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Cartilage Restoration in the Patellofemoral Joint

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Take-Home Points

  • Careful evaluation is key in attributing knee pain to patellofemoral cartilage lesions-that is, in making a "diagnosis by exclusion".
  • Initial treatment is nonoperative management focused on weight loss and extensive "core-to-floor" rehabilitation.
  • Optimization of anatomy and biomechanics is crucial.
  • Factors important in surgical decision-making incude defect location and size, subchondral bone status, unipolar vs bipolar lesions, and previous cartilage procedure.
  • The most commonly used surgical procedures-autologous chondrocyte implantation, osteochondral autograft transfer, and osteochondral allograft-have demonstrated improved intermediate-term outcomes.

Patellofemoral (PF) pain is often a component of more general anterior knee pain. One source of PF pain is chondral lesions. As these lesions are commonly seen on magnetic resonance imaging (MRI) and during arthroscopy, it is necessary to differentiate incidental and symptomatic lesions.1 In addition, the correlation between symptoms and lesion presence and severity is poor.

PF pain is multifactorial (structural lesions, malalignment, deconditioning, muscle imbalance and overuse) and can coexist with other lesions in the knee (ligament tears, meniscal injuries, and cartilage lesions in other compartments). Therefore, careful evaluation is key in attributing knee pain to PF cartilage lesions—that is, in making a "diagnosis by exclusion."

From the start, it must be appreciated that the vast majority of patients will not require surgery, and many who require surgery for pain will not require cartilage restoration. One key to success with PF patients is a good working relationship with an experienced physical therapist.

Etiology

The primary causes of PF cartilage lesions are patellar instability, chronic maltracking without instability, direct trauma, repetitive microtrauma, and idiopathic.

Patellar Instability

Patients with patellar instability often present with underlying anatomical risk factors (eg, trochlear dysplasia, increased Q-angle/tibial tubercle-trochlear groove [TT-TG] distance, patella alta, and unbalanced medial and lateral soft tissues2). These factors should be addressed before surgery.

Patellar instability can cause cartilage damage during the dislocation event or by chronic subluxation. Cartilage becomes damaged in up to 96% of patellar dislocations.3 Most commonly, the damage consists of fissuring and/or fibrillation, but chondral and osteochondral fractures can occur as well. During dislocation, the medial patella strikes the lateral aspect of the femur, and, as the knee collapses into flexion, the lateral aspect of the proximal lateral femoral condyle (weight-bearing area) can sustain damage. In the patella, typically the injury is distal-medial (occasionally crossing the median ridge). A shear lesion may involve the chondral surface or be osteochondral (Figure 1A).

Figure 1.
In an osteochondral lesion, the area of cartilage damage is often larger than the bony fragment indicates (Figure 1A), and even small fractures visible on radiographs can portend extensive cartilage damage. In addition, isolated cartilage flaps can occur; if suspected, they should be assessed with MRI. The extent of cartilage damage is related to the magnitude of energy required to cause the dislocation and/or to the frequency of events. In more normal anatomy, more energy is required to provoke a dislocation, and damage to articular cartilage is greater. In recurrent patellar dislocation, each event can cause additional injury, and the size of the lesion tends to increase with the number of dislocations.4 Patellar dislocation can result in chronic patellar subluxation, or dislocations that often lead to recurrent or chronic patellar instability. With recurrent instability, the medial patellar facet becomes damaged as it displaces out of the trochlea during subluxation and dislocation events. With lateral patellar maltracking, the contact area is reduced. With overall similar PF forces, a smaller contact area results in increased point loading, thus increasing stress and promoting cartilage wear.

Chronic Maltracking Without Instability

Chronic maltracking is usually related to anatomical abnormalities, which include the same factors that can cause patellar instability. A common combination is trochlear dysplasia, increased TT-TG or TT-posterior cruciate ligament distance, and lateral soft-tissue contracture. These are often seen in PF joints that progress to lateral PF arthritis. As lateral PF arthritis progresses, lateral soft-tissue contracture worsens, compounding symptoms of laterally based pain. With respect to cartilage repair, these joints can be treated if recognized early; however, once osteoarthritis is fully established in the joint, facetectomy or PF replacement may be necessary.

Direct Trauma

With the knee in flexion during a direct trauma over the patella (eg, fall or dashboard trauma), all zones of cartilage and subchondral bone in both patella and trochlea can be injured, leading to macrostructural damage, chondral/osteochondral fracture, or, with a subcritical force, microstructural damage and chondrocyte death, subsequently causing cartilage degeneration (cartilage may look normal initially; the matrix takes months to years to deteriorate). Direct trauma usually occurs with the knee flexed. Therefore, these lesions typically are located in the distal trochlea and superior pole of the patella.

Repetitive Microtrauma

Minor injuries, which by themselves do not immediately cause apparent chondral or osteochondral fractures, may eventually exceed the capacity of natural cartilage homeostasis and result in repetitive microtrauma. Common causes are repeated jumping (as in basketball and volleyball) and prolonged flexed-knee position (eg, what a baseball catcher experiences), which may also be associated with other lesions caused by extensor apparatus overload (eg, quadriceps tendon or patellar tendon tendinitis, and fat pad impingement syndrome).

Idiopathic

In a subset of patients with osteochondritis dissecans, the patella is the lesion site. In another subset, idiopathic lesions may be related to a genetic predisposition to osteoarthritis and may not be restricted to the PF joint. In some cases, the PF joint is the first compartment to degenerate and is the most symptomatic in a setting of truly tricompartmental disease. In these cases, treating only the PF lesion can result in functional failure, owing to disease progression in other compartments. Even mild disease in other compartments should be carefully evaluated.

History and Physical Examination

Patients often report a history of anterior knee pain that worsens with stair use, prolonged sitting, and flexed-knee activities (eg, squatting). Compared with pain alone, swelling, though not specific to cartilage disease, is more suspicious for a cartilage etiology. Identifying the cartilage defect as the sole source of pain is particularly difficult in patients with recurrent patellar instability. In these patients, pain and swelling, even between instability episodes, suggest that cartilage damage is at least a component of the symptomology.

Important diagnostic components of physical examination are gait analysis, tibiofemoral alignment, and patellar alignment in all 3 planes, both static and functional. Patella-specific measurements include medial-lateral position and quadrants of excursion, lateral tilt, and patella alta, as well as J-sign and subluxation with quadriceps contraction in extension.

It is also important to document effusion; crepitus; active and passive range of motion (spine, hips, knees); site of pain or tenderness to palpation (medial, lateral, distal, retropatellar) and whether it matches the complaints and the location of the cartilage lesion; results of the grind test (placing downward force on the patella during flexion and extension) and whether they match the flexion angle of the tenderness and the flexion angle in which the cartilage lesion has increased PF contact; ligamentous and soft-tissue stability or imbalance (tibiofemoral and patellar; apprehension test, glide test, tilt test); and muscle strength, flexibility, and atrophy of the core (abdomen, dorsal and hip muscles) and lower extremities (quadriceps, hamstrings, gastrocnemius).

Imaging

Imaging should be used to evaluate both PF alignment and the cartilage lesions. For alignment, standard radiographs (weight-bearing knee sequence and axial view; full limb length when needed), computed tomography, and MRI can be used.

Meaningful evaluation requires MRI with cartilage-specific sequences, including standard spin-echo (SE) and gradient-recalled echo (GRE), fast SE, and, for cartilage morphology, T2-weighted fat suppression (FS) and 3-dimensional SE and GRE.5 For evaluation of cartilage function and metabolism, the collagen network, and proteoglycan content in the knee cartilage matrix, consideration should be given to compositional assessment techniques, such as T2 mapping, delayed gadolinium-enhanced MRI of cartilage, T1ρ imaging, sodium imaging, and diffusion-weighted sequences.5 Use of the latter functional sequences is still debatable, and these sequences are not widely available.

Treatment

In general, the initial approach is nonoperative management focused on weight loss and extensive core-to-floor rehabilitation, unless surgery is specifically indicated (eg, for loose body removal or osteochondral fracture reattachment). Rehabilitation focuses on achieving adequate range of motion of the spine, hips, and knees along with muscle strength and flexibility of the core (abdomen, dorsal and hip muscles) and lower limbs (quadriceps, hamstrings, gastrocnemius). Rehabilitation is not defined by time but rather by development of an optimized soft-tissue envelope that decreases joint reactive forces. The full process can take 6 to 9 months, but there should be some improvement by 3 months.

Corticosteroid, hyaluronic acid,6 or platelet-rich plasma7 injections can provide temporary relief and facilitate rehabilitation in the setting of pain inhibition. As stand-alone treatment, injections are more suitable for more diffuse degenerative lesions in older and low-demand patients than for focal traumatic lesions in young and high-demand patients.

Surgery is indicated for full-thickness or nearly full-thickness lesions (International Cartilage Repair Society grade 3a or higher) >1 cm2 after failed conservative treatment.

Optimization of anatomy and biomechanics is crucial, as persistent abnormalities lead to high rates of failure of cartilage procedures, and correction of those factors results in outcomes similar to those of patients without such abnormal anatomy.8 The procedures most commonly used to improve patellar tracking or unloading in the PF compartment are lateral retinacular lengthening and TT transfer: medialization and/or distalization for correction of malalignment, and straight anteriorization or anteromedialization for unloading. These procedures can improve symptoms and function in lateral and distal patellar and trochlear lesions even without the addition of a cartilage restoration procedure.

Factors that are important in surgical decision-making include defect location and size, subchondral bone status, unipolar vs bipolar lesions, and previous cartilage procedure.

Location. The shapes of the patella and trochlea vary much more than the shapes of the condyles and plateaus. This variability complicates morphology matching, particularly with involvement of the central TG and median patellar ridge. Therefore, focal contained lesions of the patella and trochlea may be more technically amenable to cell therapy techniques than to osteochondral procedures, which require contour matching between donor and recipient

Size. Although small lesions in the femoral condyles can be considered for microfracture (MFx) or osteochondral autograft transfer (OAT), MFx is less suitable because of poor results in the PF joint, and OAT because of donor-site morbidity in the trochlea.

Subchondral bone status. When subchondral bone is compromised, such as with bone loss, cysts, or significant bone edema, the entire osteochondral unit should be treated. Here, OAT and osteochondral allograft (OCA) are the preferred treatments, depending on lesion size.

Unipolar vs bipolar lesions. Compared with unipolar lesions, bipolar lesions tend to have worse outcomes. Therefore, an associated unloading procedure (TT osteotomy) should be given special consideration. Autologous chondrocyte implantation (ACI) appears to have better outcomes than OCA for bipolar PF lesions.9,10

Previous surgery. Although a failed cartilage procedure can negatively affect ACI outcomes, particularly in the presence of intralesional osteophytes,11 it does not affect OCA outcomes.12 Therefore, after previous MFx, OCA instead of ACI may be considered.

Fragment Fixation

Viable fragments from traumatic lesions (direct trauma or patellar dislocation) or osteochondritis dissecans should be repaired if possible, particularly in young patients. In a fragment that contains a substantial amount of bone, compression screws provide stable fixation. More recently, it has been recognized that fixation of predominantly cartilaginous fragments can be successful13 (Figure 1B). Débridement of soft tissue in the lesion bed and on the fragment is important in facilitating healing, as is removal of sclerotic bone.

MFx

Although MFx can have good outcomes in small contained femoral condyle lesions, in the PF joint treatment has been more challenging, and clinical outcomes have been poor (increased subchondral edema, increased effusion).14 In addition, deterioration becomes significant after 36 months. Therefore, MFx should be restricted to small (<2 cm2), well-contained trochlear defects, particularly in low-demand patients.

ACI and Matrix-Induced ACI

As stated, ACI (Figure 2) is suitable for PF joints because it intrinsically respects the complex anatomy.

Figure 2.
Multiple case series with midterm and long-term follow-up have found improved outcomes for patella and trochlea.8,15 With careful assessment and correction of malalignment, outcomes are similar to those of patients with normal anatomy.8 Results tend to be better for unipolar lesions than for bipolar lesions.15 TT osteotomy is a useful adjunct in correcting malalignment and unloading the PF compartment, even more so in the bipolar lesion setting. Previous procedures that violate the subchondral bone increase the risk of failure of subsequent ACI 3- to 7-fold, particularly in the presence of persistent subchondral abnormalities, such as intralesional osteophytes, cysts, and significant edema.11

OAT

As mentioned, donor-site morbidity may compromise final outcomes of harvest and implantation in the PF joint. Nonetheless, in carefully selected patients with small lesions that are limited to 1 facet (not including the patellar ridge or the TG) and that require only 1 plug (Figure 3), OAT can have good clinical results.16

Figure 3.

OCA

Two techniques can be used with OCA in the PF joint. The dowel technique, in which circular plugs are implanted, is predominantly used for defects that do not cross the midline (those located in their entirety on the medial or lateral aspect of the patella or trochlea). Central defects, which can be treated with the dowel technique as well, are technically more challenging to match perfectly, because of the complex geometry of the median ridge and the TG (Figure 4).

Figure 4.
The shell technique is an alternative that can be used to treat very large defects. The chondral defect area and subchondral bone are removed with an oscillating saw, using the same plane as for patellar resurfacing (total knee arthroplasty or PF arthroplasty). A matching graft is created with a similar cut, made freehand.

Experimental and Emerging Technologies

Biocartilage

Biocartilage, a dehydrated, micronized allogeneic cartilage scaffold implanted with platelet-rich plasma and fibrin glue added over a contained MFx-treated defect, can be used in the patella and trochlea and has the same indications as MFx (small lesions, contained lesions). There are limited clinical studies of short- or long-term outcomes.

Fresh and Viable OCA

Fresh OCA (ProChondrix; AlloSource) and viable/cryopreserved OCA (Cartiform; Arthrex) are thin osteochondral scaffolds that contain viable chondrocytes and growth factors. They can be implanted alone or used with MFx, and are indicated for lesions measuring 1 cm2 to 3 cm2. Aside from a case report,17 there are no clinical studies on outcomes.

Bone Marrow Aspirate Concentrate Implantation

Bone marrow aspirate concentrate from centrifuged iliac crest–harvested aspirate containing mesenchymal stem cells with chondrogenic potential is applied under a synthetic scaffold. Indications are the same as for ACI. Medium-term follow-up studies in the PF joint have shown good results, similar to those obtained with matrix-induced ACI.18

Particulated Juvenile Allograft Cartilage

Particulated juvenile allograft cartilage (DeNovo NT Graft; Zimmer Biomet) is minced cartilage allograft (from juvenile donors) that has been cut into cubes (~1 mm3). Indications are for patellar and trochlear lesions 1 cm2 to 6 cm2. For both the trochlea and the patella, short-term outcomes have been good.19,20

Rehabilitation After Surgery

Isolated PF cartilage restoration generally does not require prolonged weight-bearing restrictions, and ambulation with the knee locked in full extension is permitted as tolerated. Concurrent TT osteotomy, however, requires protection with 4 to 6 weeks of toe-touch weight-bearing to minimize the risk of tibial fracture.

Conclusion

Comprehensive preoperative assessment is essential and should include a thorough core-to-floor physical examination as well as PF-specific imaging. Treatment of symptomatic chondral lesions in the PF joint requires specific technical and postoperative management, which differs significantly from management involving the condyles. Attending to all these details makes the outcomes of PF cartilage treatment reproducible. These outcomes may rival those of condylar treatment.

References

1. Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy. 1997;13(4):456-460.

2. Steensen RN, Bentley JC, Trinh TQ, Backes JR, Wiltfong RE. The prevalence and combined prevalences of anatomic factors associated with recurrent patellar dislocation: a magnetic resonance imaging study. Am J Sports Med. 2015;43(4):921-927.

3. Nomura E, Inoue M. Cartilage lesions of the patella in recurrent patellar dislocation. Am J Sports Med. 2004;32(2):498-502.

4. Vollnberg B, Koehlitz T, Jung T, et al. Prevalence of cartilage lesions and early osteoarthritis in patients with patellar dislocation. Eur Radiol. 2012;22(11):2347-2356.

5. Crema MD, Roemer FW, Marra MD, et al. Articular cartilage in the knee: current MR imaging techniques and applications in clinical practice and research. Radiographics. 2011;31(1):37-61.

6. Campbell KA, Erickson BJ, Saltzman BM, et al. Is local viscosupplementation injection clinically superior to other therapies in the treatment of osteoarthritis of the knee: a systematic review of overlapping meta-analyses. Arthroscopy. 2015;31(10):2036-2045.e14.

7. Saltzman BM, Jain A, Campbell KA, et al. Does the use of platelet-rich plasma at the time of surgery improve clinical outcomes in arthroscopic rotator cuff repair when compared with control cohorts? A systematic review of meta-analyses. Arthroscopy. 2016;32(5):906-918.

8. Gomoll AH, Gillogly SD, Cole BJ, et al. Autologous chondrocyte implantation in the patella: a multicenter experience. Am J Sports Med. 2014;42(5):1074-1081.

9. Meric G, Gracitelli GC, Gortz S, De Young AJ, Bugbee WD. Fresh osteochondral allograft transplantation for bipolar reciprocal osteochondral lesions of the knee. Am J Sports Med. 2015;43(3):709-714.

10. Peterson L, Vasiliadis HS, Brittberg M, Lindahl A. Autologous chondrocyte implantation: a long-term follow-up. Am J Sports Med. 2010;38(6):1117-1124.

11. Minas T, Gomoll AH, Rosenberger R, Royce RO, Bryant T. Increased failure rate of autologous chondrocyte implantation after previous treatment with marrow stimulation techniques. Am J Sports Med. 2009;37(5):902-908.

12. Gracitelli GC, Meric G, Briggs DT, et al. Fresh osteochondral allografts in the knee: comparison of primary transplantation versus transplantation after failure of previous subchondral marrow stimulation. Am J Sports Med. 2015;43(4):885-891.

13. Anderson CN, Magnussen RA, Block JJ, Anderson AF, Spindler KP. Operative fixation of chondral loose bodies in osteochondritis dissecans in the knee: a report of 5 cases. Orthop J Sports Med. 2013;1(2):2325967113496546.

14. Kreuz PC, Steinwachs MR, Erggelet C, et al. Results after microfracture of full-thickness chondral defects in different compartments in the knee. Osteoarthritis Cartilage. 2006;14(11):1119-1125.

15. Vasiliadis HS, Lindahl A, Georgoulis AD, Peterson L. Malalignment and cartilage lesions in the patellofemoral joint treated with autologous chondrocyte implantation. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):452-457.

16. Astur DC, Arliani GG, Binz M, et al. Autologous osteochondral transplantation for treating patellar chondral injuries: evaluation, treatment, and outcomes of a two-year follow-up study. J Bone Joint Surg Am. 2014;96(10):816-823.

17. Hoffman JK, Geraghty S, Protzman NM. Articular cartilage repair using marrow simulation augmented with a viable chondral allograft: 9-month postoperative histological evaluation. Case Rep Orthop. 2015;2015:617365.

18. Gobbi A, Chaurasia S, Karnatzikos G, Nakamura N. Matrix-induced autologous chondrocyte implantation versus multipotent stem cells for the treatment of large patellofemoral chondral lesions: a nonrandomized prospective trial. Cartilage. 2015;6(2):82-97.

19. Farr J, Tabet SK, Margerrison E, Cole BJ. Clinical, radiographic, and histological outcomes after cartilage repair with particulated juvenile articular cartilage: a 2-year prospective study. Am J Sports Med. 2014;42(6):1417-1425.

20. Tompkins M, Hamann JC, Diduch DR, et al. Preliminary results of a novel single-stage cartilage restoration technique: particulated juvenile articular cartilage allograft for chondral defects of the patella. Arthroscopy. 2013;29(10):1661-1670.

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Authors' Disclosure Statement: Dr. Gomoll reports that he is a paid consultant/advisory board member for Vericel, Joint Restoration Foundation, LifeNet, Smith & Nephew, and NuTech Medical. Dr. Farr reports that he is a paid consultant/advisory board member for Arthrex, Osiris Therapeutics, Vericel, and Zimmer Biomet; receives research/institutional support from Arthrex, RTI Biologics, Vericel, and Zimmer Biomet; and holds a design patent for a DePuy Synthes patellofemoral arthroplasty device. Dr. Hinckel reports no actual or potential conflict of interest in relation to this article.

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Authors' Disclosure Statement: Dr. Gomoll reports that he is a paid consultant/advisory board member for Vericel, Joint Restoration Foundation, LifeNet, Smith & Nephew, and NuTech Medical. Dr. Farr reports that he is a paid consultant/advisory board member for Arthrex, Osiris Therapeutics, Vericel, and Zimmer Biomet; receives research/institutional support from Arthrex, RTI Biologics, Vericel, and Zimmer Biomet; and holds a design patent for a DePuy Synthes patellofemoral arthroplasty device. Dr. Hinckel reports no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors' Disclosure Statement: Dr. Gomoll reports that he is a paid consultant/advisory board member for Vericel, Joint Restoration Foundation, LifeNet, Smith & Nephew, and NuTech Medical. Dr. Farr reports that he is a paid consultant/advisory board member for Arthrex, Osiris Therapeutics, Vericel, and Zimmer Biomet; receives research/institutional support from Arthrex, RTI Biologics, Vericel, and Zimmer Biomet; and holds a design patent for a DePuy Synthes patellofemoral arthroplasty device. Dr. Hinckel reports no actual or potential conflict of interest in relation to this article.

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Take-Home Points

  • Careful evaluation is key in attributing knee pain to patellofemoral cartilage lesions-that is, in making a "diagnosis by exclusion".
  • Initial treatment is nonoperative management focused on weight loss and extensive "core-to-floor" rehabilitation.
  • Optimization of anatomy and biomechanics is crucial.
  • Factors important in surgical decision-making incude defect location and size, subchondral bone status, unipolar vs bipolar lesions, and previous cartilage procedure.
  • The most commonly used surgical procedures-autologous chondrocyte implantation, osteochondral autograft transfer, and osteochondral allograft-have demonstrated improved intermediate-term outcomes.

Patellofemoral (PF) pain is often a component of more general anterior knee pain. One source of PF pain is chondral lesions. As these lesions are commonly seen on magnetic resonance imaging (MRI) and during arthroscopy, it is necessary to differentiate incidental and symptomatic lesions.1 In addition, the correlation between symptoms and lesion presence and severity is poor.

PF pain is multifactorial (structural lesions, malalignment, deconditioning, muscle imbalance and overuse) and can coexist with other lesions in the knee (ligament tears, meniscal injuries, and cartilage lesions in other compartments). Therefore, careful evaluation is key in attributing knee pain to PF cartilage lesions—that is, in making a "diagnosis by exclusion."

From the start, it must be appreciated that the vast majority of patients will not require surgery, and many who require surgery for pain will not require cartilage restoration. One key to success with PF patients is a good working relationship with an experienced physical therapist.

Etiology

The primary causes of PF cartilage lesions are patellar instability, chronic maltracking without instability, direct trauma, repetitive microtrauma, and idiopathic.

Patellar Instability

Patients with patellar instability often present with underlying anatomical risk factors (eg, trochlear dysplasia, increased Q-angle/tibial tubercle-trochlear groove [TT-TG] distance, patella alta, and unbalanced medial and lateral soft tissues2). These factors should be addressed before surgery.

Patellar instability can cause cartilage damage during the dislocation event or by chronic subluxation. Cartilage becomes damaged in up to 96% of patellar dislocations.3 Most commonly, the damage consists of fissuring and/or fibrillation, but chondral and osteochondral fractures can occur as well. During dislocation, the medial patella strikes the lateral aspect of the femur, and, as the knee collapses into flexion, the lateral aspect of the proximal lateral femoral condyle (weight-bearing area) can sustain damage. In the patella, typically the injury is distal-medial (occasionally crossing the median ridge). A shear lesion may involve the chondral surface or be osteochondral (Figure 1A).

Figure 1.
In an osteochondral lesion, the area of cartilage damage is often larger than the bony fragment indicates (Figure 1A), and even small fractures visible on radiographs can portend extensive cartilage damage. In addition, isolated cartilage flaps can occur; if suspected, they should be assessed with MRI. The extent of cartilage damage is related to the magnitude of energy required to cause the dislocation and/or to the frequency of events. In more normal anatomy, more energy is required to provoke a dislocation, and damage to articular cartilage is greater. In recurrent patellar dislocation, each event can cause additional injury, and the size of the lesion tends to increase with the number of dislocations.4 Patellar dislocation can result in chronic patellar subluxation, or dislocations that often lead to recurrent or chronic patellar instability. With recurrent instability, the medial patellar facet becomes damaged as it displaces out of the trochlea during subluxation and dislocation events. With lateral patellar maltracking, the contact area is reduced. With overall similar PF forces, a smaller contact area results in increased point loading, thus increasing stress and promoting cartilage wear.

Chronic Maltracking Without Instability

Chronic maltracking is usually related to anatomical abnormalities, which include the same factors that can cause patellar instability. A common combination is trochlear dysplasia, increased TT-TG or TT-posterior cruciate ligament distance, and lateral soft-tissue contracture. These are often seen in PF joints that progress to lateral PF arthritis. As lateral PF arthritis progresses, lateral soft-tissue contracture worsens, compounding symptoms of laterally based pain. With respect to cartilage repair, these joints can be treated if recognized early; however, once osteoarthritis is fully established in the joint, facetectomy or PF replacement may be necessary.

Direct Trauma

With the knee in flexion during a direct trauma over the patella (eg, fall or dashboard trauma), all zones of cartilage and subchondral bone in both patella and trochlea can be injured, leading to macrostructural damage, chondral/osteochondral fracture, or, with a subcritical force, microstructural damage and chondrocyte death, subsequently causing cartilage degeneration (cartilage may look normal initially; the matrix takes months to years to deteriorate). Direct trauma usually occurs with the knee flexed. Therefore, these lesions typically are located in the distal trochlea and superior pole of the patella.

Repetitive Microtrauma

Minor injuries, which by themselves do not immediately cause apparent chondral or osteochondral fractures, may eventually exceed the capacity of natural cartilage homeostasis and result in repetitive microtrauma. Common causes are repeated jumping (as in basketball and volleyball) and prolonged flexed-knee position (eg, what a baseball catcher experiences), which may also be associated with other lesions caused by extensor apparatus overload (eg, quadriceps tendon or patellar tendon tendinitis, and fat pad impingement syndrome).

Idiopathic

In a subset of patients with osteochondritis dissecans, the patella is the lesion site. In another subset, idiopathic lesions may be related to a genetic predisposition to osteoarthritis and may not be restricted to the PF joint. In some cases, the PF joint is the first compartment to degenerate and is the most symptomatic in a setting of truly tricompartmental disease. In these cases, treating only the PF lesion can result in functional failure, owing to disease progression in other compartments. Even mild disease in other compartments should be carefully evaluated.

History and Physical Examination

Patients often report a history of anterior knee pain that worsens with stair use, prolonged sitting, and flexed-knee activities (eg, squatting). Compared with pain alone, swelling, though not specific to cartilage disease, is more suspicious for a cartilage etiology. Identifying the cartilage defect as the sole source of pain is particularly difficult in patients with recurrent patellar instability. In these patients, pain and swelling, even between instability episodes, suggest that cartilage damage is at least a component of the symptomology.

Important diagnostic components of physical examination are gait analysis, tibiofemoral alignment, and patellar alignment in all 3 planes, both static and functional. Patella-specific measurements include medial-lateral position and quadrants of excursion, lateral tilt, and patella alta, as well as J-sign and subluxation with quadriceps contraction in extension.

It is also important to document effusion; crepitus; active and passive range of motion (spine, hips, knees); site of pain or tenderness to palpation (medial, lateral, distal, retropatellar) and whether it matches the complaints and the location of the cartilage lesion; results of the grind test (placing downward force on the patella during flexion and extension) and whether they match the flexion angle of the tenderness and the flexion angle in which the cartilage lesion has increased PF contact; ligamentous and soft-tissue stability or imbalance (tibiofemoral and patellar; apprehension test, glide test, tilt test); and muscle strength, flexibility, and atrophy of the core (abdomen, dorsal and hip muscles) and lower extremities (quadriceps, hamstrings, gastrocnemius).

Imaging

Imaging should be used to evaluate both PF alignment and the cartilage lesions. For alignment, standard radiographs (weight-bearing knee sequence and axial view; full limb length when needed), computed tomography, and MRI can be used.

Meaningful evaluation requires MRI with cartilage-specific sequences, including standard spin-echo (SE) and gradient-recalled echo (GRE), fast SE, and, for cartilage morphology, T2-weighted fat suppression (FS) and 3-dimensional SE and GRE.5 For evaluation of cartilage function and metabolism, the collagen network, and proteoglycan content in the knee cartilage matrix, consideration should be given to compositional assessment techniques, such as T2 mapping, delayed gadolinium-enhanced MRI of cartilage, T1ρ imaging, sodium imaging, and diffusion-weighted sequences.5 Use of the latter functional sequences is still debatable, and these sequences are not widely available.

Treatment

In general, the initial approach is nonoperative management focused on weight loss and extensive core-to-floor rehabilitation, unless surgery is specifically indicated (eg, for loose body removal or osteochondral fracture reattachment). Rehabilitation focuses on achieving adequate range of motion of the spine, hips, and knees along with muscle strength and flexibility of the core (abdomen, dorsal and hip muscles) and lower limbs (quadriceps, hamstrings, gastrocnemius). Rehabilitation is not defined by time but rather by development of an optimized soft-tissue envelope that decreases joint reactive forces. The full process can take 6 to 9 months, but there should be some improvement by 3 months.

Corticosteroid, hyaluronic acid,6 or platelet-rich plasma7 injections can provide temporary relief and facilitate rehabilitation in the setting of pain inhibition. As stand-alone treatment, injections are more suitable for more diffuse degenerative lesions in older and low-demand patients than for focal traumatic lesions in young and high-demand patients.

Surgery is indicated for full-thickness or nearly full-thickness lesions (International Cartilage Repair Society grade 3a or higher) >1 cm2 after failed conservative treatment.

Optimization of anatomy and biomechanics is crucial, as persistent abnormalities lead to high rates of failure of cartilage procedures, and correction of those factors results in outcomes similar to those of patients without such abnormal anatomy.8 The procedures most commonly used to improve patellar tracking or unloading in the PF compartment are lateral retinacular lengthening and TT transfer: medialization and/or distalization for correction of malalignment, and straight anteriorization or anteromedialization for unloading. These procedures can improve symptoms and function in lateral and distal patellar and trochlear lesions even without the addition of a cartilage restoration procedure.

Factors that are important in surgical decision-making include defect location and size, subchondral bone status, unipolar vs bipolar lesions, and previous cartilage procedure.

Location. The shapes of the patella and trochlea vary much more than the shapes of the condyles and plateaus. This variability complicates morphology matching, particularly with involvement of the central TG and median patellar ridge. Therefore, focal contained lesions of the patella and trochlea may be more technically amenable to cell therapy techniques than to osteochondral procedures, which require contour matching between donor and recipient

Size. Although small lesions in the femoral condyles can be considered for microfracture (MFx) or osteochondral autograft transfer (OAT), MFx is less suitable because of poor results in the PF joint, and OAT because of donor-site morbidity in the trochlea.

Subchondral bone status. When subchondral bone is compromised, such as with bone loss, cysts, or significant bone edema, the entire osteochondral unit should be treated. Here, OAT and osteochondral allograft (OCA) are the preferred treatments, depending on lesion size.

Unipolar vs bipolar lesions. Compared with unipolar lesions, bipolar lesions tend to have worse outcomes. Therefore, an associated unloading procedure (TT osteotomy) should be given special consideration. Autologous chondrocyte implantation (ACI) appears to have better outcomes than OCA for bipolar PF lesions.9,10

Previous surgery. Although a failed cartilage procedure can negatively affect ACI outcomes, particularly in the presence of intralesional osteophytes,11 it does not affect OCA outcomes.12 Therefore, after previous MFx, OCA instead of ACI may be considered.

Fragment Fixation

Viable fragments from traumatic lesions (direct trauma or patellar dislocation) or osteochondritis dissecans should be repaired if possible, particularly in young patients. In a fragment that contains a substantial amount of bone, compression screws provide stable fixation. More recently, it has been recognized that fixation of predominantly cartilaginous fragments can be successful13 (Figure 1B). Débridement of soft tissue in the lesion bed and on the fragment is important in facilitating healing, as is removal of sclerotic bone.

MFx

Although MFx can have good outcomes in small contained femoral condyle lesions, in the PF joint treatment has been more challenging, and clinical outcomes have been poor (increased subchondral edema, increased effusion).14 In addition, deterioration becomes significant after 36 months. Therefore, MFx should be restricted to small (<2 cm2), well-contained trochlear defects, particularly in low-demand patients.

ACI and Matrix-Induced ACI

As stated, ACI (Figure 2) is suitable for PF joints because it intrinsically respects the complex anatomy.

Figure 2.
Multiple case series with midterm and long-term follow-up have found improved outcomes for patella and trochlea.8,15 With careful assessment and correction of malalignment, outcomes are similar to those of patients with normal anatomy.8 Results tend to be better for unipolar lesions than for bipolar lesions.15 TT osteotomy is a useful adjunct in correcting malalignment and unloading the PF compartment, even more so in the bipolar lesion setting. Previous procedures that violate the subchondral bone increase the risk of failure of subsequent ACI 3- to 7-fold, particularly in the presence of persistent subchondral abnormalities, such as intralesional osteophytes, cysts, and significant edema.11

OAT

As mentioned, donor-site morbidity may compromise final outcomes of harvest and implantation in the PF joint. Nonetheless, in carefully selected patients with small lesions that are limited to 1 facet (not including the patellar ridge or the TG) and that require only 1 plug (Figure 3), OAT can have good clinical results.16

Figure 3.

OCA

Two techniques can be used with OCA in the PF joint. The dowel technique, in which circular plugs are implanted, is predominantly used for defects that do not cross the midline (those located in their entirety on the medial or lateral aspect of the patella or trochlea). Central defects, which can be treated with the dowel technique as well, are technically more challenging to match perfectly, because of the complex geometry of the median ridge and the TG (Figure 4).

Figure 4.
The shell technique is an alternative that can be used to treat very large defects. The chondral defect area and subchondral bone are removed with an oscillating saw, using the same plane as for patellar resurfacing (total knee arthroplasty or PF arthroplasty). A matching graft is created with a similar cut, made freehand.

Experimental and Emerging Technologies

Biocartilage

Biocartilage, a dehydrated, micronized allogeneic cartilage scaffold implanted with platelet-rich plasma and fibrin glue added over a contained MFx-treated defect, can be used in the patella and trochlea and has the same indications as MFx (small lesions, contained lesions). There are limited clinical studies of short- or long-term outcomes.

Fresh and Viable OCA

Fresh OCA (ProChondrix; AlloSource) and viable/cryopreserved OCA (Cartiform; Arthrex) are thin osteochondral scaffolds that contain viable chondrocytes and growth factors. They can be implanted alone or used with MFx, and are indicated for lesions measuring 1 cm2 to 3 cm2. Aside from a case report,17 there are no clinical studies on outcomes.

Bone Marrow Aspirate Concentrate Implantation

Bone marrow aspirate concentrate from centrifuged iliac crest–harvested aspirate containing mesenchymal stem cells with chondrogenic potential is applied under a synthetic scaffold. Indications are the same as for ACI. Medium-term follow-up studies in the PF joint have shown good results, similar to those obtained with matrix-induced ACI.18

Particulated Juvenile Allograft Cartilage

Particulated juvenile allograft cartilage (DeNovo NT Graft; Zimmer Biomet) is minced cartilage allograft (from juvenile donors) that has been cut into cubes (~1 mm3). Indications are for patellar and trochlear lesions 1 cm2 to 6 cm2. For both the trochlea and the patella, short-term outcomes have been good.19,20

Rehabilitation After Surgery

Isolated PF cartilage restoration generally does not require prolonged weight-bearing restrictions, and ambulation with the knee locked in full extension is permitted as tolerated. Concurrent TT osteotomy, however, requires protection with 4 to 6 weeks of toe-touch weight-bearing to minimize the risk of tibial fracture.

Conclusion

Comprehensive preoperative assessment is essential and should include a thorough core-to-floor physical examination as well as PF-specific imaging. Treatment of symptomatic chondral lesions in the PF joint requires specific technical and postoperative management, which differs significantly from management involving the condyles. Attending to all these details makes the outcomes of PF cartilage treatment reproducible. These outcomes may rival those of condylar treatment.

Take-Home Points

  • Careful evaluation is key in attributing knee pain to patellofemoral cartilage lesions-that is, in making a "diagnosis by exclusion".
  • Initial treatment is nonoperative management focused on weight loss and extensive "core-to-floor" rehabilitation.
  • Optimization of anatomy and biomechanics is crucial.
  • Factors important in surgical decision-making incude defect location and size, subchondral bone status, unipolar vs bipolar lesions, and previous cartilage procedure.
  • The most commonly used surgical procedures-autologous chondrocyte implantation, osteochondral autograft transfer, and osteochondral allograft-have demonstrated improved intermediate-term outcomes.

Patellofemoral (PF) pain is often a component of more general anterior knee pain. One source of PF pain is chondral lesions. As these lesions are commonly seen on magnetic resonance imaging (MRI) and during arthroscopy, it is necessary to differentiate incidental and symptomatic lesions.1 In addition, the correlation between symptoms and lesion presence and severity is poor.

PF pain is multifactorial (structural lesions, malalignment, deconditioning, muscle imbalance and overuse) and can coexist with other lesions in the knee (ligament tears, meniscal injuries, and cartilage lesions in other compartments). Therefore, careful evaluation is key in attributing knee pain to PF cartilage lesions—that is, in making a "diagnosis by exclusion."

From the start, it must be appreciated that the vast majority of patients will not require surgery, and many who require surgery for pain will not require cartilage restoration. One key to success with PF patients is a good working relationship with an experienced physical therapist.

Etiology

The primary causes of PF cartilage lesions are patellar instability, chronic maltracking without instability, direct trauma, repetitive microtrauma, and idiopathic.

Patellar Instability

Patients with patellar instability often present with underlying anatomical risk factors (eg, trochlear dysplasia, increased Q-angle/tibial tubercle-trochlear groove [TT-TG] distance, patella alta, and unbalanced medial and lateral soft tissues2). These factors should be addressed before surgery.

Patellar instability can cause cartilage damage during the dislocation event or by chronic subluxation. Cartilage becomes damaged in up to 96% of patellar dislocations.3 Most commonly, the damage consists of fissuring and/or fibrillation, but chondral and osteochondral fractures can occur as well. During dislocation, the medial patella strikes the lateral aspect of the femur, and, as the knee collapses into flexion, the lateral aspect of the proximal lateral femoral condyle (weight-bearing area) can sustain damage. In the patella, typically the injury is distal-medial (occasionally crossing the median ridge). A shear lesion may involve the chondral surface or be osteochondral (Figure 1A).

Figure 1.
In an osteochondral lesion, the area of cartilage damage is often larger than the bony fragment indicates (Figure 1A), and even small fractures visible on radiographs can portend extensive cartilage damage. In addition, isolated cartilage flaps can occur; if suspected, they should be assessed with MRI. The extent of cartilage damage is related to the magnitude of energy required to cause the dislocation and/or to the frequency of events. In more normal anatomy, more energy is required to provoke a dislocation, and damage to articular cartilage is greater. In recurrent patellar dislocation, each event can cause additional injury, and the size of the lesion tends to increase with the number of dislocations.4 Patellar dislocation can result in chronic patellar subluxation, or dislocations that often lead to recurrent or chronic patellar instability. With recurrent instability, the medial patellar facet becomes damaged as it displaces out of the trochlea during subluxation and dislocation events. With lateral patellar maltracking, the contact area is reduced. With overall similar PF forces, a smaller contact area results in increased point loading, thus increasing stress and promoting cartilage wear.

Chronic Maltracking Without Instability

Chronic maltracking is usually related to anatomical abnormalities, which include the same factors that can cause patellar instability. A common combination is trochlear dysplasia, increased TT-TG or TT-posterior cruciate ligament distance, and lateral soft-tissue contracture. These are often seen in PF joints that progress to lateral PF arthritis. As lateral PF arthritis progresses, lateral soft-tissue contracture worsens, compounding symptoms of laterally based pain. With respect to cartilage repair, these joints can be treated if recognized early; however, once osteoarthritis is fully established in the joint, facetectomy or PF replacement may be necessary.

Direct Trauma

With the knee in flexion during a direct trauma over the patella (eg, fall or dashboard trauma), all zones of cartilage and subchondral bone in both patella and trochlea can be injured, leading to macrostructural damage, chondral/osteochondral fracture, or, with a subcritical force, microstructural damage and chondrocyte death, subsequently causing cartilage degeneration (cartilage may look normal initially; the matrix takes months to years to deteriorate). Direct trauma usually occurs with the knee flexed. Therefore, these lesions typically are located in the distal trochlea and superior pole of the patella.

Repetitive Microtrauma

Minor injuries, which by themselves do not immediately cause apparent chondral or osteochondral fractures, may eventually exceed the capacity of natural cartilage homeostasis and result in repetitive microtrauma. Common causes are repeated jumping (as in basketball and volleyball) and prolonged flexed-knee position (eg, what a baseball catcher experiences), which may also be associated with other lesions caused by extensor apparatus overload (eg, quadriceps tendon or patellar tendon tendinitis, and fat pad impingement syndrome).

Idiopathic

In a subset of patients with osteochondritis dissecans, the patella is the lesion site. In another subset, idiopathic lesions may be related to a genetic predisposition to osteoarthritis and may not be restricted to the PF joint. In some cases, the PF joint is the first compartment to degenerate and is the most symptomatic in a setting of truly tricompartmental disease. In these cases, treating only the PF lesion can result in functional failure, owing to disease progression in other compartments. Even mild disease in other compartments should be carefully evaluated.

History and Physical Examination

Patients often report a history of anterior knee pain that worsens with stair use, prolonged sitting, and flexed-knee activities (eg, squatting). Compared with pain alone, swelling, though not specific to cartilage disease, is more suspicious for a cartilage etiology. Identifying the cartilage defect as the sole source of pain is particularly difficult in patients with recurrent patellar instability. In these patients, pain and swelling, even between instability episodes, suggest that cartilage damage is at least a component of the symptomology.

Important diagnostic components of physical examination are gait analysis, tibiofemoral alignment, and patellar alignment in all 3 planes, both static and functional. Patella-specific measurements include medial-lateral position and quadrants of excursion, lateral tilt, and patella alta, as well as J-sign and subluxation with quadriceps contraction in extension.

It is also important to document effusion; crepitus; active and passive range of motion (spine, hips, knees); site of pain or tenderness to palpation (medial, lateral, distal, retropatellar) and whether it matches the complaints and the location of the cartilage lesion; results of the grind test (placing downward force on the patella during flexion and extension) and whether they match the flexion angle of the tenderness and the flexion angle in which the cartilage lesion has increased PF contact; ligamentous and soft-tissue stability or imbalance (tibiofemoral and patellar; apprehension test, glide test, tilt test); and muscle strength, flexibility, and atrophy of the core (abdomen, dorsal and hip muscles) and lower extremities (quadriceps, hamstrings, gastrocnemius).

Imaging

Imaging should be used to evaluate both PF alignment and the cartilage lesions. For alignment, standard radiographs (weight-bearing knee sequence and axial view; full limb length when needed), computed tomography, and MRI can be used.

Meaningful evaluation requires MRI with cartilage-specific sequences, including standard spin-echo (SE) and gradient-recalled echo (GRE), fast SE, and, for cartilage morphology, T2-weighted fat suppression (FS) and 3-dimensional SE and GRE.5 For evaluation of cartilage function and metabolism, the collagen network, and proteoglycan content in the knee cartilage matrix, consideration should be given to compositional assessment techniques, such as T2 mapping, delayed gadolinium-enhanced MRI of cartilage, T1ρ imaging, sodium imaging, and diffusion-weighted sequences.5 Use of the latter functional sequences is still debatable, and these sequences are not widely available.

Treatment

In general, the initial approach is nonoperative management focused on weight loss and extensive core-to-floor rehabilitation, unless surgery is specifically indicated (eg, for loose body removal or osteochondral fracture reattachment). Rehabilitation focuses on achieving adequate range of motion of the spine, hips, and knees along with muscle strength and flexibility of the core (abdomen, dorsal and hip muscles) and lower limbs (quadriceps, hamstrings, gastrocnemius). Rehabilitation is not defined by time but rather by development of an optimized soft-tissue envelope that decreases joint reactive forces. The full process can take 6 to 9 months, but there should be some improvement by 3 months.

Corticosteroid, hyaluronic acid,6 or platelet-rich plasma7 injections can provide temporary relief and facilitate rehabilitation in the setting of pain inhibition. As stand-alone treatment, injections are more suitable for more diffuse degenerative lesions in older and low-demand patients than for focal traumatic lesions in young and high-demand patients.

Surgery is indicated for full-thickness or nearly full-thickness lesions (International Cartilage Repair Society grade 3a or higher) >1 cm2 after failed conservative treatment.

Optimization of anatomy and biomechanics is crucial, as persistent abnormalities lead to high rates of failure of cartilage procedures, and correction of those factors results in outcomes similar to those of patients without such abnormal anatomy.8 The procedures most commonly used to improve patellar tracking or unloading in the PF compartment are lateral retinacular lengthening and TT transfer: medialization and/or distalization for correction of malalignment, and straight anteriorization or anteromedialization for unloading. These procedures can improve symptoms and function in lateral and distal patellar and trochlear lesions even without the addition of a cartilage restoration procedure.

Factors that are important in surgical decision-making include defect location and size, subchondral bone status, unipolar vs bipolar lesions, and previous cartilage procedure.

Location. The shapes of the patella and trochlea vary much more than the shapes of the condyles and plateaus. This variability complicates morphology matching, particularly with involvement of the central TG and median patellar ridge. Therefore, focal contained lesions of the patella and trochlea may be more technically amenable to cell therapy techniques than to osteochondral procedures, which require contour matching between donor and recipient

Size. Although small lesions in the femoral condyles can be considered for microfracture (MFx) or osteochondral autograft transfer (OAT), MFx is less suitable because of poor results in the PF joint, and OAT because of donor-site morbidity in the trochlea.

Subchondral bone status. When subchondral bone is compromised, such as with bone loss, cysts, or significant bone edema, the entire osteochondral unit should be treated. Here, OAT and osteochondral allograft (OCA) are the preferred treatments, depending on lesion size.

Unipolar vs bipolar lesions. Compared with unipolar lesions, bipolar lesions tend to have worse outcomes. Therefore, an associated unloading procedure (TT osteotomy) should be given special consideration. Autologous chondrocyte implantation (ACI) appears to have better outcomes than OCA for bipolar PF lesions.9,10

Previous surgery. Although a failed cartilage procedure can negatively affect ACI outcomes, particularly in the presence of intralesional osteophytes,11 it does not affect OCA outcomes.12 Therefore, after previous MFx, OCA instead of ACI may be considered.

Fragment Fixation

Viable fragments from traumatic lesions (direct trauma or patellar dislocation) or osteochondritis dissecans should be repaired if possible, particularly in young patients. In a fragment that contains a substantial amount of bone, compression screws provide stable fixation. More recently, it has been recognized that fixation of predominantly cartilaginous fragments can be successful13 (Figure 1B). Débridement of soft tissue in the lesion bed and on the fragment is important in facilitating healing, as is removal of sclerotic bone.

MFx

Although MFx can have good outcomes in small contained femoral condyle lesions, in the PF joint treatment has been more challenging, and clinical outcomes have been poor (increased subchondral edema, increased effusion).14 In addition, deterioration becomes significant after 36 months. Therefore, MFx should be restricted to small (<2 cm2), well-contained trochlear defects, particularly in low-demand patients.

ACI and Matrix-Induced ACI

As stated, ACI (Figure 2) is suitable for PF joints because it intrinsically respects the complex anatomy.

Figure 2.
Multiple case series with midterm and long-term follow-up have found improved outcomes for patella and trochlea.8,15 With careful assessment and correction of malalignment, outcomes are similar to those of patients with normal anatomy.8 Results tend to be better for unipolar lesions than for bipolar lesions.15 TT osteotomy is a useful adjunct in correcting malalignment and unloading the PF compartment, even more so in the bipolar lesion setting. Previous procedures that violate the subchondral bone increase the risk of failure of subsequent ACI 3- to 7-fold, particularly in the presence of persistent subchondral abnormalities, such as intralesional osteophytes, cysts, and significant edema.11

OAT

As mentioned, donor-site morbidity may compromise final outcomes of harvest and implantation in the PF joint. Nonetheless, in carefully selected patients with small lesions that are limited to 1 facet (not including the patellar ridge or the TG) and that require only 1 plug (Figure 3), OAT can have good clinical results.16

Figure 3.

OCA

Two techniques can be used with OCA in the PF joint. The dowel technique, in which circular plugs are implanted, is predominantly used for defects that do not cross the midline (those located in their entirety on the medial or lateral aspect of the patella or trochlea). Central defects, which can be treated with the dowel technique as well, are technically more challenging to match perfectly, because of the complex geometry of the median ridge and the TG (Figure 4).

Figure 4.
The shell technique is an alternative that can be used to treat very large defects. The chondral defect area and subchondral bone are removed with an oscillating saw, using the same plane as for patellar resurfacing (total knee arthroplasty or PF arthroplasty). A matching graft is created with a similar cut, made freehand.

Experimental and Emerging Technologies

Biocartilage

Biocartilage, a dehydrated, micronized allogeneic cartilage scaffold implanted with platelet-rich plasma and fibrin glue added over a contained MFx-treated defect, can be used in the patella and trochlea and has the same indications as MFx (small lesions, contained lesions). There are limited clinical studies of short- or long-term outcomes.

Fresh and Viable OCA

Fresh OCA (ProChondrix; AlloSource) and viable/cryopreserved OCA (Cartiform; Arthrex) are thin osteochondral scaffolds that contain viable chondrocytes and growth factors. They can be implanted alone or used with MFx, and are indicated for lesions measuring 1 cm2 to 3 cm2. Aside from a case report,17 there are no clinical studies on outcomes.

Bone Marrow Aspirate Concentrate Implantation

Bone marrow aspirate concentrate from centrifuged iliac crest–harvested aspirate containing mesenchymal stem cells with chondrogenic potential is applied under a synthetic scaffold. Indications are the same as for ACI. Medium-term follow-up studies in the PF joint have shown good results, similar to those obtained with matrix-induced ACI.18

Particulated Juvenile Allograft Cartilage

Particulated juvenile allograft cartilage (DeNovo NT Graft; Zimmer Biomet) is minced cartilage allograft (from juvenile donors) that has been cut into cubes (~1 mm3). Indications are for patellar and trochlear lesions 1 cm2 to 6 cm2. For both the trochlea and the patella, short-term outcomes have been good.19,20

Rehabilitation After Surgery

Isolated PF cartilage restoration generally does not require prolonged weight-bearing restrictions, and ambulation with the knee locked in full extension is permitted as tolerated. Concurrent TT osteotomy, however, requires protection with 4 to 6 weeks of toe-touch weight-bearing to minimize the risk of tibial fracture.

Conclusion

Comprehensive preoperative assessment is essential and should include a thorough core-to-floor physical examination as well as PF-specific imaging. Treatment of symptomatic chondral lesions in the PF joint requires specific technical and postoperative management, which differs significantly from management involving the condyles. Attending to all these details makes the outcomes of PF cartilage treatment reproducible. These outcomes may rival those of condylar treatment.

References

1. Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy. 1997;13(4):456-460.

2. Steensen RN, Bentley JC, Trinh TQ, Backes JR, Wiltfong RE. The prevalence and combined prevalences of anatomic factors associated with recurrent patellar dislocation: a magnetic resonance imaging study. Am J Sports Med. 2015;43(4):921-927.

3. Nomura E, Inoue M. Cartilage lesions of the patella in recurrent patellar dislocation. Am J Sports Med. 2004;32(2):498-502.

4. Vollnberg B, Koehlitz T, Jung T, et al. Prevalence of cartilage lesions and early osteoarthritis in patients with patellar dislocation. Eur Radiol. 2012;22(11):2347-2356.

5. Crema MD, Roemer FW, Marra MD, et al. Articular cartilage in the knee: current MR imaging techniques and applications in clinical practice and research. Radiographics. 2011;31(1):37-61.

6. Campbell KA, Erickson BJ, Saltzman BM, et al. Is local viscosupplementation injection clinically superior to other therapies in the treatment of osteoarthritis of the knee: a systematic review of overlapping meta-analyses. Arthroscopy. 2015;31(10):2036-2045.e14.

7. Saltzman BM, Jain A, Campbell KA, et al. Does the use of platelet-rich plasma at the time of surgery improve clinical outcomes in arthroscopic rotator cuff repair when compared with control cohorts? A systematic review of meta-analyses. Arthroscopy. 2016;32(5):906-918.

8. Gomoll AH, Gillogly SD, Cole BJ, et al. Autologous chondrocyte implantation in the patella: a multicenter experience. Am J Sports Med. 2014;42(5):1074-1081.

9. Meric G, Gracitelli GC, Gortz S, De Young AJ, Bugbee WD. Fresh osteochondral allograft transplantation for bipolar reciprocal osteochondral lesions of the knee. Am J Sports Med. 2015;43(3):709-714.

10. Peterson L, Vasiliadis HS, Brittberg M, Lindahl A. Autologous chondrocyte implantation: a long-term follow-up. Am J Sports Med. 2010;38(6):1117-1124.

11. Minas T, Gomoll AH, Rosenberger R, Royce RO, Bryant T. Increased failure rate of autologous chondrocyte implantation after previous treatment with marrow stimulation techniques. Am J Sports Med. 2009;37(5):902-908.

12. Gracitelli GC, Meric G, Briggs DT, et al. Fresh osteochondral allografts in the knee: comparison of primary transplantation versus transplantation after failure of previous subchondral marrow stimulation. Am J Sports Med. 2015;43(4):885-891.

13. Anderson CN, Magnussen RA, Block JJ, Anderson AF, Spindler KP. Operative fixation of chondral loose bodies in osteochondritis dissecans in the knee: a report of 5 cases. Orthop J Sports Med. 2013;1(2):2325967113496546.

14. Kreuz PC, Steinwachs MR, Erggelet C, et al. Results after microfracture of full-thickness chondral defects in different compartments in the knee. Osteoarthritis Cartilage. 2006;14(11):1119-1125.

15. Vasiliadis HS, Lindahl A, Georgoulis AD, Peterson L. Malalignment and cartilage lesions in the patellofemoral joint treated with autologous chondrocyte implantation. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):452-457.

16. Astur DC, Arliani GG, Binz M, et al. Autologous osteochondral transplantation for treating patellar chondral injuries: evaluation, treatment, and outcomes of a two-year follow-up study. J Bone Joint Surg Am. 2014;96(10):816-823.

17. Hoffman JK, Geraghty S, Protzman NM. Articular cartilage repair using marrow simulation augmented with a viable chondral allograft: 9-month postoperative histological evaluation. Case Rep Orthop. 2015;2015:617365.

18. Gobbi A, Chaurasia S, Karnatzikos G, Nakamura N. Matrix-induced autologous chondrocyte implantation versus multipotent stem cells for the treatment of large patellofemoral chondral lesions: a nonrandomized prospective trial. Cartilage. 2015;6(2):82-97.

19. Farr J, Tabet SK, Margerrison E, Cole BJ. Clinical, radiographic, and histological outcomes after cartilage repair with particulated juvenile articular cartilage: a 2-year prospective study. Am J Sports Med. 2014;42(6):1417-1425.

20. Tompkins M, Hamann JC, Diduch DR, et al. Preliminary results of a novel single-stage cartilage restoration technique: particulated juvenile articular cartilage allograft for chondral defects of the patella. Arthroscopy. 2013;29(10):1661-1670.

References

1. Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy. 1997;13(4):456-460.

2. Steensen RN, Bentley JC, Trinh TQ, Backes JR, Wiltfong RE. The prevalence and combined prevalences of anatomic factors associated with recurrent patellar dislocation: a magnetic resonance imaging study. Am J Sports Med. 2015;43(4):921-927.

3. Nomura E, Inoue M. Cartilage lesions of the patella in recurrent patellar dislocation. Am J Sports Med. 2004;32(2):498-502.

4. Vollnberg B, Koehlitz T, Jung T, et al. Prevalence of cartilage lesions and early osteoarthritis in patients with patellar dislocation. Eur Radiol. 2012;22(11):2347-2356.

5. Crema MD, Roemer FW, Marra MD, et al. Articular cartilage in the knee: current MR imaging techniques and applications in clinical practice and research. Radiographics. 2011;31(1):37-61.

6. Campbell KA, Erickson BJ, Saltzman BM, et al. Is local viscosupplementation injection clinically superior to other therapies in the treatment of osteoarthritis of the knee: a systematic review of overlapping meta-analyses. Arthroscopy. 2015;31(10):2036-2045.e14.

7. Saltzman BM, Jain A, Campbell KA, et al. Does the use of platelet-rich plasma at the time of surgery improve clinical outcomes in arthroscopic rotator cuff repair when compared with control cohorts? A systematic review of meta-analyses. Arthroscopy. 2016;32(5):906-918.

8. Gomoll AH, Gillogly SD, Cole BJ, et al. Autologous chondrocyte implantation in the patella: a multicenter experience. Am J Sports Med. 2014;42(5):1074-1081.

9. Meric G, Gracitelli GC, Gortz S, De Young AJ, Bugbee WD. Fresh osteochondral allograft transplantation for bipolar reciprocal osteochondral lesions of the knee. Am J Sports Med. 2015;43(3):709-714.

10. Peterson L, Vasiliadis HS, Brittberg M, Lindahl A. Autologous chondrocyte implantation: a long-term follow-up. Am J Sports Med. 2010;38(6):1117-1124.

11. Minas T, Gomoll AH, Rosenberger R, Royce RO, Bryant T. Increased failure rate of autologous chondrocyte implantation after previous treatment with marrow stimulation techniques. Am J Sports Med. 2009;37(5):902-908.

12. Gracitelli GC, Meric G, Briggs DT, et al. Fresh osteochondral allografts in the knee: comparison of primary transplantation versus transplantation after failure of previous subchondral marrow stimulation. Am J Sports Med. 2015;43(4):885-891.

13. Anderson CN, Magnussen RA, Block JJ, Anderson AF, Spindler KP. Operative fixation of chondral loose bodies in osteochondritis dissecans in the knee: a report of 5 cases. Orthop J Sports Med. 2013;1(2):2325967113496546.

14. Kreuz PC, Steinwachs MR, Erggelet C, et al. Results after microfracture of full-thickness chondral defects in different compartments in the knee. Osteoarthritis Cartilage. 2006;14(11):1119-1125.

15. Vasiliadis HS, Lindahl A, Georgoulis AD, Peterson L. Malalignment and cartilage lesions in the patellofemoral joint treated with autologous chondrocyte implantation. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):452-457.

16. Astur DC, Arliani GG, Binz M, et al. Autologous osteochondral transplantation for treating patellar chondral injuries: evaluation, treatment, and outcomes of a two-year follow-up study. J Bone Joint Surg Am. 2014;96(10):816-823.

17. Hoffman JK, Geraghty S, Protzman NM. Articular cartilage repair using marrow simulation augmented with a viable chondral allograft: 9-month postoperative histological evaluation. Case Rep Orthop. 2015;2015:617365.

18. Gobbi A, Chaurasia S, Karnatzikos G, Nakamura N. Matrix-induced autologous chondrocyte implantation versus multipotent stem cells for the treatment of large patellofemoral chondral lesions: a nonrandomized prospective trial. Cartilage. 2015;6(2):82-97.

19. Farr J, Tabet SK, Margerrison E, Cole BJ. Clinical, radiographic, and histological outcomes after cartilage repair with particulated juvenile articular cartilage: a 2-year prospective study. Am J Sports Med. 2014;42(6):1417-1425.

20. Tompkins M, Hamann JC, Diduch DR, et al. Preliminary results of a novel single-stage cartilage restoration technique: particulated juvenile articular cartilage allograft for chondral defects of the patella. Arthroscopy. 2013;29(10):1661-1670.

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The American Journal of Orthopedics - 46(5)
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Practice Makes Perfect?

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Changed

It is human nature to practice things that we are already good at doing. If you’re a golfer, then you know what I’m talking about. I hit the driver over and over again on the range, but never practice hitting the bad lie in the bunker, or the half-swing wedge from a tight lie. I sink hundreds of 3 footers, but can’t putt into this range from 50 feet. I’ve gotten much better at golf since I started playing, but my scores have hardly gone down.

Why? It’s the things I never practice that usually come back to bite me during the round, making it impossible to avoid double bogeys and driving up my score. It’s these areas where I have the most room for improvement, and if I simply made the effort to practice them, I could see a real impact on my handicap.

I think a similar thing happens in our orthopedic practices. I read everything I can on the anterior cruciate ligament, yet I already feel comfortable with my reconstruction technique. I skim, or avoid reading altogether, articles about topics I don’t like to treat, like the hand or spine. Yet, I still see these things every day in my practice and on call. If my depth of knowledge in these areas was as good as it is in sports medicine, I could provide better, more immediate care to my patients, rather than refer them to subspecialists.

A perfect orthopedic example would be the patellofemoral joint. One of the least enjoyable patient encounters for me is the young adult with normal alignment and intractable anterior knee pain that does not respond to nonoperative treatment. I’m concerned any surgical intervention may make them worse and I’m often left without much to offer the patient.

It’s for this reason AJO has partnered with Dr. Jack Farr to produce the patellofemoral issue; to provide a comprehensive guide to the latest thinking in the treatment of patellofemoral disorders (see the March/April 2017 issue). We solicited so much outstanding content, that a single issue could not hold all of the articles. In this issue, our patellofemoral series continues with 3 outstanding articles. Magnussen presents "Patella Alta Sees You, Do You See It?" and Hinckel and colleagues have authored a guide to patellofemoral cartilage restoration. Unal and colleagues follow-up with a review of the lateral retinaculum.

In our "Codes to Know" section, we reexamine diagnostic arthroscopy, a code most of us have billed infrequently. New technologies, however, have made it possible to peer into the joint in the office, and McMillan and colleagues teach us how to make it economically feasible, even for employed physicians.

Finally, we have a number of great articles on difficult problems—the stiff elbow, complex distal radius fractures, and intraoperative acetabular fractures during total hip arthroplasty.

Please enjoy this issue and think about what topics you tend to shy away from. I’m willing to bet you can add the most to your practice by studying up on these topics. As always, please provide your feedback to our editorial team so that we can continue to make improvements to our journal. We envision a change in the way orthopedists utilize a journal in their practice, and are continuously looking for ways to make AJO a more relevant tool for improving your patient care and workflow. We are working hard to give our readers the journal they deserve, but in my spare time, I’ll be brushing up on trochleoplasties and half-swing wedges.

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It is human nature to practice things that we are already good at doing. If you’re a golfer, then you know what I’m talking about. I hit the driver over and over again on the range, but never practice hitting the bad lie in the bunker, or the half-swing wedge from a tight lie. I sink hundreds of 3 footers, but can’t putt into this range from 50 feet. I’ve gotten much better at golf since I started playing, but my scores have hardly gone down.

Why? It’s the things I never practice that usually come back to bite me during the round, making it impossible to avoid double bogeys and driving up my score. It’s these areas where I have the most room for improvement, and if I simply made the effort to practice them, I could see a real impact on my handicap.

I think a similar thing happens in our orthopedic practices. I read everything I can on the anterior cruciate ligament, yet I already feel comfortable with my reconstruction technique. I skim, or avoid reading altogether, articles about topics I don’t like to treat, like the hand or spine. Yet, I still see these things every day in my practice and on call. If my depth of knowledge in these areas was as good as it is in sports medicine, I could provide better, more immediate care to my patients, rather than refer them to subspecialists.

A perfect orthopedic example would be the patellofemoral joint. One of the least enjoyable patient encounters for me is the young adult with normal alignment and intractable anterior knee pain that does not respond to nonoperative treatment. I’m concerned any surgical intervention may make them worse and I’m often left without much to offer the patient.

It’s for this reason AJO has partnered with Dr. Jack Farr to produce the patellofemoral issue; to provide a comprehensive guide to the latest thinking in the treatment of patellofemoral disorders (see the March/April 2017 issue). We solicited so much outstanding content, that a single issue could not hold all of the articles. In this issue, our patellofemoral series continues with 3 outstanding articles. Magnussen presents "Patella Alta Sees You, Do You See It?" and Hinckel and colleagues have authored a guide to patellofemoral cartilage restoration. Unal and colleagues follow-up with a review of the lateral retinaculum.

In our "Codes to Know" section, we reexamine diagnostic arthroscopy, a code most of us have billed infrequently. New technologies, however, have made it possible to peer into the joint in the office, and McMillan and colleagues teach us how to make it economically feasible, even for employed physicians.

Finally, we have a number of great articles on difficult problems—the stiff elbow, complex distal radius fractures, and intraoperative acetabular fractures during total hip arthroplasty.

Please enjoy this issue and think about what topics you tend to shy away from. I’m willing to bet you can add the most to your practice by studying up on these topics. As always, please provide your feedback to our editorial team so that we can continue to make improvements to our journal. We envision a change in the way orthopedists utilize a journal in their practice, and are continuously looking for ways to make AJO a more relevant tool for improving your patient care and workflow. We are working hard to give our readers the journal they deserve, but in my spare time, I’ll be brushing up on trochleoplasties and half-swing wedges.

It is human nature to practice things that we are already good at doing. If you’re a golfer, then you know what I’m talking about. I hit the driver over and over again on the range, but never practice hitting the bad lie in the bunker, or the half-swing wedge from a tight lie. I sink hundreds of 3 footers, but can’t putt into this range from 50 feet. I’ve gotten much better at golf since I started playing, but my scores have hardly gone down.

Why? It’s the things I never practice that usually come back to bite me during the round, making it impossible to avoid double bogeys and driving up my score. It’s these areas where I have the most room for improvement, and if I simply made the effort to practice them, I could see a real impact on my handicap.

I think a similar thing happens in our orthopedic practices. I read everything I can on the anterior cruciate ligament, yet I already feel comfortable with my reconstruction technique. I skim, or avoid reading altogether, articles about topics I don’t like to treat, like the hand or spine. Yet, I still see these things every day in my practice and on call. If my depth of knowledge in these areas was as good as it is in sports medicine, I could provide better, more immediate care to my patients, rather than refer them to subspecialists.

A perfect orthopedic example would be the patellofemoral joint. One of the least enjoyable patient encounters for me is the young adult with normal alignment and intractable anterior knee pain that does not respond to nonoperative treatment. I’m concerned any surgical intervention may make them worse and I’m often left without much to offer the patient.

It’s for this reason AJO has partnered with Dr. Jack Farr to produce the patellofemoral issue; to provide a comprehensive guide to the latest thinking in the treatment of patellofemoral disorders (see the March/April 2017 issue). We solicited so much outstanding content, that a single issue could not hold all of the articles. In this issue, our patellofemoral series continues with 3 outstanding articles. Magnussen presents "Patella Alta Sees You, Do You See It?" and Hinckel and colleagues have authored a guide to patellofemoral cartilage restoration. Unal and colleagues follow-up with a review of the lateral retinaculum.

In our "Codes to Know" section, we reexamine diagnostic arthroscopy, a code most of us have billed infrequently. New technologies, however, have made it possible to peer into the joint in the office, and McMillan and colleagues teach us how to make it economically feasible, even for employed physicians.

Finally, we have a number of great articles on difficult problems—the stiff elbow, complex distal radius fractures, and intraoperative acetabular fractures during total hip arthroplasty.

Please enjoy this issue and think about what topics you tend to shy away from. I’m willing to bet you can add the most to your practice by studying up on these topics. As always, please provide your feedback to our editorial team so that we can continue to make improvements to our journal. We envision a change in the way orthopedists utilize a journal in their practice, and are continuously looking for ways to make AJO a more relevant tool for improving your patient care and workflow. We are working hard to give our readers the journal they deserve, but in my spare time, I’ll be brushing up on trochleoplasties and half-swing wedges.

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Pronator Teres Myotendinous Tear

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I read with interest the article "Pronator Teres Myotendinous Tear" by Drs. Qayyum, Villacis, and Jobin (Am J Orthop. 2017;46(2):E105-E107), and I commend the authors for their interesting exploration of this unusual injury.

I would like to note that this pathology was previously reported by our group in 2015.1 We now have a 2-year follow-up on this patient, and he has remained asymptomatic since his return to golf. Since this article was published, we have been contacted by 3 patients (one of whom is a radiologist who interpreted his own magnetic resonance imaging) describing similar mechanisms of injury, symptoms, imaging findings, and recovery with nonoperative management. This suggests that pronator teres rupture may have been previously unrecognized or underreported.

It is interesting that this patient was injured when his club stuck in the ground while our patient reported taking only a small divot during his injury. From these differing mechanisms it is unclear whether forceful contraction or sudden loading is the largest risk factor for obtaining this injury, and this could be a point for further research. As awareness of this injury pattern spreads, we look forward to seeing larger series and establishing the success rate of nonoperative treatment and the risk factors for its failure.

Brooks W. Ficke, MD

Brent A. Ponce, MD

Birmingham, AL

Authors' Response

We appreciate Dr. Ficke’s comments regarding his experience treating pronator teres injuries and agree that they are likely under-recognized and possibly underreported. We are uncertain which mechanisms during the golf swing strains the pronator teres to the point of injury, but it may be a combination of muscular fatigue, forceful contraction, and sudden resistance to concentric loading during the club striking the ground. In our experience, these injuries do appear to heal without observable deficit. Our patient is back golfing regularly without any arm symptoms and actually had an improvement in his golf handicap this season.

Charles M. Jobin, MD

Usama Qayyum, MBBS

Diego Villacis, MD

New York, NY

References

1. Ficke BW, Larrison MC, Ponce BA. Isolated rupture of the pronator teres in an amateur golfer: a case report. Int J Orthop. 2015;2(6):481-483.

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I read with interest the article "Pronator Teres Myotendinous Tear" by Drs. Qayyum, Villacis, and Jobin (Am J Orthop. 2017;46(2):E105-E107), and I commend the authors for their interesting exploration of this unusual injury.

I would like to note that this pathology was previously reported by our group in 2015.1 We now have a 2-year follow-up on this patient, and he has remained asymptomatic since his return to golf. Since this article was published, we have been contacted by 3 patients (one of whom is a radiologist who interpreted his own magnetic resonance imaging) describing similar mechanisms of injury, symptoms, imaging findings, and recovery with nonoperative management. This suggests that pronator teres rupture may have been previously unrecognized or underreported.

It is interesting that this patient was injured when his club stuck in the ground while our patient reported taking only a small divot during his injury. From these differing mechanisms it is unclear whether forceful contraction or sudden loading is the largest risk factor for obtaining this injury, and this could be a point for further research. As awareness of this injury pattern spreads, we look forward to seeing larger series and establishing the success rate of nonoperative treatment and the risk factors for its failure.

Brooks W. Ficke, MD

Brent A. Ponce, MD

Birmingham, AL

Authors' Response

We appreciate Dr. Ficke’s comments regarding his experience treating pronator teres injuries and agree that they are likely under-recognized and possibly underreported. We are uncertain which mechanisms during the golf swing strains the pronator teres to the point of injury, but it may be a combination of muscular fatigue, forceful contraction, and sudden resistance to concentric loading during the club striking the ground. In our experience, these injuries do appear to heal without observable deficit. Our patient is back golfing regularly without any arm symptoms and actually had an improvement in his golf handicap this season.

Charles M. Jobin, MD

Usama Qayyum, MBBS

Diego Villacis, MD

New York, NY

I read with interest the article "Pronator Teres Myotendinous Tear" by Drs. Qayyum, Villacis, and Jobin (Am J Orthop. 2017;46(2):E105-E107), and I commend the authors for their interesting exploration of this unusual injury.

I would like to note that this pathology was previously reported by our group in 2015.1 We now have a 2-year follow-up on this patient, and he has remained asymptomatic since his return to golf. Since this article was published, we have been contacted by 3 patients (one of whom is a radiologist who interpreted his own magnetic resonance imaging) describing similar mechanisms of injury, symptoms, imaging findings, and recovery with nonoperative management. This suggests that pronator teres rupture may have been previously unrecognized or underreported.

It is interesting that this patient was injured when his club stuck in the ground while our patient reported taking only a small divot during his injury. From these differing mechanisms it is unclear whether forceful contraction or sudden loading is the largest risk factor for obtaining this injury, and this could be a point for further research. As awareness of this injury pattern spreads, we look forward to seeing larger series and establishing the success rate of nonoperative treatment and the risk factors for its failure.

Brooks W. Ficke, MD

Brent A. Ponce, MD

Birmingham, AL

Authors' Response

We appreciate Dr. Ficke’s comments regarding his experience treating pronator teres injuries and agree that they are likely under-recognized and possibly underreported. We are uncertain which mechanisms during the golf swing strains the pronator teres to the point of injury, but it may be a combination of muscular fatigue, forceful contraction, and sudden resistance to concentric loading during the club striking the ground. In our experience, these injuries do appear to heal without observable deficit. Our patient is back golfing regularly without any arm symptoms and actually had an improvement in his golf handicap this season.

Charles M. Jobin, MD

Usama Qayyum, MBBS

Diego Villacis, MD

New York, NY

References

1. Ficke BW, Larrison MC, Ponce BA. Isolated rupture of the pronator teres in an amateur golfer: a case report. Int J Orthop. 2015;2(6):481-483.

References

1. Ficke BW, Larrison MC, Ponce BA. Isolated rupture of the pronator teres in an amateur golfer: a case report. Int J Orthop. 2015;2(6):481-483.

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Percutaneous Release of Trigger Digits

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Take-Home Points

  • The author had a 90% success rate with no complications in treating almost 600 trigger digits.
  • All digits can be safely treated, including multiple fingers on one hand, all in an office setting.
  • Percutaneous trigger release appears to be a safe and reliable alternative to open surgery.
  • Success rate, discomfort, and cost may make a percutaneous trigger release preferable to even a trial of corticosteroid injection.
  • A failed percutaneous release can be successfully treated with an open release, if needed.

Trigger finger, or stenosing flexor tenosynovitis, is a condition characterized by clicking or locking during finger movement, sometimes resulting in the freezing of a digit in flexion or extension1 (Figure 1). [[{"fid":"202300","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"1"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"1":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":""}}}]]Tendon inflammation is thought to cause constriction of the tendon sheath and bunching of the fibrous bundles of the first annular (A1) pulley, often creating a palpable nodule at the base of the digit.2,3 Many patients experience intermittent joint pain and swelling, which may progress to triggering or complete locking of the digit.1 One of the most common conditions treated by hand surgeons, trigger finger is most often reported in the dominant hand of women in their sixth decade of life and has been associated with several conditions, including diabetes and rheumatoid arthritis.4-6 Other researchers have indicated the thumb and ring finger are most commonly affected, though all fingers can potentially trigger.7,8

Initial treatment often involves injecting corticosteroid into the flexor tendon sheath, at or proximal to the annular pulley system, to reduce inflammation and the fibrous nodule.3 Another injection study found an initial success rate of 57% with a single injection, and 86% with a second injection, but patients were monitored for only 6 months, a period that may have been too short for symptom recurrence.7

On failure of steroid injections, patients typically are treated with open tendon sheath incision.9 This procedure, usually performed in a hospital or outpatient surgery setting, requires postoperative wound care, including dressing changes, suture removal, possible hand therapy, and follow-up physician visits. Operative treatment involves making a 1-cm to 2-cm incision, releasing the A1 pulley, and skin suturing.7,8,10 The most common postoperative complaint is incisional tenderness, though long-term scar pain, infection, nerve injury, and disease recurrence have been reported.8 Overall, the procedure is very successful, providing up to 100% symptom relief.7,8,10

Endoscopic release of trigger finger has also been described as an effective operative treatment. This technique involves passing a small cannula through a palmar incision—using an endoscope and retrograde knife within this 2.7-mm tunnel.10 With this treatment, reduced visibility may increase the risk of nerve injury.10 Although generally successful, endoscopic release requires anesthesia and expensive instruments and has a significant learning curve.8,10

More recently, percutaneous release of trigger finger has been described as a definitive, in-office treatment.5,6,11,12 Percutaneous release has the obvious advantages of no open incision, less scarring, less discomfort, and shorter recovery. Several studies have found comparable success rates for open and percutaneous procedures but consistently shorter recovery with the percutaneous technique.7,8,12 Given its lower recurrence rate (vs steroid injections) and shorter recovery and lower cost (vs a surgical procedure), percutaneous treatment of stenosing tenosynovitis appears to be a safe, highly successful, and minimally invasive treatment method.8 This study represents a single surgeon’s experience with percutaneous tendon sheath incision over a 10-year period.

Methods

Patients presented with symptoms of stenosing flexor tenosynovitis with severity ranging from intermittent triggering to frank locking of the digit. Most patients underwent prior conservative treatment, including corticosteroid injections and hand therapy. With each patient, the senior author discussed the pathophysiology of trigger digit; treatment options, including observation, hand therapy, corticosteroid injection, percutaneous release, and open release; and potential risks and complications. The treatment path—initial corticosteroid injection, percutaneous release, or open release—was left up to the patient. The only exclusion criterion was prior surgery to the involved digit, and there was no discrimination by finger, symptomatic period, or severity. Each released digit was recorded independently. In no case was anticoagulant therapy discontinued.
A complete medical history was obtained for each patient.

Over a 10-year period (March 2003-December 2013), percutaneous release was performed on 596 trigger fingers in 429 patients, 18 years old or older. Of these patients, 279 were female. Mean age was 62 years (range, 26-97 years). Of the 531 releases with handedness recorded, 56.3% were performed on trigger digits on dominant hands (Table 1). [[{"fid":"202302","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"2"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"2":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 1.","field_file_image_credit[und][0][value]":""}}}]]Mean duration of symptoms before percutaneous release was 9.7 months (range, 0.5-132 months). Of the 596 digits, 69 were reported to have previously sustained trauma, and 161 had been unsuccessfully treated with one or more cortisone injections before undergoing release. Of the suspected comorbidities examined, carpal tunnel syndrome was previously diagnosed in 79 patients and diabetes in 56 patients.1

Of the 429 patients, 313 had a single digit released and 116 had multiple digits released. Of the 116 patients in the multiple-release group, 80 had 2 fingers released, 24 had 3 released, 7 had 4 released, and 5 had 5 released. The 596 released trigger fingers consisted of 188 thumbs, 41 index fingers, 185 middle fingers, 140 ring fingers, and 42 small fingers.

Surgical Technique

In-office percutaneous trigger finger releases were performed with a local anesthetic. One milliliter of lidocaine 1% injection was used to anesthetize the skin, the subcutaneous tissues, and the flexor tendon sheath at the level of the A1 pulley. As described by Pandey and colleagues,6 the proper location of the pulley was confirmed using specific surface landmarks on each digit. After waiting several minutes to allow the anesthetic to take effect, the surgeon inserted an 18-gauge needle into the center of the pulley with the digit held in extension (Figure 2). [[{"fid":"202303","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"3"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"3":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":""}}}]]The needle was carefully moved longitudinally along the length of the pulley with the bevel of the needle parallel to the tendon. A grating sensation was felt as the fibers of the pulley were cut. Several needle passes were made until the pulley was felt to have been released. Complete release was determined by loss of the grating sensation, along with complete relief of any further symptoms of triggering. The puncture site was cleaned and covered with a light sterile dressing (watch the Video online). There was no postoperative immobilization, and patients were encouraged to immediately return to normal use of the digit. Hand therapy was not prescribed, and pain medications were not dispensed. A 1-week follow-up appointment was scheduled, and patients were advised to return for evaluation in the event of any recurring symptoms (eg, triggering, swelling, stiffness, pain).

Results

were successfully released with 1 percutaneous procedure (recurrence or failure rate, 9.9%). The thumb was the digit most reliably released (success rate, 94.7%) (Table 2). [[{"fid":"202306","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"4"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"4":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 2.","field_file_image_credit[und][0][value]":""}}}]]Patients with recurrent or unresolved symptoms were given the options of a second percutaneous release or an open surgical procedure. Of the 59 digits unsuccessfully released, as identified by persistent triggering or locking of the digit, 17 were treated with a second percutaneous release (15 were successful), and 40 underwent open tendon sheath incision as a second procedure (success rate, 100%); triggering persisted in the remaining 2 digits, and these were considered failures (the 2 patients did not pursue further treatment).

There were no complications: infection; nerve, artery, or tendon injury; or chronic pain. Some patients had mild stiffness, swelling, or pain for a few days after the procedure, and these effects typically resolved without treatment. In 29 digits, persistent pain or swelling without triggering was successfully treated with a corticosteroid injection.

Discussion

[[{"fid":"202307","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"5"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Table 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"5":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Table 3.","field_file_image_credit[und][0][value]":""}}}]]Over a 10-year period, 596 percutaneous trigger finger releases were sequentially performed by a single surgeon. The 90% success rate compares favorably with rates found in other studies (Table 3).5-9,12-14 The surgeon’s success rates for individual years vary and demonstrate no clear trend or learning curve with the procedure (Figure 3). There were no significant complications. Patient satisfaction with the procedure was high.[[{"fid":"202308","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"6"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"6":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":""}}}]]

There were no injuries to digital nerves, arteries, or flexor tendons, either early or late, and no reports of infections or long-term pain or loss of motion. Although it is quite probable that in some procedures the longitudinal passes of the 18-gauge needle may have also slightly cut into the flexor tendon after passing through the A1 pulley, the direction of the needle passes was in line with the direction of the collagen fibers of the tendon, and thus any inadvertent superficial abrasion would not have structurally weakened the tendon. Of the 40 digits that underwent open release after incomplete or failed percutaneous release, none showed significant longitudinal lacerations of the superficialis tendon. During these revision surgeries, the typical intraoperative finding was incomplete release of the A1 pulley, usually at the distal end. Although loss of the grating sensation or relief of further triggering symptoms was considered adequate evidence of a successful release in this study, small tendon attachments could remain and potentially could lead to recurrent triggering. Given the high success rate achieved with the large sample, however, these 2 factors are considered appropriate indicators of successful release.

It is unclear why there was a relatively consistent 10% failure rate and why it did not decrease over the 10-year study period. Although the technique used does not have a significant learning curve, it appears that digits are not actively triggering at time of procedure have a higher failure rate. When a patient’s digit is actively triggering, assessment of the success of the procedure is relatively straightforward, whereas when a digit intermittently triggers and locks and is not symptomatic in the office, success cannot be immediately determined.

No specific digit was significantly more prone to failed releases, though the small finger had the lowest success rate (85.7%). Given that only 56.4% of patients experienced triggering on the dominant hand, there is not enough evidence to suggest a significant relationship between likelihood of a trigger digit and a patient’s hand dominance. Similarly, there was no correlation between the duration of symptoms and the success of the percutaneous procedure.

Investigation of the relationship between the previously suggested comorbidities of carpal tunnel syndrome and diabetes was also inconclusive. Only 79 (18%) of 429 patients reported having carpal tunnel syndrome, and even fewer, 56 (13.0%), reported having diabetes. Only 69 of the 596 treated digits reportedly had sustained trauma before developing triggering symptoms, and only 12 of the 69 were unsuccessfully released. In addition, of the 161 digits in which one or more steroid injections failed to resolve triggering symptoms, 158 (87.3%) were successfully released with 1 percutaneous procedure. Collectively, these data show percutaneous release can effectively eliminate triggering symptoms in a digit that has sustained injury or that has been unsuccessfully treated with nonoperative methods. Failed percutaneous release subsequently can be reliably treated with an open procedure, and results are excellent.

This study had several limitations. It was retrospective, nonblinded, and did not compare outcomes of percutaneous release with those of an open procedure. Data are presented to support the efficacy and safety of percutaneous release as a treatment option. Another limitation is that pre-release treatment was not controlled. Patients had been treated with a variety of nonoperative methods, including use of anti-inflammatory medication, hand therapy, splinting, and one or more corticosteroid injections, both at our office and elsewhere.

Percutaneous release appears to have an advantage in terms of pain relief, but the study did not evaluate or control for procedure discomfort. However, patients who had been treated with a corticosteroid injection before percutaneous release consistently refused corticosteroid injections for subsequent trigger digits, citing the dramatic pain reduction achieved with release relative to injection. Similarly, all patients who had a trigger digit treated with open tendon sheath incision in the past indicated a strong preference for the percutaneous release.

Follow-up on this patient population was inconsistent and incomplete. Many patients did not return, presumably because they considered the procedure a success and thought follow-up was unnecessary. However, some patients may have had a recurrence or an incomplete release and gone elsewhere for treatment.

The results of this study, to date the largest study on percutaneous release of trigger finger, provide more evidence of the safety and efficacy of this procedure as a treatment option. The success rate of percutaneous release is high, surpasses that of nonoperative treatments such as steroid injections, and approaches that of open and endoscopic surgical alternatives. Some of the obvious advantages of percutaneous release are less visible scarring, fewer incision-related complications, and shorter rehabilitation.10 In addition, post-procedure pain is possibly reduced, symptom relief is comparable, operative time is significantly shorter,8 and percutaneous release is easily performed in the office setting.

Percutaneous release is a viable treatment option for stenosing flexor tenosynovitis, regardless of previously used nonoperative treatment methods, duration or severity of symptoms, or trigger digit treated.

References

1. Makkouk AH, Oetgen ME, Swigart CR, Dodds SD. Trigger finger: etiology, evaluation, and treatment. Curr Rev Musculoskelet Med. 2008;1(2):92-96.

2. Fahey JJ, Bollinger JA. Trigger-finger in adults and children. J Bone Joint Surg Am. 1954;36(6):1200-1218.

3. Marks MR, Gunther SF. Efficacy of cortisone injection in treatment of trigger fingers and thumbs. J Hand Surg Am. 1989;14(4):722-727.

4. Chammas M, Bousquet P, Renard E, Poirier JL, Jaffiol C, Allieu Y. Dupuytren’s disease, carpal tunnel syndrome, trigger finger, and diabetes mellitus. J Hand Surg Am. 1995;20(1):109-114.

5. Habbu R, Putman MD, Adams JE. Percutaneous release of the A1 pulley: a cadaver study. J Hand Surg Am. 2012;37(11):2273-2277.

6. Pandey BK, Sharma S, Manandhar RR, Pradhan RL, Lakhey S, Rijal KP. Percutaneous trigger finger release. Nepal Orthop Assoc J. 2010;1(1):1-5.

7. Sato ES, Gomes dos Santos JB, Belloti JC, Albertoni WM, Faloppa F. Treatment of trigger finger: randomized clinical trial comparing the methods of corticosteroid injection, percutaneous release and open surgery. Rheumatology. 2012;51(1):93-99.

8. Dierks U, Hoffmann R, Meek MF. Open versus percutaneous release of the A1-pulley for stenosing tendovaginitis: a prospective randomized trial. Tech Hand Up Extrem Surg. 2008;12(3):183-187.

9. Tanaka J. Percutaneous trigger finger release. Tech Hand Up Extrem Surg. 1999;3(1):52-57.

10. Pegoli L, Cavalli E, Cortese P, Parolo C, Pajardi G. A comparison of endoscopic and open trigger finger release. Hand Surg. 2008;13(3):147-151.

11. Ryzewicz M, Wolf JM. Trigger digits: principles, management, and complications. J Hand Surg Am. 2006;31(1):135-146.

12. Schramm JM, Nguyen M, Wongworawat MD. The safety of percutaneous trigger finger release. Hand. 2008;3(1):44-46.

13. Paulius KL, Maguina P. Ultrasound-assisted percutaneous trigger finger release: is it safe? Hand. 2009;4(1):35-37.

14. Cihantimur B, Akin S, Ozcan M. Percutaneous treatment of trigger finger. 34 fingers followed 0.5-2 years. Acta Orthop Scand. 1998;69(2):167-168.

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Take-Home Points

  • The author had a 90% success rate with no complications in treating almost 600 trigger digits.
  • All digits can be safely treated, including multiple fingers on one hand, all in an office setting.
  • Percutaneous trigger release appears to be a safe and reliable alternative to open surgery.
  • Success rate, discomfort, and cost may make a percutaneous trigger release preferable to even a trial of corticosteroid injection.
  • A failed percutaneous release can be successfully treated with an open release, if needed.

Trigger finger, or stenosing flexor tenosynovitis, is a condition characterized by clicking or locking during finger movement, sometimes resulting in the freezing of a digit in flexion or extension1 (Figure 1). [[{"fid":"202300","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"1"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"1":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":""}}}]]Tendon inflammation is thought to cause constriction of the tendon sheath and bunching of the fibrous bundles of the first annular (A1) pulley, often creating a palpable nodule at the base of the digit.2,3 Many patients experience intermittent joint pain and swelling, which may progress to triggering or complete locking of the digit.1 One of the most common conditions treated by hand surgeons, trigger finger is most often reported in the dominant hand of women in their sixth decade of life and has been associated with several conditions, including diabetes and rheumatoid arthritis.4-6 Other researchers have indicated the thumb and ring finger are most commonly affected, though all fingers can potentially trigger.7,8

Initial treatment often involves injecting corticosteroid into the flexor tendon sheath, at or proximal to the annular pulley system, to reduce inflammation and the fibrous nodule.3 Another injection study found an initial success rate of 57% with a single injection, and 86% with a second injection, but patients were monitored for only 6 months, a period that may have been too short for symptom recurrence.7

On failure of steroid injections, patients typically are treated with open tendon sheath incision.9 This procedure, usually performed in a hospital or outpatient surgery setting, requires postoperative wound care, including dressing changes, suture removal, possible hand therapy, and follow-up physician visits. Operative treatment involves making a 1-cm to 2-cm incision, releasing the A1 pulley, and skin suturing.7,8,10 The most common postoperative complaint is incisional tenderness, though long-term scar pain, infection, nerve injury, and disease recurrence have been reported.8 Overall, the procedure is very successful, providing up to 100% symptom relief.7,8,10

Endoscopic release of trigger finger has also been described as an effective operative treatment. This technique involves passing a small cannula through a palmar incision—using an endoscope and retrograde knife within this 2.7-mm tunnel.10 With this treatment, reduced visibility may increase the risk of nerve injury.10 Although generally successful, endoscopic release requires anesthesia and expensive instruments and has a significant learning curve.8,10

More recently, percutaneous release of trigger finger has been described as a definitive, in-office treatment.5,6,11,12 Percutaneous release has the obvious advantages of no open incision, less scarring, less discomfort, and shorter recovery. Several studies have found comparable success rates for open and percutaneous procedures but consistently shorter recovery with the percutaneous technique.7,8,12 Given its lower recurrence rate (vs steroid injections) and shorter recovery and lower cost (vs a surgical procedure), percutaneous treatment of stenosing tenosynovitis appears to be a safe, highly successful, and minimally invasive treatment method.8 This study represents a single surgeon’s experience with percutaneous tendon sheath incision over a 10-year period.

Methods

Patients presented with symptoms of stenosing flexor tenosynovitis with severity ranging from intermittent triggering to frank locking of the digit. Most patients underwent prior conservative treatment, including corticosteroid injections and hand therapy. With each patient, the senior author discussed the pathophysiology of trigger digit; treatment options, including observation, hand therapy, corticosteroid injection, percutaneous release, and open release; and potential risks and complications. The treatment path—initial corticosteroid injection, percutaneous release, or open release—was left up to the patient. The only exclusion criterion was prior surgery to the involved digit, and there was no discrimination by finger, symptomatic period, or severity. Each released digit was recorded independently. In no case was anticoagulant therapy discontinued.
A complete medical history was obtained for each patient.

Over a 10-year period (March 2003-December 2013), percutaneous release was performed on 596 trigger fingers in 429 patients, 18 years old or older. Of these patients, 279 were female. Mean age was 62 years (range, 26-97 years). Of the 531 releases with handedness recorded, 56.3% were performed on trigger digits on dominant hands (Table 1). [[{"fid":"202302","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"2"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"2":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 1.","field_file_image_credit[und][0][value]":""}}}]]Mean duration of symptoms before percutaneous release was 9.7 months (range, 0.5-132 months). Of the 596 digits, 69 were reported to have previously sustained trauma, and 161 had been unsuccessfully treated with one or more cortisone injections before undergoing release. Of the suspected comorbidities examined, carpal tunnel syndrome was previously diagnosed in 79 patients and diabetes in 56 patients.1

Of the 429 patients, 313 had a single digit released and 116 had multiple digits released. Of the 116 patients in the multiple-release group, 80 had 2 fingers released, 24 had 3 released, 7 had 4 released, and 5 had 5 released. The 596 released trigger fingers consisted of 188 thumbs, 41 index fingers, 185 middle fingers, 140 ring fingers, and 42 small fingers.

Surgical Technique

In-office percutaneous trigger finger releases were performed with a local anesthetic. One milliliter of lidocaine 1% injection was used to anesthetize the skin, the subcutaneous tissues, and the flexor tendon sheath at the level of the A1 pulley. As described by Pandey and colleagues,6 the proper location of the pulley was confirmed using specific surface landmarks on each digit. After waiting several minutes to allow the anesthetic to take effect, the surgeon inserted an 18-gauge needle into the center of the pulley with the digit held in extension (Figure 2). [[{"fid":"202303","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"3"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"3":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":""}}}]]The needle was carefully moved longitudinally along the length of the pulley with the bevel of the needle parallel to the tendon. A grating sensation was felt as the fibers of the pulley were cut. Several needle passes were made until the pulley was felt to have been released. Complete release was determined by loss of the grating sensation, along with complete relief of any further symptoms of triggering. The puncture site was cleaned and covered with a light sterile dressing (watch the Video online). There was no postoperative immobilization, and patients were encouraged to immediately return to normal use of the digit. Hand therapy was not prescribed, and pain medications were not dispensed. A 1-week follow-up appointment was scheduled, and patients were advised to return for evaluation in the event of any recurring symptoms (eg, triggering, swelling, stiffness, pain).

Results

were successfully released with 1 percutaneous procedure (recurrence or failure rate, 9.9%). The thumb was the digit most reliably released (success rate, 94.7%) (Table 2). [[{"fid":"202306","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"4"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"4":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 2.","field_file_image_credit[und][0][value]":""}}}]]Patients with recurrent or unresolved symptoms were given the options of a second percutaneous release or an open surgical procedure. Of the 59 digits unsuccessfully released, as identified by persistent triggering or locking of the digit, 17 were treated with a second percutaneous release (15 were successful), and 40 underwent open tendon sheath incision as a second procedure (success rate, 100%); triggering persisted in the remaining 2 digits, and these were considered failures (the 2 patients did not pursue further treatment).

There were no complications: infection; nerve, artery, or tendon injury; or chronic pain. Some patients had mild stiffness, swelling, or pain for a few days after the procedure, and these effects typically resolved without treatment. In 29 digits, persistent pain or swelling without triggering was successfully treated with a corticosteroid injection.

Discussion

[[{"fid":"202307","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"5"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Table 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"5":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Table 3.","field_file_image_credit[und][0][value]":""}}}]]Over a 10-year period, 596 percutaneous trigger finger releases were sequentially performed by a single surgeon. The 90% success rate compares favorably with rates found in other studies (Table 3).5-9,12-14 The surgeon’s success rates for individual years vary and demonstrate no clear trend or learning curve with the procedure (Figure 3). There were no significant complications. Patient satisfaction with the procedure was high.[[{"fid":"202308","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"6"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"6":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":""}}}]]

There were no injuries to digital nerves, arteries, or flexor tendons, either early or late, and no reports of infections or long-term pain or loss of motion. Although it is quite probable that in some procedures the longitudinal passes of the 18-gauge needle may have also slightly cut into the flexor tendon after passing through the A1 pulley, the direction of the needle passes was in line with the direction of the collagen fibers of the tendon, and thus any inadvertent superficial abrasion would not have structurally weakened the tendon. Of the 40 digits that underwent open release after incomplete or failed percutaneous release, none showed significant longitudinal lacerations of the superficialis tendon. During these revision surgeries, the typical intraoperative finding was incomplete release of the A1 pulley, usually at the distal end. Although loss of the grating sensation or relief of further triggering symptoms was considered adequate evidence of a successful release in this study, small tendon attachments could remain and potentially could lead to recurrent triggering. Given the high success rate achieved with the large sample, however, these 2 factors are considered appropriate indicators of successful release.

It is unclear why there was a relatively consistent 10% failure rate and why it did not decrease over the 10-year study period. Although the technique used does not have a significant learning curve, it appears that digits are not actively triggering at time of procedure have a higher failure rate. When a patient’s digit is actively triggering, assessment of the success of the procedure is relatively straightforward, whereas when a digit intermittently triggers and locks and is not symptomatic in the office, success cannot be immediately determined.

No specific digit was significantly more prone to failed releases, though the small finger had the lowest success rate (85.7%). Given that only 56.4% of patients experienced triggering on the dominant hand, there is not enough evidence to suggest a significant relationship between likelihood of a trigger digit and a patient’s hand dominance. Similarly, there was no correlation between the duration of symptoms and the success of the percutaneous procedure.

Investigation of the relationship between the previously suggested comorbidities of carpal tunnel syndrome and diabetes was also inconclusive. Only 79 (18%) of 429 patients reported having carpal tunnel syndrome, and even fewer, 56 (13.0%), reported having diabetes. Only 69 of the 596 treated digits reportedly had sustained trauma before developing triggering symptoms, and only 12 of the 69 were unsuccessfully released. In addition, of the 161 digits in which one or more steroid injections failed to resolve triggering symptoms, 158 (87.3%) were successfully released with 1 percutaneous procedure. Collectively, these data show percutaneous release can effectively eliminate triggering symptoms in a digit that has sustained injury or that has been unsuccessfully treated with nonoperative methods. Failed percutaneous release subsequently can be reliably treated with an open procedure, and results are excellent.

This study had several limitations. It was retrospective, nonblinded, and did not compare outcomes of percutaneous release with those of an open procedure. Data are presented to support the efficacy and safety of percutaneous release as a treatment option. Another limitation is that pre-release treatment was not controlled. Patients had been treated with a variety of nonoperative methods, including use of anti-inflammatory medication, hand therapy, splinting, and one or more corticosteroid injections, both at our office and elsewhere.

Percutaneous release appears to have an advantage in terms of pain relief, but the study did not evaluate or control for procedure discomfort. However, patients who had been treated with a corticosteroid injection before percutaneous release consistently refused corticosteroid injections for subsequent trigger digits, citing the dramatic pain reduction achieved with release relative to injection. Similarly, all patients who had a trigger digit treated with open tendon sheath incision in the past indicated a strong preference for the percutaneous release.

Follow-up on this patient population was inconsistent and incomplete. Many patients did not return, presumably because they considered the procedure a success and thought follow-up was unnecessary. However, some patients may have had a recurrence or an incomplete release and gone elsewhere for treatment.

The results of this study, to date the largest study on percutaneous release of trigger finger, provide more evidence of the safety and efficacy of this procedure as a treatment option. The success rate of percutaneous release is high, surpasses that of nonoperative treatments such as steroid injections, and approaches that of open and endoscopic surgical alternatives. Some of the obvious advantages of percutaneous release are less visible scarring, fewer incision-related complications, and shorter rehabilitation.10 In addition, post-procedure pain is possibly reduced, symptom relief is comparable, operative time is significantly shorter,8 and percutaneous release is easily performed in the office setting.

Percutaneous release is a viable treatment option for stenosing flexor tenosynovitis, regardless of previously used nonoperative treatment methods, duration or severity of symptoms, or trigger digit treated.

Take-Home Points

  • The author had a 90% success rate with no complications in treating almost 600 trigger digits.
  • All digits can be safely treated, including multiple fingers on one hand, all in an office setting.
  • Percutaneous trigger release appears to be a safe and reliable alternative to open surgery.
  • Success rate, discomfort, and cost may make a percutaneous trigger release preferable to even a trial of corticosteroid injection.
  • A failed percutaneous release can be successfully treated with an open release, if needed.

Trigger finger, or stenosing flexor tenosynovitis, is a condition characterized by clicking or locking during finger movement, sometimes resulting in the freezing of a digit in flexion or extension1 (Figure 1). [[{"fid":"202300","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"1"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"1":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":""}}}]]Tendon inflammation is thought to cause constriction of the tendon sheath and bunching of the fibrous bundles of the first annular (A1) pulley, often creating a palpable nodule at the base of the digit.2,3 Many patients experience intermittent joint pain and swelling, which may progress to triggering or complete locking of the digit.1 One of the most common conditions treated by hand surgeons, trigger finger is most often reported in the dominant hand of women in their sixth decade of life and has been associated with several conditions, including diabetes and rheumatoid arthritis.4-6 Other researchers have indicated the thumb and ring finger are most commonly affected, though all fingers can potentially trigger.7,8

Initial treatment often involves injecting corticosteroid into the flexor tendon sheath, at or proximal to the annular pulley system, to reduce inflammation and the fibrous nodule.3 Another injection study found an initial success rate of 57% with a single injection, and 86% with a second injection, but patients were monitored for only 6 months, a period that may have been too short for symptom recurrence.7

On failure of steroid injections, patients typically are treated with open tendon sheath incision.9 This procedure, usually performed in a hospital or outpatient surgery setting, requires postoperative wound care, including dressing changes, suture removal, possible hand therapy, and follow-up physician visits. Operative treatment involves making a 1-cm to 2-cm incision, releasing the A1 pulley, and skin suturing.7,8,10 The most common postoperative complaint is incisional tenderness, though long-term scar pain, infection, nerve injury, and disease recurrence have been reported.8 Overall, the procedure is very successful, providing up to 100% symptom relief.7,8,10

Endoscopic release of trigger finger has also been described as an effective operative treatment. This technique involves passing a small cannula through a palmar incision—using an endoscope and retrograde knife within this 2.7-mm tunnel.10 With this treatment, reduced visibility may increase the risk of nerve injury.10 Although generally successful, endoscopic release requires anesthesia and expensive instruments and has a significant learning curve.8,10

More recently, percutaneous release of trigger finger has been described as a definitive, in-office treatment.5,6,11,12 Percutaneous release has the obvious advantages of no open incision, less scarring, less discomfort, and shorter recovery. Several studies have found comparable success rates for open and percutaneous procedures but consistently shorter recovery with the percutaneous technique.7,8,12 Given its lower recurrence rate (vs steroid injections) and shorter recovery and lower cost (vs a surgical procedure), percutaneous treatment of stenosing tenosynovitis appears to be a safe, highly successful, and minimally invasive treatment method.8 This study represents a single surgeon’s experience with percutaneous tendon sheath incision over a 10-year period.

Methods

Patients presented with symptoms of stenosing flexor tenosynovitis with severity ranging from intermittent triggering to frank locking of the digit. Most patients underwent prior conservative treatment, including corticosteroid injections and hand therapy. With each patient, the senior author discussed the pathophysiology of trigger digit; treatment options, including observation, hand therapy, corticosteroid injection, percutaneous release, and open release; and potential risks and complications. The treatment path—initial corticosteroid injection, percutaneous release, or open release—was left up to the patient. The only exclusion criterion was prior surgery to the involved digit, and there was no discrimination by finger, symptomatic period, or severity. Each released digit was recorded independently. In no case was anticoagulant therapy discontinued.
A complete medical history was obtained for each patient.

Over a 10-year period (March 2003-December 2013), percutaneous release was performed on 596 trigger fingers in 429 patients, 18 years old or older. Of these patients, 279 were female. Mean age was 62 years (range, 26-97 years). Of the 531 releases with handedness recorded, 56.3% were performed on trigger digits on dominant hands (Table 1). [[{"fid":"202302","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"2"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"2":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 1.","field_file_image_credit[und][0][value]":""}}}]]Mean duration of symptoms before percutaneous release was 9.7 months (range, 0.5-132 months). Of the 596 digits, 69 were reported to have previously sustained trauma, and 161 had been unsuccessfully treated with one or more cortisone injections before undergoing release. Of the suspected comorbidities examined, carpal tunnel syndrome was previously diagnosed in 79 patients and diabetes in 56 patients.1

Of the 429 patients, 313 had a single digit released and 116 had multiple digits released. Of the 116 patients in the multiple-release group, 80 had 2 fingers released, 24 had 3 released, 7 had 4 released, and 5 had 5 released. The 596 released trigger fingers consisted of 188 thumbs, 41 index fingers, 185 middle fingers, 140 ring fingers, and 42 small fingers.

Surgical Technique

In-office percutaneous trigger finger releases were performed with a local anesthetic. One milliliter of lidocaine 1% injection was used to anesthetize the skin, the subcutaneous tissues, and the flexor tendon sheath at the level of the A1 pulley. As described by Pandey and colleagues,6 the proper location of the pulley was confirmed using specific surface landmarks on each digit. After waiting several minutes to allow the anesthetic to take effect, the surgeon inserted an 18-gauge needle into the center of the pulley with the digit held in extension (Figure 2). [[{"fid":"202303","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"3"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"3":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":""}}}]]The needle was carefully moved longitudinally along the length of the pulley with the bevel of the needle parallel to the tendon. A grating sensation was felt as the fibers of the pulley were cut. Several needle passes were made until the pulley was felt to have been released. Complete release was determined by loss of the grating sensation, along with complete relief of any further symptoms of triggering. The puncture site was cleaned and covered with a light sterile dressing (watch the Video online). There was no postoperative immobilization, and patients were encouraged to immediately return to normal use of the digit. Hand therapy was not prescribed, and pain medications were not dispensed. A 1-week follow-up appointment was scheduled, and patients were advised to return for evaluation in the event of any recurring symptoms (eg, triggering, swelling, stiffness, pain).

Results

were successfully released with 1 percutaneous procedure (recurrence or failure rate, 9.9%). The thumb was the digit most reliably released (success rate, 94.7%) (Table 2). [[{"fid":"202306","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"4"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"4":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table 2.","field_file_image_credit[und][0][value]":""}}}]]Patients with recurrent or unresolved symptoms were given the options of a second percutaneous release or an open surgical procedure. Of the 59 digits unsuccessfully released, as identified by persistent triggering or locking of the digit, 17 were treated with a second percutaneous release (15 were successful), and 40 underwent open tendon sheath incision as a second procedure (success rate, 100%); triggering persisted in the remaining 2 digits, and these were considered failures (the 2 patients did not pursue further treatment).

There were no complications: infection; nerve, artery, or tendon injury; or chronic pain. Some patients had mild stiffness, swelling, or pain for a few days after the procedure, and these effects typically resolved without treatment. In 29 digits, persistent pain or swelling without triggering was successfully treated with a corticosteroid injection.

Discussion

[[{"fid":"202307","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"5"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Table 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"5":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Table 3.","field_file_image_credit[und][0][value]":""}}}]]Over a 10-year period, 596 percutaneous trigger finger releases were sequentially performed by a single surgeon. The 90% success rate compares favorably with rates found in other studies (Table 3).5-9,12-14 The surgeon’s success rates for individual years vary and demonstrate no clear trend or learning curve with the procedure (Figure 3). There were no significant complications. Patient satisfaction with the procedure was high.[[{"fid":"202308","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"6"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"6":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":""}}}]]

There were no injuries to digital nerves, arteries, or flexor tendons, either early or late, and no reports of infections or long-term pain or loss of motion. Although it is quite probable that in some procedures the longitudinal passes of the 18-gauge needle may have also slightly cut into the flexor tendon after passing through the A1 pulley, the direction of the needle passes was in line with the direction of the collagen fibers of the tendon, and thus any inadvertent superficial abrasion would not have structurally weakened the tendon. Of the 40 digits that underwent open release after incomplete or failed percutaneous release, none showed significant longitudinal lacerations of the superficialis tendon. During these revision surgeries, the typical intraoperative finding was incomplete release of the A1 pulley, usually at the distal end. Although loss of the grating sensation or relief of further triggering symptoms was considered adequate evidence of a successful release in this study, small tendon attachments could remain and potentially could lead to recurrent triggering. Given the high success rate achieved with the large sample, however, these 2 factors are considered appropriate indicators of successful release.

It is unclear why there was a relatively consistent 10% failure rate and why it did not decrease over the 10-year study period. Although the technique used does not have a significant learning curve, it appears that digits are not actively triggering at time of procedure have a higher failure rate. When a patient’s digit is actively triggering, assessment of the success of the procedure is relatively straightforward, whereas when a digit intermittently triggers and locks and is not symptomatic in the office, success cannot be immediately determined.

No specific digit was significantly more prone to failed releases, though the small finger had the lowest success rate (85.7%). Given that only 56.4% of patients experienced triggering on the dominant hand, there is not enough evidence to suggest a significant relationship between likelihood of a trigger digit and a patient’s hand dominance. Similarly, there was no correlation between the duration of symptoms and the success of the percutaneous procedure.

Investigation of the relationship between the previously suggested comorbidities of carpal tunnel syndrome and diabetes was also inconclusive. Only 79 (18%) of 429 patients reported having carpal tunnel syndrome, and even fewer, 56 (13.0%), reported having diabetes. Only 69 of the 596 treated digits reportedly had sustained trauma before developing triggering symptoms, and only 12 of the 69 were unsuccessfully released. In addition, of the 161 digits in which one or more steroid injections failed to resolve triggering symptoms, 158 (87.3%) were successfully released with 1 percutaneous procedure. Collectively, these data show percutaneous release can effectively eliminate triggering symptoms in a digit that has sustained injury or that has been unsuccessfully treated with nonoperative methods. Failed percutaneous release subsequently can be reliably treated with an open procedure, and results are excellent.

This study had several limitations. It was retrospective, nonblinded, and did not compare outcomes of percutaneous release with those of an open procedure. Data are presented to support the efficacy and safety of percutaneous release as a treatment option. Another limitation is that pre-release treatment was not controlled. Patients had been treated with a variety of nonoperative methods, including use of anti-inflammatory medication, hand therapy, splinting, and one or more corticosteroid injections, both at our office and elsewhere.

Percutaneous release appears to have an advantage in terms of pain relief, but the study did not evaluate or control for procedure discomfort. However, patients who had been treated with a corticosteroid injection before percutaneous release consistently refused corticosteroid injections for subsequent trigger digits, citing the dramatic pain reduction achieved with release relative to injection. Similarly, all patients who had a trigger digit treated with open tendon sheath incision in the past indicated a strong preference for the percutaneous release.

Follow-up on this patient population was inconsistent and incomplete. Many patients did not return, presumably because they considered the procedure a success and thought follow-up was unnecessary. However, some patients may have had a recurrence or an incomplete release and gone elsewhere for treatment.

The results of this study, to date the largest study on percutaneous release of trigger finger, provide more evidence of the safety and efficacy of this procedure as a treatment option. The success rate of percutaneous release is high, surpasses that of nonoperative treatments such as steroid injections, and approaches that of open and endoscopic surgical alternatives. Some of the obvious advantages of percutaneous release are less visible scarring, fewer incision-related complications, and shorter rehabilitation.10 In addition, post-procedure pain is possibly reduced, symptom relief is comparable, operative time is significantly shorter,8 and percutaneous release is easily performed in the office setting.

Percutaneous release is a viable treatment option for stenosing flexor tenosynovitis, regardless of previously used nonoperative treatment methods, duration or severity of symptoms, or trigger digit treated.

References

1. Makkouk AH, Oetgen ME, Swigart CR, Dodds SD. Trigger finger: etiology, evaluation, and treatment. Curr Rev Musculoskelet Med. 2008;1(2):92-96.

2. Fahey JJ, Bollinger JA. Trigger-finger in adults and children. J Bone Joint Surg Am. 1954;36(6):1200-1218.

3. Marks MR, Gunther SF. Efficacy of cortisone injection in treatment of trigger fingers and thumbs. J Hand Surg Am. 1989;14(4):722-727.

4. Chammas M, Bousquet P, Renard E, Poirier JL, Jaffiol C, Allieu Y. Dupuytren’s disease, carpal tunnel syndrome, trigger finger, and diabetes mellitus. J Hand Surg Am. 1995;20(1):109-114.

5. Habbu R, Putman MD, Adams JE. Percutaneous release of the A1 pulley: a cadaver study. J Hand Surg Am. 2012;37(11):2273-2277.

6. Pandey BK, Sharma S, Manandhar RR, Pradhan RL, Lakhey S, Rijal KP. Percutaneous trigger finger release. Nepal Orthop Assoc J. 2010;1(1):1-5.

7. Sato ES, Gomes dos Santos JB, Belloti JC, Albertoni WM, Faloppa F. Treatment of trigger finger: randomized clinical trial comparing the methods of corticosteroid injection, percutaneous release and open surgery. Rheumatology. 2012;51(1):93-99.

8. Dierks U, Hoffmann R, Meek MF. Open versus percutaneous release of the A1-pulley for stenosing tendovaginitis: a prospective randomized trial. Tech Hand Up Extrem Surg. 2008;12(3):183-187.

9. Tanaka J. Percutaneous trigger finger release. Tech Hand Up Extrem Surg. 1999;3(1):52-57.

10. Pegoli L, Cavalli E, Cortese P, Parolo C, Pajardi G. A comparison of endoscopic and open trigger finger release. Hand Surg. 2008;13(3):147-151.

11. Ryzewicz M, Wolf JM. Trigger digits: principles, management, and complications. J Hand Surg Am. 2006;31(1):135-146.

12. Schramm JM, Nguyen M, Wongworawat MD. The safety of percutaneous trigger finger release. Hand. 2008;3(1):44-46.

13. Paulius KL, Maguina P. Ultrasound-assisted percutaneous trigger finger release: is it safe? Hand. 2009;4(1):35-37.

14. Cihantimur B, Akin S, Ozcan M. Percutaneous treatment of trigger finger. 34 fingers followed 0.5-2 years. Acta Orthop Scand. 1998;69(2):167-168.

References

1. Makkouk AH, Oetgen ME, Swigart CR, Dodds SD. Trigger finger: etiology, evaluation, and treatment. Curr Rev Musculoskelet Med. 2008;1(2):92-96.

2. Fahey JJ, Bollinger JA. Trigger-finger in adults and children. J Bone Joint Surg Am. 1954;36(6):1200-1218.

3. Marks MR, Gunther SF. Efficacy of cortisone injection in treatment of trigger fingers and thumbs. J Hand Surg Am. 1989;14(4):722-727.

4. Chammas M, Bousquet P, Renard E, Poirier JL, Jaffiol C, Allieu Y. Dupuytren’s disease, carpal tunnel syndrome, trigger finger, and diabetes mellitus. J Hand Surg Am. 1995;20(1):109-114.

5. Habbu R, Putman MD, Adams JE. Percutaneous release of the A1 pulley: a cadaver study. J Hand Surg Am. 2012;37(11):2273-2277.

6. Pandey BK, Sharma S, Manandhar RR, Pradhan RL, Lakhey S, Rijal KP. Percutaneous trigger finger release. Nepal Orthop Assoc J. 2010;1(1):1-5.

7. Sato ES, Gomes dos Santos JB, Belloti JC, Albertoni WM, Faloppa F. Treatment of trigger finger: randomized clinical trial comparing the methods of corticosteroid injection, percutaneous release and open surgery. Rheumatology. 2012;51(1):93-99.

8. Dierks U, Hoffmann R, Meek MF. Open versus percutaneous release of the A1-pulley for stenosing tendovaginitis: a prospective randomized trial. Tech Hand Up Extrem Surg. 2008;12(3):183-187.

9. Tanaka J. Percutaneous trigger finger release. Tech Hand Up Extrem Surg. 1999;3(1):52-57.

10. Pegoli L, Cavalli E, Cortese P, Parolo C, Pajardi G. A comparison of endoscopic and open trigger finger release. Hand Surg. 2008;13(3):147-151.

11. Ryzewicz M, Wolf JM. Trigger digits: principles, management, and complications. J Hand Surg Am. 2006;31(1):135-146.

12. Schramm JM, Nguyen M, Wongworawat MD. The safety of percutaneous trigger finger release. Hand. 2008;3(1):44-46.

13. Paulius KL, Maguina P. Ultrasound-assisted percutaneous trigger finger release: is it safe? Hand. 2009;4(1):35-37.

14. Cihantimur B, Akin S, Ozcan M. Percutaneous treatment of trigger finger. 34 fingers followed 0.5-2 years. Acta Orthop Scand. 1998;69(2):167-168.

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Postpartum Treatment of Metastatic Recurrent Giant Cell Tumor of Capitate Bone of Wrist

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Take-Home Points

  • GCT of bones of the wrist is rare. This article is the only report of a wrist GCT during pregnancy that we could identify.
  • Routine treatment usually consists of surgical excision with local adjuvant, and in the wrist, often results in reduced wrist motion.
  • GCT of the wrist is more aggressive than the more common locations in long bones, with higher local recurrence rates if treated with surgery alone.
  • Diagnosis is often delayed for GCT of the wrist, due to insufficient imaging, which should include CT or MRI.
  • For pregnant women with GCT, local adjuvant treatments can be used in addition to surgery. Following pregnancy, denosumab can be used systemically, and can be effective with metastatic or unresectable disease.

Giant cell tumor (GCT) of bone accounts for about 5% of primary bone tumors.1-3 Only 3% to 5% of GCTs occur in the hand.4,5 Wrist involvement, which is rare, most often involves the hamate bone.5-7 Capitate bone involvement is exceedingly rare.8-11 Although histologically benign, GCT can recur locally after treatment with curettage alone, and lung metastases are found in 2% to 5% of cases.2,12-14 Therefore, en bloc tumor excision is preferred in the setting of cortical erosion or soft-tissue involvement.1,4,8 Wrist joint motion is inevitably reduced, and bone graft donor-site morbidity is significant.6-8

In the unusual case reported here, GCT presented in the capitate bone and, after the patient became pregnant, recurred in the hamate and trapezoid bones with soft-tissue extension and lung metastases. The capitate was excised en bloc and reconstructed with an interposition of polymethylmethacrylate bone cement. Pulmonary metastases developed, and the GCT expanded to involve multiple carpal bones and the bases of the second through fourth metacarpals. A 10-month course of systemic chemotherapy with the RANK ligand (RANKL) inhibitor denosumab was started after the pregnancy. After this treatment, the patient underwent both tumor resection and reconstruction with autogenous bicortical iliac crest bone graft (ICBG) carefully designed to preserve range of motion and maintain the fingers in anatomical position. Treatment with denosumab was continued after surgery. Although this case offers no endpoint for postoperative chemotherapy with denosumab, preoperative treatment dramatically reduced the GCT and permitted limb-sparing reconstruction. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 19-year-old right-handed woman with atraumatic swelling of the left wrist presented to an orthopedic surgeon at an outside facility. Physical examination revealed tender fullness on the dorsum of the wrist, slightly reduced range of motion and grip strength, and a neurovascularly intact wrist. The diagnosis was periarticular cyst, and the patient underwent physical therapy. Two years later, the swelling returned, tenderness was increasing, and symptoms did not resolve with cast immobilization. A radiograph showed a lytic lesion in the capitate bone (Figure 1).[[{"fid":"202332","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"1"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"1":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":""}}}]]

GCT was diagnosed with percutaneous needle biopsy. A preoperative chest radiograph was reported normal. For initial treatment, the capitate and trapezoid bones were resected en bloc through a dorsal approach. Reconstruction consisted of limited arthrodesis using bone cement without additional fixation.

At 6-month follow-up, the patient was pregnant, and there was a recurrence of the wrist lesion. During the first 2 months of pregnancy, swelling and pain rapidly progressed, and a palpable mass formed. Radiographs showed a lytic lesion extending into the hamate bone (Figure 2), and magnetic resonance imaging (MRI) showed articular extension of the lesion with involvement of the base of the fourth metacarpal. [[{"fid":"202334","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"2"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"2":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":""}}}]]Targeted anti-RANKL therapy was not recommended (and was not available at the patient’s home hospital). The patient deferred surgical treatment because of the pregnancy, which proved otherwise uneventful and ended with a full-term delivery.

After the pregnancy, radiographs of the wrist showed complete destruction of the hamate and trapezium bones, with erosion of the bases of the second through fourth metacarpals (Figure 3A). [[{"fid":"202335","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"3"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"3":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":""}}}]]The patient presented at our institution 4 years after initial diagnosis. Computed tomography (CT) of the chest showed numerous bilateral pulmonary nodular opacities. Wrist imaging showed soft-tissue extension (Figure 3B). The diagnosis of recurrent metastatic GCT was confirmed with needle biopsies of the wrist mass and the right lung nodule.

Systemic chemotherapy was initiated with 120 mg of denosumab, given subcutaneously on days 1, 8, and 15 and then monthly during the 10 months leading up to surgery. Serum calcium was monitored during treatment and remained within the normal range the entire time, except for once at the start of therapy, when it dropped to 6.8 mg/dL. After 8 months, the soft-tissue mass, originally 8 cm × 8 cm × 6 cm, shrunk and stabilized at 5 cm × 4 cm × 4 cm (Figure 3B), and a bony shell reformed around it. Nodules in both lung fields showed response to denosumab.

Histologic examination revealed scattered osteoclast-like, multinucleated giant cells, consistent with a recurrent lesion (Figure 4). [[{"fid":"202336","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"4"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 4.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"4":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 4.","field_file_image_credit[und][0][value]":""}}}]]After 10 months of treatment with denosumab, the patient underwent resection (dorsal approach) of the residual cement, the soft-tissue mass, the affected carpal bones, half of the third metacarpal, and the second and fourth metacarpal bases. The proximal carpal row was preserved after no intra-articular involvement was verified. The closet margin was marginal; the tumor mass abutted without encompassing the flexor tendons and median nerve. The tumor was meticulously elevated from the neurovascular and tendinous structures, which were not sacrificed. Hydrogen peroxide was used for local adjuvant treatment. Bicortical autogenous ICBG was placed between the remaining scaphoid, lunate, and metacarpal bones. The second, third, and fourth metacarpal bases were stabilized on the overlapping outer table of ICBG with 2.0-mm plates and miniscrews (Figure 5A). Kirschner wires were used to stabilize the proximal bone graft and the scapholunate fossa. Cancellous bone graft was packed between the structural bone graft and neighboring unaffected carpal bones (Figure 5A). Immobilization with a short-arm thumb spica cast was maintained for 6 weeks after surgery and was followed by a 12-week rehabilitation program. The patient returned to normal activities when plain radiographs showed solid bony union (Figure 5B). Fourteen months after initial surgery, tenolysis was performed to free the extensor tendons (index, middle, and ring fingers on dorsum of left hand) from adhesions to the bone graft. At 37-month follow-up (Figure 5C), there was no clinical or radiographic evidence of progression in the wrist.[[{"fid":"202337","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"5"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 5.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"5":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 5.","field_file_image_credit[und][0][value]":""}}}]]

The patient had bilateral pulmonary metastases (Figures 6A, 6B). Treatment with denosumab produced an initial response (smaller pulmonary lesions) and subsequent stability. After 12 months of treatment with denosumab, the patient underwent left thoracotomy and wedge resection of pulmonary metastases on the left. Pathologic evaluation revealed pulmonary parenchyma with calcification and ossification and limited viable tumor. Given the dramatic effects on the left pulmonary metastases, denosumab was continued, and surgical intervention on the right was not attempted. Pulmonary metastases were stable afterward (Figure 6C).[[{"fid":"202338","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"6"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 6.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"6":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 6.","field_file_image_credit[und][0][value]":""}}}]]

At 54-month follow-up, systemic treatment with denosumab was continued. The patient had no pain in the wrist or hand and was able to use the left hand normally. There was some fissuring of the third and fourth digits over each other. However, the patient had good grip strength and was using eating utensils, picking up water bottles, and engaging in other activities without difficulty.

Discussion

GCT isolated to the carpus is rare. However, compared with GCT in the more common locations in long bones, it is also more aggressive, and its local recurrence rates are higher, probably 60% or more if treated with curettage alone.15 Therefore, excision augmented with adjuvant treatment is recommended.2,7 Use of bone cement in the hand is relatively uncommon.4,5,7-10

The diagnosis of GCT in the carpus is difficult and often delayed. The initial complaint is usually mild wrist pain after relatively mild trauma.5 The first reported case of GCT in the lunate bone was mistakenly thought to be Kienbock disease.5 Similarly, our patient was initially given a nononcologic diagnosis, which prompted conservative management.

Whether the biological behavior of GCT in the carpus differs from that of GCT in other sites is unclear. The high recurrence rates might be attributable in part to suboptimal curettage.5,6 En bloc resections of involved bone inevitably result in carpal instability or loss of wrist motion if arthrodesis is performed.4-7,11 In the present case, resection was followed by limited arthrodesis to mitigate motion losses.

Multifocal GCT in the carpal bones often affects younger patients and has a high rate of recurrence.7,16 In the present case, the patient’s pregnancy delayed treatment and allowed tumor extension into soft tissues and metacarpal bones. Given her young age, en bloc tumor resection was performed, with the proximal carpal row spared to preserve wrist motion. ICBG was carefully shaped to match the defect that remained after tumor resection.7 Supporting wrist height to prevent carpal collapse provided a stable base for remaining distal segments of the second through fourth metacarpals. After short-arm thumb spica casting and early rehabilitation, the patient recovered wrist motion and use of the involved fingers distal to the carpometacarpal joints.

In pregnant women, GCTs have been found primarily in the long bones and spine but are rare.17-21 A review of the literature (1950-present) revealed that the present article is the first report of GCT in the hand or wrist bones of a pregnant woman.18,20,21 There is no consensus as to whether surgical excision should be performed during pregnancy.18,20,21 In 1 unusual case, at 18 weeks’ gestation GCT in the distal femur was resected with curettage and bone grafting, and there were no complications.21 Therefore, pregnancy termination is not indicated for GCT.

The relationship between tumorigenesis and pregnancy is unclear.18,20,21 Empirically, pregnancy is thought to promote tumor growth.18,20 Estrogen and progesterone levels are elevated during pregnancy, potentially influencing tumor cells that are hormonally sensitive.18,20 An early report in which reverse transcription–polymerase chain reaction showed estrogen receptor expression in GCT osteoclast-like cells was followed by several studies that failed to find estrogen receptors at the protein level.19 In contrast, progesterone receptors were found in 50% of GCTs in a study.22 However, the etiopathogenic significance of this is unclear. In pregnant women, vascular endothelial growth factor, placental growth factor, and other growth factors induce osteoclast formation.23 ß-Human chorionic gonadotropin expression (ß-hCG) has been found in 58% of cases, with some showing ß-hCG elevation in the serum.24 Other studies have focused on an immunologic explanation for occurrence of GCT during pregnancy.18 Oncofetal antigens, which are similar to fetal antigens, have been found in fibrosarcoma and in an osteosarcoma cell line but not in GCT.18-20 Thus, though occurrence during pregnancy may be coincidental given the frequency of GCT in women of childbearing age, it is plausible that tumor growth may be enhanced by pregnancy. More studies are needed to understand the relationship between giant cell proliferation and pregnancy-related growth factors and hormones.

With GCT, the rate of pulmonary metastases ranges from 0% to 4%; these metastases are usually diagnosed at time of local recurrence, or 2 years to 3 years after initial GCT diagnosis.2,3,12,14,25 Lung metastases secondary to GCT in the hand or foot bones are rare; our literature review identified only 4 cases.12,14 Risk factors for lung metastasis include local recurrence, aggressive appearance (Enneking grade 3) on radiograph, Ki-67 antigen expression, and distal radius location.14 The mechanism of metastasis is unknown.12,14

Lung metastases are usually excised, but they may spontaneously evolve toward necrosis and ossification.12 In cases in which surgery is unfeasible, chemotherapy (eg, with doxorubicin) has been used to control progression.12,14 Radiation can cause sarcomatous transformation and is contraindicated. Interferon26-28 and other antiangiogenic strategies have been successfully used in systemic therapy for GCT of bone. More recently, bisphosphonates29-32 and denosumab33 have been investigated.29,32-36 The limited toxicity of denosumab makes the drug a very attractive treatment option for recurrent or unresectable GCT of bone.33 Reported rates of mortality from lung metastases have ranged from 0% to 40%.14 There is evidence that control of lung metastases during the first 3 years after diagnosis is important for favorable outcomes.2,3

Malignant stromal cells of GCT of bone have been known to secrete RANKL, which recruits osteoclasts and osteoclast precursor cells, which in turn generate aggressive osteolytic activity.33,37 Denosumab, a monoclonal antibody that inhibits RANKL, is effective in stopping osteoclastic activity. In a phase 2 trial of denosumab in the treatment of GCT of bone, 96% of treated patients with unresectable disease showed no progression at 13 months.38 In addition, 74% of treated patients who had resectable disease but were likely to have morbid surgery did not require surgery, and 62% of treated patients who underwent surgery were able to have a less morbid procedure. Forty-one percent to 58% of treated patients had a reduction in tumor size.

Denosumab is very well tolerated. The phase 2 trial found serious adverse events in 9% of patients, and in 5% of cases the drug was discontinued because of toxicity.38 Serious adverse events include osteonecrosis of jaw, hypocalcemia, and hypophosphatemia.37 Electrolyte changes with denosumab are easy to monitor and manage. Although the favorable toxicity profile of denosumab allows for long-term therapy, the data on therapy duration in patients with unresectable disease are unclear. Patients who discontinue therapy should be closely monitored, as disease can progress in this setting.37

In contrast to GCT of larger bones, GCT of the wrist is rare and typically more aggressive, and has higher local recurrence rates. In many cases, diagnosis is delayed by insufficient imaging, which optimally should include either CT or MRI (Table). [[{"fid":"202341","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"7"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"7":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table.","field_file_image_credit[und][0][value]":""}}}]]For pregnant women with GCT, options include surgical resection with curettage and local adjuvant treatment. After pregnancy, denosumab can be used systemically, and can be effective with metastatic or unresectable disease. Surgical treatment in the wrist can be challenging when partial or complete resections of carpal bones are required. Occupational therapy is recommended for optimization of hand function after surgery.

References

1. Balke M, Ahrens H, Streitbuerger A, et al. Treatment options for recurrent giant cell tumors of bone. J Cancer Res Clin Oncol. 2009;135(1):149-158.

2. Klenke FM, Wenger DE, Inwards CY, Rose PS, Sim FH. Giant cell tumor of bone risk factors for recurrence. Clin Orthop Relat Res. 2011;469(2):591-599.

3. Klenke FM, Wenger DE, Inwards CY, Rose PS, Sim FH. Recurrent giant cell tumor of long bones: analysis of surgical management. Clin Orthop Relat Res. 2011;469(4):1181-1187.

4. Averill RM, Smith RJ, Campbell CJ. Giant-cell tumors of the bones of the hand. J Hand Surg Am. 1980;5(1):39-50.

5. Shigematsu K, Kobata Y, Yajima H, Kawamura K, Maegawa N, Takakura Y. Giant-cell tumors of the carpus. J Hand Surg Am. 2006;31(7):1214-1219.

6. Gupta GG, Lucas GL, Pirela-Cruz M. Multifocal giant cell tumor of the capitate, hamate, and triquetrum: a case report. J Hand Surg Am. 1995;20(6):1003-1006.

7. Tarng YW, Yang SW, Hsu CJ. Surgical treatment of multifocal giant cell tumor of carpal bones with preservation of wrist function: case report. J Hand Surg Am. 2009;34(2):262-265.

8. Angelini A, Mavrogenis AF, Ruggieri P. Giant cell tumor of the capitate. Musculoskelet Surg. 2011;95(1):45-48.

9. Howard FM, Lassen K. Giant cell tumor of the capitate. J Hand Surg Am. 1984;9(2):272-274.

10. McDonald DJ, Schajowicz F. Giant cell tumor of the capitate. A case report. Clin Orthop Relat Res. 1992(279):264-268.

11. Wilson SC, Cascio BM, Plauche HR. Giant-cell tumor of the capitate. Orthopedics. 2001;24(11):1085-1086.

12. Combalia-Aleu A, Sastre S, Fernández-de-Retana P, Tomás X, Palacin A. Giant cell tumor of the talus with pulmonary metastasis: seven years follow up. Foot. 2006;16(2):107-111.

13. Donthineni R, Boriani L, Ofluoglu O, Bandiera S. Metastatic behaviour of giant cell tumour of the spine. Int Orthop. 2009;33(2):497-501.

14. Jacopin S, Viehweger E, Glard Y, et al. Fatal lung metastasis secondary to index finger giant cell tumor in an 8-year-old child. Orthop Traumatol Surg Res. 2010;96(3):310-313.

15. Plate AM, Lee SJ, Steiner G, Posner MA. Tumor-like lesions and benign tumors of the hand and wrist. J Am Acad Orthop Surg. 2003;11(2):129-141.

16. Moreel P, Le Viet D. Failure of initial surgical treatment of a giant cell tumor of the capitate and its salvage: a case report [in French]. Chir Main. 2006;25(6):315-318.

17. Caillouette JC, Mattar N. Massive peripheral giant-cell reparative granuloma of the jaw: a pregnancy dependent tumor. Trans Pac Coast Obstet Gynecol Soc. 1978;45:78-81.

18. Kathiresan AS, Johnson JN, Hood BJ, Montoya SP, Vanni S, Gonzalez-Quintero VH. Giant cell bone tumor of the thoracic spine presenting in late pregnancy. Obstet Gynecol. 2011;118(2 pt 2):428-431.

19. Komiya S, Zenmyo M, Inoue A. Bone tumors in the pelvis presenting growth during pregnancy. Arch Orthop Trauma Surg. 1999;119(1-2):22-29.

20. Ross AE, Bojescul JA, Kuklo TR. Giant cell tumor: a case report of recurrence during pregnancy. Spine. 2005;30(12):E332-3E35.

21. Sharma JB, Chanana C, Rastogi, et al. Successful pregnancy outcome with elective caesarean section following two attempts of surgical excision of large giant cell tumor of the lower limb during pregnancy. Arch Gynecol Obstet. 2006;274(5):313-315.

22. Demertzis N, Kotsiandri F, Giotis I, Apostolikas N. Giant-cell tumors of bone and progesterone receptors. Orthopedics. 2003;26(12):1209-1212.

23. Taylor RM, Kashima TG, Knowles HJ, Athanasou NA. VEGF, FLT3 ligand, PlGF and HGF can substitute for M-CSF to induce human osteoclast formation: implications for giant cell tumour pathobiology. Lab Invest. 2012;92(10):1398-1406.

24. Lawless ME, Jour G, Hoch BL, Rendi MH. Beta-human chorionic gonadotropin expression in recurrent and metastatic giant cell tumors of bone: a potential mimicker of germ cell tumor. Int J Surg Pathol. 2014;22(7):617-622.

25. Viswanathan S, Jambhekar NA. Metastatic giant cell tumor of bone: are there associated factors and best treatment modalities? Clin Orthop Relat Res. 2010;468(3):827-833.

26. Kaban LB, Troulis MJ, Ebb D, August M, Hornicek FJ, Dodson TB. Antiangiogenic therapy with interferon alpha for giant cell lesions of the jaws. J Oral Maxillofac Surg. 2002;60(10):1103-1111.

27. Kaiser U, Neumann K, Havemann K. Generalised giant-cell tumour of bone: successful treatment of pulmonary metastases with interferon alpha, a case report. J Cancer Res Clin Oncol. 1993;119(5):301-303.

28. Dickerman JD. Interferon and giant cell tumors. Pediatrics. 1999;103(6 pt 1):1282-1283.

29. Balke M, Campanacci L, Gebert C, et al. Bisphosphonate treatment of aggressive primary, recurrent and metastatic giant cell tumour of bone. BMC Cancer. 2010;10:462.

30. Gille O, Oliveira Bde A, Guerin P, Lepreux S, Richez C, Vital JM. Regression of giant cell tumor of the cervical spine with bisphosphonate as single therapy. Spine. 2012;37(6):E396-E399.

31. Moriceau G, Ory B, Gobin B, et al. Therapeutic approach of primary bone tumours by bisphosphonates. Curr Pharm Des. 2010;16(27):2981-2987.

32. Tse LF, Wong KC, Kumta SM, Huang L, Chow TC, Griffith JF. Bisphosphonates reduce local recurrence in extremity giant cell tumor of bone: a case–control study. Bone. 2008;42(1):68-73.

33. Thomas D, Henshaw R, Skubitz K, et al. Denosumab in patients with giant-cell tumour of bone: an open-label, phase 2 study. Lancet Oncol. 2010;11(3):275-280.

34. Balke M, Hardes J. Denosumab: a breakthrough in treatment of giant-cell tumour of bone? Lancet Oncol. 2010;11(3):218-219.

35. Kyrgidis A, Toulis K. Safety and efficacy of denosumab in giant-cell tumour of bone. Lancet Oncol. 2010;11(6):513-514.

36. Thomas D, Carriere P, Jacobs I. Safety of denosumab in giant-cell tumour of bone. Lancet Oncol. 2010;11(9):815.

37. Skubitz KM. Giant cell tumor of bone: current treatment options. Curr Treat Options Oncol. 2014;15(3):507-518.

38. Chawla S, Henshaw R, Seeger L, et al. Safety and efficacy of denosumab for adults and skeletally mature adolescents with giant cell tumour of bone: interim analysis of an open-label, parallel-group, phase 2 study. Lancet Oncol. 2013;14(9):901-908.

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Take-Home Points

  • GCT of bones of the wrist is rare. This article is the only report of a wrist GCT during pregnancy that we could identify.
  • Routine treatment usually consists of surgical excision with local adjuvant, and in the wrist, often results in reduced wrist motion.
  • GCT of the wrist is more aggressive than the more common locations in long bones, with higher local recurrence rates if treated with surgery alone.
  • Diagnosis is often delayed for GCT of the wrist, due to insufficient imaging, which should include CT or MRI.
  • For pregnant women with GCT, local adjuvant treatments can be used in addition to surgery. Following pregnancy, denosumab can be used systemically, and can be effective with metastatic or unresectable disease.

Giant cell tumor (GCT) of bone accounts for about 5% of primary bone tumors.1-3 Only 3% to 5% of GCTs occur in the hand.4,5 Wrist involvement, which is rare, most often involves the hamate bone.5-7 Capitate bone involvement is exceedingly rare.8-11 Although histologically benign, GCT can recur locally after treatment with curettage alone, and lung metastases are found in 2% to 5% of cases.2,12-14 Therefore, en bloc tumor excision is preferred in the setting of cortical erosion or soft-tissue involvement.1,4,8 Wrist joint motion is inevitably reduced, and bone graft donor-site morbidity is significant.6-8

In the unusual case reported here, GCT presented in the capitate bone and, after the patient became pregnant, recurred in the hamate and trapezoid bones with soft-tissue extension and lung metastases. The capitate was excised en bloc and reconstructed with an interposition of polymethylmethacrylate bone cement. Pulmonary metastases developed, and the GCT expanded to involve multiple carpal bones and the bases of the second through fourth metacarpals. A 10-month course of systemic chemotherapy with the RANK ligand (RANKL) inhibitor denosumab was started after the pregnancy. After this treatment, the patient underwent both tumor resection and reconstruction with autogenous bicortical iliac crest bone graft (ICBG) carefully designed to preserve range of motion and maintain the fingers in anatomical position. Treatment with denosumab was continued after surgery. Although this case offers no endpoint for postoperative chemotherapy with denosumab, preoperative treatment dramatically reduced the GCT and permitted limb-sparing reconstruction. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 19-year-old right-handed woman with atraumatic swelling of the left wrist presented to an orthopedic surgeon at an outside facility. Physical examination revealed tender fullness on the dorsum of the wrist, slightly reduced range of motion and grip strength, and a neurovascularly intact wrist. The diagnosis was periarticular cyst, and the patient underwent physical therapy. Two years later, the swelling returned, tenderness was increasing, and symptoms did not resolve with cast immobilization. A radiograph showed a lytic lesion in the capitate bone (Figure 1).[[{"fid":"202332","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"1"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"1":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":""}}}]]

GCT was diagnosed with percutaneous needle biopsy. A preoperative chest radiograph was reported normal. For initial treatment, the capitate and trapezoid bones were resected en bloc through a dorsal approach. Reconstruction consisted of limited arthrodesis using bone cement without additional fixation.

At 6-month follow-up, the patient was pregnant, and there was a recurrence of the wrist lesion. During the first 2 months of pregnancy, swelling and pain rapidly progressed, and a palpable mass formed. Radiographs showed a lytic lesion extending into the hamate bone (Figure 2), and magnetic resonance imaging (MRI) showed articular extension of the lesion with involvement of the base of the fourth metacarpal. [[{"fid":"202334","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"2"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"2":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":""}}}]]Targeted anti-RANKL therapy was not recommended (and was not available at the patient’s home hospital). The patient deferred surgical treatment because of the pregnancy, which proved otherwise uneventful and ended with a full-term delivery.

After the pregnancy, radiographs of the wrist showed complete destruction of the hamate and trapezium bones, with erosion of the bases of the second through fourth metacarpals (Figure 3A). [[{"fid":"202335","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"3"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"3":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":""}}}]]The patient presented at our institution 4 years after initial diagnosis. Computed tomography (CT) of the chest showed numerous bilateral pulmonary nodular opacities. Wrist imaging showed soft-tissue extension (Figure 3B). The diagnosis of recurrent metastatic GCT was confirmed with needle biopsies of the wrist mass and the right lung nodule.

Systemic chemotherapy was initiated with 120 mg of denosumab, given subcutaneously on days 1, 8, and 15 and then monthly during the 10 months leading up to surgery. Serum calcium was monitored during treatment and remained within the normal range the entire time, except for once at the start of therapy, when it dropped to 6.8 mg/dL. After 8 months, the soft-tissue mass, originally 8 cm × 8 cm × 6 cm, shrunk and stabilized at 5 cm × 4 cm × 4 cm (Figure 3B), and a bony shell reformed around it. Nodules in both lung fields showed response to denosumab.

Histologic examination revealed scattered osteoclast-like, multinucleated giant cells, consistent with a recurrent lesion (Figure 4). [[{"fid":"202336","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"4"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 4.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"4":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 4.","field_file_image_credit[und][0][value]":""}}}]]After 10 months of treatment with denosumab, the patient underwent resection (dorsal approach) of the residual cement, the soft-tissue mass, the affected carpal bones, half of the third metacarpal, and the second and fourth metacarpal bases. The proximal carpal row was preserved after no intra-articular involvement was verified. The closet margin was marginal; the tumor mass abutted without encompassing the flexor tendons and median nerve. The tumor was meticulously elevated from the neurovascular and tendinous structures, which were not sacrificed. Hydrogen peroxide was used for local adjuvant treatment. Bicortical autogenous ICBG was placed between the remaining scaphoid, lunate, and metacarpal bones. The second, third, and fourth metacarpal bases were stabilized on the overlapping outer table of ICBG with 2.0-mm plates and miniscrews (Figure 5A). Kirschner wires were used to stabilize the proximal bone graft and the scapholunate fossa. Cancellous bone graft was packed between the structural bone graft and neighboring unaffected carpal bones (Figure 5A). Immobilization with a short-arm thumb spica cast was maintained for 6 weeks after surgery and was followed by a 12-week rehabilitation program. The patient returned to normal activities when plain radiographs showed solid bony union (Figure 5B). Fourteen months after initial surgery, tenolysis was performed to free the extensor tendons (index, middle, and ring fingers on dorsum of left hand) from adhesions to the bone graft. At 37-month follow-up (Figure 5C), there was no clinical or radiographic evidence of progression in the wrist.[[{"fid":"202337","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"5"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 5.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"5":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 5.","field_file_image_credit[und][0][value]":""}}}]]

The patient had bilateral pulmonary metastases (Figures 6A, 6B). Treatment with denosumab produced an initial response (smaller pulmonary lesions) and subsequent stability. After 12 months of treatment with denosumab, the patient underwent left thoracotomy and wedge resection of pulmonary metastases on the left. Pathologic evaluation revealed pulmonary parenchyma with calcification and ossification and limited viable tumor. Given the dramatic effects on the left pulmonary metastases, denosumab was continued, and surgical intervention on the right was not attempted. Pulmonary metastases were stable afterward (Figure 6C).[[{"fid":"202338","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"6"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 6.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"6":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 6.","field_file_image_credit[und][0][value]":""}}}]]

At 54-month follow-up, systemic treatment with denosumab was continued. The patient had no pain in the wrist or hand and was able to use the left hand normally. There was some fissuring of the third and fourth digits over each other. However, the patient had good grip strength and was using eating utensils, picking up water bottles, and engaging in other activities without difficulty.

Discussion

GCT isolated to the carpus is rare. However, compared with GCT in the more common locations in long bones, it is also more aggressive, and its local recurrence rates are higher, probably 60% or more if treated with curettage alone.15 Therefore, excision augmented with adjuvant treatment is recommended.2,7 Use of bone cement in the hand is relatively uncommon.4,5,7-10

The diagnosis of GCT in the carpus is difficult and often delayed. The initial complaint is usually mild wrist pain after relatively mild trauma.5 The first reported case of GCT in the lunate bone was mistakenly thought to be Kienbock disease.5 Similarly, our patient was initially given a nononcologic diagnosis, which prompted conservative management.

Whether the biological behavior of GCT in the carpus differs from that of GCT in other sites is unclear. The high recurrence rates might be attributable in part to suboptimal curettage.5,6 En bloc resections of involved bone inevitably result in carpal instability or loss of wrist motion if arthrodesis is performed.4-7,11 In the present case, resection was followed by limited arthrodesis to mitigate motion losses.

Multifocal GCT in the carpal bones often affects younger patients and has a high rate of recurrence.7,16 In the present case, the patient’s pregnancy delayed treatment and allowed tumor extension into soft tissues and metacarpal bones. Given her young age, en bloc tumor resection was performed, with the proximal carpal row spared to preserve wrist motion. ICBG was carefully shaped to match the defect that remained after tumor resection.7 Supporting wrist height to prevent carpal collapse provided a stable base for remaining distal segments of the second through fourth metacarpals. After short-arm thumb spica casting and early rehabilitation, the patient recovered wrist motion and use of the involved fingers distal to the carpometacarpal joints.

In pregnant women, GCTs have been found primarily in the long bones and spine but are rare.17-21 A review of the literature (1950-present) revealed that the present article is the first report of GCT in the hand or wrist bones of a pregnant woman.18,20,21 There is no consensus as to whether surgical excision should be performed during pregnancy.18,20,21 In 1 unusual case, at 18 weeks’ gestation GCT in the distal femur was resected with curettage and bone grafting, and there were no complications.21 Therefore, pregnancy termination is not indicated for GCT.

The relationship between tumorigenesis and pregnancy is unclear.18,20,21 Empirically, pregnancy is thought to promote tumor growth.18,20 Estrogen and progesterone levels are elevated during pregnancy, potentially influencing tumor cells that are hormonally sensitive.18,20 An early report in which reverse transcription–polymerase chain reaction showed estrogen receptor expression in GCT osteoclast-like cells was followed by several studies that failed to find estrogen receptors at the protein level.19 In contrast, progesterone receptors were found in 50% of GCTs in a study.22 However, the etiopathogenic significance of this is unclear. In pregnant women, vascular endothelial growth factor, placental growth factor, and other growth factors induce osteoclast formation.23 ß-Human chorionic gonadotropin expression (ß-hCG) has been found in 58% of cases, with some showing ß-hCG elevation in the serum.24 Other studies have focused on an immunologic explanation for occurrence of GCT during pregnancy.18 Oncofetal antigens, which are similar to fetal antigens, have been found in fibrosarcoma and in an osteosarcoma cell line but not in GCT.18-20 Thus, though occurrence during pregnancy may be coincidental given the frequency of GCT in women of childbearing age, it is plausible that tumor growth may be enhanced by pregnancy. More studies are needed to understand the relationship between giant cell proliferation and pregnancy-related growth factors and hormones.

With GCT, the rate of pulmonary metastases ranges from 0% to 4%; these metastases are usually diagnosed at time of local recurrence, or 2 years to 3 years after initial GCT diagnosis.2,3,12,14,25 Lung metastases secondary to GCT in the hand or foot bones are rare; our literature review identified only 4 cases.12,14 Risk factors for lung metastasis include local recurrence, aggressive appearance (Enneking grade 3) on radiograph, Ki-67 antigen expression, and distal radius location.14 The mechanism of metastasis is unknown.12,14

Lung metastases are usually excised, but they may spontaneously evolve toward necrosis and ossification.12 In cases in which surgery is unfeasible, chemotherapy (eg, with doxorubicin) has been used to control progression.12,14 Radiation can cause sarcomatous transformation and is contraindicated. Interferon26-28 and other antiangiogenic strategies have been successfully used in systemic therapy for GCT of bone. More recently, bisphosphonates29-32 and denosumab33 have been investigated.29,32-36 The limited toxicity of denosumab makes the drug a very attractive treatment option for recurrent or unresectable GCT of bone.33 Reported rates of mortality from lung metastases have ranged from 0% to 40%.14 There is evidence that control of lung metastases during the first 3 years after diagnosis is important for favorable outcomes.2,3

Malignant stromal cells of GCT of bone have been known to secrete RANKL, which recruits osteoclasts and osteoclast precursor cells, which in turn generate aggressive osteolytic activity.33,37 Denosumab, a monoclonal antibody that inhibits RANKL, is effective in stopping osteoclastic activity. In a phase 2 trial of denosumab in the treatment of GCT of bone, 96% of treated patients with unresectable disease showed no progression at 13 months.38 In addition, 74% of treated patients who had resectable disease but were likely to have morbid surgery did not require surgery, and 62% of treated patients who underwent surgery were able to have a less morbid procedure. Forty-one percent to 58% of treated patients had a reduction in tumor size.

Denosumab is very well tolerated. The phase 2 trial found serious adverse events in 9% of patients, and in 5% of cases the drug was discontinued because of toxicity.38 Serious adverse events include osteonecrosis of jaw, hypocalcemia, and hypophosphatemia.37 Electrolyte changes with denosumab are easy to monitor and manage. Although the favorable toxicity profile of denosumab allows for long-term therapy, the data on therapy duration in patients with unresectable disease are unclear. Patients who discontinue therapy should be closely monitored, as disease can progress in this setting.37

In contrast to GCT of larger bones, GCT of the wrist is rare and typically more aggressive, and has higher local recurrence rates. In many cases, diagnosis is delayed by insufficient imaging, which optimally should include either CT or MRI (Table). [[{"fid":"202341","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"7"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"7":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table.","field_file_image_credit[und][0][value]":""}}}]]For pregnant women with GCT, options include surgical resection with curettage and local adjuvant treatment. After pregnancy, denosumab can be used systemically, and can be effective with metastatic or unresectable disease. Surgical treatment in the wrist can be challenging when partial or complete resections of carpal bones are required. Occupational therapy is recommended for optimization of hand function after surgery.

Take-Home Points

  • GCT of bones of the wrist is rare. This article is the only report of a wrist GCT during pregnancy that we could identify.
  • Routine treatment usually consists of surgical excision with local adjuvant, and in the wrist, often results in reduced wrist motion.
  • GCT of the wrist is more aggressive than the more common locations in long bones, with higher local recurrence rates if treated with surgery alone.
  • Diagnosis is often delayed for GCT of the wrist, due to insufficient imaging, which should include CT or MRI.
  • For pregnant women with GCT, local adjuvant treatments can be used in addition to surgery. Following pregnancy, denosumab can be used systemically, and can be effective with metastatic or unresectable disease.

Giant cell tumor (GCT) of bone accounts for about 5% of primary bone tumors.1-3 Only 3% to 5% of GCTs occur in the hand.4,5 Wrist involvement, which is rare, most often involves the hamate bone.5-7 Capitate bone involvement is exceedingly rare.8-11 Although histologically benign, GCT can recur locally after treatment with curettage alone, and lung metastases are found in 2% to 5% of cases.2,12-14 Therefore, en bloc tumor excision is preferred in the setting of cortical erosion or soft-tissue involvement.1,4,8 Wrist joint motion is inevitably reduced, and bone graft donor-site morbidity is significant.6-8

In the unusual case reported here, GCT presented in the capitate bone and, after the patient became pregnant, recurred in the hamate and trapezoid bones with soft-tissue extension and lung metastases. The capitate was excised en bloc and reconstructed with an interposition of polymethylmethacrylate bone cement. Pulmonary metastases developed, and the GCT expanded to involve multiple carpal bones and the bases of the second through fourth metacarpals. A 10-month course of systemic chemotherapy with the RANK ligand (RANKL) inhibitor denosumab was started after the pregnancy. After this treatment, the patient underwent both tumor resection and reconstruction with autogenous bicortical iliac crest bone graft (ICBG) carefully designed to preserve range of motion and maintain the fingers in anatomical position. Treatment with denosumab was continued after surgery. Although this case offers no endpoint for postoperative chemotherapy with denosumab, preoperative treatment dramatically reduced the GCT and permitted limb-sparing reconstruction. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 19-year-old right-handed woman with atraumatic swelling of the left wrist presented to an orthopedic surgeon at an outside facility. Physical examination revealed tender fullness on the dorsum of the wrist, slightly reduced range of motion and grip strength, and a neurovascularly intact wrist. The diagnosis was periarticular cyst, and the patient underwent physical therapy. Two years later, the swelling returned, tenderness was increasing, and symptoms did not resolve with cast immobilization. A radiograph showed a lytic lesion in the capitate bone (Figure 1).[[{"fid":"202332","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"1"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"1":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 1.","field_file_image_credit[und][0][value]":""}}}]]

GCT was diagnosed with percutaneous needle biopsy. A preoperative chest radiograph was reported normal. For initial treatment, the capitate and trapezoid bones were resected en bloc through a dorsal approach. Reconstruction consisted of limited arthrodesis using bone cement without additional fixation.

At 6-month follow-up, the patient was pregnant, and there was a recurrence of the wrist lesion. During the first 2 months of pregnancy, swelling and pain rapidly progressed, and a palpable mass formed. Radiographs showed a lytic lesion extending into the hamate bone (Figure 2), and magnetic resonance imaging (MRI) showed articular extension of the lesion with involvement of the base of the fourth metacarpal. [[{"fid":"202334","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"2"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"2":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 2.","field_file_image_credit[und][0][value]":""}}}]]Targeted anti-RANKL therapy was not recommended (and was not available at the patient’s home hospital). The patient deferred surgical treatment because of the pregnancy, which proved otherwise uneventful and ended with a full-term delivery.

After the pregnancy, radiographs of the wrist showed complete destruction of the hamate and trapezium bones, with erosion of the bases of the second through fourth metacarpals (Figure 3A). [[{"fid":"202335","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"3"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"3":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 3.","field_file_image_credit[und][0][value]":""}}}]]The patient presented at our institution 4 years after initial diagnosis. Computed tomography (CT) of the chest showed numerous bilateral pulmonary nodular opacities. Wrist imaging showed soft-tissue extension (Figure 3B). The diagnosis of recurrent metastatic GCT was confirmed with needle biopsies of the wrist mass and the right lung nodule.

Systemic chemotherapy was initiated with 120 mg of denosumab, given subcutaneously on days 1, 8, and 15 and then monthly during the 10 months leading up to surgery. Serum calcium was monitored during treatment and remained within the normal range the entire time, except for once at the start of therapy, when it dropped to 6.8 mg/dL. After 8 months, the soft-tissue mass, originally 8 cm × 8 cm × 6 cm, shrunk and stabilized at 5 cm × 4 cm × 4 cm (Figure 3B), and a bony shell reformed around it. Nodules in both lung fields showed response to denosumab.

Histologic examination revealed scattered osteoclast-like, multinucleated giant cells, consistent with a recurrent lesion (Figure 4). [[{"fid":"202336","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"4"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 4.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"4":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 4.","field_file_image_credit[und][0][value]":""}}}]]After 10 months of treatment with denosumab, the patient underwent resection (dorsal approach) of the residual cement, the soft-tissue mass, the affected carpal bones, half of the third metacarpal, and the second and fourth metacarpal bases. The proximal carpal row was preserved after no intra-articular involvement was verified. The closet margin was marginal; the tumor mass abutted without encompassing the flexor tendons and median nerve. The tumor was meticulously elevated from the neurovascular and tendinous structures, which were not sacrificed. Hydrogen peroxide was used for local adjuvant treatment. Bicortical autogenous ICBG was placed between the remaining scaphoid, lunate, and metacarpal bones. The second, third, and fourth metacarpal bases were stabilized on the overlapping outer table of ICBG with 2.0-mm plates and miniscrews (Figure 5A). Kirschner wires were used to stabilize the proximal bone graft and the scapholunate fossa. Cancellous bone graft was packed between the structural bone graft and neighboring unaffected carpal bones (Figure 5A). Immobilization with a short-arm thumb spica cast was maintained for 6 weeks after surgery and was followed by a 12-week rehabilitation program. The patient returned to normal activities when plain radiographs showed solid bony union (Figure 5B). Fourteen months after initial surgery, tenolysis was performed to free the extensor tendons (index, middle, and ring fingers on dorsum of left hand) from adhesions to the bone graft. At 37-month follow-up (Figure 5C), there was no clinical or radiographic evidence of progression in the wrist.[[{"fid":"202337","view_mode":"medstat_image_flush_left","attributes":{"class":"media-element file-medstat-image-flush-left","data-delta":"5"},"fields":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 5.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"5":{"format":"medstat_image_flush_left","field_file_image_caption[und][0][value]":"Figure 5.","field_file_image_credit[und][0][value]":""}}}]]

The patient had bilateral pulmonary metastases (Figures 6A, 6B). Treatment with denosumab produced an initial response (smaller pulmonary lesions) and subsequent stability. After 12 months of treatment with denosumab, the patient underwent left thoracotomy and wedge resection of pulmonary metastases on the left. Pathologic evaluation revealed pulmonary parenchyma with calcification and ossification and limited viable tumor. Given the dramatic effects on the left pulmonary metastases, denosumab was continued, and surgical intervention on the right was not attempted. Pulmonary metastases were stable afterward (Figure 6C).[[{"fid":"202338","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"6"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 6.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"6":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Figure 6.","field_file_image_credit[und][0][value]":""}}}]]

At 54-month follow-up, systemic treatment with denosumab was continued. The patient had no pain in the wrist or hand and was able to use the left hand normally. There was some fissuring of the third and fourth digits over each other. However, the patient had good grip strength and was using eating utensils, picking up water bottles, and engaging in other activities without difficulty.

Discussion

GCT isolated to the carpus is rare. However, compared with GCT in the more common locations in long bones, it is also more aggressive, and its local recurrence rates are higher, probably 60% or more if treated with curettage alone.15 Therefore, excision augmented with adjuvant treatment is recommended.2,7 Use of bone cement in the hand is relatively uncommon.4,5,7-10

The diagnosis of GCT in the carpus is difficult and often delayed. The initial complaint is usually mild wrist pain after relatively mild trauma.5 The first reported case of GCT in the lunate bone was mistakenly thought to be Kienbock disease.5 Similarly, our patient was initially given a nononcologic diagnosis, which prompted conservative management.

Whether the biological behavior of GCT in the carpus differs from that of GCT in other sites is unclear. The high recurrence rates might be attributable in part to suboptimal curettage.5,6 En bloc resections of involved bone inevitably result in carpal instability or loss of wrist motion if arthrodesis is performed.4-7,11 In the present case, resection was followed by limited arthrodesis to mitigate motion losses.

Multifocal GCT in the carpal bones often affects younger patients and has a high rate of recurrence.7,16 In the present case, the patient’s pregnancy delayed treatment and allowed tumor extension into soft tissues and metacarpal bones. Given her young age, en bloc tumor resection was performed, with the proximal carpal row spared to preserve wrist motion. ICBG was carefully shaped to match the defect that remained after tumor resection.7 Supporting wrist height to prevent carpal collapse provided a stable base for remaining distal segments of the second through fourth metacarpals. After short-arm thumb spica casting and early rehabilitation, the patient recovered wrist motion and use of the involved fingers distal to the carpometacarpal joints.

In pregnant women, GCTs have been found primarily in the long bones and spine but are rare.17-21 A review of the literature (1950-present) revealed that the present article is the first report of GCT in the hand or wrist bones of a pregnant woman.18,20,21 There is no consensus as to whether surgical excision should be performed during pregnancy.18,20,21 In 1 unusual case, at 18 weeks’ gestation GCT in the distal femur was resected with curettage and bone grafting, and there were no complications.21 Therefore, pregnancy termination is not indicated for GCT.

The relationship between tumorigenesis and pregnancy is unclear.18,20,21 Empirically, pregnancy is thought to promote tumor growth.18,20 Estrogen and progesterone levels are elevated during pregnancy, potentially influencing tumor cells that are hormonally sensitive.18,20 An early report in which reverse transcription–polymerase chain reaction showed estrogen receptor expression in GCT osteoclast-like cells was followed by several studies that failed to find estrogen receptors at the protein level.19 In contrast, progesterone receptors were found in 50% of GCTs in a study.22 However, the etiopathogenic significance of this is unclear. In pregnant women, vascular endothelial growth factor, placental growth factor, and other growth factors induce osteoclast formation.23 ß-Human chorionic gonadotropin expression (ß-hCG) has been found in 58% of cases, with some showing ß-hCG elevation in the serum.24 Other studies have focused on an immunologic explanation for occurrence of GCT during pregnancy.18 Oncofetal antigens, which are similar to fetal antigens, have been found in fibrosarcoma and in an osteosarcoma cell line but not in GCT.18-20 Thus, though occurrence during pregnancy may be coincidental given the frequency of GCT in women of childbearing age, it is plausible that tumor growth may be enhanced by pregnancy. More studies are needed to understand the relationship between giant cell proliferation and pregnancy-related growth factors and hormones.

With GCT, the rate of pulmonary metastases ranges from 0% to 4%; these metastases are usually diagnosed at time of local recurrence, or 2 years to 3 years after initial GCT diagnosis.2,3,12,14,25 Lung metastases secondary to GCT in the hand or foot bones are rare; our literature review identified only 4 cases.12,14 Risk factors for lung metastasis include local recurrence, aggressive appearance (Enneking grade 3) on radiograph, Ki-67 antigen expression, and distal radius location.14 The mechanism of metastasis is unknown.12,14

Lung metastases are usually excised, but they may spontaneously evolve toward necrosis and ossification.12 In cases in which surgery is unfeasible, chemotherapy (eg, with doxorubicin) has been used to control progression.12,14 Radiation can cause sarcomatous transformation and is contraindicated. Interferon26-28 and other antiangiogenic strategies have been successfully used in systemic therapy for GCT of bone. More recently, bisphosphonates29-32 and denosumab33 have been investigated.29,32-36 The limited toxicity of denosumab makes the drug a very attractive treatment option for recurrent or unresectable GCT of bone.33 Reported rates of mortality from lung metastases have ranged from 0% to 40%.14 There is evidence that control of lung metastases during the first 3 years after diagnosis is important for favorable outcomes.2,3

Malignant stromal cells of GCT of bone have been known to secrete RANKL, which recruits osteoclasts and osteoclast precursor cells, which in turn generate aggressive osteolytic activity.33,37 Denosumab, a monoclonal antibody that inhibits RANKL, is effective in stopping osteoclastic activity. In a phase 2 trial of denosumab in the treatment of GCT of bone, 96% of treated patients with unresectable disease showed no progression at 13 months.38 In addition, 74% of treated patients who had resectable disease but were likely to have morbid surgery did not require surgery, and 62% of treated patients who underwent surgery were able to have a less morbid procedure. Forty-one percent to 58% of treated patients had a reduction in tumor size.

Denosumab is very well tolerated. The phase 2 trial found serious adverse events in 9% of patients, and in 5% of cases the drug was discontinued because of toxicity.38 Serious adverse events include osteonecrosis of jaw, hypocalcemia, and hypophosphatemia.37 Electrolyte changes with denosumab are easy to monitor and manage. Although the favorable toxicity profile of denosumab allows for long-term therapy, the data on therapy duration in patients with unresectable disease are unclear. Patients who discontinue therapy should be closely monitored, as disease can progress in this setting.37

In contrast to GCT of larger bones, GCT of the wrist is rare and typically more aggressive, and has higher local recurrence rates. In many cases, diagnosis is delayed by insufficient imaging, which optimally should include either CT or MRI (Table). [[{"fid":"202341","view_mode":"medstat_image_flush_right","attributes":{"class":"media-element file-medstat-image-flush-right","data-delta":"7"},"fields":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table.","field_file_image_credit[und][0][value]":"","field_file_image_caption[und][0][format]":"plain_text","field_file_image_credit[und][0][format]":"plain_text"},"type":"media","field_deltas":{"7":{"format":"medstat_image_flush_right","field_file_image_caption[und][0][value]":"Table.","field_file_image_credit[und][0][value]":""}}}]]For pregnant women with GCT, options include surgical resection with curettage and local adjuvant treatment. After pregnancy, denosumab can be used systemically, and can be effective with metastatic or unresectable disease. Surgical treatment in the wrist can be challenging when partial or complete resections of carpal bones are required. Occupational therapy is recommended for optimization of hand function after surgery.

References

1. Balke M, Ahrens H, Streitbuerger A, et al. Treatment options for recurrent giant cell tumors of bone. J Cancer Res Clin Oncol. 2009;135(1):149-158.

2. Klenke FM, Wenger DE, Inwards CY, Rose PS, Sim FH. Giant cell tumor of bone risk factors for recurrence. Clin Orthop Relat Res. 2011;469(2):591-599.

3. Klenke FM, Wenger DE, Inwards CY, Rose PS, Sim FH. Recurrent giant cell tumor of long bones: analysis of surgical management. Clin Orthop Relat Res. 2011;469(4):1181-1187.

4. Averill RM, Smith RJ, Campbell CJ. Giant-cell tumors of the bones of the hand. J Hand Surg Am. 1980;5(1):39-50.

5. Shigematsu K, Kobata Y, Yajima H, Kawamura K, Maegawa N, Takakura Y. Giant-cell tumors of the carpus. J Hand Surg Am. 2006;31(7):1214-1219.

6. Gupta GG, Lucas GL, Pirela-Cruz M. Multifocal giant cell tumor of the capitate, hamate, and triquetrum: a case report. J Hand Surg Am. 1995;20(6):1003-1006.

7. Tarng YW, Yang SW, Hsu CJ. Surgical treatment of multifocal giant cell tumor of carpal bones with preservation of wrist function: case report. J Hand Surg Am. 2009;34(2):262-265.

8. Angelini A, Mavrogenis AF, Ruggieri P. Giant cell tumor of the capitate. Musculoskelet Surg. 2011;95(1):45-48.

9. Howard FM, Lassen K. Giant cell tumor of the capitate. J Hand Surg Am. 1984;9(2):272-274.

10. McDonald DJ, Schajowicz F. Giant cell tumor of the capitate. A case report. Clin Orthop Relat Res. 1992(279):264-268.

11. Wilson SC, Cascio BM, Plauche HR. Giant-cell tumor of the capitate. Orthopedics. 2001;24(11):1085-1086.

12. Combalia-Aleu A, Sastre S, Fernández-de-Retana P, Tomás X, Palacin A. Giant cell tumor of the talus with pulmonary metastasis: seven years follow up. Foot. 2006;16(2):107-111.

13. Donthineni R, Boriani L, Ofluoglu O, Bandiera S. Metastatic behaviour of giant cell tumour of the spine. Int Orthop. 2009;33(2):497-501.

14. Jacopin S, Viehweger E, Glard Y, et al. Fatal lung metastasis secondary to index finger giant cell tumor in an 8-year-old child. Orthop Traumatol Surg Res. 2010;96(3):310-313.

15. Plate AM, Lee SJ, Steiner G, Posner MA. Tumor-like lesions and benign tumors of the hand and wrist. J Am Acad Orthop Surg. 2003;11(2):129-141.

16. Moreel P, Le Viet D. Failure of initial surgical treatment of a giant cell tumor of the capitate and its salvage: a case report [in French]. Chir Main. 2006;25(6):315-318.

17. Caillouette JC, Mattar N. Massive peripheral giant-cell reparative granuloma of the jaw: a pregnancy dependent tumor. Trans Pac Coast Obstet Gynecol Soc. 1978;45:78-81.

18. Kathiresan AS, Johnson JN, Hood BJ, Montoya SP, Vanni S, Gonzalez-Quintero VH. Giant cell bone tumor of the thoracic spine presenting in late pregnancy. Obstet Gynecol. 2011;118(2 pt 2):428-431.

19. Komiya S, Zenmyo M, Inoue A. Bone tumors in the pelvis presenting growth during pregnancy. Arch Orthop Trauma Surg. 1999;119(1-2):22-29.

20. Ross AE, Bojescul JA, Kuklo TR. Giant cell tumor: a case report of recurrence during pregnancy. Spine. 2005;30(12):E332-3E35.

21. Sharma JB, Chanana C, Rastogi, et al. Successful pregnancy outcome with elective caesarean section following two attempts of surgical excision of large giant cell tumor of the lower limb during pregnancy. Arch Gynecol Obstet. 2006;274(5):313-315.

22. Demertzis N, Kotsiandri F, Giotis I, Apostolikas N. Giant-cell tumors of bone and progesterone receptors. Orthopedics. 2003;26(12):1209-1212.

23. Taylor RM, Kashima TG, Knowles HJ, Athanasou NA. VEGF, FLT3 ligand, PlGF and HGF can substitute for M-CSF to induce human osteoclast formation: implications for giant cell tumour pathobiology. Lab Invest. 2012;92(10):1398-1406.

24. Lawless ME, Jour G, Hoch BL, Rendi MH. Beta-human chorionic gonadotropin expression in recurrent and metastatic giant cell tumors of bone: a potential mimicker of germ cell tumor. Int J Surg Pathol. 2014;22(7):617-622.

25. Viswanathan S, Jambhekar NA. Metastatic giant cell tumor of bone: are there associated factors and best treatment modalities? Clin Orthop Relat Res. 2010;468(3):827-833.

26. Kaban LB, Troulis MJ, Ebb D, August M, Hornicek FJ, Dodson TB. Antiangiogenic therapy with interferon alpha for giant cell lesions of the jaws. J Oral Maxillofac Surg. 2002;60(10):1103-1111.

27. Kaiser U, Neumann K, Havemann K. Generalised giant-cell tumour of bone: successful treatment of pulmonary metastases with interferon alpha, a case report. J Cancer Res Clin Oncol. 1993;119(5):301-303.

28. Dickerman JD. Interferon and giant cell tumors. Pediatrics. 1999;103(6 pt 1):1282-1283.

29. Balke M, Campanacci L, Gebert C, et al. Bisphosphonate treatment of aggressive primary, recurrent and metastatic giant cell tumour of bone. BMC Cancer. 2010;10:462.

30. Gille O, Oliveira Bde A, Guerin P, Lepreux S, Richez C, Vital JM. Regression of giant cell tumor of the cervical spine with bisphosphonate as single therapy. Spine. 2012;37(6):E396-E399.

31. Moriceau G, Ory B, Gobin B, et al. Therapeutic approach of primary bone tumours by bisphosphonates. Curr Pharm Des. 2010;16(27):2981-2987.

32. Tse LF, Wong KC, Kumta SM, Huang L, Chow TC, Griffith JF. Bisphosphonates reduce local recurrence in extremity giant cell tumor of bone: a case–control study. Bone. 2008;42(1):68-73.

33. Thomas D, Henshaw R, Skubitz K, et al. Denosumab in patients with giant-cell tumour of bone: an open-label, phase 2 study. Lancet Oncol. 2010;11(3):275-280.

34. Balke M, Hardes J. Denosumab: a breakthrough in treatment of giant-cell tumour of bone? Lancet Oncol. 2010;11(3):218-219.

35. Kyrgidis A, Toulis K. Safety and efficacy of denosumab in giant-cell tumour of bone. Lancet Oncol. 2010;11(6):513-514.

36. Thomas D, Carriere P, Jacobs I. Safety of denosumab in giant-cell tumour of bone. Lancet Oncol. 2010;11(9):815.

37. Skubitz KM. Giant cell tumor of bone: current treatment options. Curr Treat Options Oncol. 2014;15(3):507-518.

38. Chawla S, Henshaw R, Seeger L, et al. Safety and efficacy of denosumab for adults and skeletally mature adolescents with giant cell tumour of bone: interim analysis of an open-label, parallel-group, phase 2 study. Lancet Oncol. 2013;14(9):901-908.

References

1. Balke M, Ahrens H, Streitbuerger A, et al. Treatment options for recurrent giant cell tumors of bone. J Cancer Res Clin Oncol. 2009;135(1):149-158.

2. Klenke FM, Wenger DE, Inwards CY, Rose PS, Sim FH. Giant cell tumor of bone risk factors for recurrence. Clin Orthop Relat Res. 2011;469(2):591-599.

3. Klenke FM, Wenger DE, Inwards CY, Rose PS, Sim FH. Recurrent giant cell tumor of long bones: analysis of surgical management. Clin Orthop Relat Res. 2011;469(4):1181-1187.

4. Averill RM, Smith RJ, Campbell CJ. Giant-cell tumors of the bones of the hand. J Hand Surg Am. 1980;5(1):39-50.

5. Shigematsu K, Kobata Y, Yajima H, Kawamura K, Maegawa N, Takakura Y. Giant-cell tumors of the carpus. J Hand Surg Am. 2006;31(7):1214-1219.

6. Gupta GG, Lucas GL, Pirela-Cruz M. Multifocal giant cell tumor of the capitate, hamate, and triquetrum: a case report. J Hand Surg Am. 1995;20(6):1003-1006.

7. Tarng YW, Yang SW, Hsu CJ. Surgical treatment of multifocal giant cell tumor of carpal bones with preservation of wrist function: case report. J Hand Surg Am. 2009;34(2):262-265.

8. Angelini A, Mavrogenis AF, Ruggieri P. Giant cell tumor of the capitate. Musculoskelet Surg. 2011;95(1):45-48.

9. Howard FM, Lassen K. Giant cell tumor of the capitate. J Hand Surg Am. 1984;9(2):272-274.

10. McDonald DJ, Schajowicz F. Giant cell tumor of the capitate. A case report. Clin Orthop Relat Res. 1992(279):264-268.

11. Wilson SC, Cascio BM, Plauche HR. Giant-cell tumor of the capitate. Orthopedics. 2001;24(11):1085-1086.

12. Combalia-Aleu A, Sastre S, Fernández-de-Retana P, Tomás X, Palacin A. Giant cell tumor of the talus with pulmonary metastasis: seven years follow up. Foot. 2006;16(2):107-111.

13. Donthineni R, Boriani L, Ofluoglu O, Bandiera S. Metastatic behaviour of giant cell tumour of the spine. Int Orthop. 2009;33(2):497-501.

14. Jacopin S, Viehweger E, Glard Y, et al. Fatal lung metastasis secondary to index finger giant cell tumor in an 8-year-old child. Orthop Traumatol Surg Res. 2010;96(3):310-313.

15. Plate AM, Lee SJ, Steiner G, Posner MA. Tumor-like lesions and benign tumors of the hand and wrist. J Am Acad Orthop Surg. 2003;11(2):129-141.

16. Moreel P, Le Viet D. Failure of initial surgical treatment of a giant cell tumor of the capitate and its salvage: a case report [in French]. Chir Main. 2006;25(6):315-318.

17. Caillouette JC, Mattar N. Massive peripheral giant-cell reparative granuloma of the jaw: a pregnancy dependent tumor. Trans Pac Coast Obstet Gynecol Soc. 1978;45:78-81.

18. Kathiresan AS, Johnson JN, Hood BJ, Montoya SP, Vanni S, Gonzalez-Quintero VH. Giant cell bone tumor of the thoracic spine presenting in late pregnancy. Obstet Gynecol. 2011;118(2 pt 2):428-431.

19. Komiya S, Zenmyo M, Inoue A. Bone tumors in the pelvis presenting growth during pregnancy. Arch Orthop Trauma Surg. 1999;119(1-2):22-29.

20. Ross AE, Bojescul JA, Kuklo TR. Giant cell tumor: a case report of recurrence during pregnancy. Spine. 2005;30(12):E332-3E35.

21. Sharma JB, Chanana C, Rastogi, et al. Successful pregnancy outcome with elective caesarean section following two attempts of surgical excision of large giant cell tumor of the lower limb during pregnancy. Arch Gynecol Obstet. 2006;274(5):313-315.

22. Demertzis N, Kotsiandri F, Giotis I, Apostolikas N. Giant-cell tumors of bone and progesterone receptors. Orthopedics. 2003;26(12):1209-1212.

23. Taylor RM, Kashima TG, Knowles HJ, Athanasou NA. VEGF, FLT3 ligand, PlGF and HGF can substitute for M-CSF to induce human osteoclast formation: implications for giant cell tumour pathobiology. Lab Invest. 2012;92(10):1398-1406.

24. Lawless ME, Jour G, Hoch BL, Rendi MH. Beta-human chorionic gonadotropin expression in recurrent and metastatic giant cell tumors of bone: a potential mimicker of germ cell tumor. Int J Surg Pathol. 2014;22(7):617-622.

25. Viswanathan S, Jambhekar NA. Metastatic giant cell tumor of bone: are there associated factors and best treatment modalities? Clin Orthop Relat Res. 2010;468(3):827-833.

26. Kaban LB, Troulis MJ, Ebb D, August M, Hornicek FJ, Dodson TB. Antiangiogenic therapy with interferon alpha for giant cell lesions of the jaws. J Oral Maxillofac Surg. 2002;60(10):1103-1111.

27. Kaiser U, Neumann K, Havemann K. Generalised giant-cell tumour of bone: successful treatment of pulmonary metastases with interferon alpha, a case report. J Cancer Res Clin Oncol. 1993;119(5):301-303.

28. Dickerman JD. Interferon and giant cell tumors. Pediatrics. 1999;103(6 pt 1):1282-1283.

29. Balke M, Campanacci L, Gebert C, et al. Bisphosphonate treatment of aggressive primary, recurrent and metastatic giant cell tumour of bone. BMC Cancer. 2010;10:462.

30. Gille O, Oliveira Bde A, Guerin P, Lepreux S, Richez C, Vital JM. Regression of giant cell tumor of the cervical spine with bisphosphonate as single therapy. Spine. 2012;37(6):E396-E399.

31. Moriceau G, Ory B, Gobin B, et al. Therapeutic approach of primary bone tumours by bisphosphonates. Curr Pharm Des. 2010;16(27):2981-2987.

32. Tse LF, Wong KC, Kumta SM, Huang L, Chow TC, Griffith JF. Bisphosphonates reduce local recurrence in extremity giant cell tumor of bone: a case–control study. Bone. 2008;42(1):68-73.

33. Thomas D, Henshaw R, Skubitz K, et al. Denosumab in patients with giant-cell tumour of bone: an open-label, phase 2 study. Lancet Oncol. 2010;11(3):275-280.

34. Balke M, Hardes J. Denosumab: a breakthrough in treatment of giant-cell tumour of bone? Lancet Oncol. 2010;11(3):218-219.

35. Kyrgidis A, Toulis K. Safety and efficacy of denosumab in giant-cell tumour of bone. Lancet Oncol. 2010;11(6):513-514.

36. Thomas D, Carriere P, Jacobs I. Safety of denosumab in giant-cell tumour of bone. Lancet Oncol. 2010;11(9):815.

37. Skubitz KM. Giant cell tumor of bone: current treatment options. Curr Treat Options Oncol. 2014;15(3):507-518.

38. Chawla S, Henshaw R, Seeger L, et al. Safety and efficacy of denosumab for adults and skeletally mature adolescents with giant cell tumour of bone: interim analysis of an open-label, parallel-group, phase 2 study. Lancet Oncol. 2013;14(9):901-908.

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The American Journal of Orthopedics - 46(4)
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Patient Preference Before and After Arthroscopic Rotator Cuff Repair: Which Is More Important, Pain Relief or Strength Return?

Article Type
Changed

Take-Home Points

  • Pain relief and return of strength are important satisfaction variables for patients undergoing ARCR.
  • Pain relief and strength return are equally desirable in the majority (50%) of the patients before and after ARCR.
  • Overall, patient preference for strength return dominates pain relief in long-term.
  • Increasing age is associated with a stronger preference for pain relief.
  • Improved understanding of patient expectations after ARCR will promote meaningful changes in patient satisfaction.

A rotator cuff tear (RCT) can cause significant pain, weakness, stiffness, and loss of function in the shoulder. In most patients, arthroscopic rotator cuff repair (ARCR) provides significant and reproducible pain relief and variable return of shoulder strength and function.1-4 ARCR outcomes are well described and well represented by validated outcome measures.5-9 However, these outcomes do not always correlate with patient satisfaction. For example, after ARCR, 2 patients with similar outcome scores may have different satisfaction levels.

Patient satisfaction involves multiple factors and varies with the patient’s preoperative expectations and the degree to which the surgery matches the patient’s desired outcomes.10-15 In clinical studies, Tashjian and colleagues,10 Henn and colleagues,11 and O’Holleran and colleagues12 found patient satisfaction correlated most highly with postoperative shoulder pain, shoulder function, general health status, and outcome scores. However, our understanding of patients’ desired outcomes and expectations of ARCR is limited, particularly regarding the importance of pain relief and strength return relative to each other. We believe patients’ preoperative expectations are influenced by their self-assessments of symptom severity and by their understanding of the outcomes of surgical procedures and of the information they receive from their surgeons during preoperative evaluation.

We conducted an observational study to determine patients’ preoperative preferences and the importance of post-ARCR pain relief and strength return relative to each other. After surgery, preferences and ratings of pain relief and strength return were reevaluated to determine if they were altered by outcomes. We also studied the influence of multiple factors, including severity of preoperative symptoms (pain, weakness), age, sex, occupation, and active sports involvement, on patients’ preoperative ratings of the importance of post-ARCR improvements in pain relief and strength return. We hypothesized that patients would vary in how they preoperatively value and desire post-ARCR pain relief and strength return.

Materials and Methods

The simple shoulder questionnaire (Figure) designed for this study had 12 items. Patients subjectively assessed the severity of their symptoms (pain level, shoulder weakness) and rated the importance of both pain relief and strength return to their occupational and personal life.

Figure.
They quantified their perceived level of pain over the preceding 7 days by rating it 0 (no pain) to 10 (worst pain imaginable). Preoperative pain level was evaluated to determine if patients with the worst pain would rate the importance of pain relief and strength return differently. Patients also rated their painful shoulder’s strength deficit as a percentage of the contralateral shoulder’s strength. In addition, patients rated the importance of pain relief and strength return from 0 (not important) to 10 (very important). Strength-to-pain difference (SPD) was calculated by subtracting the pain relief preference from the strength return preference, with positive values indicating a preference for strength return and negative values indicating a preference for pain relief.

Before patients underwent surgery for symptomatic suspected RCTs, they were approached to participate in this prospective study. Sixty-five patients provided informed consent on forms approved by an Institutional Review Board. Inclusion criteria were suspected unilateral rotator cuff pathology and willingness to participate. Of the 65 patients, 60 underwent ARCR without another procedure, such as shoulder instability repair, SLAP (superior labrum anterior-to-posterior) repair, or distal clavicle excision; the other 5 patients elected nonoperative treatment and were excluded from review. At a mean (SD) follow-up of 5.2 (0.2) years, the 60 patients who had surgery completed the questionnaire again and rated the importance of pain relief and strength return relative to each other.

Patients with RCTs were divided according to age, sex, shoulder dominance, occupation type, and active sports involvement. Standard definitions for occupation types were used: blue-collar, manual labor jobs; white-collar, salaried/educated positions; and retired.

Matched-pairs t tests were used to compare preoperative and postoperative continuous variables (strength return preference, pain relief preference, SPD). One-way analysis of variance (ANOVA) was used to compare categorical variables (sex, shoulder dominance, active sports involvement) with continuous variables (SPD), and bivariate regression was used to compare groups with continuous data (age, SPD). In cases involving more than 2 groups (occupation types), the Tukey honestly significant difference (HSD) test was used to evaluate intergroup differences. P < .05 was used for statistical significance.

 

 

Results

ARCR Outcomes

After ARCR, there was significant improvement in patient-reported pain and subjective strength scores. Mean (SD) pain score improved from 5.9 (2.3) to 1.3 (2.3) after ARCR (P < .001), and mean (SD) strength improved from 46% (22%) of normal to 84% (17%) of normal (P < .001).

Importance of Post-ARCR Pain Relief and Strength Return

Analysis of preoperative questionnaire responses

revealed that, of 60 patients, 29 (48.3%) considered pain relief and strength return equally important, 20 (33.3%) valued postoperative strength return was more important, and 11 patients (18.3%) rated pain relief was more important than strength return. After a mean (SD) follow-up of 5.2 (0.2) years, 33 patients (55 %) valued pain relief and strength return as equally important, 17 patients (28.3%) preferred a strength recovery, and 10 patients (16.7%) preferred pain relief.

Overall patient ratings were significantly higher for strength return compared to pain relief before surgery, mean (SD), 9.2 (2.1) and 8.6 (2.3) (P = .02), and afterward, 8.9 (1.9) and 8.2 (3.1) (P = .03) (Table 1).

Table 1.
Although SPD was lower after surgery (relative increase in importance of analgesia at postoperative time point), the value was not significant (P = .73). There was a weak positive correlation between patient-reported preoperative pain and importance of pain relief ratings (r = 0.05, P < .001), but there was no significant correlation between postoperative values (r = 0.01, P = .73). Also, there was no significant correlation between importance of strength return rating and strength deficits reported before surgery (r = 0.22, P = .09) or afterward (r = 0.21, P = .11).

Subgroup Analyses

Sex and Age. Of the 60 patients, 43 were male and 17 female. Mean (SD) preoperative SPD was 1.0 (2.7) for males and 0.7 (2.3) females; the difference was not significant (P = .61). After surgery, females emphasized strength return over pain relief more than males did: Mean (SD) SPD was significantly higher (P = .04) for females, 1.7 (3.0), than for males, 0.4 (2.5). There were no preoperative–postoperative differences (P = .33) for males or females (Table 2).

Table 2.
Before surgery, increasing age was associated with lower SPD, indicating a stronger preference for pain relief over strength return (r = 0.33, P = .01). There was no association between age and SPD after surgery (r = 0.2, P = .12).

Hand Dominance. RCT was found in the dominant shoulder of 31 patients (52%). Shoulder dominance did not affect SPD: Mean (SD) preoperative SPD was 1.3 (2.3) for dominant shoulders and 0.5 (2.7) for nondominant shoulders (P = .21), and postoperative SPD was 0.7 (2.6) for dominant and 0.9 (2.8) for nondominant (P = .79). SPD did not change from before surgery to after surgery for dominant (P = .14) or nondominant (P = .28) shoulders (Table 2).

Active Sports Participation. Thirty-two patients (53%) reported preoperative involvement in sports; 35 (58%) reported postoperative involvement (P = .37). Mean (SD) preoperative SPD was 1.4 (3.0) for involved patients and 0.3 (1.7) for uninvolved patients (P = .09), and postoperative SPD was 0.6 (2.8) for involved patients and 1.0 (2.6) for uninvolved patients (P = .53). SPD did not change from before surgery to after surgery for involved (P = .17) or uninvolved (P = .26) patients (Table 2).

Occupation Type. There were 9 blue-collar workers (15%), 32 white-collar workers (53%), and 19 retirees (32%). Mean (SD) preoperative SPD was 2.8 (4.2) for blue-collar workers, 1.2 (2.1) for white-collar workers, and –0.4 (0.4) for retirees. There were no significant differences in preoperative SPD between blue-collar and white-collar workers (P = .19) or between white-collar workers and retirees (P = .06), but there was a significant difference between blue-collar workers and retirees (P = .004). Mean (SD) postoperative SPD was 1.3 (2.7) for blue-collar workers, 1.2 (3.1) for white-collar workers, and –0.3 (1.6) for retirees. There were no significant differences between blue-collar and white-collar workers (P = .99), white-collar workers and retirees (P = .13), or blue-collar workers and retirees (P = .3).

Discussion

In this study, we wanted to determine patients’ pre- and postoperative preferences for pain relief and strength return after ARCR. Preoperative and postoperative preference analysis of the 60 patients who underwent ARCR revealed that the majority valued pain relief and strength return equally. However, overall, there was higher ratings for strength return in long term after ARCR, irrespective of age, sex, preoperative levels of shoulder pain and weakness, and preoperative and postoperative sports involvement.

Patients’ preoperative expectations are a function of their assessment of their symptoms, their perceptions of expected surgical outcomes, and their understanding of preoperative discussion with their surgeons. In this study, patients self-assessed their shoulder symptoms and their effect on their occupational and personal life. They also rated the importance of post-ARCR pain relief and strength return relative to each other. To assess whether surgical outcomes affected perceptions of pain relief and strength return, patients completed the questionnaire before and after surgery. Overall, patients rated postoperative strength return over pain relief on long-term (5 years).

Subgroup analysis revealed a weak positive correlation between patient-reported preoperative pain scores and ratings of the importance of pain relief after surgery, but there was no correlation between postoperative pain scores and ratings of the importance of pain relief after surgery. This finding was surprising because we thought pain relief would be more important than strength return for patients with higher pain scores.1-3,16-21 We would like to clarify a point about this study: That patients preferred strength return over pain relief does not mean they did not care about pain relief. A substantial subset of patients (~50%) valued pain relief and strength return equally. In rotator cuff pathology, pain and weakness are to an extent interrelated. Shoulder pain that limits a patient’s ability to perform a strenuous task can be perceived as shoulder weakness, which may explain why, despite having higher pain scores, patients preferred strength return over pain relief. Increasing age showed a positive correlation with preference for pain relief, which explains the finding that retirees preferred pain relief over strength return. We used SPD to express the preference for strength return over pain relief before and after ARCR. Unfortunately, SPD may not be used to quantitatively define the preference for strength return over pain relief.

Patient satisfaction after RCR involves multiple factors and has been well studied. In a retrospective analysis of 112 patients, Tashjian and colleagues10 found that patient satisfaction was affected by preoperative expectations, marital status, disability status, preoperative pain function, and general health status after RCR. They also found a positive but weak correlation between patient satisfaction and functional outcome scores, including visual analog scale (VAS), Simple Shoulder Test (SST), and Disabilities of the Arm, Shoulder, and Hand (DASH) scores. Henn and colleagues11 evaluated 125 patients who underwent primary RCR for a chronic RCT. Higher preoperative expectations correlated with better postoperative VAS, SST, DASH, and Short Form 36 performance, irrespective of worker compensation status, symptom duration, number of patient comorbidities, tear size, repair technique, and number of previous operations. In a prospective cohort analysis of 311 RCR patients, O’Holleran and colleagues12 found that decreased patient satisfaction was associated with postoperative pain and dysfunction. Furthermore, willingness to recommend surgery to another person was significantly related to patient satisfaction. In the present study, we did not correlate preoperative expectations with postoperative outcome scores or evaluate the effect of other known factors on RCR outcomes. Our main goal was to understand ARCR patients’ preoperative and postoperative evaluations of the importance of pain relief and strength return relative to each other. Improved understanding of patients’ expectations will allow us to identify disparities between expectations and outcomes.

Our study had several limitations. First, our questionnaire was not validated. However, we used it only as an assessment tool, to collect data, and do not propose using it to assess ARCR outcomes. Second, objective strength measurements were not performed, before or after surgery, and therefore patients’ perceptions of weakness were not tested. Third, we did not correlate preoperative or postoperative shoulder outcome scores with patients’ expectations. Our intention was to understand how ARCR patients rate the importance of pain relief and strength return relative to each other. Fourth, we did not correlate patients’ expectations of strength return and pain relief with preoperative tear size or postoperative retear status.

Our observational study results showed that, before undergoing ARCR, most patients valued postoperative pain relief and strength return equally. However, there was an overall preference for strength return over pain relief. Furthermore, this preference held up irrespective of age, sex, sports involvement, or preoperative symptom severity. These findings add to our understanding of patients’ preoperative expectations of ARCR.


Am J Orthop. 2017;46(4):E244-E250. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

References

1. Cole BJ, McCarty LP 3rd, Kang RW, Alford W, Lewis PB, Hayden JK. Arthroscopic rotator cuff repair: prospective functional outcome and repair integrity at minimum 2-year follow-up. J Shoulder Elbow Surg. 2007;16(5):579-585.

2. Huijsmans PE, Pritchard MP, Berghs BM, van Rooyen KS, Wallace AL, de Beer JF. Arthroscopic rotator cuff repair with double-row fixation. J Bone Joint Surg Am. 2007;89(6):1248-1257.

3. Wilson F, Hinov V, Adams G. Arthroscopic repair of full-thickness tears of the rotator cuff: 2- to 14-year follow-up. Arthroscopy. 2002;18(2):136-144.

4. Denard PJ, Jiwani AZ, Lädermann A, Burkhart SS. Long-term outcome of a consecutive series of subscapularis tendon tears repaired arthroscopically. Arthroscopy. 2012;28(11):1587-1591.

5. Richards RR, An KN, Bigliani LU, et al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg. 1994;3(6):347-352.

6. Roach KE, Budiman-Mak E, Songsiridej N, Lertratanakul Y. Development of a shoulder pain and disability index. Arthritis Care Res. 1991;4(4):143-149.

7. Constant CR, Murley AH. A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res. 1987;(214):160-164.

8. Michener LA, McClure PW, Sennett BJ. American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form, patient self-report section: reliability, validity, and responsiveness. J Shoulder Elbow Surg. 2002;11(6):587-594.

9. Romeo AA, Bach BR Jr, O’Halloran KL. Scoring systems for shoulder conditions. Am J Sports Med. 1996;24(4):472-476.

10. Tashjian RZ, Bradley MP, Tocci S, Rey J, Henn RF, Green A. Factors influencing patient satisfaction after rotator cuff repair. J Shoulder Elbow Surg. 2007;16(6):752-758.

11. Henn RF 3rd, Kang L, Tashjian RZ, Green A. Patients’ preoperative expectations predict the outcome of rotator cuff repair. J Bone Joint Surg Am. 2007;89(9):1913-1919.

12. O’Holleran JD, Kocher MS, Horan MP, Briggs KK, Hawkins RJ. Determinants of patient satisfaction with outcome after rotator cuff surgery. J Bone Joint Surg Am. 2005;87(1):121-126.

13. Namdari S, Donegan RP, Chamberlain AM, Galatz LM, Yamaguchi K, Keener JD. Factors affecting outcome after structural failure of repaired rotator cuff tears. J Bone Joint Surg Am. 2014;96(2):99-105.

14. Nho SJ, Brown BS, Lyman S, Adler RS, Altchek DW, MacGillivray JD. Prospective analysis of arthroscopic rotator cuff repair: prognostic factors affecting clinical and ultrasound outcome. J Shoulder Elbow Surg. 2009;18(1):13-20.

15. Sonnabend DH, Watson EM. Structural factors affecting the outcome of rotator cuff repair. J Shoulder Elbow Surg. 2002;11(3):212-218.

16. Boileau P, Brassart N, Watkinson DJ, Carles M, Hatzidakis AM, Krishnan SG. Arthroscopic repair of full-thickness tears of the supraspinatus: does the tendon really heal? J Bone Joint Surg Am. 2005;87(6):1229-1240.

17. Sugaya H, Maeda K, Matsuki K, Moriishi J. Repair integrity and functional outcome after arthroscopic double-row rotator cuff repair. A prospective outcome study. J Bone Joint Surg Am. 2007;89(5):953-960.

18. DeFranco MJ, Bershadsky B, Ciccone J, Yum JK, Iannotti JP. Functional outcome of arthroscopic rotator cuff repairs: a correlation of anatomic and clinical results. J Shoulder Elbow Surg. 2007;16(6):759-765.

19. Galatz LM, Ball CM, Teefey SA, Middleton WD, Yamaguchi K. The outcome and repair integrity of completely arthroscopically repaired large and massive rotator cuff tears. J Bone Joint Surg Am. 2004;86(2):219-224.

20. Harryman DT 2nd, Mack LA, Wang KY, Jackins SE, Richardson ML, Matsen FA 3rd. Repairs of the rotator cuff. Correlation of functional results with integrity of the cuff. J Bone Joint Surg Am. 1991;73(7):982-989.

21. Romeo AA, Hang DW, Bach BR Jr, Shott S. Repair of full thickness rotator cuff tears. Gender, age, and other factors affecting outcome. Clin Orthop Relat Res. 1999;(367):243-255.

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Take-Home Points

  • Pain relief and return of strength are important satisfaction variables for patients undergoing ARCR.
  • Pain relief and strength return are equally desirable in the majority (50%) of the patients before and after ARCR.
  • Overall, patient preference for strength return dominates pain relief in long-term.
  • Increasing age is associated with a stronger preference for pain relief.
  • Improved understanding of patient expectations after ARCR will promote meaningful changes in patient satisfaction.

A rotator cuff tear (RCT) can cause significant pain, weakness, stiffness, and loss of function in the shoulder. In most patients, arthroscopic rotator cuff repair (ARCR) provides significant and reproducible pain relief and variable return of shoulder strength and function.1-4 ARCR outcomes are well described and well represented by validated outcome measures.5-9 However, these outcomes do not always correlate with patient satisfaction. For example, after ARCR, 2 patients with similar outcome scores may have different satisfaction levels.

Patient satisfaction involves multiple factors and varies with the patient’s preoperative expectations and the degree to which the surgery matches the patient’s desired outcomes.10-15 In clinical studies, Tashjian and colleagues,10 Henn and colleagues,11 and O’Holleran and colleagues12 found patient satisfaction correlated most highly with postoperative shoulder pain, shoulder function, general health status, and outcome scores. However, our understanding of patients’ desired outcomes and expectations of ARCR is limited, particularly regarding the importance of pain relief and strength return relative to each other. We believe patients’ preoperative expectations are influenced by their self-assessments of symptom severity and by their understanding of the outcomes of surgical procedures and of the information they receive from their surgeons during preoperative evaluation.

We conducted an observational study to determine patients’ preoperative preferences and the importance of post-ARCR pain relief and strength return relative to each other. After surgery, preferences and ratings of pain relief and strength return were reevaluated to determine if they were altered by outcomes. We also studied the influence of multiple factors, including severity of preoperative symptoms (pain, weakness), age, sex, occupation, and active sports involvement, on patients’ preoperative ratings of the importance of post-ARCR improvements in pain relief and strength return. We hypothesized that patients would vary in how they preoperatively value and desire post-ARCR pain relief and strength return.

Materials and Methods

The simple shoulder questionnaire (Figure) designed for this study had 12 items. Patients subjectively assessed the severity of their symptoms (pain level, shoulder weakness) and rated the importance of both pain relief and strength return to their occupational and personal life.

Figure.
They quantified their perceived level of pain over the preceding 7 days by rating it 0 (no pain) to 10 (worst pain imaginable). Preoperative pain level was evaluated to determine if patients with the worst pain would rate the importance of pain relief and strength return differently. Patients also rated their painful shoulder’s strength deficit as a percentage of the contralateral shoulder’s strength. In addition, patients rated the importance of pain relief and strength return from 0 (not important) to 10 (very important). Strength-to-pain difference (SPD) was calculated by subtracting the pain relief preference from the strength return preference, with positive values indicating a preference for strength return and negative values indicating a preference for pain relief.

Before patients underwent surgery for symptomatic suspected RCTs, they were approached to participate in this prospective study. Sixty-five patients provided informed consent on forms approved by an Institutional Review Board. Inclusion criteria were suspected unilateral rotator cuff pathology and willingness to participate. Of the 65 patients, 60 underwent ARCR without another procedure, such as shoulder instability repair, SLAP (superior labrum anterior-to-posterior) repair, or distal clavicle excision; the other 5 patients elected nonoperative treatment and were excluded from review. At a mean (SD) follow-up of 5.2 (0.2) years, the 60 patients who had surgery completed the questionnaire again and rated the importance of pain relief and strength return relative to each other.

Patients with RCTs were divided according to age, sex, shoulder dominance, occupation type, and active sports involvement. Standard definitions for occupation types were used: blue-collar, manual labor jobs; white-collar, salaried/educated positions; and retired.

Matched-pairs t tests were used to compare preoperative and postoperative continuous variables (strength return preference, pain relief preference, SPD). One-way analysis of variance (ANOVA) was used to compare categorical variables (sex, shoulder dominance, active sports involvement) with continuous variables (SPD), and bivariate regression was used to compare groups with continuous data (age, SPD). In cases involving more than 2 groups (occupation types), the Tukey honestly significant difference (HSD) test was used to evaluate intergroup differences. P < .05 was used for statistical significance.

 

 

Results

ARCR Outcomes

After ARCR, there was significant improvement in patient-reported pain and subjective strength scores. Mean (SD) pain score improved from 5.9 (2.3) to 1.3 (2.3) after ARCR (P < .001), and mean (SD) strength improved from 46% (22%) of normal to 84% (17%) of normal (P < .001).

Importance of Post-ARCR Pain Relief and Strength Return

Analysis of preoperative questionnaire responses

revealed that, of 60 patients, 29 (48.3%) considered pain relief and strength return equally important, 20 (33.3%) valued postoperative strength return was more important, and 11 patients (18.3%) rated pain relief was more important than strength return. After a mean (SD) follow-up of 5.2 (0.2) years, 33 patients (55 %) valued pain relief and strength return as equally important, 17 patients (28.3%) preferred a strength recovery, and 10 patients (16.7%) preferred pain relief.

Overall patient ratings were significantly higher for strength return compared to pain relief before surgery, mean (SD), 9.2 (2.1) and 8.6 (2.3) (P = .02), and afterward, 8.9 (1.9) and 8.2 (3.1) (P = .03) (Table 1).

Table 1.
Although SPD was lower after surgery (relative increase in importance of analgesia at postoperative time point), the value was not significant (P = .73). There was a weak positive correlation between patient-reported preoperative pain and importance of pain relief ratings (r = 0.05, P < .001), but there was no significant correlation between postoperative values (r = 0.01, P = .73). Also, there was no significant correlation between importance of strength return rating and strength deficits reported before surgery (r = 0.22, P = .09) or afterward (r = 0.21, P = .11).

Subgroup Analyses

Sex and Age. Of the 60 patients, 43 were male and 17 female. Mean (SD) preoperative SPD was 1.0 (2.7) for males and 0.7 (2.3) females; the difference was not significant (P = .61). After surgery, females emphasized strength return over pain relief more than males did: Mean (SD) SPD was significantly higher (P = .04) for females, 1.7 (3.0), than for males, 0.4 (2.5). There were no preoperative–postoperative differences (P = .33) for males or females (Table 2).

Table 2.
Before surgery, increasing age was associated with lower SPD, indicating a stronger preference for pain relief over strength return (r = 0.33, P = .01). There was no association between age and SPD after surgery (r = 0.2, P = .12).

Hand Dominance. RCT was found in the dominant shoulder of 31 patients (52%). Shoulder dominance did not affect SPD: Mean (SD) preoperative SPD was 1.3 (2.3) for dominant shoulders and 0.5 (2.7) for nondominant shoulders (P = .21), and postoperative SPD was 0.7 (2.6) for dominant and 0.9 (2.8) for nondominant (P = .79). SPD did not change from before surgery to after surgery for dominant (P = .14) or nondominant (P = .28) shoulders (Table 2).

Active Sports Participation. Thirty-two patients (53%) reported preoperative involvement in sports; 35 (58%) reported postoperative involvement (P = .37). Mean (SD) preoperative SPD was 1.4 (3.0) for involved patients and 0.3 (1.7) for uninvolved patients (P = .09), and postoperative SPD was 0.6 (2.8) for involved patients and 1.0 (2.6) for uninvolved patients (P = .53). SPD did not change from before surgery to after surgery for involved (P = .17) or uninvolved (P = .26) patients (Table 2).

Occupation Type. There were 9 blue-collar workers (15%), 32 white-collar workers (53%), and 19 retirees (32%). Mean (SD) preoperative SPD was 2.8 (4.2) for blue-collar workers, 1.2 (2.1) for white-collar workers, and –0.4 (0.4) for retirees. There were no significant differences in preoperative SPD between blue-collar and white-collar workers (P = .19) or between white-collar workers and retirees (P = .06), but there was a significant difference between blue-collar workers and retirees (P = .004). Mean (SD) postoperative SPD was 1.3 (2.7) for blue-collar workers, 1.2 (3.1) for white-collar workers, and –0.3 (1.6) for retirees. There were no significant differences between blue-collar and white-collar workers (P = .99), white-collar workers and retirees (P = .13), or blue-collar workers and retirees (P = .3).

Discussion

In this study, we wanted to determine patients’ pre- and postoperative preferences for pain relief and strength return after ARCR. Preoperative and postoperative preference analysis of the 60 patients who underwent ARCR revealed that the majority valued pain relief and strength return equally. However, overall, there was higher ratings for strength return in long term after ARCR, irrespective of age, sex, preoperative levels of shoulder pain and weakness, and preoperative and postoperative sports involvement.

Patients’ preoperative expectations are a function of their assessment of their symptoms, their perceptions of expected surgical outcomes, and their understanding of preoperative discussion with their surgeons. In this study, patients self-assessed their shoulder symptoms and their effect on their occupational and personal life. They also rated the importance of post-ARCR pain relief and strength return relative to each other. To assess whether surgical outcomes affected perceptions of pain relief and strength return, patients completed the questionnaire before and after surgery. Overall, patients rated postoperative strength return over pain relief on long-term (5 years).

Subgroup analysis revealed a weak positive correlation between patient-reported preoperative pain scores and ratings of the importance of pain relief after surgery, but there was no correlation between postoperative pain scores and ratings of the importance of pain relief after surgery. This finding was surprising because we thought pain relief would be more important than strength return for patients with higher pain scores.1-3,16-21 We would like to clarify a point about this study: That patients preferred strength return over pain relief does not mean they did not care about pain relief. A substantial subset of patients (~50%) valued pain relief and strength return equally. In rotator cuff pathology, pain and weakness are to an extent interrelated. Shoulder pain that limits a patient’s ability to perform a strenuous task can be perceived as shoulder weakness, which may explain why, despite having higher pain scores, patients preferred strength return over pain relief. Increasing age showed a positive correlation with preference for pain relief, which explains the finding that retirees preferred pain relief over strength return. We used SPD to express the preference for strength return over pain relief before and after ARCR. Unfortunately, SPD may not be used to quantitatively define the preference for strength return over pain relief.

Patient satisfaction after RCR involves multiple factors and has been well studied. In a retrospective analysis of 112 patients, Tashjian and colleagues10 found that patient satisfaction was affected by preoperative expectations, marital status, disability status, preoperative pain function, and general health status after RCR. They also found a positive but weak correlation between patient satisfaction and functional outcome scores, including visual analog scale (VAS), Simple Shoulder Test (SST), and Disabilities of the Arm, Shoulder, and Hand (DASH) scores. Henn and colleagues11 evaluated 125 patients who underwent primary RCR for a chronic RCT. Higher preoperative expectations correlated with better postoperative VAS, SST, DASH, and Short Form 36 performance, irrespective of worker compensation status, symptom duration, number of patient comorbidities, tear size, repair technique, and number of previous operations. In a prospective cohort analysis of 311 RCR patients, O’Holleran and colleagues12 found that decreased patient satisfaction was associated with postoperative pain and dysfunction. Furthermore, willingness to recommend surgery to another person was significantly related to patient satisfaction. In the present study, we did not correlate preoperative expectations with postoperative outcome scores or evaluate the effect of other known factors on RCR outcomes. Our main goal was to understand ARCR patients’ preoperative and postoperative evaluations of the importance of pain relief and strength return relative to each other. Improved understanding of patients’ expectations will allow us to identify disparities between expectations and outcomes.

Our study had several limitations. First, our questionnaire was not validated. However, we used it only as an assessment tool, to collect data, and do not propose using it to assess ARCR outcomes. Second, objective strength measurements were not performed, before or after surgery, and therefore patients’ perceptions of weakness were not tested. Third, we did not correlate preoperative or postoperative shoulder outcome scores with patients’ expectations. Our intention was to understand how ARCR patients rate the importance of pain relief and strength return relative to each other. Fourth, we did not correlate patients’ expectations of strength return and pain relief with preoperative tear size or postoperative retear status.

Our observational study results showed that, before undergoing ARCR, most patients valued postoperative pain relief and strength return equally. However, there was an overall preference for strength return over pain relief. Furthermore, this preference held up irrespective of age, sex, sports involvement, or preoperative symptom severity. These findings add to our understanding of patients’ preoperative expectations of ARCR.


Am J Orthop. 2017;46(4):E244-E250. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

Take-Home Points

  • Pain relief and return of strength are important satisfaction variables for patients undergoing ARCR.
  • Pain relief and strength return are equally desirable in the majority (50%) of the patients before and after ARCR.
  • Overall, patient preference for strength return dominates pain relief in long-term.
  • Increasing age is associated with a stronger preference for pain relief.
  • Improved understanding of patient expectations after ARCR will promote meaningful changes in patient satisfaction.

A rotator cuff tear (RCT) can cause significant pain, weakness, stiffness, and loss of function in the shoulder. In most patients, arthroscopic rotator cuff repair (ARCR) provides significant and reproducible pain relief and variable return of shoulder strength and function.1-4 ARCR outcomes are well described and well represented by validated outcome measures.5-9 However, these outcomes do not always correlate with patient satisfaction. For example, after ARCR, 2 patients with similar outcome scores may have different satisfaction levels.

Patient satisfaction involves multiple factors and varies with the patient’s preoperative expectations and the degree to which the surgery matches the patient’s desired outcomes.10-15 In clinical studies, Tashjian and colleagues,10 Henn and colleagues,11 and O’Holleran and colleagues12 found patient satisfaction correlated most highly with postoperative shoulder pain, shoulder function, general health status, and outcome scores. However, our understanding of patients’ desired outcomes and expectations of ARCR is limited, particularly regarding the importance of pain relief and strength return relative to each other. We believe patients’ preoperative expectations are influenced by their self-assessments of symptom severity and by their understanding of the outcomes of surgical procedures and of the information they receive from their surgeons during preoperative evaluation.

We conducted an observational study to determine patients’ preoperative preferences and the importance of post-ARCR pain relief and strength return relative to each other. After surgery, preferences and ratings of pain relief and strength return were reevaluated to determine if they were altered by outcomes. We also studied the influence of multiple factors, including severity of preoperative symptoms (pain, weakness), age, sex, occupation, and active sports involvement, on patients’ preoperative ratings of the importance of post-ARCR improvements in pain relief and strength return. We hypothesized that patients would vary in how they preoperatively value and desire post-ARCR pain relief and strength return.

Materials and Methods

The simple shoulder questionnaire (Figure) designed for this study had 12 items. Patients subjectively assessed the severity of their symptoms (pain level, shoulder weakness) and rated the importance of both pain relief and strength return to their occupational and personal life.

Figure.
They quantified their perceived level of pain over the preceding 7 days by rating it 0 (no pain) to 10 (worst pain imaginable). Preoperative pain level was evaluated to determine if patients with the worst pain would rate the importance of pain relief and strength return differently. Patients also rated their painful shoulder’s strength deficit as a percentage of the contralateral shoulder’s strength. In addition, patients rated the importance of pain relief and strength return from 0 (not important) to 10 (very important). Strength-to-pain difference (SPD) was calculated by subtracting the pain relief preference from the strength return preference, with positive values indicating a preference for strength return and negative values indicating a preference for pain relief.

Before patients underwent surgery for symptomatic suspected RCTs, they were approached to participate in this prospective study. Sixty-five patients provided informed consent on forms approved by an Institutional Review Board. Inclusion criteria were suspected unilateral rotator cuff pathology and willingness to participate. Of the 65 patients, 60 underwent ARCR without another procedure, such as shoulder instability repair, SLAP (superior labrum anterior-to-posterior) repair, or distal clavicle excision; the other 5 patients elected nonoperative treatment and were excluded from review. At a mean (SD) follow-up of 5.2 (0.2) years, the 60 patients who had surgery completed the questionnaire again and rated the importance of pain relief and strength return relative to each other.

Patients with RCTs were divided according to age, sex, shoulder dominance, occupation type, and active sports involvement. Standard definitions for occupation types were used: blue-collar, manual labor jobs; white-collar, salaried/educated positions; and retired.

Matched-pairs t tests were used to compare preoperative and postoperative continuous variables (strength return preference, pain relief preference, SPD). One-way analysis of variance (ANOVA) was used to compare categorical variables (sex, shoulder dominance, active sports involvement) with continuous variables (SPD), and bivariate regression was used to compare groups with continuous data (age, SPD). In cases involving more than 2 groups (occupation types), the Tukey honestly significant difference (HSD) test was used to evaluate intergroup differences. P < .05 was used for statistical significance.

 

 

Results

ARCR Outcomes

After ARCR, there was significant improvement in patient-reported pain and subjective strength scores. Mean (SD) pain score improved from 5.9 (2.3) to 1.3 (2.3) after ARCR (P < .001), and mean (SD) strength improved from 46% (22%) of normal to 84% (17%) of normal (P < .001).

Importance of Post-ARCR Pain Relief and Strength Return

Analysis of preoperative questionnaire responses

revealed that, of 60 patients, 29 (48.3%) considered pain relief and strength return equally important, 20 (33.3%) valued postoperative strength return was more important, and 11 patients (18.3%) rated pain relief was more important than strength return. After a mean (SD) follow-up of 5.2 (0.2) years, 33 patients (55 %) valued pain relief and strength return as equally important, 17 patients (28.3%) preferred a strength recovery, and 10 patients (16.7%) preferred pain relief.

Overall patient ratings were significantly higher for strength return compared to pain relief before surgery, mean (SD), 9.2 (2.1) and 8.6 (2.3) (P = .02), and afterward, 8.9 (1.9) and 8.2 (3.1) (P = .03) (Table 1).

Table 1.
Although SPD was lower after surgery (relative increase in importance of analgesia at postoperative time point), the value was not significant (P = .73). There was a weak positive correlation between patient-reported preoperative pain and importance of pain relief ratings (r = 0.05, P < .001), but there was no significant correlation between postoperative values (r = 0.01, P = .73). Also, there was no significant correlation between importance of strength return rating and strength deficits reported before surgery (r = 0.22, P = .09) or afterward (r = 0.21, P = .11).

Subgroup Analyses

Sex and Age. Of the 60 patients, 43 were male and 17 female. Mean (SD) preoperative SPD was 1.0 (2.7) for males and 0.7 (2.3) females; the difference was not significant (P = .61). After surgery, females emphasized strength return over pain relief more than males did: Mean (SD) SPD was significantly higher (P = .04) for females, 1.7 (3.0), than for males, 0.4 (2.5). There were no preoperative–postoperative differences (P = .33) for males or females (Table 2).

Table 2.
Before surgery, increasing age was associated with lower SPD, indicating a stronger preference for pain relief over strength return (r = 0.33, P = .01). There was no association between age and SPD after surgery (r = 0.2, P = .12).

Hand Dominance. RCT was found in the dominant shoulder of 31 patients (52%). Shoulder dominance did not affect SPD: Mean (SD) preoperative SPD was 1.3 (2.3) for dominant shoulders and 0.5 (2.7) for nondominant shoulders (P = .21), and postoperative SPD was 0.7 (2.6) for dominant and 0.9 (2.8) for nondominant (P = .79). SPD did not change from before surgery to after surgery for dominant (P = .14) or nondominant (P = .28) shoulders (Table 2).

Active Sports Participation. Thirty-two patients (53%) reported preoperative involvement in sports; 35 (58%) reported postoperative involvement (P = .37). Mean (SD) preoperative SPD was 1.4 (3.0) for involved patients and 0.3 (1.7) for uninvolved patients (P = .09), and postoperative SPD was 0.6 (2.8) for involved patients and 1.0 (2.6) for uninvolved patients (P = .53). SPD did not change from before surgery to after surgery for involved (P = .17) or uninvolved (P = .26) patients (Table 2).

Occupation Type. There were 9 blue-collar workers (15%), 32 white-collar workers (53%), and 19 retirees (32%). Mean (SD) preoperative SPD was 2.8 (4.2) for blue-collar workers, 1.2 (2.1) for white-collar workers, and –0.4 (0.4) for retirees. There were no significant differences in preoperative SPD between blue-collar and white-collar workers (P = .19) or between white-collar workers and retirees (P = .06), but there was a significant difference between blue-collar workers and retirees (P = .004). Mean (SD) postoperative SPD was 1.3 (2.7) for blue-collar workers, 1.2 (3.1) for white-collar workers, and –0.3 (1.6) for retirees. There were no significant differences between blue-collar and white-collar workers (P = .99), white-collar workers and retirees (P = .13), or blue-collar workers and retirees (P = .3).

Discussion

In this study, we wanted to determine patients’ pre- and postoperative preferences for pain relief and strength return after ARCR. Preoperative and postoperative preference analysis of the 60 patients who underwent ARCR revealed that the majority valued pain relief and strength return equally. However, overall, there was higher ratings for strength return in long term after ARCR, irrespective of age, sex, preoperative levels of shoulder pain and weakness, and preoperative and postoperative sports involvement.

Patients’ preoperative expectations are a function of their assessment of their symptoms, their perceptions of expected surgical outcomes, and their understanding of preoperative discussion with their surgeons. In this study, patients self-assessed their shoulder symptoms and their effect on their occupational and personal life. They also rated the importance of post-ARCR pain relief and strength return relative to each other. To assess whether surgical outcomes affected perceptions of pain relief and strength return, patients completed the questionnaire before and after surgery. Overall, patients rated postoperative strength return over pain relief on long-term (5 years).

Subgroup analysis revealed a weak positive correlation between patient-reported preoperative pain scores and ratings of the importance of pain relief after surgery, but there was no correlation between postoperative pain scores and ratings of the importance of pain relief after surgery. This finding was surprising because we thought pain relief would be more important than strength return for patients with higher pain scores.1-3,16-21 We would like to clarify a point about this study: That patients preferred strength return over pain relief does not mean they did not care about pain relief. A substantial subset of patients (~50%) valued pain relief and strength return equally. In rotator cuff pathology, pain and weakness are to an extent interrelated. Shoulder pain that limits a patient’s ability to perform a strenuous task can be perceived as shoulder weakness, which may explain why, despite having higher pain scores, patients preferred strength return over pain relief. Increasing age showed a positive correlation with preference for pain relief, which explains the finding that retirees preferred pain relief over strength return. We used SPD to express the preference for strength return over pain relief before and after ARCR. Unfortunately, SPD may not be used to quantitatively define the preference for strength return over pain relief.

Patient satisfaction after RCR involves multiple factors and has been well studied. In a retrospective analysis of 112 patients, Tashjian and colleagues10 found that patient satisfaction was affected by preoperative expectations, marital status, disability status, preoperative pain function, and general health status after RCR. They also found a positive but weak correlation between patient satisfaction and functional outcome scores, including visual analog scale (VAS), Simple Shoulder Test (SST), and Disabilities of the Arm, Shoulder, and Hand (DASH) scores. Henn and colleagues11 evaluated 125 patients who underwent primary RCR for a chronic RCT. Higher preoperative expectations correlated with better postoperative VAS, SST, DASH, and Short Form 36 performance, irrespective of worker compensation status, symptom duration, number of patient comorbidities, tear size, repair technique, and number of previous operations. In a prospective cohort analysis of 311 RCR patients, O’Holleran and colleagues12 found that decreased patient satisfaction was associated with postoperative pain and dysfunction. Furthermore, willingness to recommend surgery to another person was significantly related to patient satisfaction. In the present study, we did not correlate preoperative expectations with postoperative outcome scores or evaluate the effect of other known factors on RCR outcomes. Our main goal was to understand ARCR patients’ preoperative and postoperative evaluations of the importance of pain relief and strength return relative to each other. Improved understanding of patients’ expectations will allow us to identify disparities between expectations and outcomes.

Our study had several limitations. First, our questionnaire was not validated. However, we used it only as an assessment tool, to collect data, and do not propose using it to assess ARCR outcomes. Second, objective strength measurements were not performed, before or after surgery, and therefore patients’ perceptions of weakness were not tested. Third, we did not correlate preoperative or postoperative shoulder outcome scores with patients’ expectations. Our intention was to understand how ARCR patients rate the importance of pain relief and strength return relative to each other. Fourth, we did not correlate patients’ expectations of strength return and pain relief with preoperative tear size or postoperative retear status.

Our observational study results showed that, before undergoing ARCR, most patients valued postoperative pain relief and strength return equally. However, there was an overall preference for strength return over pain relief. Furthermore, this preference held up irrespective of age, sex, sports involvement, or preoperative symptom severity. These findings add to our understanding of patients’ preoperative expectations of ARCR.


Am J Orthop. 2017;46(4):E244-E250. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

References

1. Cole BJ, McCarty LP 3rd, Kang RW, Alford W, Lewis PB, Hayden JK. Arthroscopic rotator cuff repair: prospective functional outcome and repair integrity at minimum 2-year follow-up. J Shoulder Elbow Surg. 2007;16(5):579-585.

2. Huijsmans PE, Pritchard MP, Berghs BM, van Rooyen KS, Wallace AL, de Beer JF. Arthroscopic rotator cuff repair with double-row fixation. J Bone Joint Surg Am. 2007;89(6):1248-1257.

3. Wilson F, Hinov V, Adams G. Arthroscopic repair of full-thickness tears of the rotator cuff: 2- to 14-year follow-up. Arthroscopy. 2002;18(2):136-144.

4. Denard PJ, Jiwani AZ, Lädermann A, Burkhart SS. Long-term outcome of a consecutive series of subscapularis tendon tears repaired arthroscopically. Arthroscopy. 2012;28(11):1587-1591.

5. Richards RR, An KN, Bigliani LU, et al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg. 1994;3(6):347-352.

6. Roach KE, Budiman-Mak E, Songsiridej N, Lertratanakul Y. Development of a shoulder pain and disability index. Arthritis Care Res. 1991;4(4):143-149.

7. Constant CR, Murley AH. A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res. 1987;(214):160-164.

8. Michener LA, McClure PW, Sennett BJ. American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form, patient self-report section: reliability, validity, and responsiveness. J Shoulder Elbow Surg. 2002;11(6):587-594.

9. Romeo AA, Bach BR Jr, O’Halloran KL. Scoring systems for shoulder conditions. Am J Sports Med. 1996;24(4):472-476.

10. Tashjian RZ, Bradley MP, Tocci S, Rey J, Henn RF, Green A. Factors influencing patient satisfaction after rotator cuff repair. J Shoulder Elbow Surg. 2007;16(6):752-758.

11. Henn RF 3rd, Kang L, Tashjian RZ, Green A. Patients’ preoperative expectations predict the outcome of rotator cuff repair. J Bone Joint Surg Am. 2007;89(9):1913-1919.

12. O’Holleran JD, Kocher MS, Horan MP, Briggs KK, Hawkins RJ. Determinants of patient satisfaction with outcome after rotator cuff surgery. J Bone Joint Surg Am. 2005;87(1):121-126.

13. Namdari S, Donegan RP, Chamberlain AM, Galatz LM, Yamaguchi K, Keener JD. Factors affecting outcome after structural failure of repaired rotator cuff tears. J Bone Joint Surg Am. 2014;96(2):99-105.

14. Nho SJ, Brown BS, Lyman S, Adler RS, Altchek DW, MacGillivray JD. Prospective analysis of arthroscopic rotator cuff repair: prognostic factors affecting clinical and ultrasound outcome. J Shoulder Elbow Surg. 2009;18(1):13-20.

15. Sonnabend DH, Watson EM. Structural factors affecting the outcome of rotator cuff repair. J Shoulder Elbow Surg. 2002;11(3):212-218.

16. Boileau P, Brassart N, Watkinson DJ, Carles M, Hatzidakis AM, Krishnan SG. Arthroscopic repair of full-thickness tears of the supraspinatus: does the tendon really heal? J Bone Joint Surg Am. 2005;87(6):1229-1240.

17. Sugaya H, Maeda K, Matsuki K, Moriishi J. Repair integrity and functional outcome after arthroscopic double-row rotator cuff repair. A prospective outcome study. J Bone Joint Surg Am. 2007;89(5):953-960.

18. DeFranco MJ, Bershadsky B, Ciccone J, Yum JK, Iannotti JP. Functional outcome of arthroscopic rotator cuff repairs: a correlation of anatomic and clinical results. J Shoulder Elbow Surg. 2007;16(6):759-765.

19. Galatz LM, Ball CM, Teefey SA, Middleton WD, Yamaguchi K. The outcome and repair integrity of completely arthroscopically repaired large and massive rotator cuff tears. J Bone Joint Surg Am. 2004;86(2):219-224.

20. Harryman DT 2nd, Mack LA, Wang KY, Jackins SE, Richardson ML, Matsen FA 3rd. Repairs of the rotator cuff. Correlation of functional results with integrity of the cuff. J Bone Joint Surg Am. 1991;73(7):982-989.

21. Romeo AA, Hang DW, Bach BR Jr, Shott S. Repair of full thickness rotator cuff tears. Gender, age, and other factors affecting outcome. Clin Orthop Relat Res. 1999;(367):243-255.

References

1. Cole BJ, McCarty LP 3rd, Kang RW, Alford W, Lewis PB, Hayden JK. Arthroscopic rotator cuff repair: prospective functional outcome and repair integrity at minimum 2-year follow-up. J Shoulder Elbow Surg. 2007;16(5):579-585.

2. Huijsmans PE, Pritchard MP, Berghs BM, van Rooyen KS, Wallace AL, de Beer JF. Arthroscopic rotator cuff repair with double-row fixation. J Bone Joint Surg Am. 2007;89(6):1248-1257.

3. Wilson F, Hinov V, Adams G. Arthroscopic repair of full-thickness tears of the rotator cuff: 2- to 14-year follow-up. Arthroscopy. 2002;18(2):136-144.

4. Denard PJ, Jiwani AZ, Lädermann A, Burkhart SS. Long-term outcome of a consecutive series of subscapularis tendon tears repaired arthroscopically. Arthroscopy. 2012;28(11):1587-1591.

5. Richards RR, An KN, Bigliani LU, et al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg. 1994;3(6):347-352.

6. Roach KE, Budiman-Mak E, Songsiridej N, Lertratanakul Y. Development of a shoulder pain and disability index. Arthritis Care Res. 1991;4(4):143-149.

7. Constant CR, Murley AH. A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res. 1987;(214):160-164.

8. Michener LA, McClure PW, Sennett BJ. American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form, patient self-report section: reliability, validity, and responsiveness. J Shoulder Elbow Surg. 2002;11(6):587-594.

9. Romeo AA, Bach BR Jr, O’Halloran KL. Scoring systems for shoulder conditions. Am J Sports Med. 1996;24(4):472-476.

10. Tashjian RZ, Bradley MP, Tocci S, Rey J, Henn RF, Green A. Factors influencing patient satisfaction after rotator cuff repair. J Shoulder Elbow Surg. 2007;16(6):752-758.

11. Henn RF 3rd, Kang L, Tashjian RZ, Green A. Patients’ preoperative expectations predict the outcome of rotator cuff repair. J Bone Joint Surg Am. 2007;89(9):1913-1919.

12. O’Holleran JD, Kocher MS, Horan MP, Briggs KK, Hawkins RJ. Determinants of patient satisfaction with outcome after rotator cuff surgery. J Bone Joint Surg Am. 2005;87(1):121-126.

13. Namdari S, Donegan RP, Chamberlain AM, Galatz LM, Yamaguchi K, Keener JD. Factors affecting outcome after structural failure of repaired rotator cuff tears. J Bone Joint Surg Am. 2014;96(2):99-105.

14. Nho SJ, Brown BS, Lyman S, Adler RS, Altchek DW, MacGillivray JD. Prospective analysis of arthroscopic rotator cuff repair: prognostic factors affecting clinical and ultrasound outcome. J Shoulder Elbow Surg. 2009;18(1):13-20.

15. Sonnabend DH, Watson EM. Structural factors affecting the outcome of rotator cuff repair. J Shoulder Elbow Surg. 2002;11(3):212-218.

16. Boileau P, Brassart N, Watkinson DJ, Carles M, Hatzidakis AM, Krishnan SG. Arthroscopic repair of full-thickness tears of the supraspinatus: does the tendon really heal? J Bone Joint Surg Am. 2005;87(6):1229-1240.

17. Sugaya H, Maeda K, Matsuki K, Moriishi J. Repair integrity and functional outcome after arthroscopic double-row rotator cuff repair. A prospective outcome study. J Bone Joint Surg Am. 2007;89(5):953-960.

18. DeFranco MJ, Bershadsky B, Ciccone J, Yum JK, Iannotti JP. Functional outcome of arthroscopic rotator cuff repairs: a correlation of anatomic and clinical results. J Shoulder Elbow Surg. 2007;16(6):759-765.

19. Galatz LM, Ball CM, Teefey SA, Middleton WD, Yamaguchi K. The outcome and repair integrity of completely arthroscopically repaired large and massive rotator cuff tears. J Bone Joint Surg Am. 2004;86(2):219-224.

20. Harryman DT 2nd, Mack LA, Wang KY, Jackins SE, Richardson ML, Matsen FA 3rd. Repairs of the rotator cuff. Correlation of functional results with integrity of the cuff. J Bone Joint Surg Am. 1991;73(7):982-989.

21. Romeo AA, Hang DW, Bach BR Jr, Shott S. Repair of full thickness rotator cuff tears. Gender, age, and other factors affecting outcome. Clin Orthop Relat Res. 1999;(367):243-255.

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Comparison of Anterior and Posterior Cortico­steroid Injections for Pain Relief and Functional Improvement in Shoulder Impingement Syndrome

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Take-Home Points

  • When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.

  • Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months

  • CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used.

  • Clinical response to CSI may not depend on injection accuracy.

  • Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

Shoulder pain, a common clinical problem, occurs in 7% to 34% of the general population and in 21% of people older than 70 years.1 Subacromial impingement refers to shoulder pain resulting from mechanical impingement of the rotator cuff underneath the coracoacromial arch between the acromion and the humeral head.2,3 Subacromial impingement syndrome (SIS) is the most common cause of shoulder pain, resulting in significant functional deficits and disability.3

Treatment options for SIS include conservative modalities such as use of nonsteroidal anti-inflammatory drugs, physical therapy (PT), and subacromial corticosteroid injections (CSIs). Studies have found short- and long-term improvement in pain, function, and range of motion after CSI.4-8 Subacromial CSI can be administered through an anterior or a posterior route.4,9 There have been several studies of the accuracy of anterior and posterior CSIs,10-12 with 2 studies finding similar accuracy for these routes.10,11 However, there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12

Although the accuracy of anterior and posterior routes has been studied, their effect on clinical outcomes has not. We conducted a study to understand the effects of anterior and posterior CSIs on SIS. As one of the accuracy studies suggested anterior CSI is more accurate—the anterior route was theorized to provide easier access to the subacromial space12—we hypothesized patients treated with anterior CSI would have superior clinical outcomes 6 months after injection.12,13

Materials and Methods

Study Participants and Randomization

After this study received Institutional Review Board approval, patients with shoulder pain of more than 3 months’ duration and consistent with SIS were screened for inclusion. Eligible patients had pain in the anterior biceps and over the top of the shoulder with overhead activities as well as one or more clinical findings on physical examination: Hawkins-Kennedy sign, Neer sign, painful arc, and infraspinatus pain (pain with external rotation).

Patients were excluded if their history included prior subacromial CSI, adhesive capsulitis (inability to passively abduct shoulder to 90° with scapular stabilization), calcific tendonitis, radiographic evidence of os acromiale, cervical radiculopathy, Spurling sign, neck pain, radiating arm pain or numbness, sensory deficits, or neck and upper extremity motor dysfunction. Also excluded were patients with full-thickness rotator cuff tear, weakness on arm elevation, positive "drop arm sign," or high-riding humerus on standing shoulder radiograph. Patients who had work-related injuries or who were involved in worker compensation were excluded as well.

Enrolled patients were randomly assigned (with use of a computer-based random number generator) to receive either anterior CSI or posterior CSI.

Injection Procedures

All patients were administered 5 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone by 2 board-certified orthopedic surgeons using a 22-gauge 1½-inch needle. For patients who received their subacromial CSI by the anterior route, the arm was held in 0° of abduction and 20° of external rotation. The needle was inserted medial to the humeral head, lateral to the coracoid process, beginning 1 cm inferior to the clavicle with the needle directed posteriorly and laterally toward the acromion.10 For patients who received their CSI by the posterior route, the arm was held in 0° of abduction, the posterolateral corner of the acromion was identified by palpation, and the needle was inserted 1 cm inferior and medial to this point with the needle directed anteriorly and laterally toward the acromion.10,12 In both groups, the subacromial space was identified when a drop in pressure was felt during needle insertion. Accuracy was assessed post hoc by asking patients to grade their response to the injection on a visual analog scale (VAS); VAS score was used as a surrogate for improvement. All patients had a positive Neer test: Pain decreased with impingement maneuvers immediately after injection.

All patients were referred for PT provided according to an evidence-based rehabilitation protocol.14 This program emphasized range of motion with shoulder shrugs, scapular retraction, and pendulum exercises; flexibility with stretching exercises targeting the anterior and posterior aspects of the shoulder and cane stretching for forward elevation and external rotation; and strength with strengthening exercises involving the rotator cuff and scapular stabilizers.

Outcome Measures

Pain was measured with VAS scores and function with Single Assessment Numeric Evaluation (SANE) scores. The VAS is a validated outcome measure of pain intensity. A numeric version of the VAS was used: Patients selected the whole number, from 0 (no pain) to 10 (worst possible pain), that best reflected their pain intensity. On SANE, another validated outcome measure, patients rated their shoulder function as a percentage of normal, from 0% (no function possible) to 100% (perfect).15 Before injection, all patients were administered the VAS and SANE questionnaires to establish their baseline pain level and opinion of shoulder function. These measures were repeated 1, 3, and 6 months after injection. Telephone interviews were conducted at 1 month and 6 months. Patients were asked to return to clinic 3 months after injection as part of the standard of care. At 3 months, 47 (86%) of the 55 patients returned for follow-up and were administered the VAS and SANE questionnaires; the other 8 completed the questionnaires by telephone. At each time point, patients were asked to report on their participation in PT and/or adherence to their home exercise program.

Statistical Analysis

Power analysis performed with Student t test and a 2-sided level of P = .05 compared VAS pain scores between the anterior and posterior injection routes and found a mean (SD) difference of 1.4 (1.7).16 Power calculations made with nQuery Advisor Version 7.0 (Statistical Solutions) indicated a total sample size of 60 patients (30/group) would provide 80% power for detecting a significant difference assuming a 20% dropout rate.

Two-way mixed-model analysis of variance (ANOVA) was used to compare the anterior and posterior routes for statistical differences in both VAS pain scores and SANE function scores at baseline and 1, 3, and 6 months after injection. Likewise, time at baseline (just before injection)was compared with follow-up (1, 3, 6 months) with 2-way mixed-model ANOVA adjusting for anterior or posterior route. Multivariate analysis was performed to evaluate differences between baseline and 6-month follow-up with respect to anterior and posterior injection routes, controlling for age, sex, and body mass index (BMI) for VAS and SANE scores. Parametric testing methods were used for statistical analysis, which was performed with IBM SPSS Statistics Version 21.0 (IBM Corp). Significance was set at P < .05.

Results

Patient Characteristics

Of the 55 patients enrolled, 25 (46%) received anterior subacromial CSI and 30 (54%) received posterior CSI. All enrolled patients had a positive Neer impingement test immediately after injection. Mean (SD) age was 48 (9.3) years for anterior group patients and 48 (9.0) years for posterior group patients. There was no significant difference in age or BMI between the 2 groups (Table).

Table.

Five patients (9%) were excluded from the study after randomization and CSI: 2 for a full-thickness rotator cuff tear, 1 for a Bankart lesion, 1 for adhesive capsulitis, and 1 for a worker compensation claim.

One month after injection, 41 patients (75%) reported having engaged in PT as prescribed. Of the 47 patients (86%) who returned for the 3-month follow-up, 25 (46%) reported having engaged in PT between 1 month and 3 months after injection. Fourteen patients (26%) reported attending PT between 3 and 6 months post-injection.

Outcome Measures

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in VAS scores between the anterior and posterior groups at any time point (P = .45). Both groups had highly significant pain reductions (anterior, F = 9.71, P < .001; posterior, F = 13.46, P < .001). Figure 1 shows mean VAS scores and significant reductions in pain 1, 3, and 6 months after injection (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of pain reduction over time, as indicated by a nonsignificant (P = .50) difference in slopes. These pain score reductions were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 1.

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in SANE scores between the anterior and posterior groups, except for a higher mean score in the anterior group at 3 months
(P = .02). There were no other group differences (P > .10 for all). Both groups had highly significant improvements in function (anterior, F = 17.34,
P < .001; posterior, F = 13.57, P < .001). Figure 2 shows mean SANE scores and significant improvement at 1, 3, and 6 months (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of improved function over time, as indicated by a nonsignificant (P = .51) difference in slopes. These function score improvements were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 2.

From the results of this prospective randomized study, we concluded subacromial CSI significantly reduces pain and improves function regardless of route used. In addition, age, sex, and BMI do not significantly affect the efficacy of either anterior CSI or posterior CSI.

Discussion

In patients with SIS, anterior CSI and posterior CSI provided significant improvements in pain and function 1, 3, and 6 months after injection. These effects were independent of age, sex, BMI, and PT participation. There were no significant differences in outcomes between injection routes.

When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.4-8 Although clinical outcomes are inconsistent, CSI can be used to address SIS symptoms in appropriate patients. Specifically, Blair and colleagues6 found that, CSI consisting of 4 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone was effective in alleviating shoulder pain and improving shoulder range of motion. Other authors have similarly reported improved outcomes after subacromial injection and short-term follow-up with PT.4,7,8 Our findings are consistent with these reports: CSI coupled with a structured rehabilitation program is effective in alleviating symptoms associated with acute or subacute SIS.

Numerous studies have found improved clinical outcomes after anterior CSI and after posterior CSI,6-8 but no study has directly compared the clinical impact of anterior CSI with that of posterior CSI—which suggests injection route may not affect ultimate clinical outcomes.

CSI accuracy has been studied extensively.10-12,17-20 Although 2 studies found similar accuracy for anterior and posterior routes,10,11 there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12 Collectively, these studies expose the inherent difficulty in treating shoulder pain with localized subacromial injection. Therapy may fail because of errant needle positioning. Two prospective studies found improved clinical outcomes with successful delivery of medication into the subacromial space.17,18 Poor clinical outcomes may result from inaccurate CSI.

In contrast to other clinical studies, our study found that injection route was not associated with differences in clinical response. In a prospective randomized clinical trial in which 75 patients received a subacromial injection, Marder and colleagues12 found anterior routes 84% accurate and posterior routes 56% accurate; they concluded acromion anatomy and subacromial bursa anatomy make posterior injections more difficult. As theorized by Gruson and colleagues,13 with use of an anterior route, the needle enters inferior to the concavity of the acromion and provides easier access to the subacromial space. This idea is in line with Marder and colleagues’12 conclusion that subacromial bursa anatomy provides a favorable environment for accurate CSI.

If accuracy is positively correlated with clinical improvement and anterior routes are more accurate, there should be a difference in response to posterior injections. Our results provide evidence that clinical response to CSI may not depend on injection accuracy. Perhaps merely placing the corticosteroid near the bursa is adequate for improving symptoms or perhaps some of the clinical improvement is due to the systemic effect of corticosteroids. These possibilities require further analysis.

Establishing the efficacy of CSI in SIS is difficult. The literature includes various study designs, different CSI indications and medication formulations, and varying emphasis on the role of organized PT. Rehabilitation has been found to alleviate joint pain by reducing inflammation,14 but data do not universally support this finding.21,22 Nevertheless, use of PT might explain the divergence in clinical outcomes reported by Marder and colleagues,12 who found anterior CSI more accurate than posterior CSI. In our practice, PT is recommended for all SIS patients, not only those who have CSI. Thus, our findings are framed within the context of successful CSI but may include patients who improved with PT alone. This issue raises the question of whether subacromial CSI should be guided by ultrasound. Ultrasound guidance can improve CSI accuracy and clinical outcomes,23-25 though the value of this benefit is debated.26

This study had several limitations. First, pain relief was patient reported. Second, the treatment plan involved CSI with PT but did not control for CSI used alone. PT, which is part of the standard of care for patients with SIS, added another degree of complexity to the study. Third, there may have been some variability in SIS severity (stage 1, 2, or 3). Fourth, although the study design controlled for various shoulder pathologies, advanced imaging, which could have provided diagnosis confirmation, was not available for all patients. Therefore, concurrent conditions may have confounded results. However, randomization was used to try to minimize this effect. Fifth, although injection routes were randomly assigned, the trial was not blinded. Sixth, the study was underpowered by 1 patient, as there was an estimated 20% dropout rate over 3 and 6 months of follow-up. However, we do not think our results were significantly affected.

Although more research is needed to fully describe the role of subacromial CSI in SIS, our study findings suggested that CSI using either an anterior or a posterior route creates a window of symptomatic relief in which patients may be able to engage in PT.

Conclusion

Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months. No differences were found between anterior and posterior CSIs. In the context of this study, CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used. Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

References

1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain. Cochrane Database Syst Rev. 2003;(1):CD004016.

2. