A Clinical Approach to Low Back Pain
Rohan Moffatt, MBBS, CAQ Sports Medicine, Assistant Professor, Department of Family and
Community Medicine, University of Maryland School of Medicine
Background
Back Pain is the third most common reason for a visit to a doctor in the United States [1]. The vast
majority of patients with back related symptoms were seen in a primary care office (40-50%) with
another 15-30% of patients being seen in Hospital outpatient departments and Emergency departments
combined [3]. Sixty one percent of patients with recent-onset (<12 weeks) back pain sought care during
their most recent episode [16]. Due to the extensiveness of back symptoms, for the purpose of this
discussion, the focus will be on Lower Back Pain (LBP). This is defined as pain which is located between
the region bordered by the costal margins superiorly and the gluteal folds inferiorly. LBP may be
associated with pain radiating down one or both lower extremities in the distribution of the sciatic nerve
L4-S2 (sciatica). The lifetime prevalence of LBP approaches 85% in the United States with an annual
prevalence of 15-45% [9]. The mean lifetime prevalence of LBP globally was 39% with countries like
China (46-48%), Nepal (49%), Cuba (50%) and Pakistan (51%) accounting for lower global lifetime
prevalence [10]. The median overall prevalence of LBP was higher for females in comparison to males
across all age groups globally. No significant gender difference exist for annual and lifetime prevalence
[10]
. The mean prevalence of LBP peaks between ages 40-69 years with the prevalence of benign back
pain decreasing with increasing age [10,11] Dionne et al demonstrated though that the elderly population
experience or report less frequently benign or mild pain (either due to increase pain tolerance or decreased
pain perception, cognitive impairment, depression). This group of patients do experience a higher
prevalence of severe or disabling pain [11]. The prevalence of LBP is low in children at 1-6% [12] but
increases dramatically to 18-50% in adolescents [12,13]. Most LBP resolves within 6 weeks. Pain is
characterized as acute if it last for less than six weeks, subacute from six weeks but less than three months
and chronic if lasting more than three months. Fifteen to 20% of patients will develop protracted pain.
Two to 8% will become chronic pain [9]. Chronic LBP is the leading cause of disability in Americans
younger than 45 years [15]. Direct and indirect medical cost is between 50 to 100 billion dollars per annum
with 75% of the cost being generated by 5% of patients with temporary or permanent disabling back pain
[14]
. A similar pattern was noted in the Quebec Province of Canada where 7.4% of patients with LBP who
were absent from work for 6 months accounted for 75% of lost days, medical cost and indemnity
payments [17]. If a patient is disabled for more than 6 months then there is a less than 50% chance of return
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to work. If LBP is disabling for 2 years then return to work is almost unlikely [9]. The economic burden
and prevalence makes LBP a condition of importance for which significant implications for care are
derived.
Risk factors
Numerous risk factors have been identified for which an increased likelihood exist for the development of
LBP. These include age with a peak occurring in the middle age group range [10,11]. Studies have revealed
that genetic factors play a role in the heritability of LBP in monozygotic twins [18,19]. Other risk factors
include obesity [19], tobacco smoking, poor posture (due to weakness of trunk extensors in comparison to
flexors), occupation (manual labor, vibration exposure, prolonged standing or sitting[20] and job
dissatisfaction) and lower educational level [4].
Diagnosis
History
This should be focused on identifying risk factors for LBP and red flags for more serious causes of pain.
It is appropriate to note the age of patient, characterise the nature of pain by location, onset, duration,
radiation, nocturnal occurrence, severity and modifying factors. The examiner will want to determine if
current or past history of trauma might be related to LBP. Positive tobacco use in social history as well
the current use of oral corticosteroids both have implications for osteoporosis. Enquire about previous
surgical procedures on the lower back, past medical history of cancer as well as screen for depression and
anxiety which both may impact recovery. Red flags that warrant urgent attention include LBP in an
immunocompromised patient, presence of fever, unexplained weight loss, intravenous drug abuse, saddle
anesthesia, bowel/bladder dysfunction, unexplained weakness, paresthesia and colicky pain [24].
The examiner can also probe for barriers to recovery from LBP, sometimes referred to as “yellow flags”.
These include fear and avoidance beliefs [5], heightened emotional activity, depression, dysthymia, anxiety
disorders [6], personality disorders, predisposition to somatoform pain disorder and childhood sexual
abuse.
Physical examination
First observe the patient’s gait and ability to independently maneuver their surroundings during
interview. This might provide some objective insight into the the patient’s functional status. Make note of
the patient’s attire, posture and overall demeanor. Observe for signs of nutritional inadequacies as well as
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checking the body mass index. Check the patient’s temperature, blood pressure and peripheral pulses for
any significant radio-femoral delays. The patient’s ability to walk on tip-toes or on heels provides gross
assessment of S1-2 and L4-5 nerve roots respectively. Systematic evaluation of the cardiovascular,
gastrointestinal (inclusive of a rectal exam for sphincter tone, saddle anesthesia) and lymphatics should
ensue. With the patient standing, evaluate the back for signs of asymmetry, scoliosis, increased lordosis
or surgical scars. Palpate the back for any bony tenderness or muscle spasms. The examiner should
include palpation of the sacroiliac joints as part of the evaluation of LBP. While standing with both feet
together, observe for range of motions deficits elicited from active forward flexion at the waist (Schober
test), passive rotation of the shoulders and pelvis in the same plane in either directions. Axial loading of
the spine by direct pressure on the head should be performed while standing. Facet joint related pain is
aggravated with hyperextension of spine and relieved with flexion which is opposite to discogenic related
pain. In the supine position, check for limb length discrepancy and range of motion of the hips. A straight
leg raise (SLR) test should be performed by passively flexing the hip while maintaining extension of the
knee. The accuracy of the SLR test is inconsistent and false positives may inflate the sensitivity of the
test[21]. The SLR test can also be performed with the patient sitting by extending the knee joint. The
bowstring test is a modification of the SLR test. Once a level of discomfort is achieved with the supine
SLR test, the knee is flexed enough just to relieve the pain. At that point, pressure is applied to the
popliteal fossa which may cause a recurrence of symptoms (a positive test result). Perform the FABER
test which involves Flexion, ABduction & External Rotation of the hip to identify pain originating from
the sacroiliac joints. A neurological examination should conclude the physical examination with special
attention placed on strength evaluation, deep tendon reflexes and sensory deficits Table 1.
Waddell et al described five categories upon which back pain with psychological component can be
identified. Some of the individual components that form the basis of his criteria were described earlier.
These include TENDERNESS from light palpation or in a non-anatomic distribution, SIMULATION of
movements such as axial loading/passive rotation of torso while standing causing pain, DISTRACTION
of the patient while rechecking SLR, REGIONAL DISTURBANCES marked by sensory loss or
weakness in a non neurological or anatomical pattern and OVERREACTION characterized by
disproportionate pain response, dramatic grimacing, bracing and clutching painful area for more than 3
seconds. It is still possible for the patient to have an organic cause of pain with positive Waddell criteria.
Table 1. Dermatomal sensory, reflex and functional muscle test
Root
Muscle Action
Sensory Loss
L2
Hip flexion
Mid-anterior thigh
Reflex
3
L3
Knee extension
Lateral thigh to medial femoral condyle
Patellar
L4
Ankle dorsiflexion
Medial malleolus
Patellar
L5
Great toe extension
Lateral leg and dorsum of foot
Medial hamstring
S1
Ankle plantarflexion
Lateral aspect of calcaneus
Achilles
Differential Diagnosis
These can be classified into mechanical, systemic and referred pain. Mechanical conditions are
responsible for 98% of the causes of LBP[22]
Mechanical
Degenerative disc disease (with or without radiculopathy), lumbar stenosis, cauda equina syndrome,
myofascial (sprains or strains), facet joint arthropathy, vertebral fractures, spondylosis, spondylolysis and
spondylolisthesis (pars interarticularis defects), hip joint pain, sacroiliac joint pain (sacroiliitis)
Systemic
Myelopathy, myositis, spinal segmental & lumbopelvic dystonia, lumbosacral plexopathy (diabetes,
vasculitis, malignancy), mononeuropathy, primary or metastatic neoplasms, seronegative
spondyloarthropathy (Reiter's syndrome, Ankylosing spondylitis), Metabolic bone disease (paget's
disease, osteoporosis)
Referred
Gastrointestinal (pancreatitis, pancreatic cancer, cholecystitis, intestinal obstruction, peptic ulcer disease),
genitourinary (nephrolithiasis, pyelonephritis, prostatitis), Cardiovascular (thoracic or abdominal aortic
aneurysm), Hip joint disorders (osteoarthritis, avascular necrosis).
Other less understood but well documented pain syndromes responsible for LBP include Failed Back
Surgery Syndrome (FBSS) and Complex Regional Pain Syndrome (CRPS)
Investigations
Hematological studies where indicated by history and examination include CBC, ESR, CRP, Alkaline
phosphatase, serum calcium and parathyroid hormone. SPEP and UPEP should be ordered if multiple
myeloma is being entertained. A urinalysis with microscopy may assist with ruling out conditions related
to the urinary tract.
Imaging studies are usually not required initially for the evaluation of non specific LBP[23]. These are
usually reserved for pain which do not respond to the usual mode of treatment, persisting for over six
weeks. There are certain instances however when imaging studies should be ordered at initial evaluation
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of the patient with LBP. These include the presence of red flags as described earlier, a history of acute
trauma and a past medical history of cancer. Initial testing should include plain radiographs of the
Lumbosacral spine (AP, lateral and oblique), pelvic x-ray if indicated by history or examination. If these
initial test prove non-diagnostic or in the presence of neurological findings then a MRI scan is warranted.
Patients with previous Lumbar spine surgeries might benefit more from a CT myelogram to avoid
distorted MRI images caused from hardware in-situ. Other diagnostic test which may be indicated based
on history and examination include Electromyogram (EMG), Somatosensory evoked potential testing
(SSEP), Nerve conduction study (NCS) and a bone scan.
Treatment
All patients should be provided with evidenced based information on LBP with regards to expected
course, advise on remaining physically active and self care options [23]. It has been demonstrated that
controlled exercises helps to restore function, reduce pain, distress and illness related behavior thus
promoting a return to work [27]. Non pharmacological therapies with good evidence of moderate efficacy
for chronic or subacute low back pain are cognitive-behavioral therapy, exercise, spinal manipulation and
interdisciplinary rehabilitation. Superficial heat was the only therapy with good evidence of efficacy for
the treatment acute low back pain [25].
Pharmacological options available for the treatment of LBP include acetaminophen, Nonsteroidal antiinflammatory drugs (NSAIDs), Cyclooxygenase 2 (COX 2) inhibitors, oral corticosteroids, Opioids,
muscle relaxants (benzodiazepines and non-benzodiazepines), antiepileptic drugs (AED), antidepressants
and topical (lidocaine, diclofenac).
NSAIDs, COX2 inhibitors and oral corticosteroids are anti-inflammatory and inhibit the production of
cytokines that are responsible for pain generation and tissue edema.
Opioid analgesia act by inhibiting the ascending pain pathways at the level of the spinal cord thus
producing analgesic effect. When considering the level and duration of opiod analgesia to prescribe, the
physician should rely on the patient’s achievement of vocational, recreational and social goals as better
measures of medication efficacy than the subjective report of pain relief. All patients being considered for
opioid therapy should have screening assessment performed to identify risk factors for adverse outcome,
developing abuse or addiction. Currently available screening tools include National Institute of Drug
Abuse (NIDA) quick screen, The Opioid Risk Tool (ORT), The Diagnosis, Intractability, Risk, Efficacy
(DIRE) tool and The Screener and Opioid Assessment for Patients with Pain-Revised (SOAPP-R).
Skeletal muscle relaxants and antispasmodics are centrally acting medications which promote
generalized muscle relaxation and sleep. Short term use is recommended due to the increased potential for
dependence and side effects.
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AEDs and antidepressants are neuromodulators which act centrally to alter the interpretation of pain.
Gabapentin is the most popular of the AEDs however dose will have to be titrated to effect. The antidepressants commonly used for LBP include Tricyclic Antidepressants (TCA), Selective Serotonin
Reuptake Inhibitors (SSRI) and Serotonin-Norepinephrine Reuptake Inhibitors (SNRI).
There is good evidence in support of acetaminophen, NSAIDs, Skeletal Muscle relaxants for acute LBP
and TCA for chronic LBP. However the evidence is fair in support of opioids, tramadol, Benzodiazepine
and gabapentin being effective for pain relief. No evidence has been found in support of systemic
corticosteroid use in the treatment of LBP [26]. Acupuncture therapy provides a viable alternative to oral
options for the management of LBP.
Interventional therapy are reserved for LBP with a specific cause. Intra-articular facet joint block and
radiofrequency medial branch neurotomy are used to treat facet joint arthropathy related pain. Epidural
corticosteroid injections are used for treatment of spinal stenosis. Vertebral body fracture can be treated
with vertebroplasty. Spinal cord stimulators have been shown to be effective for FBSS and CRPS.
Surgery is recommended for the treatment of LBP secondary to significant intervertebral disc herniation
resulting in compression of neural tissues.
Prevention
The following recommendations on preventing LBP are evidenced based and were obtained from
systematic searches of scientific literature. Strong scientific evidence exist in support of the following
recommendations:
Physical exercise helps to reduce the occurrence, duration of LBP and limit work absence [8,28]. Back
schools which teach lifting techniques, offer advice on biomechanics and optimal postures are not
recommended. Lumbar supports and back belts are no more helpful than no intervention and hence not
recommended for use in the prevention of back pain. The use of shoe orthoses is not recommended for the
prevention of LBP [28].
Low scientific evidence exist in support of pain reduction with change from a firm to a medium-firm
mattress [28].
Referrals
Patients with cauda equina syndrome, acute vertebral fractures, cord compression, progressive
neurological deficits and the suspicion for infection will require urgent referral for treatment.
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