慢性非癌性疼痛的治疗方法
Lancet 2011; 377: 2226–35
See Editorial page 2151 This is the second in a Series of
three papers about pain Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA,
USA (Prof D C Turk PhD,
H D Wilson PhD,
Prof A Cahana MD)
Correspondence to: Prof Dennis C Turk, University
of Washington, Seattle, WA
98195, USA
turkdc@https://www.docsj.com/doc/bd9730587.html, Pain 2
Treatment of chronic non-cancer pain
Dennis C Turk,Hilary D Wilson,Alex Cahana
Chronic pain is a pervasive problem that a? ects the patient, their signi? cant others, and society in many ways. The past decade has seen advances in our understanding of the mechanisms underlying pain and in the availability of techn ically advan ced diagn ostic procedures; however, the most n otable therapeutic chan ges have n ot been the development of novel evidenced-based methods, but rather changing trends in applications and practices within the available clinical armamentarium. We provide a general overview of empirical evidence for the most commonly used interventions in the management of chronic non-cancer pain, including pharmacological, interventional, physical, psychological, rehabilitative, an d altern ative modalities. Overall, curren tly available treatmen ts provide modest improvements in pain and minimum improvements in physical and emotional functioning. The quality of evidence is mediocre and has not improved substantially during the past decade. There is a crucial need for assessment of combination treatments, identi? cation of indicators of treatment response, and assessment of the bene? t of matching of treatments to patient characteristics.
Introduction
WHO estimates that 20% of individuals worldwide have
some degree of chronic pain.1 The presence of chronic
pain has both direct health-care and associated indirect
(eg, disability payments, lost productivity) costs. For
example, estimates for the total cost of chronic pain
exceed US$210 billion annually in the USA.2 These large
amounts are not unique to the USA. In the UK, back
pain alone is estimated to cost society $26–49 billion each
year.3 For most of those a? ected, the presence of chronic
pain compromises all aspects of their lives and the lives
of their signi? cant others (? gure 1). Despite important
advances in understanding of the neurophysiology of
pain, the increasing availability of advanced diag-
nostic procedures, and the application of sophisticated
thera p eutic modalities and approaches, currently
available treatments for chronic pain rarely result in
complete resolution of symptoms. Thus, people with
chronic pain will continue to live with some level of pain
irrespective of the treatment or treatments they receive
for the foreseeable future.
Chronic non-cancer pain is typically de? ned as pain
lasting longer than 3 months or beyond the expected
period of healing of tissue pathology.4 Pain severity,
however, is not correlated with the amount of damage
and symptoms can persist long after tissue damage from
an antecedent injury resolves.4 Research suggests that
chronic non-cancer pain can develop as a result of
persistent stimulation of or changes to nociceptors due
to localised tissue damage from an acute injury or
disease (eg, osteoarthritis), or damage to the peripheral
or central nervous system, or both (eg, painful diabetic
neuropathy, poststroke pain, spinal cord injury), which Key messages
? Chronic pain is a pervasive health issue that exerts a
substantial social and economic burden on both the
a? ected individual and society
? Mechanisms underlying chronic pain include a complex
interaction of physiological, emotional, cognitive, social,
and environmental factors
? Treatment options include pharmacological approaches;
interventional techniques including nerve blocks, surgery,
implantable drug-delivery systems, and spinal-cord
stimulators; exercise and physical rehabilitation;
psychological treatments; interdisciplinary treatment; and
complementary and alternative treatments
? In view of the complex nature of chronic pain, treatment
often necessitates use of a blend of di? erent approaches
? Overall, present treatment options result in modest
improvements at best, and part of chronic pain
management should include dialogue with the patient
about realistic expectations of pain relief, and bring focus
to improvement of function
Search strategy and selection criteria
We searched Medline (between 2000, and July, 2010),
Embase (2000–10), and Cochrane (2005–10) using the search
terms “chronic pain” or “chronic non-cancer pain”, and
limited the ? eld to “title/abstract”. We focused mainly on
meta-analyses, systematic reviews, and guidelines published
within the past 5 years; however, we also made use of the
reference lists of articles identi? ed by this search strategy,
highly regarded older publications, and the authors’ personal
reference lists. From this list we selected references that
addressed categories of musculoskeletal (primarily
osteoarthritis), neuropathic (primarily post-herpetic
neuralgia and diabetic painful neuropathy), chronic
widespread (primarily ? bromyalgia), and low-back pain,
favouring the most recent guidelines and comprehensive
reviews. Four new references, published after July, 2010, were
added during the peer-review process.
might not be readily detectable with currently available diagnostic technologies.5
Pain does not occur in a vacuum. Individuals’ unique genotypes, previous learning histories, environmental and socioeconomic resources, cognitive, emotional, and behavioural factors, and physical pathology interact to mediate and moderate the experience of pain (? gure 2).6 Thus, to understand and treat patients with pain requires that consideration be given to all contributing facets. This complexity has bedevilled health-care providers, people experiencing pain, their signi?cant others, and society since earliest recorded history. We provide a brief overview of, and evidence for the e?ectiveness of, the most commonly prescribed treatments for chronic non-cancer pain.
Treatment overview
A growing array of pharmaceutical, surgical, neuro-augmentative, somatic, behavioural, rehabilitative, and
complementary and alternative treatment options are available for the management of patients with chronic pain. However, overall treatment e? ectiveness remains inconsistent and fairly poor. Moreover, even when treatments e?ectively reduce pain, they often do not produce concomitant improvements in physical and emotional functioning and overall health-related quality of life.7
The focus of this paper is to provide an overview of current practices and concerns in the management of patients with chronic non-cancer pain. Notably, chronic non-cancer pain is a broad category, and disorders tend to be classi? ed on the basis of anatomy (eg, body location), cause (eg, nociceptive, neuropathic), neurophysiology, or body system involved.4 Various classes of pain disorders have potentially distinct underlying mechanisms, and as a result drawing of overarching conclusions on any one particular treatment modality is di? cult. Management options, however, overlap substantially, so we present results on the basis of therapeutic modality. We provide a contemporary survey of some of the most common pharmacological, interventional, and non-interventional treatments. A comprehensive systematic review of the e?ectiveness of treatments for speci?c diagnoses is beyond the scope of this report. We focus mainly on the categories of musculoskeletal pain (eg, osteoarthritis), neuropathic pain (eg, postherpetic neuralgia and diabetic painful neuropathy), chronic widespread pain (eg, ?bromyalgia), and non-speci?c low-back pain on the basis of their prevalence in clinical practice and in research into treatment.
Pharmacological treatments
Background
Oral drugs have been the mainstay of treatment for pain during past centuries, and the use of drugs to treat pain has expanded exponentially in recent years, with increases in expenditures of 188% between 1996 and 2005.7 We review evidence for classes of drugs most commonly
used for treatment of chronic non-cancer pain.
Opioids
Retail sales for opioids, the most common class of drug
prescribed in the USA, increased by 176% from 1997
to 2006.8 Despite this striking escalation, their use remains
controversial both with respect to e? cacy and adverse
physical e?ects and to aberrant behaviours.9,10 A meta-
analysis of 41 randomised controlled trials11 evaluating the
e? ectiveness of opioids for the treatment of various forms
of chronic non-cancer pain, including osteoarthritis,
diabetic painful neuropathy, low-back pain, and
rheumatoid arthritis, concluded that on average opioids
result in a small improvement in pain severity and
functional improvement compared with placebo, and
similar reductions in pain, but less improvement in
function compared with other analgesic drugs. On the
basis of similar conclusions from a systematic review of
the use of opioids in osteoarthritis, Neush and colleagues12
concluded that opioids should not be routinely used.
G uidelines from both the Neuropathic Pain Special
Interest G roup of the International Association for the
Study of Pain13 and the European Federation of
Neurological Societies Task Force14 recommend opioids as
second-line or third-line treatment that can be considered
for ? rst-line treatment in speci? c clinical circumstances,
such as during episodic exacerbation of severe neuropathic
pain. On the basis of scarcity of evidence, opioids are not
strongly recommended for use in patients with
?bromyalgia in any of the three most recent evidence-
based guidelines published by professional societies for
the management of this disorder.15–17
Tramadol, a combination of a serotonin and nor-
adrenaline reuptake inhibitor and a μ-opioid agonist, is
notable because its mechanism of action is distinct from
those of other opioids. Tramadol reduces pain
substantially in osteoarthritis,18? bromyalgia,19,20 and
Figure 1: The e?ect and burden of chronic pain
Chronic pain a? ects every aspect of a patient’s life, contributing to a loss of both physical and emotional function, a? ecting a patient’s levels of activity (ability to work at home and job and engage in social and recreational pursuits); additionally, there are often serious economic consequences as a result of health-care bills and potential loss or decrease in ? nancial income.
neuropathic pain.21 There is insu? cient evidence to establish whether tramadol is more e? ective compared with other opioids. Tapentadol, another dual-action substance that acts as both a noradrenaline reuptake inhibitor and μ-opioid agonist, was recently approved by the US Food and Drug Administration (FDA) for use in acute pain;22 however, there is a dearth of evidence with respect to the e? cacy of its use in chronic non-cancer pain.23 Serotonin syndrome, a potentially life-threatening adverse event that can occur in patients as a result of too much serotonin in the body, is an additional side-e? ect to be monitored in patients taking these drugs.
Side-e?ects associated with opioids (eg, nausea, constipation, somnolence) contribute to attrition during randomised controlled trials and are often important enough to prevent patients from remaining on opioid treatment. In a meta-analysis of 17 studies24 concerning e? cacy of long-term opioid use for chronic non-cancer pain, 44% of patients abandon treatment 7–24 months into open-label extensions.24 A few patients opting to remain on long-term opioid treatment can develop opioid-induced hyperalgesia, which occurs when patients taking opioids become hypersensitive to nociceptive stimuli.25 Opioid-induced hyperalgesia is postulated to result from changes in the peripheral and central nervous system that lead to facilitation of nociceptive pathways.25
Aside from the physical adverse events, opioids carry a substantial risk of misuse. Studies of patients with chronic non-cancer pain taking opioids on a long-term basis suggest that as many as 45% could be engaging in aberrant drug-taking behaviours.26 In the USA, the misuse of prescription opioids is the fastest growing form of drug misuse and is the leading cause of accidental overdose and mortality,27 and there is increasing concern about diversion and criminal tra? cking by patients and physicians. Emergency room visits involving narcotic analgesic substances increased 274% in 11 years, from 1995 to 2005, and from 1999 to 2004, the number of all poisoning deaths increased 54%,28 whereas the number of methadone-related deaths rose 390%.29 These concerns, as well as restricted e? cacy, have resulted in some re-assessment and debate regarding practices surrounding opioid use. Manchikanti and colleagues30 provide a detailed discussion of the complexities and complications of therapeutic use, misuse, and non-medical use of prescription opioids.
Non-steroidal anti-in? ammatory drugs
The e?cacy of non-steroidal anti-in? ammatory drugs (NSAIDs) has been reported for patients with osteoarthritis and rheumatoid arthritis31 and back pain.32 NSAIDs are generally accepted to be ine? ective for neuropathic pain; however, this belief is not founded on published evidence, and research is needed to establish the e?cacy of NSAIDs for this class of disorders.33 NSAIDs are not included in any of the three most recent guidelines for treatment of ? bromyalgia.15–17
NSAID gastropathy is regarded as one of the most common serious adverse drug events a? ecting people in industrialised nations.34 Selective cyclo-oxygenase (COX)-2 inhibitors have fewer gastrointestinal side-e?ects than do traditional NSAIDs, but they are associated with increased cardiovascular risk.32 Careful scrutiny for the development of adverse reactions should be undertaken, particularly with long-term use. Paracetamol is a slightly weaker analgesic than NSAIDs, but is a reasonable alternative because of reduced gastrointestinal complications and low cost.35 The widespread use of paracetamol, combined with the small margin of safety between therapeutic and toxic dose, often result in unintentional overdose.36 On the basis of growing rates of unintentional overdose and hepatic failure associated with paracetamol, the FDA revised the drug’s warning label in April, 2010.
Antidepressant drugs
Antidepressants have diverse e?ects that might contribute to their analgesic e? ect, including e? ects on N-methyl-D-aspartate (NMDA) and adenosine receptors, sodium channels, and serotonin, noradrenaline, and opioid systems. Meta-analyses suggest that antidepressants are superior to placebo for the treatment of chronic non-cancer pain, resulting in moderate symptom reduction.35 E?cacy is most well researched for neuropathic pain, ? bromyalgia, low-back pain, and headaches.37 Evidence is particularly strong for use of antidepressants in neuropathic pain.38
Tricyclic antidepressants (TCAs), such as amitriptyline and cyclobenzaprine, have the longest track record of any antidepressants in treatment of chronic non-cancer pain. They primarily work by directly blocking the reuptake of
Figure 2: Factors contributing to pain severity
Pain severity is not accounted for solely by degree of physiological pathology, but is the result of a complex interaction among individuals’ unique previous histories, any physiological abnormalities, their cognitive perceptions of nociception, emotional factors, their coping styles, and social and ? nancial resources.
serotonin and noradrenaline. TCAs have important side-e? ect pro?les including cardiovascular events (eg, hypertension, postural hypotension, arrhythmias) and falls in elderly adults; moreover, tolerability is an important issue because high doses can become toxic. A recent systematic review37 concluded that the evidence supports use of TCAs in neuropathic pain, ? bromyalgia, low-back pain, headaches, and irritable bowel syndrome. Selective serotonin reuptake inhibitors (SSRIs) were developed to speci? cally target serotonin in an e? ort to decrease side-e?ects associated with the more broadly acting TCAs. Trials evaluating the e? cacy of these more highly selective serotonin drugs, including ? uoxetine and citalopram, are less consistent than those with dual e?ects on noradrenaline and serotonin; however, bene? cial e? ects have been reported.37,39
Recent trials have focused on the new selective serotonin and noradrenaline reuptake inhibitors (SNRIs). These drugs target both serotonin and noradrenaline, but do not interact with adrenergic, cholinergic, or sodium channels in the way that TCAs do, thereby avoiding some of the side-e? ect and tolerability issues. Evidence suggests that the SNRIs duloxetine40 and milnacipran41 are well tolerated and e? ectively reduce the functional e? ect of ? bromyalgia. Duloxetine has been recommended by the UK National Institute of Health and Clinical Excellence (NICE) as a ? rst-line treatment for patients with neuropathic pain.42 Additional research is needed to evaluate the e? cacy of SNRIs in other pain disorders.
