmerich, 2006) (Nielsen, 2006) (Chan, 2004) (Gold, 2007)
Cardiovascular disease: A non-pharmacological choice should be the first option in patients with cardiac risk factors. It is then suggested that acetaminophen or aspirin be used for short-term needs. An opioid also remains a short-term alternative for analgesia. If long-term or high-dose therapy is required, naproxen appears to be the preferred choice of NSAID. Progressive medications include introducing an NSAID with Cox-2 activity. Cardiovascular risk does appear to extend to all non-aspirin NSAIDs, with the highest risk found for the Cox-2 agents. (Johnsen, 2005) (Lanas, 2006) (Antman, 2007)
Use with Aspirin for cardioprotective effect: The GI protective effect of Cox-2 agents is diminished in patients taking low-dose aspirin. (Laine, 2007) Ibuprofen appears to attenuate the antiplatlet effect of enteric-coated aspirin and should be taken 30 minutes after ASA or 8 hours before. (Antman, 2007)
Use of NSAIDs and SSRIs: The concurrent use of SSRIs and NSAIDs is associated with moderate excess relative risk of serious upper GI events when compared to NSAIDs alone. This risk was higher for non-selective NSAIDs when compared to Cox-2 selective agents (adjusted odds ratio of 1.77 and 1.33, respectively). (Helin-Salmivaara, 2007)
Nucleoplasty
Not recommended. Given the extremely low level of evidence available for Nucleoplasty (Coblation Nucleoplasty), and the lack of clinical trials, it is recommended that this procedure be regarded as experimental at this time. (Manchikanti, 2003) (Boswell, 2007) (ArthroCare Corp, Sunnyvale, CA, introduced the Micro DisCoblator in 2003 to enable minimally invasive disc decompression. Total 2003 Revenue $119 million. Company literature: “The Nucleoplasty procedure uses a minimally-invasive catheter to create a pathway into the disc. Radio wave signals are sent through the transmitter into the nucleus of the herniated disc. The radio waves produce a low-temperature ionized gas that breaks up molecular bonds in the spongy nucleus, removing tissue volume. The Nucleoplasty procedure uses an FDA-cleared device, and is a clinically proven treatment with over 20,000 patients treated.”)
Number needed to treat (NNT) Recommended as a measure of absolute risk in evaluating drug therapies. This is the average number of patients that need to be treated in order to have improvement in one patient. As an example, for every 4 patients treated with neuropathic pain, pain relief described as good is found in 1 patient. The NNT is a useful and relatively simple tool for practicing evidence-based medicine. This calculation can be applied to intervention studies and reflects the number of additional patients who need to receive an intervention to prevent 1 additional outcome. In this recent study, using NNT was superior to achieve participant consent versus other explanations. (Halvorsen, 2007)
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