5
Myth and Reality of Sacroiliac Joint Pathology
Kristen E. Jones and David W. Polly, Jr.
■ Introduction
Sacroiliac (SI) joint dysfunction is a significant source of disability that is an often-overlooked cause of low back pain, buttock pain, and leg pain.1–3 The burden of SI joint pain is higher than many commonly disabling medical conditions such as chronic obstructive pulmonary disease (COPD) and angina.4 Diagnosis of SI joint pain is often difficult because of significant overlap with referred pain from disorders of the lumbar spine and hip. Correct identification of SI joint pain requires dedicated physical examination maneuvers and diagnostic injection sequences, followed by a trial of nonoperative management. However, there are significant annual direct medical costs associated with nonsurgical management of SI joint dysfunction.5 A recent prospective multicenter randomized controlled trial has shown the superiority of SI joint minimally invasive fusion to nonoperative management at 1-year follow-up.6 Spine surgeons and spine care providers must have a thorough understanding of SI joint anatomy and physiology in order to correctly diagnose spinal disorders and to understand the connection between the spine and the SI joint. The complex structural and biomechanical interactions of the SI joint require ongoing attempts to better understand, correctly diagnose, and effectively treat this difficult pathology.
■ Anatomy and Biomechanics
As the largest axial joint in the human body, the SI joint functions to transmit loads from the trunk and spine to the lower extremities. The SI joint provides some flexible adaptation of the bony pelvis via articulation with the sacral aspect of the spine. Each SI joint is diarthrodial, with sinusoidal, auricular-shaped surfaces containing both fibrocartilage and hyaline cartilage.7,8 The SI joint surface forms an angle oblique to the sagittal plane and is typically present between sacral segments S1, S2, and S3 and the ilium.8 Because the sacrum is triangular in shape, widest and thickest at its superior aspect, it functionally wedges between the iliac wings and resists against vertical forces.8,9 The intra-articular surfaces exhibit a coarse texture with interdigitating ridges and depressions, a biomechanical adaptation to increase the coefficient of friction across the joint and to help resist shear forces, to which the SI joint is particularly susceptible.9,10 Strong ligamentous attachments act as stabilizing forces across the joint, including the anterior and posterior SI, sacrospinous, sacrotuberous, interosseous, and iliolumbar ligaments. The gluteus maximus runs perpendicular to the joint surface, and the thoracolumbar fascia additionally acts as a stabilizing structure.7–9,11
The SI joint has mechanoreceptors and nociceptors in its articular surfaces for proprioception and pain signal transmission.12 Considerable debate exists over the pattern of SI joint innervation, with likely significant variation present from person to person. Anatomic studies have shown that a large contribution of joint innervation comes from the dorsal primary rami of the lower lumbar and upper sacral nerve roots.
Although the SI joint is encapsulated, the ventral capsule is thin. Importantly, the lumbosacral plexus lies immediately adjacent to the ventral capsule. Fluoroscopic-guided SI joint arthrography has shown that in 61% of patients with SI joint pain, intra-articular contrast extravasation occurs ventrally adjacent to the lumbosacral plexus, superiorly at the sacral ala adjacent to the L5 nerve root, or posteriorly adjacent to the dorsal sacral foramina.13 Inflammatory mediators leaking from a pathological SI joint following a similar path could irritate the lumbosacral plexus, representing one hypothesis as to why SI joint pain can cause radicular patterns of irritation in the lower extremity.12,13
Iliac motion occurs relative to the sacrum across the SI joints in a transverse axis with concomitant rotation and translation, termed nutation and counternutation, respectively. Nutation occurs with lumbar extension as the sacral base translates anteriorly and inferiorly relative to the ilium. Counternutation is the opposite, occurring with lumbar flexion when the sacral base moves posterior and superior to the ilium.2 The exact degree of movement is unknown, but a widely accepted average is approximately 3 degrees. Importantly, lumbar spine movement is tied to SI joint movement.9 Lumbar fusion constructs have been associated with an SI joint radiographic degeneration rate of up to 75% within 5 years postoperatively, presumably from increased loads across the SI joint with lack of lumbar flexion/extension.14
■ Pathophysiology
Sacroiliac joint dysfunction can result from inflammation, pregnancy, and disproportionate load from spinal forces such as occurring after lumbar fusion, traumatic injury, and degeneration.7,11 Inflammatory spondyloarthropathies such as ankylosing spondylitis commonly result in SI joint pain, and should be ruled out as a contributing factor.
Pregnancy results in hormonal-induced laxity of pelvic ligamentous structures and can contribute to significant SI joint pain.15 The SI joint exhibits structural as well as functional sexual dimorphism. Females have smaller joint surface area and lack the bony tubercle seen on the sacral aspect of most male SI joints, resulting in a completely concave sacral joint surface with fewer articulations to prevent slipping.7 For women during childbearing, mobility of the pelvic inlet and outlet is crucial and is accomplished via hormone-induced relaxation of the ligamentous structures of the symphysis pubis and SI joints. SI joint pain incidence increases significantly in pregnancy, and asymmetric laxity of the SI joint ligaments is a prognostic factor for development of pain.15
Compared with the lumbar facet joints, the SI joints are significantly more vulnerable to shearing forces, approximately 20 times more susceptible to axial compression failure, and twice as likely to fail upon axial torsion loading.2
Common traumatic injury to an SI joint results from asymmetric loading via one lower extremity’s impact, such as a misstep into a hole in the ground or a motor vehicle accident with one foot on the brake.1,2 Shearing injury via lateral pelvic impact is also common. Only the most blatant traumatic disruption is likely to be seen on imaging. Much of traumatic and degenerative pathology of the SI joint is not directly correlated with radiographic features.2,7 It is important to note that because significant SI joint pathology can be present even with negative radiographic imaging, diagnosis of SI joint dysfunction is commonly overlooked and requires a dedicated approach.
■ Diagnosis
Low back pain originates in the SI joint in 15 to 30% of patients.3 Because the SI joint commonly produces low back pain radiating to the buttocks or lower extremity, differentiating SI joint pathology from lumbar spine or hip pathology is often difficult. Patients with SI joint pain may describe a band-like distribution of low back pain, and when asked to point specifically to the painful area, they may further localize it to a region medial and inferior to the posterior superior iliac spine (PSIS), representing a positive Fortin Finger Test.1–3 After careful history taking, diagnosis of SI joint pain begins with dedicated physical examination maneuvers. Because each maneuver individually lacks sufficient specificity or sensitivity to make the diagnosis, the following combination of examination maneuvers must be completed.16
In standing position, the patient is asked to point to the greatest site of pain (Fortin Finger Test). The PSIS is then evaluated for point tenderness to palpation.
A series of six SI joint diagnostic exam maneuvers are then performed, as described elsewhere.17 Although these exam maneuvers may cause discomfort in multiple areas, it is crucial to ask patients whether each maneuver reproduces the exact type of pain that they typically experience. The patient is placed in the supine position on the examination table and pelvic gapping, flexion/abduction/external rotation, and thigh thrust maneuvers are performed (Fig. 5.1). The patient is placed in the lateral position for Gaenslen’s maneuver and pelvic compression, performed on each side. Sacral thrust is then performed with the patient prone. A full examination of the lumbosacral spine, lower extremity, and hip is also performed.
A systematic review of the validity of the diagnostic criteria for SI joint pain supports using a threshold of three positive tests that reproduce the patient’s pain to indicate that the SI joint is a major source of pain generation.16
■ Nonoperative Treatment
Physical Therapy
In a patient with three or more positive diagnostic maneuvers, conservative therapeutic intervention targeting the SI joint is begun.
This consists of specialized SI joint physical therapy that should be performed by a therapist with specific SI joint training, targeting postural control of the joints via core and pelvic stabilization exercises.1 Pelvic stabilization orthoses, such as SI belts or tape, can be used as adjuncts to rehabilitation therapy and are maximally effective when applied just superior to the greater trochanter to limit SI joint motion.1 Oral nonsteroidal anti-inflammatory medications are commonly used adjuncts during therapy.
Injections
For patients in whom conservative treatment fails to render significant improvement, the diagnosis of SI joint dysfunction warrants further investigation via diagnostic injection. Although physical exam maneuvers may be positive indicators of SI joint pain, they also invariably place stress on adjacent structures with the potential for pain-generating capacity and they do not differentiate among such structures.16 Intra-articular injection of local anesthetic can add valuable diagnostic information. Using fluoroscopic guidance, intra-articular SI joint injection of local anesthetic is performed.18 The capacity of the SI joint is ~ 1 mL.1 Selective infiltration of the intra-articular portion of the joint is the goal, and care must be taken not to allow undue extravasation of medication into structures adjacent to the joint, which will muddle the diagnostic capacity of the injection. Two separate diagnostic injections provide pain relief for SI joint dysfunction in 10 to 19% of patients with suspected SI joint pathology.1,18 Following successful diagnostic injection to confirm SI joint pain, patients may be treated with an injection of a combination of steroid and local anesthetic medication. Long-term data on this treatment are not available, and thus it is unclear which patients may benefit from repeated injection, but in general we consider a patient to have failed control with injection therapy if an injection of steroid and local anesthetic fails to provide at least 50% pain relief for 1 month, or if a patient requires more than three injections within 12 months.