Anticonvulsant drugs
The primary mechanisms of action of anticonvulsant drugs include modulation of voltage-gated calcium or sodium channels, glutamate antagonism, enhancement of the γ-aminobutyric acid (GABA) inhibitory system, or a combination of these e?ects. The best evidence supports the e? cacy of three drugs mainly used for the treatment of chronic non-cancer pain—gabapentin, pregabalin, and carbamazepine or oxcarbazepine.
Gabapentin and pregabalin act as neuromodulators by selectively binding to the α
2
δ subunit protein of calcium channels in various regions of the brain and the super? cial dorsal horn of the spinal cord. This process inhibits the release of excitatory neurotransmitters that are important in the production of pain. There is good evidence for their e? ectiveness in neuropathic pain.13,14 Pregabalin has also been shown to improve symptoms in ? bromyalgia,43 and is recommended by NICE as one of two ? rst-line treatments for patients with neuropathic pain.42 Evidence suggests that gabapentin results in a small net bene? t in patients with low-back pain due to radiculopathy, but no evidence is available for its e? ectiveness in non-speci? c low-back pain.44 The most common side-e? ects include somnolence, dizziness, fatigue, and weight gain. Carbamazepine was one of the ? rst anticonvulsant drugs to be tested in neuropathic pain. A recent review45suggests that evidence for its e? cacy is mixed, with three positive and two negative trials for either carbamazepine or the newer carbamazepine derivative, oxcarbazepine.45 Skeletal muscle relaxants
The mechanisms of action of skeletal muscle relaxants is unclear, but could be related in part to sedative e? ects. Studies have not shown signi? cant di? erences among this category of agents in their e? cacy, adverse events, or safety. Most frequently, they are recommended as adjuvant therapy for short-term relief.46 Cyclobenzaprine is the best studied muscle relaxant in musculoskeletal disorders. The drug seems to have a restricted role in the treatment of chronic non-cancer pain, with the exception of ? bromyalgia. In studies of fair quality it has consistently proven superior to placebo for ? bromyalgia, as well as pain relief, muscle spasms, and functional status in other disorders.47 Sedation is a common side-e?ect, making long-term therapy problematic.
Topical agents
Topical agents have been advocated for the treatment of chronic non-cancer pain when localised pain is present. They have the potential advantage of avoiding the systemic side-e?ects that are often associated with oral drugs. Capsaicin is an alkaloid derived from chilli peppers, and repeated application is thought to deplete substance P from primary a?erent neurons. By compari s on with placebo, topical agents e?ectively reduce pain in both neuropathic pain and musculoskeletal disorders including osteoarthritis.48 Topical salicylate has also proved superior to placebo in six trials of chronic non-cancer pain.48 Interventional treatments
Background
Interventional pain medicine involves application of various techniques that can be used to diagnose or locate an individual’s source of pain or provide therapeutic pain relief. Interventional medicine is most frequently used when a speci?c area of the spine is thought to be contributing to an individual’s pain (ie, discogenic or sacroiliac joint pain) and there is no consensus with respect to optimum diagnostic criteria. The focus of our review is therapeutic intervention, so we will not address diagnostic uses of interventional pain medicine. We refer readers to Chou and colleagues49 and Manchikanti and colleagues50 for discussion and recommendations regarding diagnostic interventions for back pain. In this section, we focus on the most common therapeutic interventions, injection therapy, surgical intervention, and implantable devices, with a primary focus on low-back pain. For a more in-depth discussion of interventional therapeutic techniques for low-back pain, we refer readers to the American Pain Society (APS)51 and the American Society of Interventional Pain Medicine52 systematic review and evidence-based guidelines.
Injection therapy
Nerve blocks involve the delivery of various anaesthetics to visceral and peripheral nerves and muscles to interrupt nociceptive input, reduce in?ammation, or destroy neurons at the source of pain. The procedures vary with respect to patient-selection criteria, location (epidural, facet joint, local site), agent, and dose. The deviations in methods make assessment of outcomes di? cult. There is no consensus about technical aspects of injection therapies, and no guidelines for optimum diagnostic criteria for patient selection, frequency, number, or timing of injections.53
In the USA, epidural steroid injections are the most commonly performed pain management procedures;54 however, evidence is not unequivocal for their use as long-term monotherapy.53,55 Recent APS guidelines report that fair evidence exists for their use in patients with radiculopathy with prolapsed lumbar disc, although there is no evidence supporting their use in non-speci? c low-back pain or failed back surgery syndrome.56 Facet injections are the second most commonly performed pain management procedure in the USA.54 Luijsterburg and colleagues57 undertook a systematic review for their use in lumbosacral radicular syndrome, and they were not clearly shown to be e? ective.However, Chou and colleagues56 conclude that there is fair evidence for their use in presumed facet joint pain. With respect to intradiscal steroid injections, they report good evidence for the use of intradiscal steroid injections in presumed discogenic low-back pain, and fair evidence in radiculopathy with prolapsed lumbar disc.56 Super? cial and deep infections are a potential side-e? ect of injection therapies.58 Rare but serious complications (cauda equine syndrome, septic facet joint arthritis, discitis, paraplegia, paraspinal abscesses, meningitis) have also been reported. The decision to use an injection therapy needs to balance the potential for some patients to bene? t against these serious adverse events and costs.
Surgery
Chronic non-cancer pain that persists despite conservative e?orts often leads to surgery. Lumbar fusion for non-radicular low-back pain with degenerative changes is one of the most rapidly increasing types of surgery. In 2001, more than 122 000 lumbar fusions were performed in the USA, a 220% increase from 1990,59 and rates of cervical fusions rose 206% from 1992 to 2005.60 Arti? cial disc replacement is one alternative to fusion surgeries. Other common surgeries include discectomy for radiculopathy with herniated lumbar disc, decompressive laminectomy for spinal stenosis, and an interspinous spacer device as an alternative to decompressive laminectomy.
In a recent systematic review61 evaluating surgery for low-back pain, evidence was rated as fair for lumbar fusion in non-radicular low-back pain with common degenerative changes. At least one of the studies included reported a signi? cantly greater pain reduction (33% reduction vs 7%) for the surgical group compared with the non-surgical group;62 however, bene? ts diminished over time with as many as 41% of patients reporting no change or a worsened quality of life up to 4·5 years after surgery.63 Evidence was regarded as good for discectomy in lumbar disc prolapse with radiculo-pathy, as well as laminectomy for spinal stenosis with or without degenerative spondylo l isthesis. High compli-cation rates and repeat procedures are realities of spinal surgery as well. Several studies show that signi? cant pain can persist after spinal surgery, an estimated 30% (93 600) will result in failed back surgery syndrome,64 and subsequent operations do not guarantee resolution of pain. In the chronic non-cancer pain population, which patients and with which characteristics are most likely to bene?t from spinal surgery is unclear.
Implantable devices
Implantable devices tend only to be considered as options when oral drugs, surgery, and injection procedures have not provided adequate improvements. Spinal-cord stimulation involves the implantation of electrodes near the spine or into peripheral nerves to modulate pain processing, resulting in inhibition of nociceptive signals. The use of this technique in carefully selected patients with refractory neuropathic pain (complex regional pain syndrome [CRPS] and radicular back pain) has been shown to reduce pain, improve quality of life, reduce analgesic consumption, and allow some patients to return to work.65 Several meta-analyses evaluating the e?cacy of spinal-cord stimulation for failed back syndrome or CRPS concluded that there was moderate evidence for improvement in pain,51,66–68 but a general need for more methodologically sound studies. The one randomised controlled trial69 reported signi? cant di?erences for pain, but not for function. Spinal-cord stimulation is also often used for low-back pain; however, in a recent systematic review, Chou and colleagues51 concluded that there are no high-quality trials that have evaluated its use in this population.
Epidural and intrathecal drug delivery systems have been used successfully to treat some patients with intractable chronic non-cancer pain, but high costs and absence of proven e? ectiveness have led to substantial controversy. Bennett and co-workers70 concluded that clinical e?cacy in large-scale randomised controlled trials using intrathecal delivery of most compounds has not been shown and variations between study designs make useful comparisons of existing studies di? cult. A more recent systematic review71 concludes that, on average, moderate reductions in pain and improvements in functioning were realised for patients with chronic non-cancer pain, although long-term e? ectiveness is unknown. Currently, morphine and ziconotide are the only FDA-approved analgesics for long-term intrathecal infusion. However, chronic use of morphine is often
associated with loss of therapeutic e?ect because of tolerance and dose-limiting side-e? ects,72 and ziconotide is associated with various adverse events associated with the CNS (eg, dizziness, abnormal gait) and data for its safety remain scarce.73
Implantation with spinal-cord stimulation or intrathecal drug delivery systems necessitates routine monitoring, replacement of the devices as needed, and re? lling of drug reservoirs. All invasive interventions have the potential to create additional medical problems that need to be treated, so there is a need to balance bene? ts against the high costs of the procedure and long-term maintenance.67
Physical, rehabilitation, and psychological approaches
Although evidence suggests that exercise can e? ectively decrease pain and improve function, improvements are small (<30% reduction in pain and <20% improvement in function).74 Systematic reviews also suggest that exercise intervention a?ects work disability status;75,76 however, no conclusions could be made about exercise type. Moreover, patient adherence can be an impediment. Exercise treatments vary widely and are often incorporated as part of multimodal and rehabilitative treatment approaches, making assessment of the e? ectiveness of exercise alone a challenge.
Psychological treatments can generally be separated into theoretically-based approaches and speci? c techniques. The most common theoretical approaches are operant conditioning and cognitive-behavioural therapy (including acceptance-based and mindfulness-based therapy). All of these approaches emphasise patient
coping, adaptation, self-management, and reduction of disability associated with symptoms, rather than elimination of physical causes of pain per se. The most commonly used psychological techniques used to achieve these goals include cognitive therapy, relaxation, and hypnosis to help patients to shift their stance from being passive, reactive, dependent, and helpless in the face of pain, to being active and resourceful in coping with their symptoms and their lives, and to replace their more typical feelings of hopelessness (panel 1).
The results of meta-analyses and systematic reviews of adult patients with chronic pain suggest that psychological treatment as a whole results in modest bene? ts in improvement of pain and physical and emotional functioning.77–82 However, evidence for the long-term e? ects is inadequate, and evidence is somewhat contradictory for e?ects on vocationally relevant outcomes.77–80 There is insu? cient evidence to recommend any one therapeutic approach or modality over another. The possibility that patients with di? erent characteristics might derive bene? ts from treatments with di? erent foci and targets is reason-able to consider.83 Psychological approaches are commonly included as components of interdisciplinary pain re-habilitation programmes (IPRPs).
Rehabilitation programmes are often thought of as a salvage approach after the alternatives described previously have proven insu? cient. Thus, patients treated at IPRPs have some of the most recalcitrant problems. Although there is no single format for IPRPs, they o?er an integrated approach that involves close coordination between physicians, psychologists, physical therapists, and other health-care providers. Most treatment facilities of this type have a generic concept and plan, and we present common components of an IPRP in panel 2.
The reduction of pain after treatment at IPRPs have been reported to be signi?cant in several meta-analyses,77,78,84 with one meta-analysis77 reporting that the mean pain reduction for patients treated at IPRPs was 37% with a concomitant signi?cant decrease (63%) in prescription pain treatment. Moreover, one early meta-analysis of 42 published studies85 reported signi? cant reductions in health-care use after treatment at IPRPs. Thomsen and colleagues86 used social records instead of self-reports to evaluate the e? cacy of an IPRP, obtaining data for disability and welfare costs for a period of 6 months before entry to a 4-month waiting list and at a 9-month follow-up after termination to evaluate the Panel 1: Common psychological and behavioural techniques used to treat chronic non-cancer pain
? Reconceptualisation of the patient’s pain from
uncontrollable to manageable
? Fostering of optimism and combating of demoralisation
? Promotion of patient feelings of success, self-control, and self-e? cacy
? Encouragement of patients to attribute success to their own role
? Education in the use of speci? c skills such as pacing, relaxation, and problem solving
? Emphasis on active patient participation and
responsibility
? Individualisation of some aspects of treatment to unique physical and psychological characteristics of the patient
Panel 2: Common components of an integrated interdisciplinary rehabilitation programme
? Physical rehabilitation
? Exercise therapy
? Cognitive restructuring with an emphasis on promotion of self-management, self-e? cacy, resourcefulness, and
activity versus passivity, reactivity, dependency, and
hopelessness
? Behavioural treatment (eg, relaxation, work to exercise quota vs pain)
? Vocational rehabilitation, where indicated
? Drug management as needed (preferably with reduction of opioid treatment)
e?cacy of an IPRP. The investigators identi? ed signi? cant
reductions in social transfers (welfare bene? ts, sickness
bene?t, and pensions). These investigators noted a
63% reduction in bene? ts during follow-up. The evidence
for the e? cacy of psychological treatments on physical
functioning is more supportive for these treatments than
for pharmacological and invasive treatment.87
The modest reductions in pain severity obtained with
psychological interventions and with IPRP studies are
similar to those noted with more traditional pharma-
cological and procedural treatment modalities.88
Although most studies have fairly short follow-up, two
meta-analyses77,85 con?rmed that the long-term e? ects
on return to work for patients treated at an IPRP and
the results were superior to those of other active
treatments. Results should be interpreted with caution
because not all clinics have the same patient mix,
di? erent measures might be used to assess outcomes,
di? erent programmes are not equally potent, studies
are conducted in countries with diverse health-care
systems, and most are not randomised controlled trials,
but rather are observational studies that have relied on
comparisons with waiting list, standard care, and
patients who were refused insurance coverage. Complementary and alternative medicine and other non-pharmacological approaches Complementary and alternative medicine (CAM)
includes a wide array of treatments that are not regarded
as part of conventional medicine. A comprehensive
review of all modalities is beyond the scope of this paper,
but we address three of the most common modalities
used, as well as those with the best evidence for treatment
of chronic non-cancer pain. The evidence that we review
is largely based on a recent systematic review89 of CAM
e?ectiveness for chronic non-cancer pain. We refer
interested readers to this review for evidence on additional
CAM modalities.
Spinal manipulation is the most commonly used CAM
therapy for low-back pain. Tan and colleagues89 concluded
on the basis of two systematic reviews that spinal
manipulation therapy is more e? ective than are sham
manipulations and treatments such as bed rest and
traction, but not more e? ective than other recommended
treatments for low-back pain. Evidence for other chronic
non-cancer pain disorders is scarce.
Massage is another modality commonly used by
patients with chronic non-cancer pain as a supplemental
treatment. Wide variations in massage techniques make
generalisation from studies di? cult. Tan and colleagues89
reviewed all published evidence for massage therapy for
chronic non-cancer pain and concluded that evidence
supports bene?t in low-back and shoulder pain, and
possibly provides bene? t for ? bromyalgia and neck pain,
but more research is needed.
Acupuncture has been used for thousands of years in
the treatment of pain, although mechanisms remain unclear. Evidence supports the e? ectiveness of acupuncture for the treatment of chronic low-back pain,90–93 and results are promising for the e? ectiveness in reduction of pain associated with ? bromyalgia and neck pain.94 There is, however, little evidence reported to support improvements in physical or emotional functioning after acupuncture treatment of patients with chronic non-cancer pain. However, acupunc-ture trials have typically not focused on function as an outcome.
Transcutaneous electric nerve stimulation (TENS) has been applied for diverse pain states since its introduction in the early 1970s, but there have been few large, randomised controlled trials to evaluate its e? ectiveness in pain management. Results from recent systematic reviews and meta-analyses draw mixed conclusions about the e? ectiveness of TENS in pain relief.95,96 The methods used in TENS (eg, bandwidth, wave-form, duration) vary widely, and these factors might contribute to inconsistent results.
Conclusions
Ideally, we would include a table summarising the conclusions about treatments for chronic non-cancer pain covering all of modalities described. However, this approach is inappropriate because drawing of conclusions between the therapeutic approaches is impossible, since the meta-analyses and systematic reviews that we used vary widely in terms of diagnostic criteria used for the di?erent conditions, outcome measures studied, criteria used to select studies for inclusion, inconsistency in some of the treatment methods, and inclusion of patients from countries with very di?erent health and economic systems. These factors make comparison within treat m ents di? cult and comparison across therapeutic modalities and approaches almost impossible. This situation could account for some of the inconsistency in the conclusions from meta-analyses on the same populations, with comparable treatments, and covering roughly the same time period. However, despite these concerns, a general conclusion about the treatment of chronic non-cancer pain is that the results presented are sobering. Even when signi? cant e? ect sizes are reported, the clinical meaningfulness of the outcomes is not always clear. Of all treatment modalities reviewed, the best evidence for pain reduction averages roughly 30% in about half of treated patients, and these pain reductions do not always occur with concurrent improvement in function. Notably, the placebo response rate for opioid trials is around 10%, and when active placebos that mimic the side-e?ects of opioids are used, the response rate increases to an average across studies of 21%.97
These results suggest that none of the most commonly prescribed treatment regimens are, by themselves, su? cient to eliminate pain and to have a major e? ect on physical and emotional function in most patients with
chronic pain. This conclusion is hardly surprising in view of the complexity of chronic pain. In the absence of a cure, there is a need to maximise symptom relief so that patients are able to lead the highest quality of life possible. If there is no proven improvement in patient pain, and physical and emotional functioning, then an alternate treatment approach should be recommended. Setting of realistic expectations with patients is also crucial. Another important consideration is that treatment response is individual, and no one approach will bene? t all patients. Matching of patients to particular treatments on the basis of relevant predictive charac-teristics would be ideal, if we had knowledge of the appropriate matching variables.98
A clear research agenda is apparent from our review. Sophisticated studies with creative placebo controls for non-pharmacological treatments are needed—for example, in the case of interventional techniques. Randomised controlled trials should also include alternative treatment comparisons that allow for comparative e?ectiveness analyses. Since none of the currently available treatments has proven to be capable of eliminating pain and restoring functioning to a high proportion of patients, attention should also be paid to the e? ectiveness of combination of various treatments (ie, combinations of several drugs, drugs with somatic treatments, pharmacological and psychological treat-ments). Trials with some combination approaches have been suggested as reasonable alternatives before more invasive procedures such as surgery.99 Despite calls for the use of combination treatments, few studies have reported on the e?cacy of combination therapy, and results showing an additive or synergistic bene? t are not conclusive for any particular combination.100,101 Finally, assessment of pain, physical and emotional functioning, patient ratings of improvement and satisfaction of events along with recording of adverse events are the recommended domains for assessment of treatment e? ectiveness.102 Unfortunately, despite this recom-mendation, pain severity continues to be the primary outcome, particularly for pharmaceutical, surgical, and intervention studies. A great need exists for research that goes beyond asking the questions of whether a particular treatment is e?ective, to addressing what treatment is e?ective, for which patients, on what outcomes, under what circumstances, and at what cost. To achieve this aim, continual measurement of patients’ core domain outcomes90 are mandatory and should become standard of care. Clinicians and investigators need to work closely together to identify unique characteristics of treatment response (measurement-based care), to translate clinical outcomes into sustainable clinical practice (value-based care).
Contributors
DCT and DHW contributed equally to the literature search, interpretation, creation of ? gures, and writing of the report. AC contributed to writing of the report.Con? icts of interest
DCT has received grants from Endo Pharmaceuticals, Ortho-McNeill Janssen, and the National Institutes of Health. He has served as a consultant to Endo Pharmaceuticals, Galderma, P? zer, and Smith & Nephew; served on an advisory board for Eli Lilly and P? zer; is a Special Government Employee of the US Food and Drug Administration (FDA), and serves as Co-chair of the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMPACT) and Associate Director of Analgesic Clinical Trials Innovations, Opportunities, and Networks (ACTION), a public-private partnership with the US FDA. HDW has received a grant from Ortho-McNeill Janssen. AC declares that he has no con? icts of interest.
Acknowledgments
We thank Christina Kemp for her assistance with the literature search. References
1 Gureje O. Persistent pain and well-being: a World Health
Organization Study in Primary Care. JAMA 1998; 280: 147–51.
2 National Research Council. Musculoskeletal disorders and the
workplace. Washington, DC, USA: National Academy Press, 2001.
3 Maniadakis N, Gray A. The economic burden of back pain
in the UK. Pain 2000; 84: 95–103.
4 Turk DC, Okifuji A. Pain terms and taxonomies of pain. In:
Fishman SM, Ballantyne JC, Rathmell JP, eds. Bonica’s
Management of Pain, 4th edn. New York, NY, USA: Lippincott
Williams & Wilkins, 2009: 13–23.
5 Thomas Cheng H. Spinal cord mechanisms of chronic pain and
clinical implications. Curr Pain Headache Rep 2010; 14: 213–20.
6 Gatchel RJ, Peng YB, Peters ML, Fuchs PN, Turk DC. The
biopsychosocial approach to chronic pain: scienti? c advances
and future directions. Psychol Bull 2007; 133: 581–624.
7 Martin BI, Deyo RA, Mirza SK, et al. Expenditures and health status
among adults with back and neck problems. JAMA 2008;
299: 656–64.
8 US Department of Justice. https://www.docsj.com/doc/bd9730587.html,/arcos/
retail_drug_summary/2006/06_rpt2.pdf (accessed May 3, 2011).
9 Chou R, Ballantyne JC, Fanciullo GJ, Fine PG, Miaskowski C.
Research gaps on use of opioids for chronic noncancer pain:
? ndings from a review of the evidence for an American Pain Society and American Academy of Pain Medicine clinical practice
guideline. J Pain 2009; 10: 147–59.
10 Stein C, Reinecke H, Sorgatz H. Opioid use in chronic noncancer
pain: guidelines revisited. Curr Opin Anaesthesiol 2010;
23: 598–601.
11 Furlan AD, Sandoval JA, Mailis-Gagnon A, Tunks E. Opioids for
chronic noncancer pain: a meta-analysis of e? ectiveness and side
e? ects. CMAJ 2006; 174: 1589–94.
12 Nuesch E, Rutjes A W, Husni E, Welch V, Juni P. Oral or
transdermal opioids for osteoarthritis of the knee or hip.
Cochrane Database Syst Rev 2009; 4: CD003115.
13 Dworkin RH, O’Connor AB, Audette J, et al. Recommendations for
the pharmacological management of neuropathic pain: an overview and literature update. Mayo Clin Proc 2010; 85 (3 suppl): S3–14.
14 Attal N, Cruccu G, Baron R, et al. EFNS guidelines on the
pharmacological treatment of neuropathic pain: 2010 revision.
Eur J Neurol 2010; 17: 1113–e88.
15 Carville SF, Arendt-Nielsen S, Bliddal H, et al. EULAR
evidence-based recommendations for the management of
? bromyalgia syndrome. Ann Rheum Dis 2008; 67: 536–41.
16 Klement A, Hauser W, Bruckle W, et al. Principles of treatment,
coordination of medical care and patient education in ? bromyalgia syndrome and chronic widespread pain. Schmerz 2008; 22: 283–94 (in German).
17 Burckhardt CS, Goldenberg DL, Cro? ord LJ, et al. Guideline for
the management of ? bromyalgia syndrome. Pain in adults and
children. APS Clinical Practice Guideline Series No. 4. Glenview, IL, USA: American Pain Society, 2005.
18 Cepeda MS, Camargo F, Zea C, Valencia L. Tramadol for
osteoarthritis. Cochrane Database Syst Rev 2006; 3: CD005522.
19 Russell IJ, Kamin M, Bennett RM, Schnitzer TJ, Green JA,
Katz WA. E? cacy of tramadol in treatment of pain in ? bromyalgia.
J Clin Rheumatol 2000; 6: 250–57.
20 Bennett RM, Kamin M, Karim R, Rosenthal N. Tramadol
and acetaminophen combination tablets in the treatment of
? bromyalgia pain: a double-blind, randomized, placebo-controlled study. Am J Med 2003; 114: 537–45.
21 Duhmke RM, Cornblath DD, Hollingshead JR. Tramadol for
neuropathic pain. Cochrane Database Syst Rev 2004; 2: CD003726.
22 Tapentadol (Nucynta)—a new analgesic. Med Lett Drugs Ther 2009;
51: 61–62.
23 Guay DR. Is tapentadol an advance on tramadol? Consult Pharm
2009; 24: 833–40.
24 Noble M, Treadwell JR, Tregear SJ, et al. Long-term opioid
management for chronic noncancer pain. Cochrane Database Syst Rev 2010; 1: CD006605.
25 Chu LF, Angst MS, Clark D. Opioid-induced hyperalgesia in
humans: molecular mechanisms and clinical considerations.
Clin J Pain 2008; 24: 479–96.
26 Michna E, Jamison RN, Pham LD, et al. Urine toxicology screening
among chronic pain patients on opioid therapy: frequency and
predictability of abnormal ? ndings. Clin J Pain 2007; 23: 173–79.
27 Compton WM, Volkow ND. Major increases in opioid analgesic
abuse in the United States: concerns and strategies.
Drug Alcohol Depend 2006; 81: 103–07.
28 Manchikanti KN, Manchikanti L, Damron KS, Pampati V,
Fellows B. Increasing deaths from opioid analgesics in the United States: an evaluation in an interventional pain management
practice. J Opioid Manag 2008; 4: 271–83.
29 Paulozzi LJ, Annest JL. US data show sharply rising drug-induced
death rates. Inj Prev 2007; 13: 130–32.
30 Manchikanti L, Singh A. Therapeutic opioids: a ten-year perspective
on the complexities and complications of the escalating use, abuse, and nonmedical use of opioids. Pain Physician 2008;
11 (2 suppl): S63–88.
31 Singh G, Triada? lopoulos G. Epidemiology of NSAID induced
gastrointestinal complications. J Rheumatol Suppl 1999; 56: 18–24. 32 Roelofs PD, Deyo RA, Koes BW, Scholten RJ, van Tulder MW.
Non-steroidal anti-in? ammatory drugs for low back pain.
Cochrane Database Syst Rev 2008; 1: CD000396.
33 Vo T, Rice AS, Dworkin RH. Non-steroidal anti-in? ammatory drugs
for neuropathic pain: how do we explain continued widespread use?
Pain 2009; 143: 169–71.
34 ri? n MR, Scheiman JM. Prospects for changing the burden
of nonsteroidal anti-in? ammatory drug toxicity. Am J Med 2001;
110: 33S–37S.
35 Kroenke K, Krebs EE, Bair MJ. Pharmacotherapy of chronic pain:
a synthesis of recommendations from systematic reviews.
Gen Hosp Psychiatry 2009; 31: 206–19.
36 Guggenheimer J, Moore PA. The therapeutic applications of and
risks associated with acetaminophen use: a review and update.
J Am Dent Assoc 2011; 142: 38–44.
37 Verdu B, Decosterd I, Buclin T, Stiefel F, Berney A. Antidepressants
for the treatment of chronic pain. Drugs 2008; 68: 2611–32.
38 Attal N, Cruccu G, Haanpaa M, et al. EFNS guidelines on
pharmacological treatment of neuropathic pain. Eur J Neurol 2006;
13: 1153–69.
39 Arnold LM. Management of psychiatric comorbidity
in ? bromyalgia. Curr Psychiatry Rep 2006; 8: 241–45.
40 Arnold LM, Clauw D, Wang F, Ahl J, Gaynor PJ, Wohlreich MM.
Flexible dosed duloxetine in the treatment of ? bromyalgia:
a randomized, double-blind, placebo-controlled trial. J Rheumatol
2010; 37: 2578–86.
41 Gendreau RM, Thorn MD, Gendreau JF, et al. E? cacy of milnacipran
in patients with ? bromyalgia. J Rheumatol 2005; 32: 1975–85.
42 Tan T, Barry P, Reken S, Baker M. Pharmacological management
of neuropathic pain in non-specialist settings: summary of NICE
guidance. BMJ 2010; 340: c1079.
43 Cro? ord LJ, Rowbotham MC, Mease PJ, et al. Pregabalin for the
treatment of ? bromyalgia syndrome: results of a randomized,
double-blind, placebo-controlled trial. Arthritis Rheum 2005;
52: 1264–73.
44 Chou R, Hu? man LH. Medications for acute and chronic low back
pain: a review of the evidence for an American Pain Society/
American College of Physicians Clinical Practice Guideline.
Ann Intern Med 2007; 147: 505–14.45 Finnerup NB, Sindrup SH, Jensen TS. The evidence for
pharmacological treatment of neuropathic pain. Pain 2010;
150: 573–81.
46 See S, Ginzburg R. Choosing a skeletal muscle relaxant.
Am Fam Physician 2008; 78: 365–70.
47 Arnold LM, Keck PE Jr, Welge JA. Antidepressant treatment of
? bromyalgia. A meta-analysis and review. Psychosomatics 2000;
41: 104–13.
48 Mason L, Moore RA, Edwards JE, McQuay HJ, Derry S, Wi? en PJ.
Systematic review of e? cacy of topical rubefacients containing
salicylates for the treatment of acute and chronic pain. BMJ 2004;
328: 995.
49 Chou R, Hu? man L. Guideline for the management of low back
pain: evidence review. Glenview, IL, USA: American Pain Society,
2009.
50 Manchikanti L, Datta S, Derby R, et al. A critical review of the
American Pain Society Clinical Practice Guidelines for
interventional techniques: Part 1. Diagnostic interventions.
Pain Physician 2010; 13: E141–74.
51 Chou R, Loeser JD, Owens DK, et al. Interventional therapies,
surgery, and interdisciplinary rehabilitation for low back pain.
Spine 2009; 34: 1066–77.
52 Manchinkanti L, Boswell MV, Singh V, Benyamin RM, Fellows B.
Comprehensive evidence-based guidelines for interventional
techniques in the management of chronic spinal pain.
Pain Physician 2009; 12: 699–802.
53 Friedly J, Nishio I, Bishop MJ, Maynard C. The relationship
between repeated epidural steroid injections and subsequent opioid use and lumbar surgery. Arch Phys Med Rehabil 2008; 89: 1011–15. 54 Manchikanti L. The growth of interventional pain management
in the new millennium: a critical analysis of utilization in the
medicare population. Pain Physician 2004; 7: 465–82.
55 Armon C, Argo? CE, Samuels J, Backonja MM. Assessment: use
of epidural steroid injections to treat radicular lumbosacral pain:
report of the Therapeutics and Technology Assessment
Subcommittee of the American Academy of Neurology. Neurology
2007; 68: 723–29.
56 Chou R, Atlas SJ, Stanos SP, Rosenquist RW. Nonsurgical
interventional therapies for low back pain. Spine 2009; 34: 1078–93.
57 Luijsterburg PA, Verhagen AP, Ostelo RW, van Os TA, Peul WC,
Koes BW. E? ectiveness of conservative treatments for the
lumbosacral radicular syndrome: a systematic review. Eur Spine J
2007; 16: 881–99.
58 Rathmell JP, Lake T, Ramundo MB. Infectious risks of chronic pain
treatments: injection therapy, surgical implants, and intradiscal
techniques. Reg Anesth Pain Med 2006; 31: 346–52.
59 Deyo RA, Gray DT, Kreuter W, Mirza S, Martin BI. United States
trends in lumbar fusion surgery for degenerative conditions. Spine 2005; 30: 1441–45.
60 Wang MC, Kreuter W, Wol? a CE, Maiman DJ, Deyo RA. Trends and
variations in cervical spine surgery in the United States: Medicare bene? ciaries, 1992 to 2005. Spine 2009; 34: 955–61.
61 Chou R, Baisden J, Carragee EJ, Resnick DK, Sha? er WO,
Loeser JD. Surgery for low back pain. A review of the evidence for an American Pain Society Clinical Practice Guideline. Spine 2009;
34: 1094–109.
62 Fritzell P, Hagg O, Wessberg P, Nordwall A. 2001 Volvo Award
Winner in Clinical Studies: lumbar fusion versus nonsurgical
treatment for chronic low back pain: a multicenter randomized
controlled trial from the Swedish Lumbar Spine Study Group. Spine 2001; 26: 2521–32.
63 DeBerard MS, Masters KS, Colledge AL, Schleusener RL,
Schlegel JD. Outcomes of posterolateral lumbar fusion in Utah
patients receiving workers’ compensation: a retrospective cohort
study. Spine 2001; 26: 738–46.
64 Hornberger J, Kumar K, Verhulst E, Clark MA, Hernandez J.
Rechargeable spinal cord stimulation versus non-rechargeable
system for patients with failed back surgery syndrome:
a cost-consequences analysis. Clin J Pain 2008; 24: 244–52.
65 Taylor RS. Spinal cord stimulation in complex regional pain
syndrome and refractory neuropathic back and leg pain/failed
back surgery syndrome: results of a systematic review and
meta-analysis. J Pain Symptom Manage 2006; 31 (4 suppl): S13–19.
66 Frey ME, Manchikanti L, Benyamin RM, Schultz DM, Smith HS,
Cohen SP. Spinal cord stimulation for patients with failed back
surgery syndrome: a systematic review. Pain Physician 2009;
12: 379–97.
67 Taylor RS, Van Buyten JP, Buchser E. Spinal cord stimulation for
chronic back and leg pain and failed back surgery syndrome:
a systematic review and analysis of prognostic factors. Spine 2005;
30: 152–60.
68 Turner JA, Loeser JD, Deyo RA, Sanders SB. Spinal cord
stimulation for patients with failed back surgery syndrome
or complex regional pain syndrome: a systematic review of
e? ectiveness and complications. Pain 2004; 108: 137–47.
69 Kemler MA, Barendse GA, van Kleef M, et al. Spinal cord
stimulation in patients with chronic re? ex sympathetic dystrophy.
N Engl J Med 2000; 343: 618–24.
70 Bennett G, Burchiel K, Buchser E, et al. Clinical guidelines for
intraspinal infusion: report of an expert panel. PolyAnalgesic
Consensus Conference 2000. J Pain Symptom Manage 2000;
20: S37–43.
71 Turner JA, Sears JM, Loeser JD. Programmable intrathecal opioid
delivery systems for chronic noncancer pain: a systematic review
of e? ectiveness and complications. Clin J Pain 2007; 23: 180–95.
72 Gerber HR. Intrathecal morphine for chronic benign pain.
Best Pract Res Clin Anaesthesiol 2003; 17: 429–42.
73 Schmidtko A, Lotsch J, Freynhagen R, Geisslinger G. Ziconotide
for treatment of severe chronic pain. Lancet 2010; 375: 1569–77.
74 van Tulder M, Malmivaara A, Hayden JA, Koes B. Statistical
signi? cance versus clinical importance: trials on exercise therapy
for chronic low back pain as example. Spine 2007; 32: 1785–90.
75 Schonstein E, Kenny DT, Keating J, Koes BW. Work conditioning,
work hardening and functional restoration for workers with back
and neck pain. Cochrane Database Syst Rev 2003; 1: CD001822.
76 Oesch P, Kool J, Hagen KB, Bachmann S. E? ectiveness of exercise
on work disability in patients with non-acute non-speci? c low back pain: systematic review and meta-analysis of randomised controlled trials. J Rehabil Med42: 193–205.
77 Ho? man BM, Papas RK, Chatko? DK, Kerns RD. Meta-analysis
of psychological interventions for chronic low back pain.
Health Psychol 2007; 26: 1–9.
78 Morley S, Eccleston C, Williams A. Systematic review and
meta-analysis of randomized controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 1999; 80: 1–13.
79 Henschke N, Ostelo RW, van Tulder MW, et al. Behavioural
treatment for chronic low-back pain. Cochrane Database Syst Rev
2010; 20: CD002014.
80 Dixon KE, Keefe FJ, Scipio CD, Perri LM, Abernethy AP.
Psychological interventions for arthritis pain management
in adults: a meta-analysis. Health Psychol 2007; 26: 241–50.
81 Montgomery GH, DuHamel KN, Redd WH. A meta-analysis
of hypnotically induced analgesia: how e? ective is hypnosis?
Int J Clin Exp Hypn 2000; 48: 138–53.
82 Jensen M, Patterson DR. Hypnotic treatment of chronic pain.
J Behav Med 2006; 29: 95–124.
83 Thieme K, Turk DC, Flor H. Responder criteria for operant
and cognitive-behavioral treatment of ? bromyalgia syndrome.
Arthritis Rheum 2007; 57: 830–36.
84 Guzman J, Esmail R, Karjalainen K, Malmivaara A, Irvin E,
Bombardier C. Multidisciplinary rehabilitation for chronic low back pain: systematic review. BMJ 2001; 322: 1511–16.85 Flor H, Fydrich T, Turk DC. E? cacy of multidisciplinary pain
treatment centers: a meta-analytic review. Pain 1992; 49: 221–30.
86 Thomsen AB, Sorensen J, Sjogren P, Eriksen J. Chronic
non-malignant pain patients and health economic consequences.
Eur J Pain 2002; 6: 341–52.
87 Nachemson AL. Newest knowledge of low back pain. A critical look.
Clin Orthop Relat Res 1992; 279: 8–20.
88 Verhaak PF, Kerssens JJ, Dekker J, Sorbi MJ, Bensing JM.
Prevalence of chronic benign pain disorder among adults: a review of the literature. Pain 1998; 77: 231–39.
89 Tan G, Craine MH, Bair MJ, et al. E? cacy of selected
complementary and alternative medicine interventions for chronic pain. J Rehabil Res Dev 2007; 44: 195–222.
90 Haake M, Muller HH, Schade-Brittinger C, et al. German
Acupuncture Trials (GERAC) for chronic low back pain:
randomized, multicenter, blinded, parallel-group trial with
3 groups. Arch Intern Med 2007; 167: 1892–98.
91 Witt CM, Ludtke R, Wegscheider K, Willich SN. Physician
characteristics and variation in treatment outcomes: are better
quali? ed and experienced physicians more successful in treating
patients with chronic pain with acupuncture? J Pain 2010;
11: 431–35.
92 Furlan AD, van Tulder M, Cherkin D, et al. Acupuncture and
dry-needling for low back pain: an updated systematic review within the framework of the cochrane collaboration. Spine 2005; 30: 944–63.
93 Manheimer E, White A, Berman B, Forys K, Ernst E. Meta-analysis:
acupuncture for low back pain. Ann Intern Med 2005; 142: 651–63. 94 Gilron I, Max MB. Combination pharmacotherapy for neuropathic
pain: current evidence and future directions. Expert Rev Neurother
2005; 5: 823–30.
95 Johnson M, Martinson M. E? cacy of electrical nerve stimulation
for chronic musculoskeletal pain: a meta-analysis of randomized
controlled trials. Pain 2007; 130: 157–65.
96 Khadilkar A, Odebiyi DO, Brosseau L, Wells GA. Transcutaneous
electrical nerve stimulation (TENS) versus placebo for chronic
low-back pain. Cochrane Database Syst Rev 2008; 4: CD003008.
97 Turk DC. Clinical e? ectiveness and cost-e? ectiveness of treatments
for patients with chronic pain. Clin J Pain 2002; 18: 355–65.
98 Turk DC. The potential of treatment matching for subgroups of
patients with chronic pain: lumping versus splitting. Clin J Pain
2005; 21: 44–55.
99 van Tulder MW, Koes B, Seitsalo S, Malmivaara A. Outcome
of invasive treatment modalities on back pain and sciatica: an
evidence-based review. Eur Spine J 2006; 15 (suppl 1): S82–92.
100 Gilron I, Bailey JM, Tu D, Holden RR, Weaver DF, Houlden RL.
Morphine, gabapentin, or their combination for neuropathic pain.
N Engl J Med 2005; 352: 1324–34.
101 Gilron I, Bailey JM, Tu D, Holden RR, Jackson AC, Houlden RL.
Nortriptyline and gabapentin, alone and in combination for
neuropathic pain: a double-blind, randomised controlled crossover trial. Lancet 2009; 374: 1252–61.
102 Dworkin, RH, Turk DC, Farrar JT, et al. Core outcome domains for chronic pain clinical trials: IMMPACT recommendations. Pain 2005; 113: 9–19.
(完整版)癌痛治疗的现状与癌痛的评估
癌痛治疗的现状与癌痛的评估 癌症疼痛 (cancer pain) 是指由癌症、癌症相关性病变及抗癌治疗所致的疼痛，常为慢性疼痛，是癌症患者的常见症状。晚期癌症患者的疼痛发生率约 60 ％～ 80 ％，其中 1 ／ 3 的患者为重度疼痛。癌症疼痛如果得不到恰当的止痛治疗将会对患者及家属的生活质量造成极其严重的影响，可造成抑郁、乏力、焦虑、失眠、全身情况恶化或严重干扰抗癌治疗的施行。进一步提高对癌症疼痛的认识、评估及治疗水平，将造福于广大癌症疼痛患者。 一、癌症疼痛治疗的现状 （一）基本情况 1982 年，世界卫生组织在意大利米兰成立世界卫生组织癌症疼痛治疗专家委员会。专家委员会经讨论一致认为应用现有的镇痛药物可以解除大多数癌症患者的疼痛，同时筹划起草癌症疼痛治疗指南。 1986 年，世界卫生组织正式出版《癌症疼痛治疗》第一版 (Cancer pain relief) 。该书作为癌症疼痛治疗指南，提出癌症疼痛药物治疗的五项基本原则：口服用药；按时给药；按阶梯给药；个体化给药；注意个体细节。按阶梯给药是指根据患者疼痛程度选择不同作用强度的镇痛药物。即轻度疼痛选择非甾体类抗炎药，中度疼痛选择弱阿片类镇痛药，重度疼痛选择强阿片类镇痛药。因此，该指南又被称为癌症三阶梯止痛治疗原则。世界卫生组织推行癌症三阶梯止痛治疗原则的倡导，得到了各国肿瘤学术界及政府管理部门的普遍赞同和支持。 1990 年，我国首次在广州与世界卫生组织共同组织全国性专题会议，开始推行世界卫生组织癌症三阶梯止痛治疗原则。 1991 年，我国卫生部颁布《关于在我国开展癌症患者三阶梯止痛治疗工作的通知》。随后十余年我国相继出台多项管理制度和政策，多次举办各种学习班和研讨会，推行世界卫生组织癌症疼痛三阶梯止痛治疗原则。经过政府部门和专家学者的共同努力，我国开展三阶梯癌痛镇痛治疗原则的努力已初见成效，我国的癌症疼痛治疗工作取得了明显的进展，医护人员在癌痛治疗的临床实践中积累了一定的经验。但是由于我国人口众多，各地区发展不平衡，工作中仍然存在很多问题，例如大量患者仍然镇痛不足、很多基层医师对于麻醉性镇痛药的使用依然心存疑虑等。因此，进一步加强癌症疼痛及非癌症疼痛知识的普及宣传，推行和完善规范化疼痛治疗工作势在必行。 （二）、癌症疼痛的原因及分类 世界卫生组织将癌症患者的疼痛分为四类，分别为肿瘤侵犯所致疼痛、抗肿瘤治疗所致疼痛、与肿瘤相关的疼痛以及与肿瘤或治疗无关的疼痛 ( 见表 ) 。多数癌症患者尤其是癌症晚期患者常合并多种类型的疼痛。 1. 肿瘤侵犯所致的疼痛：约占癌症疼痛的 80 ％。癌细胞直接浸润，压迫或转移可引起严重的癌症疼痛。
强阿片类药物治疗慢性非癌痛使用指导
前言 为了规范临床用药，充分发挥强效阿片类药物在医疗临床中的作用，最大程度地减少或者避免此类药物的相关不良反应，在参考国外相关资料和国内临床多中心研究初步结果的基础上，由国内疼痛治疗专家和药物滥用研究及药物控制专家组成的专家小组特制定出以多瑞吉为代表的《强阿片类药物治疗慢性非癌痛使用指南》。 必须指出：临床医师必须规范此类药物的临床应用，并对所有病例进行随访。《指南》也将随着临床实践和经验的不断积累，进行必要的完善。 《指南》由罗爱伦、蔡志基、李树人、许建国、黄宇光等10余位专家起草并核定。 一、慢性疼痛的定义： 既往将慢性疼痛定义为：病人无明确组织损伤,但出现持续6个月以上的疼痛。目前医学界将慢性疼痛定义为：慢性疼痛导致病人抑郁和焦虑,造成身心极大伤害，并严重影响其生活质量。慢性非癌性疼痛是十分普遍的现象，需要医治。 慢性非癌痛病人治疗是为了缓解疼痛和抑郁。临床上更加注重病人的功能恢复,应将“病人能否重返工作岗位,能否恢复正常生活"作为判定疼痛治疗是否有效的客观指标。 二、慢性非癌痛处理的原则和方法 1.基本原则：慢性非癌痛治疗的目的：缓解疼痛和改善功能状态。功能状态包括身体状态、精神状态和家庭社会关系等。有效的疼痛治疗包含多种形式的综合治疗，其中药物治疗是重要的组成部分。 2.药物治疗：世界卫生组织(WorldHealthOrganization)用于癌痛治疗的三阶梯镇 痛原则同样适用于慢性非癌痛镇痛治疗。WHO强调：慢性非癌痛治疗应采取药物和非药物结合的综合治疗方法。 3.非药物性治疗：慢性非癌痛的非药物治疗包括：理疗、针灸和心理治疗等。 三、强效阿片类药物的使用 国外大量临床资料表明：不论慢性非癌痛的病因如何，中、重度疼痛都可以使用强效阿片类药物治疗。强阿片类药物治疗伤害性疼痛疗效确切，相当一部分神经源疼痛病人使用强阿片类药物症状可得到明显缓解。因此，在其他常用治疗方法无效时，应考虑强阿片类药物治疗。 四、强阿片类药物在慢性非癌痛治疗中的指导原则
乳腺癌的护理常规
乳腺癌的相关知识和护理 乳腺癌时女性最常见的恶性肿瘤之一在我国占全身各种肿瘤的7—10%，仅次于子宫颈癌，但近年来有上升趋势，部分大城市报告乳房癌占女性恶性肿瘤的首位。 乳房癌的病因尚不清楚，但目前认为与下列因素有关，诱发因素： 1 年龄：在女性中，发病率随着年龄的增长而上升，在月经初潮前罕见，20岁前亦少见，但20岁以后发病率迅速上升，45～50岁较高，绝经后发病率继续上升，到70岁左右达最高峰。死亡率也随年龄而上升。 2 遗传因素：家族的妇女有第一级直亲家族的乳腺癌史者（母亲和姐妹），其乳腺癌的危险性是正常人群的2～3倍。 3 其他乳房疾病。 4 月经初潮年龄：初潮年龄早于13岁者发病的危险性为年龄大于17岁者的2.2倍。 5 绝经年龄：绝经年龄大于55岁者比小于45岁的危险性增加。 6 第一次怀孕年龄：危险性随着初产年龄的推迟而逐渐增高，初产年龄在35岁以后者的危险性高于无生育史者。 7 绝经后补充雌激素：在更年期长期服用雌激素可能增加乳腺癌的危险性。 8 口服避孕药。 9 食物：尤其是脂肪饮食，可以增加乳腺癌的危险性。 10 饮酒 11 体重增加可能是绝经期后妇女发生乳腺癌的重要危险因素。 (一)症状 早期常无明显的临床症状，或仅表现为轻微的乳房疼痛，性质多为钝痛或隐痛，少数为针刺样痛，疼痛不随月经周期而变化。晚期癌肿侵犯神经时则疼痛较剧烈，可放射到同侧肩、臂部。 (二)体征 1、乳房肿块 乳房肿块常是促使患者就诊的主要症状。80%以上为患者自己偶然发现，只有一小部分是查体时被医生发现。 (1)部位肿块绝大多数位于乳房外上象限，其次为内上象限、上方及中央区，
食管癌护理常规(建议收藏)
食管癌护理常规 【定义】发生于食管上皮组织的恶性肿瘤。食道癌是常见的消化道恶性肿瘤之 一。 【观察要点】1、密切观察并发症的出现：对病人疼痛的性质、体温、脉搏、血压等的变化情况要认真记录，密切观察有无异常，是否有进食、进水呛咳现象，病人有无食管穿孔、出血的有利依据,出现问题及时报告医生尽快 做好抢救治疗工作。.。..。.文档交流2、密切观察食管的反应：食管反应是食管癌病人进行放疗时最常发生的一种副反应。大部分病人在照射治疗1—2周时,常出现轻重不一的放射性食管炎。由于食管黏膜的充血、水肿，临床表现为已经出现的吞咽困难逐渐加重或进食疼痛.严重影响饮食的摄入。......文档交流 【护理措施】 1、密切观察生命体征及神志变化，定期检查肝肾功能。 2、注意视察各种并发症的先兆症状，及时发现并通知医生. 3、常见并发症包括食管穿孔、呕血、吸入性肺炎、电解质紊乱。 4、提供可口的、不油腻的、高营养的、易于咀嚼的食物，如鱼、蛋.注意少量多餐，当病人感恶心、呕吐时，暂停进食。预防性使用止吐药，观察药物疗效。加强口腔护理，保持口腔湿润、清洁,以增进食欲。。。...。文档交流 5、进餐时,让病人采取半卧位或坐位,以利吞咽。 6、病人进餐时,给病人充分的咀嚼、吞咽时间,喂饭速度不要快.
7、遵医嘱给予肠道外营养，如静滴复方氨基酸、脂肪乳剂。 8、每周监测体重。 【健康教育】 1、心理护理加强情绪护理，安慰患者，消除紧张、恐惧、抑郁、颓丧等心理，耐心做好治疗解释工作。如有脱发者，可配置发套，尽量使患者在接受化疗过程中处于最佳身心状态。..。.。.文档交流 2、营养和饮食 适量补充维生素。维生素有益于身体健康，加强人体免疫能力,食道癌的护理包括因此适量补充维生素是很必要的,术后，患者可以吃些新鲜蔬菜、水果、动物肝脏等都属于食道癌的饮食.还可以多吃些富含蛋白质饮食。其中，瘦肉、蛋类、豆类、奶类都含有各种人体所需的氨基酸，可以加强身体机能,尽早恢复健康。。。.。。.文档交流 3、用药护理 注意观察药物不良反应，如化疗时应密切观察患者胃肠道反应及骨髓抑制反应，定期复查血象。 4、心理健康 医护人员深入病房,了解各个病人的不同思想情况，针对所表现的问题，做细致的工作创造良好的住院环境,保持病室的安静和环境优美,轻重病人在条件允许下分别安置,以免病人触景生情。理解和同情病人，观察病人的情绪和行为，依具体情况有的放矢地加以安慰和开导，消除其心理障碍，对病人提出的每一个问题予以详细解答，并帮助其解决一些具体困难。此时病人若表现出一些积极反应，则预示着心理
癌性疼痛处理
癌性疼痛的处理 WHO 3-阶梯镇痛疗法 Management of Cancer Pain WHO 3 – Step Analgesic Ladder Terence L. Gutgsell, MD Hospice of the Bluegrass Lexington, KY 目标 比较，对比感受伤害性的和神经病性的疼痛 了解癌痛镇痛处理的阶梯 了解阿片类镇痛剂给药的其他途径 讲解维持镇痛时阿片类药物间互相转换的技巧 Objectives Compare, contrast nociceptive, neuropathic pain Know steps of analgesic management of cancer pain Know alternative routes for delivery of opioid analgesics Demonstrate ability to convert between opioids while maintaining analgesia 总的原则 多因素对患者反应的影响 环境心理/社会状态年龄 性别多系统疾病和障碍复合用药 General Principles Influences on patient’s response to Rx Environment Psycho/social status Age Sex Multi-system disease and disorders Polypharmacy 普遍原则 “拇指原则” 诊断可能的机制,个体化治疗 ATC和PRN用药,保持简单 反复评价,注意细节 General Principles “Rules of Thumb” Diagnose underlying mechanism Individualize treatment ATC and PRN medications
癌症疼痛诊疗规范标准
癌症疼痛诊疗规 （年版） 一、概述 疼痛是癌症患者最常见的症状之一，严重影响癌症患者的生活质量。初诊癌症患者疼痛发生率约为；晚期癌症患者的疼痛发生率约为％％，其中的患者为重度疼痛。癌症疼痛（以下简称癌痛）如果得不到缓解，患者将感到极度不适，可能会引起或加重患者的焦虑、抑郁、乏力、失眠、食欲减退等症状，严重影响患者日常活动、自理能力、交往能力及整体生活质量。 为进一步规我国癌痛诊疗行为，完善重大疾病规化诊疗体系，提高医疗机构癌痛诊疗水平，改善癌症患者生活质量，保障医疗质量和医疗安全，特制定本规。 二、癌痛病因、机制及分类 （一）癌痛病因。癌痛的原因多样，大致可分为以下三类： .肿瘤相关性疼痛：因肿瘤直接侵犯压迫局部组织，肿瘤转移累及骨等组织所致。 .抗肿瘤治疗相关性疼痛：常见于手术、创伤性检查操作、放射治疗，以及细胞毒化疗药物治疗后产生。 .非肿瘤因素性疼痛：包括其他合并症、并发症等非肿瘤因素所致的疼痛。
（二）癌痛机制与分类。 .疼痛按病理生理学机制主要分为两种类型：伤害感受性疼痛及神经病理性疼痛。 （）伤害感受性疼痛是因有害刺激作用于躯体或脏器组织，使该结构受损而导致的疼痛。伤害感受性疼痛与实际发生的组织损伤或潜在的损伤相关，是机体对损伤所表现出的生理性痛觉神经信息传导与应答的过程。伤害感受性疼痛包括躯体痛和脏痛。躯体性疼痛常表现为钝痛、锐痛或者压迫性疼痛。脏痛通常表现为定位不够准确的弥漫性疼痛和绞痛。 （）神经病理性疼痛是由于外周神经或中枢神经受损，痛觉传递神经纤维或疼痛中枢产生异常神经冲动所致。神经病理性疼痛常被表现为刺痛、烧灼样痛、放电样痛、枪击样疼痛、麻木痛、麻刺痛、枪击样疼痛。幻觉痛、中枢性坠、胀痛，常合并自发性疼痛、触诱发痛、痛觉过敏和痛觉超敏。治疗后慢性疼痛也属于神经病理性疼痛。 .疼痛按发病持续时间分为急性疼痛和慢性疼痛。癌症疼痛大多表现为慢性疼痛。与急性疼痛相比较，慢性疼痛持续时间长，病因不明确，疼痛程度与组织损伤程度可呈分离现象，可伴有痛觉过敏、异常疼痛、常规止痛治疗疗效不佳等特点。慢性疼痛与急性疼痛的发生机制既有共性也有差异。慢性疼痛的发生，除伤害感受性疼痛的基本传导调制过
癌症疼痛治疗综述
癌症疼痛的治疗 一、癌症疼痛的药物治疗 在现有疼痛治疗手段中，药物治疗是基础。严格规范按照WHO推荐的癌症疼痛病人三阶梯止痛方案，可以使90%癌症疼痛病人的疼痛得到缓解。 （一）W HO的三阶梯治疗原则 1、按阶梯给药 止痛药物的选择应根据疼痛程度由弱到强按顺序提高，除非是重度疼痛。一般首选非阿片类药物，属于三级阶梯的第一级，用于轻至中度疼痛。如疼痛继续加剧，则升高到第二级，在非阿片类药物的基础上加上弱阿片类药物。若疼痛仍未控制或继续加剧，则进入第三级，以用于中度到重度疼痛的强阿片类药物替换，也可同时加用非阿片类药，后者既能增加阿片类药物的止痛效果，又可减少阿片类药物的用量。此外辅助药物主要用于增强止痛效果，治疗疼痛加剧的并发症，在治疗特殊疼痛时辅助药物可产生独立止痛作用，因此可用于任何阶梯中。需要注意的是三阶梯应用不要过于教条，因为病人的情况复杂多变，应根据病情灵活掌握和使用镇痛药物，更多现象是需要不同药物的配伍，以求获得更好的镇痛效果。 2、口服给药 在尽可能情况下力争口服给药。因为口服给药方便、经济，无创伤性，不良反应小又能增加病人独立性。血药浓度稳定，与静脉注射用药相比同样有效，免除创伤性给药的不适，在家或医院均可使用。另外口服给药时吸收缓慢，峰值较低，不易产生药物依赖性和耐受性，从而提高病人生活质量。 所以口服给药是一种最简单、最科学的给药方式。 3、按时给药 止痛治疗应根据所用药物药代动力学的规律按时给药，而不是当疼痛达到不能忍受时才给镇痛药物（即按需给药）。因为，镇痛药物需要达到有效浓度时才具有镇痛效能，为保持止痛的连续性，需要在药物浓度下降时，及时给予药物维持有效血药浓度。按时给药可以获得稳定的镇痛效果，减少血药波动而出现的反复疼痛，推迟了药物耐受的出现，是镇痛治疗观念上的进步。 4、个体化给药 个体化原则是根据不同个体对麻醉药品敏感度的差异，既往使用止痛药的情况，及药物的药理特点确定给予药物剂量。对麻醉药品敏感度个体差异很大，所以阿片类药物没有标准量。应该说凡是能
癌性疼痛综合
定义 疼痛是一种与组织损伤或潜在组织损伤相关的、不愉快 的主观感觉和情感体验以及保护性或病理性反应。癌性 疼痛(简称癌痛) 是由癌症本身以及癌症治疗过程中产生的 疼痛。 病因 一、肿瘤自身引起疼痛 1.肿瘤浸润骨组织 2.肿瘤侵犯内脏 3.肿瘤侵犯神经系统 二、肿瘤诊断和治疗引起的疼痛 1、肿瘤诊断引起的疼痛 2、肿瘤治疗引起的疼痛 三、非肿瘤病症的合并症 四、精神与心理因素 临床表现 临床上常见癌性疼痛的表现 (1) 头痛 (2) 上肢痛 (3) 背痛: 硬膜外脊髓压迫症中在出现其他神经症状体征以前, 约有90% 以上的患者会发生剧烈的背痛。 (4) 下肢痛 (5) 放射痛 (6) 腹痛: 肠癌患者出现发作性肠梗阻, 腹痛是常见的症状, 这种腹痛紧急而复杂, (7) 会阴痛: 癌细胞浸润盆腔时, 会出现会阴部及小腹疼痛。
(8) 全身疼和暴发痛: 癌症患者的终末期可出现全身疼痛。癌痛患者在使用止痛药的过程中, 会出现暴发痛。 评估 2. 1. 1 自我评估法 (1) 口述分级评分法(Verbal Rating Scale ,VRS) ,由一系 列描述疼痛的形容词组成。 (2) 视觉模拟评分法(Visual analogue Scale ,VAS) :是诸 疼痛强度评分方法中最敏感的方法 (3) 混合法:如Mcgill 疼痛调查表(Mcgill Pain Question2 naire ,MPQ) ,Memorial 疼痛评估卡片(Memorial Pain As2 sessment Card ,MPAC) 2. 1. 2 行为评估法 2. 1. 3 生理变化测量 治疗 三阶梯方案控制癌痛癌痛的治疗必须建筑在确切的诊断基础上。在正确估价痛因及性质后,首选药物三 阶梯方案止痛。 21211 首选药———非阿片类药(第一阶梯)非甾体抗炎药: 如阿司匹林、扑热息痛、醋氨酚(paracetamal) 、双氯 芬酸钠等。主要针对轻度和中等度的周围性癌痛。对骨转移性癌痛常能止痛。这类药物对骨
医学继续教育癌症疼痛护理
第十一讲癌症疼痛护理 国际疼痛学会将疼痛定义为：“疼痛是一种与实际或潜在组织损伤相关，包括了感觉、情感、认知和社会性的方面的痛苦体验。”疼痛既是机体对创伤或疾病的反应机制，也是疾病的症状。 癌痛是指癌症、癌症相关性病变及抗癌治疗所致的疼痛，是多因素相互作用的最终结果。癌痛是肿瘤患者最常见的症状之一，据统计，53%癌症患者经历过疼痛，25%新诊断患者有疼痛，59%正在接受治疗的癌症患者发生疼痛，而晚期癌症患者的疼痛发生率可达60％-80％，其中1/3的患者为重度疼痛，33%癌症治愈患者存在与癌症或治疗相关的慢性疼痛。 如果癌症疼痛（以下简称癌痛）不能得到及时、有效的控制，患者往往感到极度不适，可能会引起或加重其食欲减退、焦虑、乏力、失眠、情绪消沉甚至患上抑郁症，以及等症状，显著影响患者的日常活动、自理能力、工作、社会交往和整体生活质量，无论病人还是家属的生活质量都无从保证。同时,也会使患者机体免疫力下降,使肿瘤有进一步发展的机会。 2001年第二届亚太地区控制癌痛研讨会提出: 消除疼痛是患者的基本权利。2002年第10届国际疼痛大会与会专家达成共识：慢性疼痛是一种疾病，同时指出：疼痛是等同于脉搏、呼吸、血压、体温的人体第五大生命体征，也就是说，医生要像关心病人的血压、脉搏、呼吸和体温一样关注病人的疼痛问
题。不要认为只要得了癌症就一定会疼，疼痛是正常现象。疼痛本身就是一种疾病，而不仅仅是癌症的症状，临床医生应予以重视。因此，止疼是每个癌症病人的基本权利，必须尊重。对癌痛患者疼痛的护理意识已被越来越多人所重视，对癌症病人癌痛的专业全面的护理是提高病人生活质量、唤起病人生活意志的重要因素。 一、癌痛的原因 癌痛的原因复杂多样大致可分为以下三类： 1.肿瘤相关性疼痛：包括原发肿瘤和继发转移瘤所致，因为肿瘤直接侵犯、压迫局部组织，或者肿瘤转移累及骨、软组织等所致。肿瘤增大、浸润、压迫或侵及神经组织、淋巴管或血管，使有关组织器官缺血、坏死、或牵拉、推移周围有关组织器官均可产生疼痛。颅内高压以及腔道性器官梗阻，积水积液等也产生疼痛。肿瘤本身坏死、破溃、继发感染或肿瘤增大刺激包膜，骨转移造成的骨皮质破坏，病理性骨折等都可产生疼痛。 2.抗肿瘤治疗相关性疼痛：常见于手术或手术后并发症可引起疼痛；创伤性操作、放射治疗、其他物理治疗以及药物治疗等抗肿瘤治疗所致。化疗药物注射引起的静脉炎，药物外渗引起的皮肤、皮下组织刺激、红肿、破溃甚至坏死；中毒性周围神经病变；胸、腹腔化疗产生的包裹粘连、增厚或牵拉引
癌症疼痛诊疗规范2011
癌症疼痛诊疗规范 （2011年版） 一、概述 疼痛是癌症患者最常见的症状之一，严重影响癌症患者的生活质量。初诊癌症患者疼痛发生率约为25%；晚期癌症患者的疼痛发生率约为60％-80％，其中1/3的患者为重度疼痛。癌症疼痛（以下简称癌痛）如果得不到缓解，患者将感到极度不适，可能会引起或加重患者的焦虑、抑郁、乏力、失眠、食欲减退等症状，严重影响患者日常活动、自理能力、交往能力及整体生活质量。 为进一步规范我国癌痛诊疗行为，完善重大疾病规范化诊疗体系，提高医疗机构癌痛诊疗水平，改善癌症患者生活质量，保障医疗质量和医疗安全，特制定本规范。 二、癌痛病因、机制及分类 （一）癌痛病因。癌痛的原因多样，大致可分为以下三类： 1.肿瘤相关性疼痛：因肿瘤直接侵犯压迫局部组织，肿瘤转移累及骨等组织所致。 2.抗肿瘤治疗相关性疼痛：常见于手术、创伤性检查操作、放射治疗，以及细胞毒化疗药物治疗后产生。 3.非肿瘤因素性疼痛：包括其他合并症、并发症等非肿瘤因素所致的疼痛。 （二）癌痛机制与分类。 1.疼痛按病理生理学机制主要分为两种类型：伤害感受性疼痛及神经病理性疼痛。 （1）伤害感受性疼痛是因有害刺激作用于躯体或脏器组织，使
该结构受损而导致的疼痛。伤害感受性疼痛与实际发生的组织损伤或潜在的损伤相关，是机体对损伤所表现出的生理性痛觉神经信息传导与应答的过程。伤害感受性疼痛包括躯体痛和内脏痛。躯体性疼痛常表现为钝痛、锐痛或者压迫性疼痛。内脏痛通常表现为定位不够准确的弥漫性疼痛和绞痛。 （2）神经病理性疼痛是由于外周神经或中枢神经受损，痛觉传递神经纤维或疼痛中枢产生异常神经冲动所致。神经病理性疼痛常被表现为刺痛、烧灼样痛、放电样痛、枪击样疼痛、麻木痛、麻刺痛。幻觉痛、中枢性坠、胀痛，常合并自发性疼痛、触诱发痛、痛觉过敏和痛觉超敏。治疗后慢性疼痛也属于神经病理性疼痛。 2.疼痛按发病持续时间分为急性疼痛和慢性疼痛。癌症疼痛大多表现为慢性疼痛。与急性疼痛相比较，慢性疼痛持续时间长，病因不明确，疼痛程度与组织损伤程度可呈分离现象，可伴有痛觉过敏、异常疼痛、常规止痛治疗疗效不佳等特点。慢性疼痛与急性疼痛的发生机制既有共性也有差异。慢性疼痛的发生，除伤害感受性疼痛的基本传导调制过程外，还可表现出不同于急性疼痛的神经病理性疼痛机制，如伤害感受器过度兴奋、受损神经异位电活动、痛觉传导中枢机制敏感性过度增强、离子通道和受体表达异常、中枢神经系统重构等。 三、癌痛评估 癌痛评估是合理、有效进行止痛治疗的前提。癌症疼痛评估应当遵循“常规、量化、全面、动态”评估的原则。 （一）常规评估原则。 癌痛常规评估是指医护人员主动询问癌症患者有无疼痛，常规评估疼痛病情，并进行相应的病历记录，应当在患者入院后8小时内完成。对于有疼痛症状的癌症患者，应当将疼痛评估列入护理常规监测
癌痛患者护理常规
成都市第七人民医院成都市肿瘤医院 癌痛患者护理常规 疼痛是癌症患者最常见的症状之一，初诊癌症患者疼痛发生率约为25％，晚期癌症患者的疼痛发生率可高达60％—80％，其中三分之一的患者为重度疼痛。癌症疼痛（以下简称癌痛）如果得不到缓解，患者将感到极度不适，可能会引起或加重患者的焦虑、抑郁、乏力、失眠、食欲减退等症状，严重影响患者日常活动、自理能力、交往能力及整体生活质量。 为进一步规范我院癌痛护理行为，改善癌症患者生活质量，保障护理质量和医疗安全，特制定本护理常规。 一、癌痛评估方法 正确评估疼痛的程度是有效治疗癌痛的关键，疼痛是患者的主观症状和感受，护理人员应该以患者的主诉为主要依据，以观察到的患者的行为及生命体征为辅助依据，结合临床目前使用的评估工具，掌握正确的评估方法，为医疗选择疼痛治疗的方法提供参考依据，有效控制癌症患者的疼痛，减轻患者的痛苦。 （一）数字分级法（NRS）：使用《疼痛程度数字评估量表》（见图1）对患者疼痛程度进行评估。将疼痛程度用0-10个数字依次表示，0表示无疼痛，10表示最剧烈的疼痛。交由患者自己选择一个最能代表自身疼痛程度的数字，或由医护人员询问患者：你的疼痛有多严重？由医护人员根据患者对疼痛的描述选择相应的数字，按照疼痛对应的数字将疼痛程度分为：轻度疼痛（1-3），中度疼痛（4-6），重度疼痛(7-10)。 （二）面部表情评估量表法
（三）主诉疼痛程度分级法（VRS） 轻度疼痛：有疼痛但可以忍受，生活正常，睡眠无干扰。中度疼痛：疼痛明显，不能忍受，要求服用镇痛药物，睡眠受干扰。重度疼痛：疼痛剧烈，不能忍受，需用镇痛药物，睡眠受严重干扰，可伴自主神经紊乱或被动体位。 二、癌痛患者筛查 （一）新入院患者： 1.每一位新入院的患者都要在2小时内完成评估。 2.癌痛评分≥4分（中度）和长期使用阿片类药物止痛处理的病员应建立《癌痛评估观察护理记录单》。 3. 《癌痛评估观察护理记录单》和《癌痛护理记录单（首页）》填写必须详细、客观。应相信病员的主诉，患者感觉有多痛就有多痛，不宜主观臆断。《癌痛护理记录单（首页）》填写完成后，请各楼层的疼痛护士审核、签名，并请病员或家属确认并签名。护理人员所评的NRS评分必须和医生所评的NRS评分保持一致。 （二）住院患者每日常规进行两次疼痛评分（固定在每日6：00、14:00），癌痛评分≥4分（中度）的建立记录《癌痛评估观察护理记录单》。 三、癌痛患者观察 （一）肿瘤住院患者每日将疼痛评分作为第五生命体征，固定时间（6：00、14:00）评估，并书写在体温单上。NRS评分应记录在电子病历体温单的相应栏内(若手绘体温单则用蓝笔记录在脉搏30~40次／分一栏对应的时间下面)。若病员发生暴发痛只需记录在《癌痛评估观察护理记录单》上，并根据使用的止痛药物或处理措施按时观察并记录。 （二）对患者疼痛及相关病情进行全面评估，包括疼痛病因及类型（躯体性、内脏性或神经病理性），疼痛发作情况（疼痛性质、加重或减轻的因素），止痛治疗情况，重要器官功能情况，心理精神情况，家庭及社会支持情况，以及既往史（如精神病史，药物滥用史）等评估疼痛及对患者情绪、睡眠、活动能力、食欲、日常生活、行走能力、与他人交往等生活质量的影响，应当重视和鼓励患者描述对止痛治疗的需求及顾虑，并根据患者病情和意愿，制定患者功能和生活质量最
晚期癌症疼痛的护理_综述
晚期癌症患者疼痛护理概论 摘要： 本文主要就近年来晚期癌症患者疼痛护理技术概况做一系统性介绍，希望能够有效指导临床护理工作者做好晚期癌症患者疼痛护理工作，帮助晚期癌症患者积极应对疼痛，提高生存质量。 关键词：晚期癌症、疼痛、护理进展 国的调查表明：在综合性医院或专科医院的各期癌症患者中，51.1%伴有不同程度的疼痛，尤其是晚期患者，75%都有疼痛问题，且92.51%的癌症患者为中度疼痛[1]，癌症疼痛给患者带来了巨大的痛苦，是患者最为恐惧和最难忍受的症状，其从心理、生理、精神等方面严重影响患者的生存质量，同时对患者家庭及社会造成巨大的危害。在护理对策中，消极、祈祷的疼痛护理对策与疼痛程度成正相关，积极、勇敢的护理对策与疼痛程度呈负相关[2]。由此可见，采取积极的护理措施以控制癌痛对提高晚期癌症患者的生活质量极其重要。 1．癌症疼痛简介。 疼痛是由实际的或潜在的组织损伤引起的一种不愉快的感觉和情感经历，是一种复杂的生理心理活动，是临床上最常见的症状之一。痛觉可作为机体受到伤害的一种警告，引起机体一系列防御性保护反应，而某些长期的剧烈疼痛，对机体已成为一种难以忍受的折磨，因此，镇痛是医务工作者面临的重要任务。 现在全世界都在关注疼痛，癌痛已成为继体温、脉搏、呼吸、血压4 大生命体征之后的第5 生命体征，日益受到重视。研究表明，中国癌性疼痛病人发病率高达50%左右，肿瘤疼痛原因包括肿瘤本身引起的疼痛占第1位约占80%、肿瘤相关或无关的疼痛综合征占10%左右、肿瘤诊断或治疗相关的疼痛占10%左右等等。另外，大部分肿瘤患者因患“绝症”后的心理改变、对肿瘤知识的缺乏、家庭社会生活的改变加重肿瘤患者的躯体疼痛，故对晚期癌痛患者的医疗护理不仅需要有效的镇痛治疗，还需要针对肿瘤疼痛的特殊护理，给予患者无微不至的关心及指导，以提高患者的生活质量[3]。 事实上，让癌症患者无痛或尽量使疼痛减轻到可以耐受的程度是完全能够做到的。只要正确评估疼痛程度，恰当使用止痛剂和有效止痛方法，90% 以上患者的疼痛可以得到缓解。通过１４００名注册护士问卷调查表明，最佳处理疼痛的主要障碍是对疼痛估计不足、处理疼痛的知识不够和患者不愿报告疼痛［4］。因此，获得疼痛护理的良好疗效，疼痛的评估和再评估是基础。 2.疼痛评估。 2.1疼痛的分级： ０级：无疼痛。Ⅰ级：轻微可以忍受的疼痛，能正常生活，饮食、睡眠基本不受干扰。Ⅱ级：中度持续或阵发性疼痛，可短时耐受，日常生活、饮食、睡眠受到不同程度的干扰。Ⅲ级：不可忍受的重度疼痛，疼痛剧烈、持续，活动受到限制，睡眠、饮食受到严重干扰，必须服用止痛药。中晚期肿瘤患者大多都是疼痛Ⅲ级。 2.2建立疼痛护理单：疼痛患者建立疼痛护理单对疼痛的观察具有重要临床意义[5]。 2.2.1疼痛护理单的容：患者的、性别、诊断、疼痛的分类( 急性、癌痛、慢性非恶性疼痛)；入院时疼痛的情况( 有无疼痛、周期性疼痛、活动性疼痛还是持续性疼痛)，疼痛的部位(A、B、C 等)，出现的日期、时间、部位、活动情
癌性疼痛
定义 1 癌性疼痛得定义 疼痛就是一种与组织损伤或潜在组织损伤相关得、不愉快 得主观感觉与情感体验以及保护性或病理性反应。癌性 疼痛（简称癌痛）就是由癌症本身以及癌症治疗过程中产生得 疼痛 病因 一、肿瘤自身引起疼痛?肿瘤自身引起得疼痛占癌性疼痛得7５％。肿瘤得生长部位决定着疼痛得发生频率,进展性肿瘤在不同时期对疼 1、肿瘤浸润骨组织: 痛程度得影响也不同：? 原发或继发肿瘤直接浸润骨组织与局部伤害感受器得激活;肿瘤压迫周围血管、软组织与神经组织；骨组织被破坏释放前列腺素。80％得原发骨肿瘤有明显疼痛。骨转移可分为局部骨转移或弥散性骨转移，疼痛得特点为持续性胀痛、刺痛或刀割样痛等。如果压迫脊髓则就是神经痛，临床治疗上区分伤害感受痛与神经痛非常重要,因后者用强效镇痛药也只能部分缓解。?2、肿瘤侵犯内脏：?肿瘤浸润内脏痛觉敏感得软组织、浆膜或包膜等；肿瘤浸润内脏血管会导致血管痉挛、闭塞；由于肿瘤压迫、阻塞导致内脏器官得坏死,其特点为持续加重得胀痛或绞痛，通常呈弥散性。?３、肿瘤侵犯神经系统：?由于肿瘤生长、压迫、浸润所引起得外周神经、神经根、脊髓或中枢神经系统损伤影响血液循环导致。疼痛大多为持续性烧灼样或针刺样疼痛,常伴有相应神经区域得感觉异常或运动障碍。约９
5％患者脊髓受侵由于转移至脊椎或脊髓得原发或继发肿瘤引起脊髓受压导致脊髓压迫症.早期可表现为神经根痛或感觉障碍，还可见于腰椎间盘突出、脊椎结核、颈椎病等。 二、肿瘤诊断与治疗引起得疼痛 1、肿瘤诊断引起得疼痛:?肿瘤在治疗诊断过程中也会引起一定程度得疼痛，如血标本得采集、腰穿、骨穿、血管造影、组织活检 2、肿等.这种疼痛对肿瘤病人来说并不具有特异性，原因明确。? 瘤治疗引起得疼痛:?临床表明几乎所有得抗肿瘤治疗都可引起疼痛。主要包括四个方面:手术治疗、放化疗与生物治疗。肿瘤治疗可引起疼痛综合征，常表现为急性疼痛,由于得神经损伤与肌肉结构得改变导致手术后疼痛得持续存在或原有疼痛得加重称术后疼痛综合征，对术后疼痛综合征若不积极处理,会发展为病变部位肌肉萎缩、功能障碍，影响患者得生存质量；由于放疗损伤神经、脊髓、导致臂丛、腰丛、骶丛纤维化、微循环障碍及脊髓得脱髓鞘病变或局部坏死导致放疗后疼痛；进行性神经损害也多伴有疼痛，造成感觉与运动神经障碍,并可出现传入神经阻滞性疼痛。对于由一系列因素造成得癌性疼痛应给予积极得治疗，目前临床上治疗癌性疼痛得药物主要采用外用止痛药，如蟾乌巴布膏、复方蟾酥膏、阿魏化痞膏、瘤痛安等经临床验证在治疗癌性疼痛方面均具有突出得疗效,得到广泛认可与应用。 三、非肿瘤病症得合并症 若肿瘤患者伴有骨质疏松、骨质增生、腰椎间盘脱出、风湿、类
癌痛患者的护理常规
癌痛患者的护理 ?疼痛是一种令人不快的感觉和情绪上的感受，伴有实质上的或潜在的组织损伤，是一种主观感觉，并非简单的生理应答，是躯体和心理的共同体验。 一、患者入院接待护士及时询问有无疼痛情况及服用镇痛药物史，督促经管医生及时开出癌痛护理医嘱。 二、责任护士8小时内完成对患者全面疼痛评估，建立疼痛评估表，根据疼痛的性质和程度在科室患者一览表上做醒目标识。 三、护士熟练掌握疼痛评估方法与工具并根据患者的病情、神志、年龄、理解 能力不同，选择不同的评估工具，对儿童和有智障的患者选用脸部表情量表。 四、入院评分小于等于3分疼痛者，每日8-10时当日责任护士评分1次、15时 分别评分1次，夜班在21点评估，并将评分结果及时记录，连续3天均小于3分时，每日8-10时评分一次；3分以上者每日责任护士在8-10时、15时分别评分1次，夜班在21点评估，直至连续3日评分在3分以下改每日一次，并将评分结果及时记录。 五、评分在3分以下的患者出现了疼痛加重的情况，及评分在3分以上时，立 即通知医生处理，处理后1小时观察疗效，并将爆发痛的评分和处理1小时后的评分记录在护理单和体温单上，评分次数由原先的1次改为3次；对于评分在3分以上的患者如果连续3日分值在3分或3分以下时，则改每日3次为1次；对于连续7日为0分的患者则停止评估疼痛；患者出现爆发痛评分。 癌痛评估原则 最重要的：1、病人的主诉（要接受、不怀疑、有反应、评估原因，不可说叫医生。） 2、病人的家庭成员或其他主要照顾者 3、行为表现如面部表情身体动作、哭泣（不建议，因对刺激反 应不同。）
最不重要的：1、测量生命体征如呼吸、血压等变化。（只有出现合并症才会变化） 如何教会患者正确使用疼痛评估量表？ 1、告知尺的含义： –1—3级表示轻度疼痛； –4-6级表示中度疼痛； –7—9级表示重度疼痛； –0级表示不痛； –10级表示剧痛； 2、确认患者是否理解，让其复述； 3、疼痛强度要有变化要告知医生； 4、告诉学会用此尺的重要性，是医生调剂量、用药的依据。 六、及时观察患者发生爆发疼情况及疼痛减轻或加重相关因素，当患者出现 爆发痛时，应及时告知医生做出相应处理，并将爆发痛的分值与镇痛处理后1小时的分值记录在评估表上的相对应的时间段上。护士能够采用热敷、转移注意力、更换体位等方法帮助患者减轻疼痛。评价疼痛缓解情况： 1、用药后、治疗后及时评价并记录疼痛缓解情况，及时反馈医生，以帮助医生合理调整用药 2、连续评价当前的疼痛及新发生的疼痛 七、协助医生达到WHO癌症三阶梯止痛治疗的原则，按根据医嘱做到口服给药、按阶梯给药、按时给药。将服药剂量与总量记录在疼痛体温单和护理疼痛护理记录单上。观察患者服药后的反应，及时汇报医生并处理。 WHO基本原则： 1. 按阶梯给药 2. 尽量口服 3. 按时给药 4. 个体化 5. 注意具体细节
癌性疼痛护理常规
癌性疼痛护理常规 定义疼痛是一种与组织损伤或潜在的组织损伤相关的不愉快的主观感觉和情感体验。疼痛既是一种生理感觉，又是对这一感觉的一种情感反应。 观察要点 1．疼痛的起始时间、持续时间、终止时间。 2．疼痛时的生命体征变化、体位、临床表现、伴随症状。 3．疼痛的原因、部位、程度、性质。 4．疼痛对患者生活的影响，如；饮食、睡眠、活动等。 5．疼痛的缓解方式 6．心理状况、大小便情况 7．患者的体重变化及营养状况 护理措施 1．密切观察患者的病情变化，发现异常及时通知医生。 2．保持病区舒适的环境，给患者创造一个良好的环境，有计划地集中操作，动作宜轻柔，置患者于舒适的体位，争取家属的配合，减少患者对医院的恐惧感，使患者保持心情愉快，可提高痛阈。 3．加强基础护理，指导帮助患者做好个人卫生，注意患者皮肤、口腔、呼吸系统、泌尿生殖系统等的护理，防止各种并发症的发生。 4．配合医生为患者实施三阶梯止痛，保证患者的疼痛得到有效缓解。 5．稳定情绪主动与患者谈心，了解患者的心理需求，解除患者的困扰，如亲人陪伴、疾病相关知识的讲解等，使其情绪稳定，坚定信心，消除引起疼痛的心理因素，减轻紧张、焦虑和疼痛。 6．及时评价和记录各项止痛措施的效果。 7．观察止痛药物的副作用，尤其注意长时间应用止痛药物者 8．给予清淡易消化饮食，保持大便通畅，应鼓励病人多饮水及多摄取富含维生素食物，必要时应用缓泻剂或灌肠。 健康教育 1.教会患者正确认识疼痛，用通俗易懂的语言，教给患者和家属有关疼痛和止痛药的知识 2.放松疗法全身松弛可以体会到轻快感，肌肉松弛可减轻疼痛感。放松方法有；音乐疗 法，转移和分散患者的注意力。 3.皮肤护理进行冷敷或热敷、按摩、触摸等松弛技术，可减轻肌肉紧张、炎症及痉挛引 起的疼痛。 4.饮食疗法进行营养护理原则是多样化、均衡化、低脂化和易消化，努力增加患者的 摄入量；若患者不能经口进食，则可考虑鼻饲，每次鼻饲量不超过200毫升，间隔时间不少于2小时；对肠道功能已丧失患者，可采用静脉高营养。 5.心理疗法 （1）提供一定的心理保证，降低焦虑和抑郁，建立正确的心理防御机制 （2）向患者进行疼痛管理宣教 （3）进行心理暗示，必要时应用精神药物和安慰剂。 副作用及对症处理 1．恶心、呕吐临床强调进食后服药方法，可减轻或避免恶心、呕吐，也可选择不同作用形式的镇吐剂来治疗，如胃复安片。 2.便秘便秘是使用美施康定常见的副作用，应鼓励病人多饮水及多摄取富含维生素食物，另外还可服用番泻叶、50℅甘油盐水等，并适当给予胃动力药，如吗丁啉等，重度便秘可给
癌性疼痛
定义 1 癌性疼痛的定义 疼痛是一种与组织损伤或潜在组织损伤相关的、不愉快 的主观感觉和情感体验以及保护性或病理性反应。癌性 疼痛(简称癌痛) 是由癌症本身以及癌症治疗过程中产生的 疼痛 病因 一、肿瘤自身引起疼痛 肿瘤自身引起的疼痛占癌性疼痛的75%。肿瘤的生长部位决定着疼痛的发生频率，进展性肿瘤在不同时期对疼痛程度的影响也不同： 1、肿瘤浸润骨组织： 原发或继发肿瘤直接浸润骨组织和局部伤害感受器的激活；肿瘤压迫周围血管、软组织和神经组织；骨组织被破坏释放前列腺素。80%的原发骨肿瘤有明显疼痛。骨转移可分为局部骨转移或弥散性骨转移，疼痛的特点为持续性胀痛、刺痛或刀割样痛等。如果压迫脊髓则是神经痛，临床治疗上区分伤害感受痛和神经痛非常重要，因后者用强效镇痛药也只能部分缓解。 2、肿瘤侵犯内脏： 肿瘤浸润内脏痛觉敏感的软组织、浆膜或包膜等；肿瘤浸润内脏血管会导致血管痉挛、闭塞；由于肿瘤压迫、阻塞导致内脏器官的坏死，其特点为持续加重的胀痛或绞痛，通常呈弥散性。 3、肿瘤侵犯神经系统：
由于肿瘤生长、压迫、浸润所引起的外周神经、神经根、脊髓或中枢神经系统损伤影响血液循环导致。疼痛大多为持续性烧灼样或针刺样疼痛，常伴有相应神经区域的感觉异常或运动障碍。约95%患者脊髓受侵由于转移至脊椎或脊髓的原发或继发肿瘤引起脊髓受压导 致脊髓压迫症。早期可表现为神经根痛或感觉障碍，还可见于腰椎间盘突出、脊椎结核、颈椎病等。 二、肿瘤诊断和治疗引起的疼痛 1、肿瘤诊断引起的疼痛： 肿瘤在治疗诊断过程中也会引起一定程度的疼痛，如血标本的采集、腰穿、骨穿、血管造影、组织活检等。这种疼痛对肿瘤病人来说并不具有特异性，原因明确。 2、肿瘤治疗引起的疼痛： 临床表明几乎所有的抗肿瘤治疗都可引起疼痛。主要包括四个方面：手术治疗、放化疗和生物治疗。肿瘤治疗可引起疼痛综合征，常表现为急性疼痛，由于的神经损伤和肌肉结构的改变导致手术后疼痛的持续存在或原有疼痛的加重称术后疼痛综合征，对术后疼痛综合征若不积极处理，会发展为病变部位肌肉萎缩、功能障碍，影响患者的生存质量；由于放疗损伤神经、脊髓、导致臂丛、腰丛、骶丛纤维化、微循环障碍及脊髓的脱髓鞘病变或局部坏死导致放疗后疼痛；进行性神经损害也多伴有疼痛，造成感觉和运动神经障碍，并可出现传入神经阻滞性疼痛。对于由一系列因素造成的癌性疼痛应给予积极的治疗，目前临床上治疗癌性疼痛的药物主要采用外用止痛药，如蟾乌巴
慢性非癌性疼痛治疗的指南
编者按现有证据表明，在阿片的使用上存在很大差异。为了改善慢性非癌症疼痛的治疗，提高病人的生活质量，减少药物滥用和挪用，提高费用效益比，美国介入疼痛医师学会(ASIPP)采用循证医学方法，制定了有关使用阿片治疗慢性非癌症疼痛的指南。指南的全文刊登在最近发表的Pain Physician杂志上。该指南主要由疼痛介入治疗医师使用。本指南没有提出硬性规定的治疗建议。现摘译其中第8.0节阿片使用原则部分供大家参考。 阿片使用的原则 序言 在疼痛介入治疗中，病人可能不仅接受阿片类止痛药的治疗，还可能接受其他控制性或非控制性药物的治疗。另外，病人还可能接受控制性药物作为介入技术的辅助治疗，或用其治疗并存的精神疾病和心理障碍。 基本观念 处方使用阿片类药物的原则是：对病人进行综合评价（法定进行生理评价，选择进行心理评价），正确记录定期评价的疗效结果，特别需要评价的是对功能状态的影响、疼痛缓解程度，发现和治疗不良事件，监测滥用行为。另外，病人还必须遵守控制
性药物协议和各个机构提出的规定指南。图1为疼痛评估和治疗的流程。表1为长期阿片类药物治疗的流程。 图1 慢性疼痛综合评估和处理的建议流程 1、评估和处理 2、病史 疼痛史 用药史 心理社会史 3、评估 生理 功能 心理社会 诊断性试验 4、印象 5、处理计划 6、其他治疗手段 7、诊断性介入技术 8、治疗性介入处理 9、再次评估 10、持续疼痛
新发疼痛 疼痛加重 11、疼痛充分缓解和功能状态改善 12、再次全面评估 13、出院或维持 评价 合适的病史和体格检查，以及基于对病人当前症状的最初评估做出的治疗决策，都是必不可少的。评估和治疗中最关键的三个要素是病史、体检和治疗决策。其他容包括会诊、协调治疗、当前问题的性质和面对面评估所需要的时间。 病史 病史包括主诉、现病史、系统回顾、过去史、家族史和/或社会史。 现病史是按时间顺序描述由最初发生到现在有关当前疾病的症状和体征的进展情况。现病史包括的容有：部位；性质、严重程度、持续时间、时间分布、背景情况、影响因素；伴发的症状和体征。
肺癌患者的护理常规(课件)
肺癌患者的护理常规 一、病因 1。吸烟吸烟是肺癌的重要危险因素。烟中含有各种致癌物质，其中苯并芘为致癌的主要物质，国内调查显示 80%－90％的男性肺癌与吸烟有关,女性约19。３%— 40％与吸烟有关. 2．职业已被确认的职业致癌因子有石棉，二氯甲醚，煤烟，焦油，烟草的加热产物等。 3。空气污染如室内被动吸烟,烧煤取暖产生的物质，城市中汽车的废气，工业废气,城市发病率大于农村. 4．电离辐射肺是对放射线敏感的器官之一,大量电离辐射可引起肺癌。 5。饮食与营养食物中维生素A含量低或血清维生素Ａ低，得肺癌的危险性高。 6.其他肺部慢性炎症、结核瘢痕、遗传因素等对肺癌的 发生可能也有一定的作用。 二、病理分类 （一）按解剖学分类 1.中央型肺癌(指发生在段支气管至主支气管的癌) ２．周围型肺癌(指发生在段支气管以下的癌）。 （二)按组织病理学分类:分为小细胞癌和非小细胞癌两大类. 1。非小细胞癌包括:1).鳞状上皮细胞癌(鳞癌）特点:最常见的肺癌. 与吸烟的关系最密切. 鳞癌细胞生长缓慢,转移较晚,手术切除机会相对较多。对化疗、放疗不如小细胞未分化癌敏感.2）大细胞未分化癌（大细胞癌）特点:恶性度较高，但转移较小细胞癌晚，手术切除机会相对较大.3）.腺癌：女性多见。特点:出现症状相对较晚。恶性度介于鳞癌与小细胞癌之间,对化疗、放疗敏感性较差。......感谢聆听 2.小细胞癌（小细胞未分化癌)特点：肺癌中恶性度最高的一种。小细胞癌对化疗、放疗较其他类型敏感。 三、临床表现 一．症状 １。呼吸系统症状
（1)咳嗽：最常见的早期症状，常以阵发性刺激性呛咳为首发症状. （2）咯血：多为持续性痰中带血，当癌肿侵犯大血管可引起大咯血。 (３）胸痛：病变累及胸膜或胸壁时,患者出现持续、固定、剧烈的胸痛。 （4）呼吸困难:因肿瘤压迫大气道引起呼吸困难。 (5)声音嘶哑：因肿瘤直接压迫或转移致纵膈淋巴结压迫喉返神经。 （6)上腔静脉阻塞综合征肿瘤压迫上腔静脉，使上腔静脉回流受阻，产生头面部,颈部,上肢水肿以及胸 前部淤血和静脉曲张，可引起头痛,头晕. 2。全身症状 (１）发热：多由继发感染引起,肿瘤坏死也可引起癌性发热，抗生素治疗效果差。 （2）食欲减退：体重下降,消瘦、明显乏力。 ３.癌肿压迫与转移 （1）中枢神经系统的转移:表现为颅内高压的征状,如头痛,呕吐,眩晕，复视，脑神经麻痹,一侧肢体无力甚至偏瘫. （2）骨转移：转移至肋骨,脊椎，骨盆时可有局部疼痛 和压痛。 （3）肝转移：表现为厌食，肝区疼痛,肝大，疼痛和腹 水. (４）淋巴转移：锁骨上淋巴结是肺癌转移的常见部位，固定而坚硬,逐渐增大，增多,可以融合，多无痛感， 淋巴结的大小不一定反应病程的早晚。 四、有关检查 （一）X线检查：是发现肺癌的重要方法之一，在肺癌的普查和诊断中占重要位置。 （二）痰液脱落细胞检查:是简单有效的早期诊断肺癌的方法之一。该检查设备简单,病人安全无痛苦。 (三）纤维支气管镜检查:可直接观察并配合刷检、活检等手段诊断肺癌。(最有效) 五、治疗要点