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19 Articles in Volume 14, Issue #9
10 Must Have Devices for Your Practice
1. Extracorporeal Shockwave Therapy
2. Pulsed Electromagnetic Fields
3. Class IV Laser
4. H-Wave Electrotherapy
5. Interferential Current Therapy
6. Class IIIb Cold Laser-Auriculotherapy
7. Shortwave Diathermy
8. Microcurrents
9. Infrared Phototherapy
10. Transcutaneous Electrical Neuromuscular Stimulation
Pain and Sleep: Understanding the Interrelationship
The Role of Endogenous Morphine and Nitric Oxide in Pain Management
Treating Pain in Patients With Chronic Kidney Disease: A Review of the Literature
Notalgia Paresthetica: An Enigmatic Condition
Preparing Patients Taking Sublingual Buprenorphine to Treat Addiction for Surgery
Editor's Memo: PAINWeek Going Forward Together
Introducing Practical Pain Management’s Newest Editorial Board Members
Ask the Expert: What are the products to prevent NSAID-related peptic ulcers?

Treating Pain in Patients With Chronic Kidney Disease: A Review of the Literature

Seventy percent of the 20 million people in the United States with chronic kidney disease report having pain. The presence of pain in these patients is association with lower quality of life, including lower functional capacity.

Patients with chronic kidney disease (CKD) often suffer from chronic pain. It may be difficult to select appropriate analgesic therapy in this population because many patients require complex medication management for the comorbidities that accompany renal disease. A reduced glomerular filtration rate (GFR) alters the normal pharmacokinetics of analgesic medications and increases the potential for toxicity, undesirable side effects, and drug interactions. Appropriate analgesic selection, dose titration, and monitoring are critical for the successful management of this population.

The Problem

More than 20 million people in the United States have CKD, including approximately 33% of adults with diabetes and 20% of adults with high blood pressure.1,2 In a recent study, 70% of CKD patients reported pain.3 Pain has been reported to be the most common symptom experienced by CKD patients, and often it is undertreated.4,5 The presence of pain in patients with moderate to severe CKD was found to be associated with lower quality of life (QOL) scores compared to the general population.3 Reduced QOL restrict patients’ functional capacity and impairs their social abilities.6 Reduced QOL may have negative effects on body mass index, blood pressure, pain levels, and medication use.7

Determining the cause of pain in patients with CKD is necessary for appropriate treatment. Aside from common causes of pain in the general population, patients with CKD have multifactorial (ischemic, neuropathic, bone, and musculoskeletal) pain conditions associated with their disease.8 They may experience pain caused by primary disease (polycystic kidney disease), bone disease (osteitis fibrosa cystica, osteomalacia, and 2-microglobulin amyloidosis), renal failure (uremic neuropathy and calciphylaxis), and comorbid conditions (cardiovascular disease, ischemic or diabetic neuropathy, and peripheral vascular disease).

Effective pain management in this population is hampered because primary care providers and nephrologists receive limited training in the assessment and treatment of chronic pain. Many physicians fail to consider the altered pharmacokinetics and adverse effects of medications in the setting of renal disease.8

Analgesic Selection

The World Health Organization (WHO) established a 3-step ladder for cancer pain management in 1986 (Table 1). Although there are no specific guidelines for the management of pain in patients with renal disease, the WHO model has been used as a guideline for the management of cancer and noncancer pain.9 The first step of pharmacologic intervention for mild pain usually employs the use of non-opioid analgesics such as acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs). For moderate levels of pain, the second step includes the addition of schedule II opioids such as codeine and hydrocodone. Tramadol may be introduced at this step. In cases where pain persists despite the use of lower-potency opioids, or if the pain is severe, the third step involves the addition of morphine, oxycodone (OxyContin, Roxicodone, others), hydromorphone (Dilaudid, Exalgo, others), methadone (Dolophine, Methadose, others), or fentanyl (Duragesic, Subsys, others).10,11

Adjuvant analgesics may be added at any step of the WHO ladder based upon the nature and etiology of the pain. In general, adjuvant agents include antidepressants for chronic pain conditions, corticosteroids for inflammatory diseases, anticonvulsants for neuropathic pain, muscle relaxants for pain associated with muscle spasm, and bisphosphonates for bone pain that is associated with metastatic disease.10,12

