Management of lower backpain

Management of lower backpain- weblink www.prodigy.nhs.uk Goals and Outcome Measures

Goals

To relieve symptoms

To recover from an acute attack (i.e. have no substantial low back pain and related disability) within 6 weeks

To maintain productive activity and minimize work loss

To prevent recurring episodes of acute low back pain and the development of chronicity

To optimize the management of chronic low back pain

Outcome measures

Pain score

Activities of daily living

Mobility

Number of days off work

Background Information

• What is it?
• How common is it?
• How do I know my patient has it?
• What else might it be?
• Complications and prognosis

What is it?

Low back pain is characterized by a range of symptoms including pain, muscle tension, or stiffness, and causes may include one or more of the following:

• Sprains
• trains
• Bad posture
• Physical injury
• Considerable leg length discrepancy

Pain is felt in the lumbar segment with or without pain in the buttocks or legs (sciatica). The person usually cannot locate the precise source of the pain.

Low back pain can present(see How do I know my patient has it?) as:

• Simple backache (over 95% of cases)
• Backache caused by nerve root pain (under 5% of cases)
• Backache secondary to serious spinal pathology (under 2% of cases)

People with low back pain can also be classified by the duration of symptoms as follows:

• Acute low back pain present for 6 weeks or less
• Chronic low back pain lasting for longer than 12 weeks

Sub-acute low back pain represents an interim period of between 6-12 weeks experienced by the relatively low percentage of people whose symptoms have not resolved within 6 weeks.[DTB, 1998b]

How common is it?

GP consultations for low back pain have been estimated at 14-15 million per year in the UK [Clinical Standards Advisory Group, 1994].

Approximately 40% of adults claim to have suffered from low back pain lasting more than 1 day in the previous 12 months [Department of Health, 1999].

Lifetime prevalence for low back pain is 60-80% [Clinical Standards Advisory Group, 1994].

How do I know my patient has it?

• Simple backache (over 95% of cases) usually presents between 20 years and 55 years; 'mechanical' pain is felt in lumbosacral area, buttocks, and thighs; the person is otherwise well.
• Nerve root pain (under 5% of cases) is usually unilateral leg pain worse than low back pain; radiates below the knee; numbness and parasthesia in same distribution; straight leg raise reproduces the leg pain; localized neurological signs.
• Serious spinal pathology (under 2% of cases) should be considered in those with previous trauma or aged under 20 years or over 55 years. There are a variety of warning symptoms, including pain of gradual onset that is unrelated to physical activity, morning stiffness, or limitation of back movements in all directions. The person should be referred to a specialist. Urgent admission is required if the development of a cauda equina syndrome is suspected - sphincter disturbances, saddle anaesthesia, widespread or progressive motor weakness in the legs, or a gait disturbance.

[DTB, 1998b; Waddell et al, 1999]

What else might it be?

Other causes of low back pain besides simple mechanical damage include:

• Degenerative changes
• Structural changes, e.g. spinal stenosis)
• Inflammatory changes, e.g. ankylosing spondylitis, rheumatoid arthritis (rare)
• Infections, e.g. pyelonephritis, bacterial osteomyelitis, tuberculous osteomyelitis, epidural abscess, brucellosis
• Neoplasms, e.g. multiple myeloma, lymphoma, secondary metastases, primary cancer (rare)
• Metabolic bone disease, e.g. osteoporotic collapse, osteomalacia, Paget's disease
• Other, e.g. gynaecological problems, sickle cell disease, vascular claudication

Complications and prognosis

• Pain can become chronic
• People with back pain may develop depression
• Some low back pain initially diagnosed as 'simple mechanical' may be due to sinister causes

• In the UK, low back pain was responsible for 150 million days being lost from work in 1 year [Clinical Standards Advisory Group, 1994]
• Some people with back pain may never return to work

Management Issues

• General issues
• General advice
• Drug management for acute low back pain
• Drug management for chronic low back pain (>12 weeks)
• Physiotherapy and other therapies
• Children and adolescents
• Which patients to refer

General issues

• Diagnostic triage should distinguish between simple backache, nerve root pain and serious spinal pathologies. It forms the basis for referral, investigation, and management (*).
• Early treatment of acute non-serious back problems, specifically mobilization and exercise, is considered to be VERY IMPORTANT in the prevention of chronic low back pain.

Risk factors for chronicity include:

• Previous history of low back pain
• Regular work loss (due to low back pain) in past 12 months
• Radiating leg pain
• Reduced straight leg raising
• Signs of nerve root involvement
• Reduced trunk muscle strength and endurance
• Poor physical fitness
• Self-rated poor health
• Heavy smoking
• Psychological distress and depressive symptoms
• Disproportionate illness behaviour
• Low job satisfaction
• Personal problems - alcohol, marital, financial
• Adversarial medico-legal proceedings

[Waddell et al, 1999]

Psychosocial factors play an important role in low back pain and disability, and influence the person's response to treatment and rehabilitation (***). Psychosocial factors may increase the risk of an individual with low back pain developing or perpetuating long-term disability, with resultant work loss and reduced quality of life. Clinical assessment of these factors involves examining:

• Attitudes and beliefs about low back pain
• Illness behaviour
• Psychological distress and depressive symptoms
• Diagnostic and treatment issues
• Family factors
• Work factors

[Waddell et al, 1999]

General advice

• Bed rest is NOT recommended for simple low back pain (i.e. for people without significant additional features such as neurological signs) and should be limited to a few days in those people forced to stay in bed by severe pain. Bed rest for 2-7 days is worse than placebo or ordinary activity. It is less effective than alternative treatments for pain relief, rate of recovery, return to daily activities, or days lost from work (***). Prolonged bed rest may lead to debilitation, chronic disability, and increasing difficulty in rehabilitation (**). There is insufficient evidence to recommend bed rest in people with chronic low back pain. [Clinical Standards Advisory Group, 1994; Waddell et al, 1999; Hagen, 2001; van Tulder and Koes, 2001]
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• Advise the person to stay active: Evidence indicates that staying active speeds symptomatic recovery from the acute attack and leads to less chronic disability and less time off work (***) [Waddell et al, 1997, 1999]. There is insufficient evidence on the effect of this advice in people with chronic low back pain.
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• Additional advice on improving posture, taking exercise, lifting, bending, sitting, driving, and choice of mattress may be helpful [Waddell et al, 1999].
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• Reassure people with acute simple low back pain that the condition is not serious and should resolve quickly [Croft et al, 1998; van den Hoogen et al, 1998].
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• Sciatica may take longer to resolve than simple backache.
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• In chronic low back pain, allowing time for the person to discuss and understand their condition is important.
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• Advice on controlled weight loss may be appropriate
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• People with low back pain may wish to know about back care (see Patient Information Leaflet).
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Drug management for acute low back pain

General points

• Analgesics provide symptomatic relief during the days or weeks in which natural recovery is expected.
• Over-the-counter products may be sufficient for many people with low back pain

Paracetamol

• Paracetamol is a good first-line analgesic for use in pain relief. Paracetamol is more effective when used regularly than as required for reducing low back pain (**).

Nonsteroidal anti-inflammatory drugs

General issues

• A nonsteroidal anti-inflammatory drug (NSAID) is appropriate for second-line use in the absence of contraindications and when paracetamol alone is inadequate. NSAIDs prescribed at regular intervals effectively reduce simple backache (***). The data available indicates that NSAIDs offer short-term benefit but there is no clear difference in efficacy between them [van Tulder et al, 2001b].
• NSAID efficacy data for the relief of nerve root pain is limited (**).
• Gastrointestinal toxicity is a particular concern with NSAIDs, especially in elderly people [CSM, 1994; Henry et al, 1996; Hernandez-Diaz and Rodriguez, 2000; Bandolier, 2000].
• Risk factors for NSAID-induced ulceration include:

• Age of 65 years and over
• Previous clinical history of gastroduodenal ulcer, gastrointestinal bleeding, or gastroduodenal perforation
• Concomitant use of medications that are known to increase the likelihood of upper gastrointestinal adverse events, e.g. corticosteroids and anticoagulants
• Presence of serious co-morbidity, such as cardiovascular disease, renal or hepatic impairment, diabetes, and hypertension
• Requirement for the prolonged use of maximum recommended doses of standard NSAIDs [NICE, 2001a].

Types of NSAID

• NSAIDs act by inhibiting cyclo-oxygenase (COX) pathways. There are at least two isoforms of cyclo-oxygenase: COX-I produces prostaglandins that help to maintain gastric mucosal integrity, and COX-II produces prostaglandins that mediate pain and inflammation. It is thought that the anti-inflammatory effect of NSAIDs is due to inhibition of COX-II
• NSAIDs can be classified according to their relative effects on COX-I and COX-II. The risk of gastrointestinal adverse effects seems to be reduced with increasing COX-II selectivity. However, other factors are involved, as some NSAIDs that are relatively COX-II selective are known to be associated with a higher incidence of gastrointestinal adverse events [Warner et al, 1999].
• Standard NSAIDs vary in their risk of causing serious gastrointestinal adverse effects. Ibuprofen has the lowest risk; diclofenac, naproxen, ketoprofen, piroxicam, and indomethacin are associated with intermediate risk; and azapropazone is associated with the highest risk [CSM, 1994; Henry et al, 1996; Bandolier, 2000; Hernandez-Diaz and Rodriguez, 2000].
• COX-II selective NSAIDS are difficult to rank on the basis of selectivity because there is a wide variation between different assay techniques. NICE identifies celecoxib, rofecoxib, meloxicam, and etodolac as being COX-II selective inhibitors [NICE, 2001a]. None is licensed for use in general (musculoskeletal) pain and inflammation.
• Topical NSAIDs: There have been no good-quality studies comparing the efficacy of topical with oral NSAIDs in people with low back pain. Topical NSAIDs have been compared with placebo, and improvements in pain relief have been found [Moore et al, 1998; Heyneman et al, 2000]. However, there is more evidence of effectiveness for oral treatment [Waddell et al, 1999; van Tulder et al, 2001b]. Gastrointestinal adverse effects are uncommon with topical NSAIDs [Heyneman et al, 2000].

Gastroprotective agents

• Proton pump inhibitors (PPIs) are generally considered to be the preferred choice for gastroprotection; they are effective and well tolerated. PPIs reduce the risk of endoscopically proven gastric ulcers by 63% and duodenal ulcers by 81% [Rostom et al, 2001]. There is a lack of data on prevention of ulcer complications. A recent study of 46 people with a previously documented severe gastrointestinal haemorrhage while on NSAIDs compared omeprazole to misoprostol [Rostom et al, 2001]. Treatment failures were defined as symptomatic ulcers, ulcer bleeding, or severe adverse effects. Fewer treatment failures occurred with omeprazole than with misoprostol (4.4% versus 30.4%, P = 0.02). However, if only ulcer bleeding or symptomatic ulcer was considered, no statistical difference was seen. This probably reflects the poor tolerability of misoprostol.
• Misoprostol reduces the risk of NSAID-induced endoscopically proven gastric ulcers by 75% and duodenal ulcers by 78% [Rostom et al, 2001]. Dosages studied have ranged from 400 to 800 micrograms daily. The 800-microgram daily dosage is associated with the lowest risk of gastric ulceration. There is no statistical difference between the higher and lower daily dosage for risk of duodenal ulcer. One large study found that misoprostol 800 micrograms daily reduced the risk of NSAID-induced ulcer complications by 40% [Silverstein et al, 1995]. Misoprostol is poorly tolerated because of gastrointestinal adverse effects, particularly diarrhoea.
• H2-receptor antagonists (H2RAs) at standard doses (equivalent to ranitidine 150 mg twice daily) reduce the risk of duodenal ulcers by 64%, but do not reduce the risk of gastric ulceration. There is some evidence that double doses of H2RAs may reduce the risk of gastric ulceration; pooled results from three trials (298 people) found a statistically significant 56% reduction in risk, although the confidence interval was wide. There is no data regarding the effectiveness of H2RAs in reducing ulcer complications. However, no H2-receptor antagonists are currently licensed for prevention of NSAID-induced gastric ulcers in the UK [Rostom et al, 2001].

