Athletic pubalgia is a syndrome that is most commonly seen in high-performance athletes. It consists of lower abdominal/inguinal pain upon activity and often progresses to include adductor pain. Athletes participating in sports requiring cutting or frequent acceleration and deceleration (e.g., soccer, ice hockey, and football) appear to be most susceptible to athletic pubalgia [18, 32]. Although the mechanism of athletic pubalgia has been debated in the literature, the majority of evidence appears to suggest that the syndrome is caused by a complex injury of the flexion/adduction apparatus of the lower abdomen and hip [43]. A number of alternative terms have been used to describe athletic pubalgia in the literature including “Gilmore’s groin” [18], “sports hernia” [21], “sportsman’s hernia” [51], and “pubic inguinal pain syndrome” [9].

Patients presenting with athletic pubalgia will most commonly complain of lower abdominal pain and proximal adductor pain. Although this pain is generally gradual in onset, it less commonly occurs as a result of an acute injury. These acute injuries are generally caused by hyperabduction of the hip and/or hyperextension of the trunk leading to a tear of the rectus abdominis [43, 57]. Athletic pubalgia appears to be much more common in males; however, an increasing proportion of females have been diagnosed in the last decade [44]. A number of physical examination maneuvers may be useful in the diagnosis of athletic pubalgia including painful resisted hip adduction in flexion and extension [36], reproduced symptoms with Valsalva maneuver [43], and reproduced symptoms with a resisted sit-up with simultaneous palpation of the inferolateral distal rectus abdominis [43]. Moreover, palpation of the proximal adductor muscles, abdominal obliques, transverse abdominis, and rectus abdominis is recommended [36].

If after a thorough history and physical examination athletic pubalgia is suspected, a plain radiograph and MRI are the recommended investigations [36]. Although there are no characteristic radiograph findings of athletic pubalgia, a plain radiograph is useful in ruling out other causes of groin pain. MRI has been shown to have high sensitivity and specificity for adductor and rectus abdominis pathology [57]. Figure 15.1 shows typical MRI findings in a patient with athletic pubalgia. It should be noted that Silvis et al. [52] found in one study that 36 % of asymptomatic professional hockey players had MRI findings consistent with athletic pubalgia. Additionally, a diagnostic ultrasound-guided intra-articular injection can be useful in ruling out intra-articular pathology as the source of the patients’ symptoms [3].

Athletic pubalgia can be managed both nonsurgically and surgically. Nonsurgical treatment recommendations include a trial of physiotherapy and rest followed by gradual reintroduction to sport activity [4, 34]. However, the current literature suggests that nonsurgical management of athletic pubalgia may offer no benefit compared with placebo [53]. On the other hand, surgical outcomes in the literature are much more positive. There have been a number of different surgical procedures described. These procedures include, but are not limited to, external oblique, transversalis fascia, and transversus abdominis repairs either with or without mesh and through either open or laparoscopic methods [6, 17, 33, 43]. The various surgical treatment options report generally positive outcomes with anywhere between 80 and 100 % rates of return to sport.

Recently, there has been evidence appearing that suggests there is an association between athletic pubalgia and FAI [22, 37, 38]. Larson et al. [37, 38] showed in a case series of 37 patients with both symptomatic athletic pubalgia and FAI that patients only had a 25 % rate of return to sport if only athletic pubalgia surgery was performed. Similarly, patients who only had hip arthroscopy performed for FAI had a relatively low (50 %) rate of return to sport. However, those patients who had procedures to correct both the athletic pubalgia and the FAI had an almost 90 % rate of unrestricted return to sport. In this study, the surgical procedure for athletic pubalgia was unspecified, and in all cases, the FAI was treated arthroscopically. The only complications reported were two superficial wound infections.

Another 38 patient case series on individuals with both FAI and athletic pubalgia reported similar findings [22]. In this study, no patients who had only athletic pubalgia correction surgery were able to return to sport; however, 100 % of patients who had surgical treatment of their athletic pubalgia followed by surgical treatment of their FAI at a later date were able to return to sport. The mean duration prior to return to play was 5.9 months. In this study, the procedure performed to treat the athletic pubalgia was not specified. The FAI was treated arthroscopically, and it was reported that 65 % of patients underwent both femoroplasty and acetabuloplasty, 21 % had only femoroplasty, and the remaining 13 % had only acetabuloplasty.