The selection of analgesics should involve consideration for the type of pain, severity, anticipated duration of treatment, side effects, and interactions with other medications. The ability to recognize the nature of pain is necessary for tailoring effective analgesic therapy. Somatic pain, which is characterized as achy and localizable, often responds well to NSAIDs and opioids. Visceral pain, which is usually deep and poorly localized, may respond to opioids, but in some instances opioids may exacerbate an underlying problem, such as a bowel obstruction. Neuropathic pain, which is characterized as burning or lancinating in nature, is frequently associated with tingling, numbness, and sensory deficits. Neuropathic pain is less responsive to opioids and more responsive to anticonvulsant and antidepressant agents.13 


Acetaminophen (Tylenol, others) is one of the most commonly prescribed medications. It is well known for its analgesic and antipyretic properties. It is recognized as a peripherally acting analgesic, although its true mechanism of action remains unclear.13 Acetaminophen has minimal anti-
inflammatory effects. It is associated with weak inhibition of cyclooxygenase (COX) enzyme isoforms COX-1 and 2.14

Since 1996, the National Kidney Foundation has supported the use of acetaminophen as the non-narcotic agent of choice for episodic treatment of mild to moderate pain in patients with CKD.7 Acetaminophen is a good analgesic for patients with advanced CKD and end-stage renal disease (ESRD), because it does not result in platelet inhibition or gastrointestinal irritation.13

It has been reported that acetaminophen may be safe to use in patients with advanced CKD, stages 4–5, without increasing the disease progression rates.15 Acetaminophen is metabolized by the liver and does not require dose adjustment in the presence of CKD. It is important to recognize that acetaminophen frequently is combined with low-potency narcotics and is found in many over-the-counter medications. The concurrent use of multiple acetaminophen-containing medications may place patients with CKD at risk for liver failure.16 Table 2 provides the recommended acetaminophen dosage reduction for patients with reduced glomerular filtration rate (GFR).17


NSAIDs inhibit prostaglandin synthesis through their effects on COX enzymes.18 COX-1 is expressed in many tissues, most notably the gastrointestinal mucosa. COX-2 is expressed primarily in locations of inflammation.19 Through these pathways, NSAID use may lead to inhibition of platelet function and irritation of the gastrointestinal mucosa, which increase the risk for bleeding, especially in patients who are uremic.13 NSAIDs are associated with direct nephrotoxic effects that include a significant decrease in GFR and renal vasoconstriction mediated by renal prostaglandin inhibition. They have been known to cause interstitial nephritis, nephrotic syndrome, and membranous glomerulonephropathy, among other conditions.13,20,21 NSAIDs have been associated with hypertension, hyponatremia, and edema due to their effects on distal renal sodium reabsorption and antidiuretic hormone secretion.13 In a meta-analysis, the hypertensive effect of NSAIDs was demonstrated to be greater for patients with pre-existing hypertension compared to patients without it.22

Use of COX-2 selective agents (coxibs, Celebrex) is thought to be associated with reduced risk for gastrointestinal and hematologic effects. Published trials comparing the effects of selective COX-2 agents against nonselective agents have excluded patients with clinically significant CKD.23,24 The gastrointestinal and hematolgoic effects of COX-2 inhibitors in vulnerable patients with ESRD has, therefore, not been established.13 Cardiovascular death in the ESRD population is a concern associated with the use of COX-2 inhibitors.25 ESRD patients with coronary artery disease should not receive COX-2 inhibitors.

Given the many risks associated with NSAIDs, they should be limited to specific indications (acute pain) and short-term use (3 to 7 days). A good example of short-term use would be for the control of symptoms associated with an acute gout flare. The time between doses should be extended as much as possible, to limit risks and side effects. NSAIDs with a half-life longer than 12 hours (i.e. meloxicam, naproxen) should be avoided because they can decrease renal blood flow, causing significant depression in GFR and acute renal failure, as well as life-threatening hyperkalemia.26


When a patient with ESRD is experiencing moderate to severe pain that persists despite treatment with non-opioids, the potential benefits of opioid medications should be considered.27 As with other pain medications, the pharmacokinetics of opioids are altered in renal failure. Most opioids are metabolized by the liver and excreted by the kidneys, so dosage adjustments often is required in patients with CKD and lower GFR rates. Here we will cover the most commonly used opioids and their recommended usage:

  • Recommended with caution: hydromorphone, fentanyl, tramadol, oxycodone, and buprenorphine
  • Recommended with caution, short-term use: morphine
  • Not recommended: codeine and meperidine


Morphine sulfate is one of the oldest naturally occurring opiates, and, therefore, is one of the most well studied opioid medications. Practitioners commonly use morphine as a standard to which other opioid medications are compared. Morphine is primarily metabolized in the liver to its primary metabolites morphine-3-glucuronide (M3G), morphine-6-glucuronide (M6G), and normorphine. It is subject to extensive first-pass metabolism, resulting in an oral bioavailability of less than 40%.28 All metabolites are primarily excreted in the urine, with up to 10% excreted unchanged. In renal failure, these metabolites are known to accumulate, leading to adverse events including myoclonus and respiratory depression.29-32 There have been case reports suggesting that patients with ESRD may be at greater risk for morphine-induced central nervous system (CNS) complications and respiratory depression.33 M3G has been shown to antagonize morphine-induced analgesia, leading to poor pain control.34,35 M6G accumulates in patients with renal failure and may cause respiratory depression. In patients with ESRD, the half-life of M6G is approximately 50 hours, compared to 3 to 5 hours in patients with normal renal function.36 Sustained release morphine formulations can have half-lives that exceed 10 hours, and so extra care should be taken when they are used. 37


Codeine is a naturally occurring methylated morphine. It is considered to be a weak opioid analgesic. Codeine commonly is used for mild to moderate pain, and it also is used as an antitussive. It is hepatically metabolized via cytochrome P450 (CYP450) to codeine-6-glucuronide, norcodeine, morphine (approximately 10%), M3G, M6G, and normorphine.38 Guay et al found that codeine and its metabolites had significantly longer half-lives in patients on hemodialysis.39 The normal half-life of codeine’s major metabolites is approximately 2.5 hours, whereas it is nearly 13 hours in patients with ESRD.36 Codeine use in renal failure patients has been associated with CNS depression and respiratory arrest.40,41 Additionally, codeine is not removed in patients on hemodialysis.36 Given the potential toxicity of codeine in patients with renal failure, its usage is not recommended.


Oxycodone is a semi-synthetic opioid indicated for the treatment of moderate to severe pain. It is available in short- and long-term formulations, and in combination products containing NSAIDs or acetaminophen. It is hepatically metabolized, via CYP450, to its primary metabolites noroxycodone and oxymorphone, with less than 10% excreted unchanged in the urine.36 Noroxycodone is thought to be inactive. However, oxymorphone (Opana, others) is a potent opioid analgesic. Its half-life is 2 to 4 hours in normal healthy patients, and is prolonged to 3 to 5 hours in patients with ESRD. Kirvela et al showed that the mean half-life of oxycodone and its metabolites was prolonged in patients with ESRD who were uremic.42

Given the reduced excretion of oxycodone metabolites, and the potential for CNS toxicity, reduced dosing is recommended. Bunn and Ashley recommend starting with the lowest dose in patients with a GFR <10 mL/min,
and increasing as tolerated to an effective dose.36 Long, however, recommends starting with 75% of the normal dose of oxycodone in patients with a GFR between 10 to 50 mL/min, and 50% dose of the normal dose in patients with a GFR <10 mL/min.43 Bunn and Ashley recommend dosing patients on hemodialysis as you would patients with a GFR <10 mL/min. These cautions should be applied to long-acting preparations and to oxymorphone.36


Hydrocodone, a semi-synthetic opioid, is derived from codeine. It is most often prescribed as a combination product with acetaminophen (Vicodin, others). The US Food and Drug Administration (FDA) recently approved an extended-release formulation called Zohydro that does not contain acetaminophen. This approval has come under some scrutiny due to concerns about the potential for misuse and abuse.44 While no definitive recommendations exist at this time, since hydrocodone is hepatically metabolized (via CYP450) to hydromorphone, it would be prudent to follow guidelines similar to those for hydromorphone.


Hydromorphone (Dilaudid, Exalgo, others) is a potent semi-synthetic opioid (hydrogenated ketone of morphine) that is 5 to 7 times more potent than morphine. Hydromorphone is metabolized in the liver to its primary metabolites hydromorphone-3-glucuronide (H3G), dihydromorphine, and dihydroisomorphine.These metabolites are excreted through the urine. In 2001, Durnin et al studied the effects of renal impairment on the pharmacokinetics of hydromorphone. They showed impaired elimination of hydromorphone metabolites in patients with moderate to severe renal impairment compared to healthy individuals.45 Additionally they showed that hemodialysis was effective at reducing plasma levels of hydromorphone.45 Babul et al also reported the accumulation of metabolites in CKD patients.46 The buildup of metabolites, particularly H3G, which is similar to morphine’s M3G, could lead to neuroexcitation and cognitive impairment.36 In a retrospective study, Lee et al showed improved side-effect profiles (decreased cognitive/drowsiness/nausea effects) in 80% of patients with CKD switched from another opioid to hydromorphone.47 Patients with CKD treated with hydromorphone should have dosing adjustments according to their level of renal impairment.


Meperidine (Demerol, others), the first synthetic opioid, was introduced into the market in 1932. It is metabolized in the liver to its primary active metabolite normeperidine. Normeperidine is a proconvulsant metabolite with neuroexcitatory properties that are observed primarily in individuals with impaired renal function.48 In 1983, Kaiko et al reported a case series of 48 patients who experienced side effects from meperidine, and 29% of these patients had renal insufficiency.49 The most frequently reported adverse effects of meperidine include seizures, myoclonus (sudden twitching or jerking), and mental status changes.50-52 Adverse effects are most effectively treated with hemodialysis (HD) and not with competitive antagonists such as naloxone.50 Meperidine should never be used in patients taking selective serotonin reuptake inhibitors or monoamine oxidase inhibitors because the combination greatly increases the risk for developing potentially fatal serotonin syndrome. Given the potential for these serious complications, meperidine is not recommended for use in CKD patients and should be avoided.


Methadone is a synthetic opioid that was developed in 1937. Methadone has the dual effect of being both a mu-opioid agonist as well as an N-methyl-D-asparate (NMDA) receptor antagonist.53 Its NMDA antagonist activity can reduce opioid tolerance and glutamate excitoxicity. Methadone has been used for both the treatment of opioid addiction and for chronic pain management. It is metabolized in the liver to its primary metabolite 2-ethylidene-1,
5-dimethyl1-3,3-diphenylpyrrolidine, which is inactive.54 It has a high oral bioavailability and typical half-life of 13 to 47 hours.36 Half-lives as long as 120 hours have been reported, due to its lipid solubility.55

Kreek et al showed that in an anuric patient on hemodialysis, 10% to 45% of methadone metabolites were excreted via the fecal route.56 Methadone is not removed by hemodialysis.36,57 Additionally there was no evidence for accumulation of methadone or metabolites in the 3 CKD patients studied.56

Prior to starting methadone, patients should have a baseline electrocardiogram. One week after starting methadone, patients should have a repeat electrocardiogram to evaluate for QT prolongation, and be regularly monitored for the risk of Torsades de Pointes, especially after dose escalations. Justo et al performed a literature review and identified renal failure as a risk factor for QT prolongation in patients treated with methadone for opioid addiction.58 In patients with normal renal function being treated with methadone for pain, one study in the review found that 5% of the patients were at serious risk for Torsades, with QTc times >500 ms.58 Clinicians should be mindful of any drug interactions (ie, ciprofloxacin [Cipro, others], escitalopram [Lexapro, others], haloperidol [Haldol, others]) that could raise methadone levels and/or increase the QT interval, increasing the risk of Torsades.59

Given the available evidence, methadone is a safe treatment option for patients with CKD when appropriately monitored. Bunn and Ashley recommend a starting dose of 50% of normal for patients with a GFR <10 mL/min, and normal dosing for patients with mild to moderate renal impairment.36 Because of the potential adverse events associated with methadone, it is recommended that only physicians familiar with its use prescribe this agent.


Fentanyl is a potent synthetic opioid with a rapid onset and short duration of action that was first synthesized in 1960. In comparison to morphine, fentanyl is much more lipophilic and 50 to 100 time more potent. It causes less histamine release and is associated with a lower incidence of constipation. It is available in multiple formulations, but the transdermal patch is most commonly used for chronic pain management, with immediate-release transmucosal formulations for breakthrough pain.60

Fentanyl undergoes rapid hepatic metabolism to its primary inactive metabolite norfentanyl.61 Less than 7% is excreted unchanged in the urine.36 Fentanyl is not removed by hemodialysis, due to its high protein binding and low water solubility.36 Koehntop et al noted decreased clearance of fentanyl in severely uremic patients (blood urea nitrogen >60 mg/dL) that resulted in postoperative respiratory depression.62 Officially, the manufacturers of the transdermal fentanyl patch cite this study and recommend against use of the patch in patients with severe renal impairment.63 There is insufficient data on the use of transdermal fentanyl in patients with mild to moderate renal impairment. Bunn and Ashley recommend dosing adjustments according to GFR.36 In consideration of its lack of active metabolites, primary hepatic metabolism, and available safety data, fentanyl can safely be used in patients with mild to moderate CKD. Dosing adjustments are suggested, and this drug should be used with caution in uremic patients. More research on the use of transdermal fentanyl in patients with chronic pain and CKD is needed.


