A 51-year-old male presents to the clinic with a complaint of low back pain (LBP), which started approximately 6 months ago. The patient is a long-distance truck driver who is obese and rarely exercises. He has not been seen for this pain by another provider but tried to manage it once with combined ibuprofen 200 mg and acetaminophen 325 mg without much relief. He has had no known injury and no other known cause. The pain is constant and worsens with activity. He rates the pain, which extends across his lower back bilaterally, a 7 on a scale from 0 to 10. He denies radiation to legs, bladder/bowel dysfunction, prior history of cancer, or numbness of/tingling in lower extremities. The patient states that he has been experiencing difficulties with prolonged driving and bending to lift heavy objects while at work. He had recent lab work including complete metabolic panel and complete blood cell count with all results within normal limits.
The patient has no other comorbidities and scored a 2 on the Patient Health Questionnaire-9 (PHQ-9). Vital signs are within normal limits. On exam, the patient has a normal gait and reproducible pain with a straight leg raise. Pain is elicited with bending forward and rotation of the back. No edema or erythema of the spine is noted. Neurologic exam is unremarkable.
Background
LBP continues to be one of the most frequent conditions leading patients to seek medical care globally despite efforts to improve management and reduce disability.1 The most common cause of disability, LBP has a global prevalence of 7.3%.2 Spinal pain is common across the lifespan, from adolescents to older adults, with greater LBP-related disability occurring with increasing age.2-5 Complaints of LBP over the prior 12 months may range from as low as 21% to as high as 68% in adults over 60 years old.4 LBP is not frequent in the first decade of life; however, adolescents between 10 and 18 years old have been estimated to report back pain as high as 33%, with LBP accounting for 68.9% of those cases.2,3 Although there are special considerations for evaluation and management in pediatric populations presenting with LBP, discussion of them is beyond the scope of this article. Attempts to diagnose the source of LBP is often difficult, as any innervated structure, including muscle, ligament, vertebra, intervertebral disk, joint, dura mater, and nerve root, may account for pain.1 Nonspecific LBP represents 90%-95% of cases with a prevalence of 18%.5 Furthermore, overreliance on imaging may result in false-positive findings that do not always correlate with patient symptoms.6-8 Recently, international frameworks and clinical practice guidelines have attempted to provide more clarity, structured guidance, and clinical reasoning on screening for, evaluation, and management of LBP.1,5,6,9,10
Pathophysiology of pain
Diagnosing the source of LBP based on a pathoanatomic model has been suggested as potentially viable in acute LBP but may not be feasible in chronic or persistent LBP.6,11,12 The International Association for the Study of Pain (IASP) expands on this difficulty by defining pain as "an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage."13 Given that no actual tissue damage is required for a patient to experience pain, there has been a push to identify the predominant pain mechanism in a patient presenting with pain versus working immediately to identify damaged tissue in such a patient.14-18
Three predominant pain mechanisms have been identified: nociceptive, neuropathic, and nociplastic pain.15-18 Nociceptive pain is typically produced by activation of peripheral nociceptors and can be attributed to pathologic processes underlying injured tissues in the musculoskeletal system such as muscles, ligaments, vertebrae, intervertebral disks, and joints.18 Key elements of the clinical cluster of nociceptive pain include 1) pain localized to the area of dysfunction, 2) clear, proportionate mechanical aggravating and easing factors, 3) intermittent and sharp pain with movement or mechanical provocation, and 4) absence of neurologic symptoms.18 Neuropathic pain is due to various complex pathophysiologic processes of the nervous system, such as spinal nerve roots.17 Key elements of the clinical cluster of peripheral neuropathic pain in patients with LBP include 1) pain referred into the limb in a dermatomal distribution; 2) pain provocation with mechanical or movement tests that compress or load neural tissue; and 3) history consistent with nerve injury, pathology, or mechanical compromise.17 Finally, nociplastic pain is due to altered nociception despite no evidence of tissue damage activating peripheral nociceptors, and it is likely secondary to central sensitization.13,16,19 Key elements of the clinical cluster of nociplastic pain include 1) disproportionate pain relative to the injury or pathology, 2) disproportionate, nonmechanical pattern of pain provocation from aggravating and easing factors, 3) presence of maladaptive biopsychosocial variables, and 4) diffuse pain on palpation.14,16
Clinical manifestations
In an effort to minimize cost and keep management of LBP patient-centered, clinical practice guidelines suggest classifying LBP based on a clustering of signs and symptoms.1,5,6,20 LBP can be classified as acute or chronic (see Common acute or chronic LBP presentations). For simplicity, acute episodes entail presence of symptoms for less than 1 month and chronic episodes entail presence of symptoms for more than 3 months.6 Local lumbar pain can be associated with a combination of any of the following: referred nociceptive pain into either leg, radicular pain into either leg, paresthesia, numbness, and/or weakness.21 The presence of leg symptoms may occur in both acute and chronic LBP. Of note, leg symptoms should not always be attributed to the sciatic nerve, as it can result from other mechanisms, such as referred nociceptive pain from the low back.21,22
Of primary concern with complaints of paresthesia, numbness, or weakness in the lower extremities is whether a radiculopathy is present.21 Radiculopathy is a neurologic condition of a spinal nerve or its roots in which neural conduction is blocked with resultant objective hypoesthesia, hyporeflexia, and/or weakness.21 Watchful waiting during a trial of conservative rehabilitation is recommended while continually reassessing sensation, reflexes, and/or strength.1,21 Improvement in objective neurologic status does not warrant a referral; however, worsening of hypoesthesia, hyporeflexia, and/or weakness would require an orthopedic or neurosurgical referral for further investigation.
Health history
Obtaining a thorough health history, including medical and psychosocial history and a review of systems, along with a physical exam is imperative when trying to identify the cause of LBP and can help rule differential diagnoses in or out. Starting with the mnemonic OLD CARTS (onset, location, duration, characteristics, aggravating and relieving factors, radiation, treatments, and severity) will help to guide the provider in classifying the type of pain.
In the past, LBP was considered to be caused by some type of trauma, but it is now known that other factors can contribute to pain.23 LBP can be caused by an injury, spinal degenerative changes, different chronic diseases affecting the spine, infectious processes, and psychosocial distress.24 Many chronic conditions such as osteoporosis, arthritis, fibromyalgia, and endometriosis can contribute to LBP and must be inquired about during the health history.
Many risk factors are associated with the development of LBP including smoking, inactivity, obesity, older age, female sex, previous LBP episodes, physically strenuous or sedentary work, job-related stress, low educational attainment, workers' compensation insurance, job dissatisfaction, and mental health factors such as anxiety and depression.2,3,23,25 The patient's social history should be reviewed for current job status and responsibilities as well as exercise regimen to help better determine the cause of the pain. Performing a PHQ-9 can also help evaluate certain mental health considerations that may be factoring into the LBP.26
Performing a medication reconciliation, including reviewing the patient's past medications, is imperative when determining possible secondary causes of LBP. Many medications can cause bone loss that can potentially lead to osteoporosis and LBP; such drugs include glucocorticoids, hormonal therapies, gonadotropin-releasing hormone antagonists, aromatase inhibitors, selective serotonin reuptake inhibitors, loop diuretics, heparins, oral anticoagulants, high doses of thyroxine, certain immunosuppressants, and proton pump inhibitors.27 Because these medications can lead to osteoporosis and have been associated with reduced vertebral bone mineral measures, a bone density scan may be useful when the patient has LBP.28
Family health history is also important when evaluating a patient for LBP. Many chronic familial conditions can contribute to LBP such as osteoarthritis and degenerative disk disease. To assess the cause thoroughly, it is essential to learn about family upbringing, values, and genetic predisposition for LBP.
Red flags
Some serious diseases and conditions may masquerade as routine musculoskeletal sources of LBP.5,6,9 Lumbar spine pathologies that may present as standard LBP include cauda equina syndrome, spinal fracture, malignancy, and spinal infection.6,9 It is therefore critical to undertake an assessment for red flags for conditions of concern to rule them out prior to diagnosing a benign musculoskeletal issue causing LBP.5,6,9 Straightforward questions should be asked to rule out these diagnoses and should include queries around bladder or bowel dysfunction, recent trauma, recent infections, history of I.V. drug use, recent weight loss, history of cancer diagnosis, and relief with rest. A recently developed international framework recommends an approach that weighs clustered red flags in a patient-centered context to determine a level of concern (low, medium, or high) for the likelihood of serious pathology underpinning the pain.9 The relative level of concern for serious pathology guides management, ranging from beginning conservative treatment to making an urgent or emergent referral.9 Failure to improve after 4 weeks and failure to achieve relief with rest are among the red flags for these conditions.9,24
Cauda equina syndrome constitutes compression of the cauda equina, most commonly as the result of large disk herniation in the lower lumbar spine. Early subjective reports can include unilateral or bilateral radicular leg pain, hypoesthesia, and/or weakness. These reports commonly precede the more serious later complaints of bowel and/or bladder incontinence and saddle paresthesia/anesthesia. Guideline-based recommendations include a lower-extremity neurologic exam assessing for dermatomal sensory loss, myotomal weakness, or deep tendon hyporeflexia.9 With high levels of concern, an emergent MRI and surgical consultation are recommended.9
The most common location of traumatic spinal fractures is between T8 and L4.9 Risk factors that may predispose patients to fracture include osteoporosis, long-term corticosteroid use, diabetes, and smoking.9 Subjective reports include immediate onset of central spinal pain following a slip, trip, or fall or after lifting something while in a flexed position. Objective exam may be limited due to severity of pain; however, range of motion (ROM) will be severely limited, with pain provoked during percussion of the involved spinous process.9 Guideline-based recommendations include referral for radiography to determine presence and severity of spinal fracture.9
A history of cancer-in particular, breast, prostate, lung, kidney, or thyroid cancer-coupled with insidious onset of progressively worsening spinal pain, night pain, and any emergent associated signs or symptoms, such as weight loss, progressive fatigue, or weakness, should raise the level of concern for spinal malignancy.9 Spinal metastases most commonly occur in the thoracic region, followed by the lumbar region.9 Guideline recommendations focus on collection of a thorough subjective history to determine level of concern raised by objective physical exam.9
Although uncommon, spinal infections are a serious condition that can mimic musculoskeletal pain. Guideline recommendations focus on determining a level of suspicion based on screening for risk factors, such as immunosuppression, recent surgery, or I.V. drug use.9 Signs and symptoms may include a triad of back pain with fever and neurologic dysfunction, although patients may not present with all three.9 Often there is an insidious onset of back pain with a progressively linear worsening of symptoms.9
Physical exam
Guideline-recommended physical assessments include lumbar ROM, straight leg raise (SLR) or slump test, and a neurologic exam.5,6 ROM assessment is performed with the patient in standing position and includes forward bending, backward bending, bilateral side bending, and bilateral rotation. ROM is likely to be limited due to pain regardless of the cause; however, the degree to which motion is limited may give the clinician insight into the severity and irritability of symptoms. Both the SLR and slump tests are designed to place tension through the lumbar spinal nerve roots to reproduce neuropathic symptoms including radicular pain, paresthesia, and/or numbness. Reproduction of these symptoms during either the SLR or slump test implicates involvement of the spinal nerve roots in the clinical presentation. With the patient in supine position, the SLR is performed by slowly flexing the hip passively with the knee straight. Alternatively, the slump test is performed with the patient in seated position. The patient is asked to slouch before passively extending the knee of the involved side to allow the provider to assess for reproduction of neuropathic symptoms in the involved leg.
ROM assessment, the SLR, and the slump test aim to reproduce the patient's concordant symptoms. The neurologic exam includes assessment of lower-extremity deep tendon reflexes (patellar and Achilles), dermatomal sensation, and myotomal strength. Any combination of segmental hyporeflexia, hypoesthesia, or myotomal weakness can aid in implicating a lumbar radiculopathy. In the absence of significant clustering of red flags, reproduction of symptoms during physical assessment suggests that the patient likely will respond favorably to conservative interventions, including rehabilitation.
Diagnostics
Routine imaging for LBP may include plain films, MRI, or computed tomography (CT).5,29 The American College of Radiology (ACR) provides specific criteria to consider prior to ordering imaging to ensure patient appropriateness.29 Routine imaging for LBP is not recommended unless there has been overt trauma with concern for fracture/dislocation or there are signs and symptoms of more serious diseases such as cancer, infection, or other conditions (see Imaging for serious pathology presenting as acute LBP).5,29,30 Recent imaging updates suggest routine imaging is not warranted and may reveal abnormalities unrelated to presenting symptoms, further complicating the clinical picture.29 In accordance with the ACR criteria, guidelines only recommend imaging if the results are likely to guide further intervention or with persistent and progressive symptoms following six weeks of conservative optimal medical management.5
MRI is sensitive in identification of disk herniation, spinal stenosis, and paravertebral masses or other tumors but may overemphasize structural lesions.29,31 The advantage of a noncontrast CT is that it can expose osteophytes and lateral disk herniations but lacks the ability to identify neural elements beyond disk herniations without contrast.29,31 Many neurosurgeons will order CT myelography of the spine as a definitive test to identify lumbar disk herniation, osteophytes, and intervertebral foraminal stenosis.31 However, this is an invasive test that may miss far lateral herniations.31 Nerve conduction studies and electromyography (EMG) are sensitive for specific nerve root or peripheral neuropathic involvement, but patients may have significant radiculopathy without EMG evidence of denervation.31
Lab work is not routinely needed unless there is a concern for infection, malignancy, ankylosing spondylitis, or axial spondyloarthritis.32 Erythrocyte sedimentation rate (ESR) and/or C-reactive protein (CRP) can be used along with plain radiography if malignancy is suspected.32 An elevated ESR or CRP would require further evaluation with a spinal MRI.32 ESR and CRP are also used if spinal infection, ankylosing spondylitis, or axial spondyloarthritis is suspected.32 Additionally, an MRI should be performed if there is concern for spinal infection.
Patients presenting with LBP should be evaluated for depression as a comorbidity. Depression is a prognostic factor for development of chronic pain.6 Additionally, LBP can be a psychosomatic symptom of depression. A diagnostic tool commonly used in practice to identify depression is the PHQ-9. Using the PHQ-9 to identify depression as a possible comorbidity may help with multimodal management of a patient with LBP.26
Management
Treatment for LBP depends on the etiology and may require an interprofessional, collaborative, and multimodal patient-centered approach.1,30,33 Clinical practice guidelines from the American College of Physicians, the Academy of Orthopaedic Physical Therapy, and those for primary care providers guide clinicians on how to best manage both acute and chronic LBP.1,5,10
Guideline-based recommendations for acute LBP include nonpharmacologic treatment.1,5,10 Regardless of discipline, patient education emphasizing more active interventions, such as aerobic conditioning or muscle strengthening, over standalone passive treatments, such as pain relieving modalities, is recommended.1,30,33 Guidelines strongly recommend referral to physical therapy as a conservative treatment option.1,5,10 Physical therapy interventions for acute LBP include patient education on self-management techniques and favorable prognosis, muscle strengthening and endurance training, and joint mobilization.1,5,10,24
For patients with chronic LBP, treatment focus changes from curing the back pain to controlling it, maintaining functioning, and preventing disability.1,5,10,24 Guideline-based recommendations for chronic LBP also include referral to physical therapy in addition to pharmacologic intervention.1,5,10 Physical therapy interventions for chronic LBP include patient education on pain neuroscience and the importance of remaining active, use of thrust or nonthrust joint mobilization, and engagement in active exercise (see Multimodal treatment recommendations).1,5,10 Exercise programs may include motor control exercises such as Pilates or yoga, core exercises, aerobic exercise, and exercises to restore function in activities of daily living.1,10 Other interventions for chronic LBP may include mindfulness-based stress reduction for relaxation, electromyography biofeedback, low-level laser therapy, cognitive behavioral therapy, and acupuncture.10
Although some guidelines do not recommend pharmacologic intervention because most patients will improve without it, the ACP strongly recommends consideration of nonsteroidal anti-inflammatory drug or skeletal muscle relaxant use for acute LBP.1,5,10 Particularly in patients with chronic LBP who do not respond favorably to conservative, nonpharmacologic interventions, the ACP recommends nonsteroidal anti-inflammatory drugs as first-line therapy and tramadol or duloxetine as second-line therapy.10
When treatment with both nonpharmacologic and pharmacologic interventions fails, then referral to other specialties may be needed. Surgery may be of little value for treating LBP but may be needed under certain circumstances, such as progressively worsening radiculopathy.31 If surgery is contraindicated, then a referral to pain management may be needed for chronic LBP or limited ability to perform activities of daily living.31
Case study continued
Following guidelines, the NP providing care does not order any diagnostic testing such as imaging or lab work. The NP provides education regarding lifestyle changes such as weight loss, diet, exercise, and proper body mechanics while driving and lifting. The provider encourages adequate dosing of ibuprofen 800 mg three times per day for pain relief with precautions for gastrointestinal bleeding. To help with strengthening muscles, improving mobility, and restoring function while at work, the provider refers the patient to physical therapy for further evaluation and treatment. The provider advises the patient to follow up in the clinic in 3 months or sooner if red flags arise.
In physical therapy, the patient is educated on pain neuroscience and the importance of remaining active, thrust or nonthrust joint mobilization to improve mobility, and active exercise. Therapy focuses on muscle strengthening, motor control exercises such as Pilates, aerobic conditioning, and restoration of function during activities of daily living.
Conclusion
LBP is one of the most common presenting complaints in adults.2-5 The NP is on the frontline, playing an integral role when caring for patients with LBP, and is vital to the diagnosis and treatment processes. Understanding the etiology of LBP is essential in its treatment and is confirmed through gathering a thorough health history, performing a complete physical assessment, and prescribing recommended interventions. It is imperative to rule out any diagnoses that may masquerade as standard musculoskeletal LBP by utilizing screening tools for identifying red flags that may indicate more serious pathologies.
Interprofessional collaborative practice provides the patient with a holistic approach for care from healthcare team members with different expertise.33 Patients with back pain may be cared for by multiple disciplines that take equal responsibility for their care. After more serious pathologies have been excluded, practice guidelines recommend conservative interventions, including physical therapy.1,10 Physical therapists are valuable team members who provide multimodal interventions, including patient education, manual therapy, and muscle-strengthening exercises. However, if there are suspicions for serious pathology or other risk factors, NPs may find it helpful to refer patients to different professional healthcare specialty providers, including orthopedists, neurologists, surgeons, or pain specialists, to improve patient outcomes.
REFERENCES