Sansone et al. [48] found that more than 60 % of patients stated that they were unsatisfied after either adductor tenotomy or rectus tenotomy for athletic pubalgia had a positive hip impingement test at postoperative follow-up. These results imply that undiagnosed FAI may be a common reason for failure of athletic pubalgia surgery.

These studies highlight the importance of ensuring that physicians consider the possibility of concurrent athletic pubalgia in the patient with FAI. The evidence suggests that hip arthroscopy or correction of the athletic pubalgia alone is unlikely to completely alleviate a patient’s symptoms with both conditions. However, the literature currently reports that in patients with both athletic pubalgia and FAI simultaneous correction of both conditions results in generally good outcomes with a high proportion of patients successfully being able to return to sport. Overall, the treatments both appear to be safe as only a very low rate of minor complications are reported after surgical treatment of patients with both FAI and athletic pubalgia.

Athletic osteitis pubis is a chronic overuse injury of the pubic symphysis and the parasymphyseal bone [27]. It should be noted that osteitis pubis can also be caused by etiologies other than mechanical sport injuries such as vaginal delivery, infection, and pelvic/perineal surgery [16]. However, for the purpose of this chapter, discussion will be limited to osteitis pubis in athletes. Patients presenting with osteitis pubis most commonly complain of central pubis pain and/or medial groin pain that is worsened with activity [27]. Patients may also have superior pubic rami, adductor, perineal, inguinal, or scrotal pain [16, 54]. Physical examination findings may include reduced external/internal rotation of the hip, adductor/abductor weakness, and a waddling, antalgic gait [40, 41].

Radiographs in patients with osteitis pubis are generally unremarkable in the acute setting, however, sclerotic or cystic changes may occur in patients with chronic osteitis pubis [48]. Bone marrow edema of the pubic symphysis on MRI is a common finding in patients with osteitis pubis [45]. That being said, one study found that 65 % of asymptomatic athletes also had bone marrow edema of the pubic symphysis on MRI [45]. Figure 15.2 shows the MRI findings in a patient with severe osteitis pubis. Steroid injections into the pubic symphysis have been recommended both as a nonsurgical treatment option and to aid in diagnosis [29]. A systematic review of treatment of osteitis pubis found that 58.6 % of patients were able to fully return to sport after management with steroid injections into the pubis symphysis [10].

Nonsurgical treatment options in the management of osteitis pubis include rest, NSAIDs, physiotherapy, steroid injections, and cross training [29, 47]. Literature rates of return to sport after nonsurgical treatment (not including steroid injection) of osteitis pubis range from 81 to 100 % with time to return to sport varying from 3 days to 24 months [27]. Nevertheless, definitive treatment of osteitis pubis relies on surgical treatment. Surgical treatment options for osteitis pubis include wedge resection [19], arthrodesis [42], pubic symphysis curettage [48], and endoscopic pubic symphysectomy [41]. Radic and Annear [48] reported 16 of 24 patients undergoing pubic symphysis curettage were able to return to sport at 2.5–12 months. Similarly Matsuda et al. [41] reported positive outcomes treating osteitis pubis with an endoscopic pubic symphysectomy. Although surgical treatment does appear to provide benefit to patients, there is currently no evidence to strongly support one form of surgical treatment over the others [27]. In fact, some authors even suggest that surgical treatment should not be performed for osteitis pubis and that for the vast majority of patients, nonsurgical treatment options are sufficient [16].

It has been suggested that FAI may cause osteitis pubis as a result of a compensatory increase in range of motion at the pubic symphysis due to the reduced range of functional range of motion of the hip [55]. In a retrospective case series, Matsuda et al. [41] reported that in patients with both symptomatic FAI and osteitis pubis, simultaneous hip arthroscopy and endoscopic pubic symphysectomy resulted in significantly improved VAS and NAHS scores as well as a mean patient satisfaction rating of 8.3 (scale 0–10). The only complications reported were two patients who had postoperative scrotal swelling which resolved spontaneously. Although the literature appears to suggest that a relationship between FAI and osteitis pubis probably exists, very limited clinical information, specifically addressing the treatment and outcomes of patients with both conditions, is reported in the literature.

Internal snapping hip syndrome is a condition in which the iliopsoas tendon moves over the iliopectineal eminence or the femoral head resulting in a snapping sensation [1, 5]. Internal snapping hip syndrome has the potential to produce labral tears and even chondral damage [2,14]. Unlike labral tears secondary to FAI, which typically produce lesions at the 1–2 o’clock position, labral tears caused by internal snapping hip syndrome typically produce a characteristic labral tear at the 3 o’clock position [7].

In addition to the snapping sound and/or sensation, patients with internal snapping hip syndrome will frequently complain of pain with repetitive twisting or flexion of the hip. Physical examination findings for internal snapping hip syndrome include a positive flexion-adduction-internal rotation (FADIR) impingement test and tenderness over the iliopsoas at the level of the anterior joint line [14]. The snapping can often be reproduced on physical exam by slowly transitioning the hip from a flexed, abducted, externally rotated position to an extended, internally rotated position with the patient supine [8]. Figure 15.3 shows how this physical exam maneuver can be completed. Alternatively with the patient in the lateral position, transitioning the hip back and forth from extension to flexion will often recreate the snapping of the hip [8]. In the diagnosis of internal snapping hip syndrome, anteroposterior pelvis and elongated neck lateral radiographs are recommended in all patients [23]. A diagnostic ultrasound can also be useful in confirming the diagnosis of internal snapping hip syndrome. Real-time ultrasound or fluoroscopy with contrast injected into the iliopsoas bursa allows the examiner to observe for a jerk in the iliopsoas tendon at the same time as a snap in the hip is heard or felt [8, 56]. Although some studies suggest that an MRI can be beneficial in the diagnosis of tendinopathies [11], other authors suggest that a good history and physical examination are typically sufficient for the diagnosis of internal snapping hip syndrome [20].

Recommended nonsurgical treatment for internal snapping hip syndrome includes physiotherapy, intra-articular injections, and/or iliopsoas bursa injection [23]. Gruen et al. (2002) found in a case series that 37 % of patients failed nonsurgical management of internal snapping hip syndrome and required surgical treatment. Ilizaliturri et al. [31] stated that surgical treatment only be considered in patients who have failed nonsurgical treatment options. A number of surgical treatment options have been described in the literature for internal snapping hip syndrome including iliopsoas tendon release at the lesser trochanter [30], at the level of the joint [15], or at the level of the peripheral compartment [31]. Iliopsoas tendon releases can be done either through open approaches or through endoscopic techniques [13, 30]. One randomized control trial found no significant clinical difference between endoscopic iliopsoas tendon release at the level of the lesser trochanter compared with at the level of the peripheral compartment and that both procedures significantly improved WOMAC scores in 100 % of patients [31]. Another study reported 100 % of patients experienced no continued snapping after iliopsoas release and that 82 % of patients experienced excellent pain relief (Gruen et al. 2002). A systematic review of surgical management of internal snapping hip syndrome found that open treatment had a 21 % rate of complications, whereas arthroscopic treatment had only a 2.3 % complication rate [35]. This systematic review found the following complications reported in the literature after surgical treatment of snapping hip syndrome: hip flexor weakness, anterior thigh paresthesia, anterolateral thigh numbness, greater trochanteric bursitis, ischial bursitis, superficial infections, and a hematoma. They also reported that among the 11 included studies, arthroscopic surgery had a 100 % success rate of resolution of snapping, whereas open procedures only had a 77 % success rate.

In one case study of 75 patients undergoing iliopsoas tendon lengthening for internal snapping hip, it was observed that 76.4 % of patients also required acetabuloplasty for pincer impingement and 52.7 % of patients required femoroplasty for cam impingement [5]. Patients with FAI may have a higher propensity for developing internal snapping hip syndrome as a result of compensatory effects secondary to the reduced functional range of motion associated with FAI [23]. Heyworth et al. [26] found that failing to address a tight iliopsoas tendon during index hip arthroscopy is a frequent cause of patients requiring revision surgery. In this study, four of the nine patients who required revision surgery after index hip arthroscopy for FAI had a psoas tendon release performed during the revision surgery. One systematic review of revision hip arthroscopies found that a psoas release was performed in 15.3 % of revision hip arthroscopies [50]. It should be noted, however, that this study was looking at revision hip arthroscopies for all index indications, not exclusively for FAI.