Pain related to joint dysfunction can be treated with joint fusion; this is a long-standing principle of musculoskeletal surgery. However, pain arising from the sacroiliac (SI) joint is difficult to diagnose. Several implant devices are available that promote fusion by simply crossing the joint space. Evidence establishing outcomes is misleading because of vague diagnostic criteria, flawed methodology, bias, and limited follow-up. Because of nonstandardized indications and historically inferior reconstruction techniques, SI joint fusion should be considered unproven. The indications and procedure in their present form are unlikely to stand up to close scrutiny or weather the test of time.
Key points
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The sacroiliac (SI) joints are load-bearing synovial-lined joints that can be affected by degenerative change and therefore in some circumstances MAY cause local pain.
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Diagnosis of painful SI joints has NOT been standardized and at the current time is best represented by (1) local pain at the sacral ala, (2) degenerative changes on imaging studies, AND (3) temporary relief from intra-articular injection of topical anesthetic agents and/or steroids.
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Current technology for SI joint fusion mimics first-generation stand-alone lumbar cages, promoting fusion simply by breaching the joint space.
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Evidence of benefit from SI fusion is poor because of imprecise diagnoses, flawed methodology, bias, and limited follow-up.
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SI fusion should be undertaken only with full disclosure to the patient that the indications and long-term results for the technique remain unproven.
Introduction
The diagnosis and treatment of low back pain is a complex process. Anatomic components are varied and numerous: bones, discs, ligaments, synovium, joints. Their interactions are even more complex. Part and parcel with these moving pieces are complicated biomechanics in which changes in one part of the system affect other parts in clinically relevant ways. This article discusses sacroiliac joint dysfunction, its clinical impact, diagnosis, and nonoperative and operative treatments with a critical appraisal of a growing trend toward SI fusion.
Introduction
The diagnosis and treatment of low back pain is a complex process. Anatomic components are varied and numerous: bones, discs, ligaments, synovium, joints. Their interactions are even more complex. Part and parcel with these moving pieces are complicated biomechanics in which changes in one part of the system affect other parts in clinically relevant ways. This article discusses sacroiliac joint dysfunction, its clinical impact, diagnosis, and nonoperative and operative treatments with a critical appraisal of a growing trend toward SI fusion.
Epidemiology
Low back pain is a common complaint in health care. In 1998 it is estimated that $26.3 billion was spent investigating and treating this complaint in the United States alone, more than tripling in 2008 to $86 billion. This dramatic cost escalation has been largely attributed to a significant increase in the number of patients seeking treatment for their low back pain symptoms over that 10-year period. In the current climate of value-based disease treatment, cost has become pivotal to health care policy. The 5-year cost to Medicare, our US federally funded health care system, specifically for treating SI joint dysfunction has already been appraised at $270 million.
In any given year, the prevalence of low back pain in the adult community is estimated to range from 1.5% to 36.0%. An individual’s lifetime risk of suffering low back pain in adulthood severe enough to warrant medical consultation is 80% to 85%. The vast majority of these episodes are self-limited, with 12-month remission rates of 54% to 90%. The heterogeneity of these data are due to varied inclusion criteria and diverse mechanisms used to identify affected individuals, making them difficult to interpret.
To effectively treat low back pain, accurate diagnoses and multidisciplinary expertise is necessary. Because of multiple etiologies and interactions, clinical history and examination remain fundamental to providing good outcomes. As an important anatomic structure in lumbo-sacral geography, sacroiliac joint dysfunction deserves at least passing consideration. Differentiation of low back pain from radicular pain is the first branch-point in the diagnostic algorithm. The identification and treatment of nerve-root–mediated discomfort is reasonably objective and structured. Outcomes are predictable. However, the other causes of back pain exist in a twilight zone of low resolution and high noise. Only careful attention to the finer signs and symptoms helps the clinician avoid random diagnoses at the patient’s expense. Location (midline or paraspinal), temporal profile, aggravating and relieving circumstances, provocative maneuvers based on anatomic substrates (eg, FABER, flexion vs extension), and psychological overlay (Waddell signs) are the primary tools available to clinicians helping to guide them through the quicksand of misguided intervention.
In those seeking treatment for low back pain, estimates of SI joint involvement range as high as 10% to 30%, more frequently associated in patients with prior lumbar fusion. However, calculating the true prevalence of SI joint dysfunction as the cause of low back pain is rife with difficulty as there are no “gold standard” criteria by which to make the diagnosis. Even the largest prevalence study relied only on clinical findings to establish the diagnosis. This 1987 study of 1293 patients with low back pain from one clinician’s practice is of limited utility: the report does not detail the specific manner of diagnosis and it reports a referred pain pattern as descriptive and therefore diagnostic. Of the 336 (23%) patients with “SI joint syndrome,” only 66 (5%) were treated with joint injection yielding an amazing good-to-excellent response rate of 95%. Specious diagnostic criteria, selective intervention, and the retrospective nature of this study make its utility questionable.
Other prevalence studies suffer from even smaller sample sizes; for example, 43 patients from a selected low back pain population yielding 7 with SI joint-mediated pain (16% prevalence) and 54 patients of whom 10 responded adequately to the diagnostic interventional treatment (18.5% prevalence). Two smaller studies made use of interventional diagnostic criteria, yielding prevalence estimates of 16% to 30%. However, these data are again from highly selected, nongeneralizable low back pain populations. The sum total of these studies further confounds the true prevalence of the disease because of inconsistent inclusion criteria, loose radiographic definitions, nonspecific clinical findings, and varied interventional techniques. Consequently, the true prevalence of SI-related low back pain is unknown.
Anatomy
The sacroiliac joints are the largest axial joints in the body connecting the sacrum (and hence the spine) to the ilium of the pelvis. They are diarthrodial, planar, synovial joints lined by hyaline cartilage. As “joints” they are relatively immobile, reciprocally transmitting forces from the upper body to the lower extremities and vice versa ( Fig. 1 ). Motion through these diarthroses is limited by the complex topography of the articular surfaces and by the multitude of strong, adjacent ligaments, including short and long dorsal sacroiliac ligaments, sacrotuberal, sacrospinous, iliolumbar, and interosseous ligaments. These ligaments connect the sacrum and the lumbar spine, dispersing forces and constraining motion, normal or dysfunctional, in the pelvis to the lumbar spine and vice versa. Many of the pelvic muscles are also connected to the joints such as gluteus maximus, biceps femoris, and piriformis also affecting joint mobility and function.
Motion in the sacroiliac joint is limited mainly to rotation around the S2 axis, more specifically called nutation and counter-nutation because of the sinusoidal rather than spherical pattern. A number of studies have measured this motion, making use of a variety of motion-capture and video techniques. The most reliable studies have been performed in cadavers, and demonstrate excursion limited to 2.5° (0.8–3.9°) of rotation and 1.6 mm of translation.
Cadaveric studies have also indicated innervation of the SI joint to arise from dorsal and ventral rami of the L5 through S4 nerve roots, supplying the articular surfaces with both unmyelinated and myelinated fibers (A-delta and C).
Potential causes of sacroiliac joint pain
Senescent changes in the joint can become apparent as early as puberty. These changes accumulate over a normal life span. Motion restriction becomes apparent in the 60s and more pervasive erosive changes in the 80s ( Fig. 2 ). Studies available to date suggest approximately half of patients with symptomatic SI joint dysfunction report an inciting history of trauma, commonly a combination of axial loading and rotation. Cumulative wear and tear is proposed to account for patients unable to pinpoint a specific cause associated with their symptoms. Other potential but rare causes proposed for SI joint degeneration and pain include pregnancy-associated ligamentous laxity with joint hypermobility, sacroiliitis associated with ankylosing spondylitis, infection, enthesis injury or enthesopathy, sprain or strain, lumbar fusion and hip arthrodesis, stress and insufficiency fractures, metabolic causes (eg, gout, hyperparathyroidism), and tumors.
Diagnosis
Despite inherent limitations, clinical history has been the mainstay for diagnosing SI joint dysfunction. Symptoms suggesting SI-mediated pain are primarily identified as buttock pain and low back pain, reportedly present in 70% to 95% of patients with SI joint pathology. However, as presenting symptoms, these complaints are clearly nonspecific and are at least as likely to indicate pain generators outside of the SI joints. To add to confusion, other studies report patients with SI joint dysfunction may deny lumbar discomfort at all. Pain from SI joint dysfunction has been described to radiate into the thigh, groin, knee, and in some opinions even the lower leg. However, not only are these symptoms nonspecific but they are more frequently encountered with pathology in and around the hip region. SI joint pain has also been proposed to be affected by changes in position; for example, sitting to standing, and to be frequently unilateral. However, if one takes time to critically appraise these reports, they quickly realize there are no pathognomonic features pointing conclusively to the SI joint as the pain generator.
A variety of diagnostic clinical maneuvers elicited by physical examination have been proposed, summarized in Table 1 . Coexistence of at least 3 of these clinical signs are proposed to confirm the SI joint as the primary source of low back pain, claiming sensitivity near 80% and specificity in the range of 85% to 95%. However, as is so typical in SI pain literature, the discerning clinician will recognize these signs to be nonspecific and indeed far more synonymous with degenerative hip disease. Not surprisingly, the role of imaging in establishing a diagnosis of SI joint pain has so far been unproven (see Fig. 1 ; Fig. 3 ).
| Maneuver | Motion |
|---|---|
| Distraction | Pressure on anterior superior iliac crest |
| FABER (Patrick) | Flexion, abduction, external rotation of the thigh/hip |
| Gaenslen | Hip hyperextension |
| Thigh thrust | Adduction of flexed affected hip |
| Gillet | Standing thigh flexion |
| Compression | Compression of the thigh from lateral position |
| Fortin finger | Patient places 1 finger on source of pain 2 times |
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