Buprenorphine is a semi-synthetic, mixed agonist–antagonist opioid receptor modulator.64 It has a role in treating opiod addiction, where it may be recognized by the brand name Suboxone. At lower doses, buprenorphine may be used to control acute and chronic moderate to severe pain (Butrans).65

Buprenorphine is metabolized in the liver to active metabolites norbuprenorphine and buprenorphine-3-glucoronide. It is excreted through the billiary system, where it is unaltered, and its metabolites are excreted by the kidneys.66 In a study by Hand et al, plasma concentrations of the metabolites norbuprenorphine and buprenorphine-3-glucuronide were found to be elevated in patients with renal disease.67 Considered far less potent analgesically, Hand and colleagues suggested that these metabolites may be insignificant.

Dahan and colleagues demonstrated that buprenorphine has a ceiling effect on respiratory depression. Anti-respiratory effects were found to level off at about 50% from initial baseline respiration rate, compared to other opiods such as fentanyl, which can cause complete apnea at comparable dosages.68 Filitz et al did not find elevated levels of buprenorphine or norbuprenorphine in patients with renal failure using transdermal buprenorphine up to 70 mcg/h. Additionally they found hemodialysis had no effect on plasma levels of buprenorphine.69

Seemingly safe in patients with renal disease, transdermal buprenorphine may have a useful role in treating conditions such as osteoarthritic pain. Continuous analgesia can be provided over 7 days in the form of Butrans (buprenorphine transdermal), with strengths up to 20 mcg/hr Transdermal delivery of buprenorphine ensures the medication is delivered systemically over a sustained period, and maintains stable plasma concentrations.70

Atypical Opioids


Tramadol is a weak mu-opioid receptor agonist and a serotonin and noradrenaline reuptake inhibitor.71 It acts both peripherally and centrally, so it is effective for both nociceptive and neuropathic pain. Tramadol also produces less sedation and respiratory depression than other opiates. It has a role in the treatment of moderate pain in patients with CKD. Tramadol is metabolized by the liver. However, its active metabolite, O-demethyl tramadol, is excreted through the kidneys. Its elimination half-life is approximately 5 hours in patients with normal renal function, but the half-life can be prolonged significantly in persons with reduced GFR.72 It lacks the abuse potential that is seen with other opioids.73 Common side effects include nausea, CNS depression, and constipation. Tramadol has been shown to cause seizures in patients who have a reduced seizure threshold, such as uremic patients.74,75 Tramadol carries a risk for potentiating serotonin syndrome, and should not be administered to patients who use SSRI or other serotonergic medications.76

Anticonvulsant Medications


Gabapentin is an antiepileptic medication that is commonly used as an adjuvant analgesic in the management of neuropathic pain. Though it is structurally related to gamma-aminobutyric acid (GABA), it does not bind to GABA receptors. Some of its activity may be mediated through its effect on voltage-gated calcium channels, but its exact mechanism of action is unclear. Gabapentin may be used for the treatment of peripheral neuropathy, postherpetic neuralgia, restless legs syndrome, and pruritis secondary to uremia.77-81

Gabapentin is known to cause many CNS side effects, including dizziness, lethargy, and ataxia (failure of muscle control in the arms and legs). Gabapentin is excreted through the kidneys, and its elimination rate is dependent on GFR.82,83 In patients with normal GFR, the starting dose is 300 mg on Day 1, 300 mg twice daily on Day 2, and 300 mg three times a day on Day 3. The dose is then increased according to response to 1.2 gram per day, given in 3 divided doses.36 Plasma levels of gabapentin can be reduced by approximately 35% after hemodialysis.84,85


Pregabalin is well known for its role in treating CNS conditions, and its effect on controlling neuropathic pain. It is an alpha-2-delta ligand, that through binding with voltage gated calcium channels, reduces calcium influx in nerves. This leads to a reduction of neurotransmitter release, including glutamate, noradrenaline, and substance P, which gives it analgesic, anxiolytic, and anticonvulsant properties. Pregabalin is inactive at GABA-A and GABA-B receptors. It is not converted metabolically into GABA or a GABA antagonist, nor does it alter GABA uptake or degradation.86,87 It is not bound to plasma proteins, nor is it significantly metabolized.

Due to these properties, over 90% of it is eliminated unchanged through the kidneys.88 Its pharmacokinetic profile is linear, with plasma levels proportionately increasing with increased doseage.89 It has demonstrated little potential to interact with other medications.90,91 Randinitis et al demonstrated that pregabalin clearance is directly proportional to creatine clearance (CrCl), and so dosage adjustment should be considered for patients with CrCl <60 mL/min.92 The authors recommend that pregabalin doses be decreased by approximately 50% for each 50% decline in CrCl.92 When treating patients on hemodialysis, increased dosage of pregabalin may be required, to maintain steady-state after each treatment.92 


Carbamazepine is another antiepileptic medication that is used as an adjuvant analgesic in the management of neuropathic pain. It acts by stabilizing voltage-gated sodium channels and selectively blocks actively firing nociceptor fibers. Unlike gabapentin, carbamazepine is eliminated by the liver. It does not require dose adjustment in patients with renal insufficiency. Carbamazepine is useful for treating trigeminal neuralgia and diabetic neuropathy. It also is effective in reducing pain associated with postherpetic neuralgia.93,94 Common adverse effects include dizziness, fatigue, and ataxia. A rare but significant side effect associated with this medication is agranulocytosis (reduced ability to make white blood cells). Patients who take the medication for extended periods should obtain a complete blood count every 2 to 4 months to monitor for agranulocytosis and aplastic anemia. For patients with normal GFR, the recommended initial dose is 100 mg, 1 to 2 times a day; usual dose increases to 200 mg given 3 to 4 times a day.36 The maximum dose is 1.6 g per day—the dose is then reduced gradually as pain goes into remission.36

Tricyclic Antidepressants

Tricyclic antidepressants (TCAs) are antidepressant medications that are used as adjuvant analgesics in the management of neuropathic pain.78 TCAs frequently have analgesic effects at lower doses than are typically used for the management of depression. When used in conjunction with opioids, TCAs have a synergistic analgesic effect that can help to lower the dose of opioid needed.13 TCAs undergo hepatic metabolism and have significant side effects that often limit their use, particularly in patients with CKD. This is related to elevated serum levels of glucuronidated metabolites of TCAs, which have been found in patients with renal disease in pharmacokinetic studies.95 TCAs commonly have anticholinergic side effects, including orthostasis, sedation, constipation, urinary retention, blurred vision, memory impairment, confusion, delirium, and dry mouth. This latter side effect is poorly tolerated in dialysis patients. TCAs intensify the thirst that is induced by fluid restriction, hyperglycemia, and hyperosmolality in patients with ESRD. Nortriptyline is a TCA that exhibits less anticholinergic effects, and is generally safer in this population. TCAs can increase the QT interval, and, therefore, these agents should be used with caution in patients with cardiac conduction abnormalities, especially in patients with CKD who commonly suffer from electrolyte disturbances such as hyperkalemia, hypocalcemia, and alkalosis.96


The WHO ladder provides an important framework for managing pain in patients with CKD. Acetaminophen has an excellent safety profile in this population, and it has a role in addressing mild to moderate pain. NSAID use should be avoided if possible in patients with CKD. If NSAID use is necessary, short-acting medications are preferred and they should be discontinued as soon as possible. Selective COX-2 inhibitors have not been well studied in patients with CKD, so caution should be exercised if they are used. Opioids often require careful monitoring for toxicity and dose adjustment because they have metabolites and altered pharmacokinetics in patients with renal failure that often cause adverse side effects. Methadone, Fentanyl, and Buprenorphine are well tolerated in this patient population and should be considered for the management of severe chronic pain. Adjuvant analgesics such as anticonvulsants and TCAs enhance the effectiveness of other analgesics, and have very important roles in pain management. Concurrent use of adjuvants can permit reduced dosage of opiates and limit unwanted side effects.

Continue Reading: Dialysis, Opioids and Pain Management

Last updated on: October 17, 2014

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