Introduction

Low back pain (LBP), either episodic or recurrent, is an extremely common symptom. However, only a very small proportion of persons having an episode of LBP seek medical attention. Back pain episodes, even when rising to clinical evaluation, are very rarely due to serious pathologic disease such as tumor, infection or fracture. In most instances the cause of LBP is unclear. In societies in which very heavy labor is a necessary component of subsistence living, LBP episodes resulting in an inability to perform heavy labor may threaten basic needs. However, in recent decades chronic LBP illness has become a major clinical and financial problem in industrialized societies. The treatment of non‐specific LBP illness is recognized as a leading cause of “low‐value care” in the United States [1]. This has been exacerbated specifically by the over‐prescription, misuse and diversion of opioid medications in the United States, where LBP is the single most common reason for prescription of opioids [2]. To a great extent, non‐specific LBP illness remains an enigmatic clinical entity. When there is neither serious systemic or local pathology, complex psychological, social or neurophysiological issues have been shown to often dominate the clinical picture.

Clinical evaluation

Most persons with LBP do not seek medical care. The majority of LBP episodes are benign and self‐ limited, although minor persistent pain or recurrences are common. In a prospective evaluation of 200 working adults, asymptomatic for LBP at baseline, followed over 5 years, nearly all subjects had at least one LBP episode during the study period [3]. In fact, there were 625 LBP episodes lasting greater than 48 hours reported: that is, middle‐aged workers experience 1–2 LBP episodes per year. This is about as common as viral upper respiratory infections. Of these only 33 episodes (5%) were evaluated by a clinician. As in usual practice, the overwhelming majority of cases had no diagnosis made and no specific treatment prescribed. Only two subjects, of over 600 episodes of LBP, were found to have serious pathology on work up both had primary radicular symptoms with neurologic findings. [3]When an initial diagnostic assessment is performed in the acute period (days to several weeks of symptoms), the focus is usually on identifying or “ruling out” serious illness rather than definitively making a pathoanatomic diagnosis. This primary diagnostic evaluation usually involves a screening for “red flags” of serious disease by history and detecting systemic disease, spinal deformity and neurologic signs by history and examination (Table 29.1). In a large primary care setting (including primary care physical therapists), less than 1% of the 1200 patients newly referred for LBP evaluations had serious pathology [4]. Obviously, in other practices with more frequent, serious underlying diseases (such as cancer, major trauma exposure or immune suppression), this may be somewhat higher (3–4%).

It is important to clearly differentiate primary back and buttock pain from primary radicular pain (indicated by predominant leg pain, sensory changes, motor weakness or bowel and bladder disturbance) because the treatment will be very different. There is rarely any surgical or invasive intervention indicated for back pain syndromes early in the clinical course. Conversely, patients with primary neurological compression syndromes (e.g. radiculopathy from disc herniation or stenosis, neurogenic claudication symptoms and cauda equina symptoms) should be more closely evaluated and effective interventions might be indicated early on or even urgently. The treatment of neurological compression syndromes is beyond the scope of this chapter.

In the patient who does not recover good function in 4–8 weeks, a secondary diagnostic survey is indicated. This follow‐on evaluation should re‐examine both serious psychosocial and neurophysiological barriers to recovery (“yellow flags”) and also definitely “rule out” those serious pathologic conditions considered initially (Table 29.1). Laboratory testing, erythrocyte sedimentation rate (ESR) or C‐reactive protein (CRP) and imaging (most efficiently with a rapid sequence sagittal magnetic resonance scan of the lumbar spine) are extremely sensitive for inflammatory disease, infection, malignancy and insufficiency fracture [5]. These tests are so sensitive that these serious conditions are usually identified even in the early stages and very few serious pathologic findings will be missed.

Most commonly, however, only common degenerative changes are found on evaluation. Because the next phase of treatment is usually non‐specific (analgesics, anti‐inflammatory medication, conditioning, supportive measures and the expectant passage of time), an anatomic diagnosis of high precision is usually not pursued. It must be emphasized that a failure to report significant recovery by this time is unusual. The clinician must be concerned there are non‐spinal issues (e.g. the illnesses is linked to a compensation dispute or is part of a widespread chronic pain illness or is complicated by major depression) that are contributing or predominating this patient’s failure to return to usual activities.

In patients who report they are still having troubles that are highly bothersome after 3–6 months of illness, further anatomic evaluation may be considered. This tertiary diagnostic evaluation may be undertaken if the primary and secondary evaluations have revealed neither serious structural pathology nor significant confounding psychosocial or neurophysiological factors. This examination may include flexion and extension radiographs looking for instability, PET‐computed tomography (CT) scan looking for occult pelvic, facet or pars fractures, gynecologic or vascular examination looking for visceral pathology (Table 29.2).

Diagnostic injections (discography, anesthetic facet or sacroiliac joint blockades) are highly controversial. There are no good validation studies to confirm the diagnostic accuracy of these studies nor is there evidence that these procedures improve symptoms. There is consensus among the American Pain Society Guidelines, American College of Occupational and Environmental Medicine Guidelines, Veterans Administration Guideline and European COST Guidelines that these diagnostics injections have weak or absent supporting evidence or are frankly not recommended. There is some evidence that the use of discography may result in worse outcomes in patients with psychological distress or compensation issues. Clinicians utilizing these tests should discuss their risks and limitations frankly with patients. More recent data on the use of discography has shown that the disc puncture and injection, even with small gauge needles and low‐pressure injections, appear to cause accelerated disc degeneration. Extreme care should be taken in when considering disc puncture in poorly validated diagnostic or therapeutic disc injections [6].

Trivial findings and the “pseudo‐diagnosis”

Too often, as a matter of convenience or poor understanding of common degenerative pathology, patients are given anatomic diagnoses that may be anatomically true but unrelated or weakly contributing to the pain syndrome. Except in cases of fulminant degenerative processes (e.g. complete disc collapse with instability or facets degeneration with loss of stabilizing function) there is little supporting evidence for diagnoses such as “discogenic pain” or “facet syndrome” [3, 7, 8]. These diagnoses are often made on the basis of minor facet or disc abnormalities or unvalidated diagnostic injections, but are almost never corroborated (Table 29.2

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