Abstract
Sacroiliac joint pain represents a frequently misdiagnosed cause of low back pain, affecting between 15% and 30% of individuals with mechanical pain below L5. Although a battery of provocation maneuvers can identify most cases of sacroiliac joint pain with reasonable specificity, the reference standard is low-volume blocks, which are associated with a false-positive rate ranging between 10% and 30%. Between 40% and 50% of cases are caused by a specific inciting event, which can include motor vehicle collisions, falls, or more insidious etiologies, such as pregnancy, spinal fusion, and leg length discrepancies. Sacroiliac joint pain may be secondary to both intraarticular and extraarticular pathology, with the latter more likely to be unilateral and affect younger individuals. Both intraarticular and extraarticular steroid blocks have been shown to provide short- to intermediate-term and are sometimes used to select patients for radiofrequency denervation or fusion. Since the lateral branches targeted during denervation innervate the ligaments, those with extraarticular pathology are more likely to benefit. Minimally invasive fusion should be reserved for individuals with dislocation or degeneration with instability who have failed more conservative therapies.
Keywords
buttock pain, iliosacral, low back pain, sacroiliac joint
Anatomy, Function, and Innervation
The sacroiliac (SI) joint complex is the largest spinal joint the body, averaging 17.5 cm 2 in size. It is most frequently classified as an auricular-shaped diarthrodial joint because it contains a fibrous joint capsule filled with synovial fluid, cartilaginous surfaces, and an intricate set of ligamentous connections. The SI joint differs from other synovial joints in that it is not readily mobile, there is discontinuity in the posterior capsule, and the thinner iliac articulation is composed of fibro- instead of hyaline cartilage.
The SI joint is supported by a network of myofascial structures that help promote movement, support, and stability. These structures include the gluteus maximus and medius, biceps femoris, piriformis, latissimus dorsi via the thoracolumbar fascia, and erector spinae. The joint is primarily designed for stability and weight bearing, although small degrees of rotation (≤3 degrees) and translation (≤2 mm) occur. Previous attempts to establish a causative relationship between pain and motion abnormalities have been unsuccessful.
The nerve supply of the SI-joint complex is very variable and a subject of great relevance for interventional pain practitioners. To summarize the literature, the lateral branches of the S1 and S2 dorsal rami innervate the posterior joint and the surrounding ligaments in nearly all individuals, giving off between one and four branches. There is a contribution from S3 in most but not all individuals, with again up to four branches being noted in some people. Whereas some cadaveric dissections indicate that people receive innervation from L5, , most studies have found this to be absent or infrequent. For S4, the literature is similarly mixed, with some studies demonstrating a neural connection in most individuals but others finding contributions to be rare. Anatomic studies have also found anastomoses to be common between segmental spinal levels. Some people receive sensory input from the SI joint through the superior gluteal nerve in addition to the lateral branches.
The innervation of the ventral SI joint is less clinically relevant but no less controversial. Whereas some cadaveric studies have reported nerve filaments stemming from the ventral rami of L4–S2, other experts cite contributions from levels as cephalad as L2. Surprisingly, some anatomic studies have failed to find any ventral neural contribution to the SI joint.
Both intraarticular and extraarticular structures can be sources of SI joint pain. Clinical studies have reported benefit from both intraarticular and extraarticular injections, with one study finding no difference in benefit between the two. An electrophysiologic study performed in cats identified mechanoreceptors in both the joint capsule and adjacent muscles, with most (26/29) residing within the capsule. Among these receptor units, 28 were classified as nociceptive and 1 proprioceptive. Broken down by region, 16 were found in the proximal third, 11 in the middle third, and two in the distal third. Immunohistochemical studies in human cadavers have also found evidence of calcitonin gene–related peptide and substance P immunoreactive nociceptors in both capsular and interosseous ligaments. Clinical studies have documented pain provocation in patients and asymptomatic volunteers with both capsular distention and ligamentous provocation ( Figs. 66.1 and 66.2 ).
Epidemiology
Several problems are inherent when ascertaining the prevalence of SI joint pain. These include but are not limited to the lack of any “gold standard” for diagnosis, perspective (i.e., interventional pain specialists generally attribute a greater proportion of low back pain [LBP] to SI joint pathology than surgeons do), the population studied, and method of diagnosis.
Several studies have utilized “double blocks” with lidocaine and bupivacaine to identify a painful SI joint. These studies have generally evaluated only patients without signs of radiculopathy whose predominant pain complaint was below L5. In the five studies using the reference standard of concordant pain relief with lidocaine and bupivacaine as the diagnostic criterion, the reported prevalence rates for SI joint pain ranged between 10% and 45%, with the incidence of false-positive results varying between 0% and 43%. One flaw with these studies is that all based their criterion response on intraarticular injections, which likely excluded individuals with predominantly extraarticular pathology ( Table 66.1 ). As already noted, these studies also excluded patients with radiculopathy. In one study that examined the prevalence of SI joint pain in patients with symptoms of radiculopathy and a herniated disc confirmed by magnetic resonance imaging (MRI), over two thirds of patients had SI joint dysfunction as identified by anatomic and pain-provocation tests. This suggests that SI joint pain often coexists with other forms of pathology.
| Authors | Subjects | Interventions | Diagnostic Criteria | Results |
|---|---|---|---|---|
| Maigne et al. | 54 patients with chronic unilateral LBP with or without radiation to posterior thigh | Intraarticular blocks using 2 mL of lidocaine and bupivacaine on separate occasions. Authors avoided anesthetizing periarticular ligaments. | ≥75% pain relief, with the bupivacaine block lasting ≥2 h. | Prevalence rate 18.5%. False-positive rate 17%. |
| Manchikanti et al. | 20 patients with chronic LBP without neurologic deficits | Intraarticular blocks with unspecified volume of lidocaine and bupivacaine on separate occasions. | Not noted. | Prevalence rate 10%. False-positive rate 20%. |
| Irwin et al. | 158 patients with chronic LBP with or without lower extremity pain | Intraarticular blocks with 2 mL of lidocaine and 2 mL bupivacaine and steroid on separate occasions. | ≥70% pain relief, with the bupivacaine block lasting ≥4 h. | Prevalence rate 27%. False-positive rate 43%. |
| Laslett et al. | 48 patients with buttock pain with or without lumbar or lower extremity symptoms, without signs of nerve root compression | Intraarticular blocks with <1.5 mL of lidocaine plus steroid and bupivacaine on separate occasions. | ≥80% pain relief with lidocaine and bupivacaine. | Prevalence rate 26%. False-positive rate 0%. |
| van der Wurff et al. | 60 patients with chronic LBP below L5 with or without lower extremity symptoms, without neurologic symptoms | Intraarticular blocks with 2 mL lidocaine and bupivacaine on separate occasions. | ≥50% pain relief with lidocaine and bupivacaine, with the bupivacaine block lasting ≥4 h. | Prevalence rate 45%. False-positive rate 12%. |
| Liliang et al. | 150 patients with chronic LBP, no neurologic deficits, and positive provocative SI joint tests | Intraarticular blocks with 2 mL lidocaine or bupivacaine mixed with steroid on separate occasions. | ≥50% pain relief lasting at least 6 weeks. | Prevalence rate 33%. False-positive rate 16%. |
| Liliang et al. | 52 patients with chronic LBP who had previously undergone lumbar or lumbosacral spinal fusions, pain below L5 and positive provocative SI-joint tests | Intraarticular blocks with 2 mL lidocaine or bupivacaine mixed with steroid on separate occasions. | ≥75% pain relief lasting between 1 and 4 h. | Prevalence rate 40%. False-positive rate 10%. |
| Cohen et al. | 39 patients with chronic LBP below L5 with tenderness over the SI joint and positive provocative tests | Intraarticular blocks with 2 mL bupivacaine mixed with steroid on separate occasions. | ≥50% pain relief lasting ≥3 h. | Prevalence 41%. False-positive rate 10%. |
Studies using different diagnostic criteria have yielded similar results. Schwarzer et al. conducted a prevalence study in 43 consecutive patients with chronic LBP predominantly below L5 using fluoroscopically guided intraarticular SI joint injections. The authors diagnosed SI joint pain based on three criteria: pain relief following intraarticular local anesthetic infiltration, ventral capsular tear on postarthrography computed tomography (CT) scanning, and concordant pain provocation during capsular distension. With analgesic response as the sole criterion for diagnosis, the prevalence of SI joint pain was found to be 30%. When 75% or more pain relief combined with a ventral capsular tear was used as the diagnostic criterion, the prevalence rate dropped to 21%. Only seven patients satisfied all three diagnostic criteria, for a lower-limit prevalence rate of 16%. Overall, SI joint pathology appears to be the primary generator in between 15% and 30% of patients with chronic axial LBP below L5, being more common in females and the elderly.
Etiology
The mechanism of injury to the SI joint complex is frequently described as a combination of axial loading and abrupt rotation. On an anatomic level, injury or pathology involving the myriad structures comprising the SI joint can lead to nociception. These include capsular or synovial disruption, ligamentous injury, myofascial pain, hypomobility or hypermobility, extraneous compression or shearing forces, cysts, abnormal joint mechanics, microfractures or macrofractures, chondromalacia, soft tissue pathology and inflammation. In patients with persistent nociceptive input, central sensitization can play a contributing role ( Table 66.2 ).
| Intraarticular | Extraarticular |
|---|---|
| Arthritis (e.g., osteoarthritis, rheumatoid) Spondyloarthropathy Trauma Infection Cystic disease | Trauma/fractures Ligamentous injury Myofascial pain Enthesopathy Pregnancy Cystic disease |
Mechanistically, there are numerous reported etiologies for SI joint pain. These causes can be classified into intraarticular and extraarticular sources. Arthritis and the spondyloarthropathies are two examples of intraarticular causes of SI joint pain. Extraarticular sources include enthesopathy, fractures, ligamentous injury, and myofascial pain. The evidence in support of different etiologies includes the fact that clinical studies have demonstrated significant pain relief following both intraarticular and periarticular SI joint injections. In one of these studies, periarticular injections were found to provide benefit in patients with spondyloarthropathy, suggesting that the two etiologies may overlap.
Distinguishing between intraarticular and extraarticular pain generators may be clinically relevant in deciding on treatment options. A recent study by Dreyfuss et al. found that multisite lateral branch blocks were more effective at blocking pain from ligamentous probing than for the discomfort elicited during capsular distension. This indicates that lateral branch radiofrequency (RF) denervation may be more likely to be effective in individuals with extraarticular pathology. In contrast to intraarticular pathology, extraarticular pain is more likely to be unilateral, to occur in younger individuals, to present with more prominent tenderness, and to be associated with a specific inciting event or biomechanical etiologies.
Numerous factors can predispose a person to develop SI joint pain. Risk factors that operate by increasing the stress borne by the SI joints include obesity, true and apparent leg-length discrepancy, gait abnormalities, persistent strain/low-grade trauma (e.g., jogging), scoliosis, pregnancy, and surgery, especially fusion of the sacrum. Spine surgery may cause postprocedural SI joint pain by increasing load bearing, weakening the surrounding ligaments, iatrogenic violation of the SI joint complex, and postsurgical hypermobility. In one study that compared presurgical and postsurgical CT scans in fusion patients and matched controls, the investigators found an almost twofold increase in SI joint degeneration in the surgical patients compared with the control subjects (75% vs. 38.2%), with the highest incidence noted with fusions that extended to the sacrum. Studies evaluating the response to diagnostic injections following spinal fusion have reported prevalence rates ranging from 32% to 43%.
Pregnancy predisposes women to SI joint pain via the combination of increased weight gain, exaggerated lordotic posture, the mechanical trauma of parturition, and hormone-induced ligamental laxity. In one large study evaluating over 300 pregnant women between 12 and 18 weeks’ gestation, 62% reported LBP, with 54% of these experiencing pelvic girdle pain situated around the SI joints and another 29% describing combination pelvic girdle and lumbar pain. Infrequently, SI subluxation may also occur during pregnancy.
Between 40% and 50% of patients with injection-confirmed SI joint pain cite a specific inciting event. In investigations by Chou et al., Schwarzer et al., and Cohen et al., the leading precipitating events in descending order for trauma-induced SI joint pain were motor vehicle collisions, falls, cumulative strain, and pregnancy.
Diagnosis and Presentation
History and Physical Exam
SI joint pain can be difficult to distinguish from other sources of LBP. Numerous studies have established that no single historical report or sign on physical exam can reliably diagnose a painful SI joint. Several reviews have sought to evaluate the validity of a battery of physical exam tests in establishing the SI joint as the primary pain generator. These reviews have generally shown that mobility and alignment tests are inadequate in identifying SI joint–mediated pain. For provocative maneuvers, the results have been mixed. Whereas some reviews have determined that a combination of provocative maneuvers can accurately discriminate between pain from the SI joint and other sources of spinal pain, others have reached equivocal or negative conclusions.
Nevertheless, clinical studies suggest that a comprehensive history and physical exam can provide important clues to etiology and inform further diagnostic workup. Some of the more common findings used to select candidates for SI joint blocks are pain predominantly localized below L5, pain exacerbated by rising from a sitting position, and tenderness overlying the joint. Several studies and reviews have found that when the area of maximal tenderness is situated close to the posterosuperior iliac spine, there is a high likelihood that the primary pain generator is the SI joint. In contrast to other causes of mechanical LBP, such as myofascial, facetogenic, and discogenic pain, SI joint pain is more likely to be unilateral and occur after a specific inciting event ( Table 66.3 ).
| Author | Patients | Findings Suggestive of Sacroiliac Joint Pain |
|---|---|---|
| Fortin et al. | 10 volunteers and 16 patients with SI joint pain. | Point of maximum discomfort within 10 cm caudal and 3 cm lateral to PSIS. |
| Murakami et al. | 38 patient responders to periarticular injections | Point of maximum discomfort within 3 cm from PSIS. |
| Schwarzer et al. | 43 patients with axial LBP. | Radiation to groin. |
| Dreyfuss et al. | 85 patients with axial LBP. | None. |
| Slipman et al. | 50 patients with axial LBP. | 94% had buttock, 72% lumbar, 28% lower leg, and 14% groin pain. |
| van der Wurff et al. | 60 patients with axial LBP. | None. |
| Jung et al. | 160 patients with SI joint arthropathies. | Buttock pain alone, extending into posterolateral thigh or into groin. |
| Laslett et al. | 48 patients with axial LBP. | Noncentralization or peripheralization of pain. |
| DePalma et al. | 127 responders to IA SI joint blocks. | Lateral midline pain. |
| Young et al. | 102 patients with nonradicular LBP. | Pain rising from sitting, nonmidline pain below L5 |
| Liliang et al. | 130 patients evaluated for SI joint pain after fusion. | Unilateral pain, 3 or more provocative maneuvers, postoperative pain different than preoperative pain. |
| Ostgaard et al. | 855 pregnant women. | Pain in the pubic symphysis. |
| LaPlante et al. | 153 patients with axial LBP. | None. |
| Kurosawa et al. | 50 patients with axial LBP who responded to periarticular SI-joint injections. | Pain from the upper joint most commonly noted near posterior superior iliac spine; pain from middle joint most commonly noted in midbuttock, pain from lower joint noted in lower buttock; 44% of patients had groin pain, which was associated with upper joint involvement. |
Pain Referral Patterns
Several investigators have sought to determine pain referral patterns emanating from SI joints. In a provocative study conducted in 10 asymptomatic volunteers, Fortin et al. found that all subjects experienced pain in the ipsilateral buttock, which sometimes radiated into the posterolateral upper thigh. In a retrospective review by Slipman et al. conducted in 50 patients with injection-confirmed SI joint pain, the authors found the most common referral patterns to be focal pain in the buttock (94%) and lower lumbar region (72%) and extension into the ipsilateral lower extremity (50%), groin area (14%), upper lumbar region (6%), and abdomen (2%). Despite the widely held view that only radicular pain extends into the lower leg, 28% of patients experienced pain radiating below the knee, with 12% reporting foot pain. Cohen et al. examined pain referral patterns in an analysis of SI joint RF denervation outcome predictors conducted in 77 patients with positive screening blocks. Of these, 43% experienced symptoms localized to the buttock and lower lumbar region, with 35% noting pain referred to the thigh(s). Consistent with Slipman et al., the authors also noted a high percentage of unusual pain patterns, with 23% reporting lower leg pain and 20% complaining of extension into the groin. Lower back or buttock pain that is referred into the groin was also described by Schwarzer et al. as being the only pattern that distinguished SI joint pain from that due to other pain generators, suggesting that it may indicate ventral joint involvement.
Because the SI joint is the largest axial joint in the body, the radiation pattern may be a by-product of the part of the joint affected. In a clinical study performed in 50 patients with injection-confirmed SI joint pain, the authors found that the upper part of the joint was most frequently associated with pain in the posterosuperior iliac spine, the middle aspect of the joint tended to be associated with pain in the midbuttock, and pain emanating from the inferior portion of the joint was most likely to be experienced in the lower buttock region. In those individuals who experienced groin pain, local anesthetic injections into the upper and middle parts of the joint were more likely to result in pain relief than injections into the lower joint. A previous study conducted in discogenic pain also suggested that the greater the magnitude of nociceptive stimulation, the more distal in the extremity the evoked pain will extend ( Fig. 66.3 ).
Radiologic Imaging
Results of studies correlating radiologic findings with the results of diagnostic blocks have been inconsistent. Studies by Slipman et al. and Maigne et al. found sensitivities of 13% and 46%, respectively, for the use of radionuclide bone scanning in the identification of an injection-confirmed painful SI joint. Despite the greater than 90% specificities in these studies, the low sensitivities indicate that bone scanning is a poor screening tool for SI joint pain (i.e., it will fail to detect most cases). The lack of a strong association between symptoms and diagnostic injections has also been noted for CT and x-ray stereophotogrammetry. In a retrospective analysis by Elgafy et al., CT imaging was found to be 57.5% sensitive and 69% specific in diagnosing SI joint pain.
MRI is the reference standard for detecting SI joint involvement in patients with spondyloarthropathies. Studies have shown over 80% sensitivity in detecting chronic sacroiliitis, including sclerosis, joint space abnormalities, and ankylosis, with contrast-enhanced and short tau inverted recovery (STIR) providing the highest sensitivity. However, MRI pathology does not seem to correlate well with clinical findings. Whereas MRI may be a more sensitive test for detecting active inflammation and concomitant structural changes, CT remains the reference standard for disease processes in which bone destruction or ossification can occur.
Injections
It is widely acknowledged that an analgesic response to an SI joint injection is the most accurate means of diagnosing a painful SI joint complex. However, without another reliable means to diagnose SI joint pain, this is impossible to prove. In studies and reviews that have sought to determine the predictive value of historical reports and physical exam signs, etiologies, and referral patterns, pain relief in response to low-volume (≤2 mL) SI joint blocks has generally been used as the reference standard. The same criteria have been used in screening patients for more invasive procedures, such as surgery and RF ablation. In almost all cases, these injections have been intraarticular. Although some of the injectate may extravasate into adjacent ligaments and muscles, diagnostic capsular injections may underestimate the true prevalence of pain from the SI joint complex by failing to anesthetize the surrounding soft tissues.
The false-positive rate of uncontrolled SI joint blocks is around 20%. This has led some experts to recommend using “double blocks” (also known as comparative local anesthetic blocks) with two local anesthetic drugs having different half-lives, or placebo-controlled blocks, as the best way to identify a painful SI joint. The main problem with this paradigm is that the correlation between the duration of benefit and the pharmacokinetics of local anesthetics is weak and inconsistent. A study performed in patients with suspected cervical facet joint pain using double comparative blocks found that this diagnostic paradigm may be associated with a significant false-negative rate, which means that many patients with the index condition would be misdiagnosed. The double-block diagnostic paradigm has also been found not to be cost-effective in selecting candidates for RF denervation. Whereas one might expect higher success rates for RF denervation when candidates are selected based on their response to double compared to single diagnostic blocks, clinical studies have not found this to be the case. A randomized, crossover study also found that the use of sedation during diagnostic SI joint blocks may increase the false-positive rate.
Treatment
Conservative
The initial treatment of SI joint pain should focus on conservative measures, ideally addressing the underlying etiology. True and functional leg-length discrepancies can be treated with shoe lifts and physical therapy, respectively. True leg-length discrepancies result in increased stress and abnormal force vectors on the ipsilateral lower extremity, which may then extend to the contralateral leg. Since these occur in a large percentage of asymptomatic individuals and many people already compensate for a lower extremity length difference by altering their gait or posture, most experts recommend starting out with inserts that correct only half the incongruity and implementing them gradually. In one study conducted in 798 patients with chronic low back or hip pain and 359 controls, Friberg found that 75% of pain patients had leg length asymmetries of at least 5 mm, versus 43.5% of the asymptomatic cohort. Functional leg-length discrepancies usually occur as a result of muscle weakness or inflexibility at the pelvis or ankle. Specific causes include pelvic obliquity, adduction or flexion contractures of the hip, and genu valgum and varum. The treatment of apparent leg-length discrepancies entails aggressive physical therapy that targets the underlying etiology. If malalignment is suspected, osteopathic or chiropractic manipulation has been reported to be of value, though prospective controlled studies are lacking. For patients with spondyloarthropathies, immunomodulating agents such as cytokine inhibitors and methotrexate may reduce disease progression, alleviate pain, and improve function.
Reviews and guidelines have found exercise to be beneficial for chronic LBP, but few studies have been performed in those with predominantly SI joint pain. Biomechanical models have shown contraction of the transversus abdominis muscle to be associated with reduced laxity of the SI joint and suggest that isolated contraction of transversely oriented musculature (e.g., pelvic floor muscles and the piriformis) can stabilize the joint. In their study, Mooney et al. found five women with injection-confirmed SI joint pain who had electromyographically documented hyperactivity of the ipsilateral gluteus muscles and contralateral latissimus muscle. After a 2.5-month exercise program, all five achieved a reduction in pain and return of electromyographic patterns to normal. In another study evaluating three different physical therapy regimens in pregnant women clinically diagnosed with SI joint pain, no difference was noted between the use of a nonelastic SI belt, home exercise, and a structured exercise program, with all groups demonstrating improvement between the end of gestation and 12-months postpartum.
In patients who do not have a correctable etiology, pharmacotherapy should be considered as part of an interdisciplinary treatment regimen, though no studies have specifically evaluated medications in individuals with SI joint pain. In persons with acute nonneuropathic back pain, both nonsteroidal antiinflammatory drugs (NSAIDs) and muscle relaxants may be effective. In patients with chronic LBP, there is weak evidence supporting the use of tricyclic antidepressants and selective norepinephrine serotonin reuptake inhibitors. For opioids, there is some evidence of short-term benefit, but reviews have generally found minimal evidence to support long-term effectiveness, improvement of function, or superiority over NSAIDs and antidepressants for LBP.
Injections
Injections with local anesthetic are the reference standard for determining whether or not someone has SI joint pain; but when steroids are added, they may also confer therapeutic benefit. There have been four randomized trials (three of which were placebo-controlled) evaluating the effectiveness SI joint steroid injections, and all demonstrated benefit. Three were performed in patients with spondyloarthropathies and one was conducted in children. Two studies by the same group of investigators evaluated periarticular injections in patients with spondyloarthropathy, which by definition involves joint pathology. However, only one of the placebo-controlled studies followed patients longer than 2 months (albeit in an open-label extension); this study enrolled only 10 patients.
A major issue surrounding the use and evaluation of SI joint injections is whether the primary source of pain is intraarticular, extraarticular, or mixed. Intraarticular SI joint pain is more likely to occur in the elderly and to be bilateral, whereas extraarticular SI joint pain is more likely to be unilateral, to occur in younger individuals, and to be associated with a specific inciting event. There have been few attempts to examine the relative benefit of intraarticular versus extraarticular SI joint injections. A retrospective study by Borowsky and Fagen including 120 patients found that combination intraarticular and extraarticular injections were superior to intraarticular injections alone, although even at 3 weeks postinjection less than half of the patients had experienced over 50% pain relief (42.5% for combination injections vs. 27.5% for intraarticular blocks). Murakami et al., in a nonrandomized comparative-effectiveness study, found that extraarticular injections guided by pain provocation with hypertonic saline provided better pain relief 5 minutes after treatment than intraarticular injections. However, the lack of any long-term follow-up, myriad methodologic flaws, and the 100% success rate in the extraarticular group indicate the need for caution in interpreting these findings. In another study evaluating the accuracy of ultrasound guidance for SI joint injections in patients with active sacroiliitis, Hartung and colleagues found that there was no difference in treatment outcomes between the 12 patients who received intraarticular injections and the 8 whose injections were situated outside of the joint, with both groups experiencing almost 50% pain relief at 4-week follow-up.
There have been a host of uncontrolled studies evaluating the long-term effects of SI joint injections. In four observational studies conducted in over 100 patients with spondyloarthropathy, when data were combined, over 85% of the subjects obtained significant pain relief lasting for an average of 10 months. Comparable results have been obtained in patients without spondyloarthropathy and with repeat injections.
Whereas good results have been anecdotally reported with “blind” injections, studies examining the “accuracy” of landmark-guided SI joint blocks have found that only between 12% and 22% of injections end up being intraarticular. Yet as alluded to earlier, it is not clear whether intraarticular or extraarticular pathology is more common or which type of injection is more beneficial. A clinical trial is currently under way to answer these questions ( ClinicalTrials.gov Identifier: NCT02096653; Tables 66.4 and 66.5 ; Fig. 66.4 ).
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