In this study, we proposed using an ultrasound-guided AIIS injection test to diagnose SSI. Although it is not possible to directly compare the advantages of this method with current imaging methods, we believe that ultrasound-guided injection of the AIIS can complement existing diagnostic methods and can better distinguish the source of pain in FAI patients. Our results also showed that using the ultrasound-guided AIIS injection may result in diagnostic results inconsistent with those of 3D-CT or MRI. In addition, we also found that intraoperative findings, MRI, or CT to diagnose SSI could not achieve consistent results.
Increasing evidence has proven that ultrasound-guided hip injection is convenient and produces little pain and can be used to locate the origin of pain [14,15,16,17]. Gao et al. reported that ultrasound-guided hip injections had high accuracy in diagnosing FAI and identifying intra-articular lesions in patients with atypical pain, even higher than MRI . Amar et al. reported that ultrasound was reliable in assessing the morphology of the AIIS . Previously, it was proposed that an anaesthetic injection into the subspine region can be diagnostic . Recently, Xu et al. reported using extra-articular subspine corticosteroid injections to diagnose SSI. Patients who experienced significant relief underwent subspine decompression and achieved significant improvement . Based on the existing evidence, we considered that using ultrasound-guided AIIS injections for the diagnosis of SSI with extra-articular symptoms would be feasible and effective.
After tentative application, we found that none of the patients with Type I AIISs reported a positive response. Hetsroni et al. considered that Type I AIISs were characterized by a lack of contribution to hip impingement . Balazs et al. reported that only 20% of patients undergoing arthroscopic surgery for hip impingement had Type I AIIS . Thus, the negative response reported by all of the patients with a Type I AIIS was in line with our expectations and proved that patients will not produce false-positive results due to the placebo effect in our method. In contrast, Aguilera-Bohorquez et al. reported that 52.2% of patients with both FAI and SSI were classified as having a Type I AIIS. However, in their study, the pain of the patients could not be established to determine whether it could be attributed to FAI or SSI . In other words, they were uncertain if a Type I AIIS was involved in the appearance of symptoms. In our study, ultrasound-guided AIIS injections helped surgeons judge whether the source of pain and limitation of hip movement was primarily from the AIIS. The results of this study proved that a Type I AIIS did not contribute to the patient’s symptoms. Among a total of 73 patients, 36 reported a positive response after an ultrasound-guided AIIS injection and received subspinal decompression in arthroscopy. Follow-up of these 73 patients is still ongoing for assessing the long-term effect of our diagnosis method.
It is worth noting that only 53.49% of patients with Type IIA AIISs and 64.71% of patients with Type IIB AIISs reported a positive response. Additionally, one of three patients reported a negative response after the ultrasound-guided AIIS injection among those with Type III AIISs. Our diagnostic method confirms the conclusion drawn by Balazs et al.  and Wong et al. ; that is, subspinous impingement is not completely due to an abnormal morphology of the AIIS. In addition, Balazs et al. thought to diagnose SSI according to the AIIS morphology, but it had high sensitivity and extremely low specificity (23%) . If our diagnostic method is used as a standard, the specificity of classification proposed by Hetsroni et al. was only 27.03%. A similar conclusion was also reported by Karns et al., who found that AIIS Types I and II were hard to subdivide and showed poor correlation with the perioperative findings. Therefore, Type II AIIS possibly represents normal AIIS morphology variants rather than pathological abnormalities .
Another point demonstrated by our study is that it is inaccurate to assess symptomatic subspine impingement according to whether the patient has superior capsular oedema on MRI. Previously, Larson noted that soft tissue hypertrophy over the medial femoral neck and synovial oedema can be observed frequently in the setting of subspine impingement . Samim et al. first determined the MRI findings associated with SSI and found that the occurrence of superior capsular oedema (75% vs. 7.1%), impingement of the distal femoral neck (90% vs. 16%), superior chondral lesions (80% vs. 45%), and distal cam (80% vs. 19%) was much higher in the SSI group than in the non-SSI group . However, according to our diagnostic method, this difference is not well reflected. Although there was a significant difference in percentage of patients with superior capsular oedema between the two groups (P = 0.036), superior capsular oedema was only reported in 38.89% of patients who reported a positive response and was not observed in any of the patients with a Type III AIIS. After evaluating the result reported by Samim et al., Guermazi proposed that possible overlapping impingement syndromes had not be considered, which meant the source of the superior capsular oedema was uncertain . The results of our study suggested that the signs of impingement on the distal femoral neck, such as superior capsular oedema, have a certain level of suggestiveness but cannot be used for diagnosis due to their low sensitivity and specificity.
SSI is usually identified as distal femoral neck contact of the AIIS in full hip flexion [13, 26]. In recent years, Karns et al. believed that the possibility of direct impingement may be very small, and the occurrence of SSI was likely due to the reduction or disappearance of the space under the anterior inferior iliac spine , challenging the diagnostic criteria mentioned above. In general, our study indicates that the occurrence of subspine impingement can be heterogeneous. If the subspinal decompression is only determined by anatomical morphology and soft tissue changes, missed diagnosis or unnecessary damage to the physiological structure of patients are possible.
Our study has several limitations. First, a universally acknowledged and unchallenged consensus or gold standard in the diagnosis of SSI is currently lacking. In view of this, we are unable to design a control group to provide more statistical support for our diagnostic method of ultrasound-guided AIIS blocking to diagnose SSI and determine the sensitivity and specificity. We expect to obtain long-term patient follow-up results to provide more evidence supporting our diagnostic method. Second, our study only included a small number of patients, especially patients with Type III AIISs. We recommend further research to focus on this rare group of patients.