People with cardiovascular disease requiring long-term NSAIDs

• A recent retrospective study found that people with cardiovascular disease who took ibuprofen as well as low-dose aspirin had a higher risk of all-cause mortality than those who only took low-dose aspirin (adjusted hazard ratio 1.93, 95% CI 1.3-2.87) [MacDonald and Wei, 2003].
• There was no difference in mortality for people taking diclofenac plus low-dose aspirin, or another nonsteroidal anti-inflammatory drug (NSAID) plus low-dose aspirin. (Note: COX-II selective NSAIDs were not included in this study.)
• The results of this study should be viewed with caution as it was not able to control for confounding factors, and only small numbers of people (303) were taking ibuprofen or diclofenac. However, until more evidence becomes available, it would seem prudent to follow the advice of the British Heart Foundation and avoid ibuprofen in people taking low-dose aspirin [British Heart Foundation, 2002]. Diclofenac is probably a better option if an NSAID is required.

Compound analgesics

• Combinations of paracetamol and weak opioids may be effective alternatives when paracetamol or NSAIDs alone do not provide adequate pain control, although no quality studies compare their relative efficacy in acute low back pain.
• Codeine is the agent of choice to be taken with paracetamol as there is more established risk: benefit data available to support its use over other weak opioids.
• Compound analgesics are often associated with an increased incidence of adverse effects. Separate prescriptions of paracetamol and codeine are preferred, to facilitate titration of the most effective and safe analgesic dose to match the individual's requirements.

[De Craen et al, 1996; Moore et al, 1997; Moore, 2001; Smith et al, 2001]

Strong opioids

• Strong opioids e.g. morphine, appear to be no more effective in relieving acute low back pain than other analgesics such as paracetamol and an NSAID (**). Strong opioids have many adverse effects, inclduing drowsiness, decreased reaction times, and potential physical dependence (**).
• Investigate severe pain requiring strong opioids.

Muscle relaxants

• Muscle relaxants effectively reduce acute low back pain (***) and muscle tension, and improve mobility [van Tulder et al, 1997]. Diazepam is widely used, inexpensive, licensed for use as a muscle relaxant, and therefore the preferred agent of choice. Muscle relaxants have significant adverse effects, including drowsiness and potential physical dependence, even after relatively short courses (i.e. 1 week) (**). For these reasons they should only be used in people who have significant spasm. The optimal course length is 3-7 days, and for a maximum of 2 weeks. Comparisons of effectiveness with NSAIDs have been inconclusive (**).

Antidepressants

• Antidepressants are not licensed for use in pain control in the UK. There are currently no randomized controlled trials of their use in acute low back pain and therefore insufficient evidence of their relative efficacy is available [Waddell et al, 1999; van Tulder and Koes, 2001].

[Clinical Standards Advisory Group, 1994; Waddell et al, 1997; van Tulder et al, 1997; Croft et al, 1998; van den Hoogen et al, 1998; Waddell et al, 1999]

Drug management for chronic low back pain (>12 weeks)

• The efficacy of drug therapy for chronic low back pain is less uncertain.
• Paracetamol with or without codeine is appropriate to provide short-term pain relief, but long-term use is not well established in chronic pain [van Tulder and Koes, 2001].
• The efficacy of NSAIDs in chronic low back pain has been assessed by only a few trials and the methodology was too different for the data to be pooled. The evidence to support their use is therefore limited [van Tulder and Koes, 2001].
• The use of strong opioid analgesics in the management of chronic, non-malignant, low back pain is controversial because of the risk of addiction. It is therefore not endorsed [Medicines Resource, 1997].
• Diazepam is appropriate for use as a muscle relaxant for a few days only, because of the danger of adverse effects and the potential to cause physical dependency [Waddell et al, 1999].
• Tricyclic antidepressants (TCAs) are not licensed for use in chronic pain, although they are widely used for chronic pain of many causes [McQuay and Moore, 1997]. A recent systematic review of the effect of antidepressants (from different classes) on chronic low back pain filtered out nine randomized placebo-controlled trials that included 504 people [Salerno et al, 2002]. The systematic review found that people treated with antidepressants demonstrated a small but significant improvement in pain severity (standardized mean difference 0.41; 95% CI +0.22 to +0.61) but there was no statistically significant improvement in the ability to perform activities of daily living (standardized mean difference 0.24; 95% CI -0.21 to +0.69). The benefit of TCAs in chronic low back pain remains controversial, but an initial 1-month trial of therapy may be worth considering [Turner and Denny, 1993; van Tulder et al, 1997; Fishbain, 2000].
• Anticonvulsants are sometimes used in the management of chronic pain but no trial data is available to support their use in chronic low back pain.
• Epidural, facet joint, and local injections with anaesthetics and/or steroids have been evaluated in chronic low back pain. Owing to a lack of well-designed trials, there is insufficient evidence to demonstrate whether they are effective. The evidence to support the use of facet joint injections appears to be particularly limited [Mathews et al, 1987; Koes et al, 1995; Nelemans et al, 2001; van Tulder and Koes, 2001].

Physiotherapy and other therapies

Manipulation:

• Can provide short-term improvement in pain and activity levels and greater satisfaction in people with simple backache (***)
• Trial data assessing the efficacy of spinal manipulation in chronic low back pain is conflicting [van Tulder and Koes, 2001]
• The optimum timing for this intervention is unclear (**)
• Is associated with very low risks if performed by appropriately qualified personnel (**)
• Is inappropriate for people with severe or progressive neurological deficit
• Should not be carried out under anaesthetic as it is not effective and is associated with an increased risk of serious neurological damage (*)
• Practitioners should always exclude people with serious neurological conditions before considering manipulation [Physiotherapy Effectiveness Bulletin. Evidence-Based Practice, 1999]

Back exercises: Systematic review evidence available indicates that specific exercises for back complaints are not useful in the treatment of acute low back pain (***). Exercises may be helpful in people with chronic low back pain (**). There are some theoretical arguments for starting exercises within 6 weeks of presentation (*). [Faas, 1995; van Tulder et al, 1997; Waddell et al, 1999]

Acupuncture: There is no evidence on the efficacy of acupuncture for acute low back pain (*). For chronic low back pain, 8 of 11 RCTs found acupuncture to be no more effective than placebo [van Tulder et al, 2000a].

Massage, ultrasound, short-wave diathermy, ice, and heat: Although physical treatments are commonly used for symptomatic relief, there is insufficient evidence on their effects on clinical outcomes in acute and chronic low back pain (**) [Waddell et al, 1999; van Tulder and Koes, 2001]. A recent Cochrane review also confirms that there is insufficient evidence to recommend massage as a single isolated treatment for non-specific low back pain [Furlan et al, 2000].

Shoe insoles and shoe lifts: There is no evidence that they provide any long-term benefit (*). Leg length differences of less than 2 cm are likely to be unimportant (*).

Transcutaneous electrical nerve stimulation (TENS): There is inconclusive evidence on the efficacy of TENS in people with acute low back problems (**) [Waddell et al, 1999; van Tulder and Koes, 2001]. A systematic review of five trials found contradictory results and therefore no evidence to support the use of TENS in the treatment of chronic low back pain (**) [Waddell et al, 1999; Caroll et al, 2001].

Lumbar corsets and supports are used in the prevention and treatment of non-specific low back pain. There is limited evidence that lumbar supports are more effective than no treatment. However, a recent systematic review found the methodological quality of comparative studies to be poor and consequently the effect of lumbar supports remains unclear [van Tulder et al, 2000c].

Traction: There is no conclusive evidence from systematic reviews that traction is effective in either acute or chronic low back pain or nerve root pain (***) [Waddell et al, 1999; van Tulder and Koes, 2001].

Back schools, where groups of people with back pain receive education and skills (e.g. exercises), supervised by a specialist. There is conflicting evidence on the effects of back schools in people with acute or chronic low back pain. However, in occupational settings back schools have been found to be more effective than no treatment in people with chronic low back pain [van Tulder et al, 2000b].

Behavioural therapy: Limited evidence has indicated that cognitive, operant, and respondent behavioural therapy improved pain relief compared with certain other interventions in acute low back pain [van Tulder and Koes, 2001]. In people with chronic low back pain, evidence has found that behavioural therapy has a moderate effect on pain and a mild effect on disability compared with no treatment [van Tulder et al, 2001a]. There is conflicting evidence on the effectiveness of behavioural therapy compared to other treatments.

Multidisciplinary programmes: These intensive physical and psychosocial programmes involve different health professionals and aim to improve function and help people to cope with their symptoms. Limited evidence has found that multidisciplinary rehabilitation, which included workplace visits for people with acute low back pain, led to a faster return to work [Effective Health Care Bulletin, 2000]. In people with severe chronic low back pain, multidisciplinary treatment improved pain relief, functional status, and return to work moderately more than traditional inpatient rehabilitation or usual care, up to 1 year [van Tulder and Koes, 2001].

Evidence for the benefit of other osteopathic or chiropractic treatments is inconclusive. Only registered members of a recognized professional association should carry out these treatments.

Children and adolescents

• Low back pain is relatively less common in adolescents and children than in adults.
• Significant underlying pathology is common.

Which patients to refer

General points

• Simple backache does not usually require specialist referral. Occasionally people with chronic problems may need referral.
• Nerve root pain does not generally require referral in the first 4 weeks, provided it is resolving.
• People with a definite psychological component to their (usually chronic) pain may benefit from a psychiatric/psychology/counselling referral. People who experience pain that does not vary during a 24-hour period are usually suffering from a pain behaviour syndrome.
• Occasionally people with chronic severe pain may be appropriately referred to pain clinics.
• Physiotherapy referral for both acute and chronic low back pain may be helpful.

Urgent referral/immediate admission

Consider prompt investigation or specialist referral (less than 4 weeks) for anyone with a red flag for possible spinal pathology, namely:

• Presentation under 20 years
• First presentation over 55 years
• Violent trauma (e.g. road traffic accident)
• Nonmechanical pain
• Thoracic pain
• Past history of carcinoma
• Corticosteroid use
• HIV infection
• Systemically unwell, weight loss
• Widespread neurological symptoms or signs
• Structural deformity

Immediate admission is needed for cauda equina syndrome:

• Sphincter disturbances
• Saddle anaesthesia
• Widespread or progressive motor weakness in the legs
• Gait disturbance

[Waddell et al, 1999]

Referral advice from the National Institute for Clinical Excellence

Referral advice: a guide to appropriate referral from general to specialist services [NICE, 2001b] contains the following advice for people with acute low back pain. The referral advice is meant to encourage local health communities to discuss referral issues and enable local referral guidelines and protocols to be produced (for further information see www.nice.org.uk/).

Almost all people with acute low back pain can be managed in primary care.

Table 1 outlines when referral to a secialist service is advised.

Table 1. Referral to a secialist service is advised if: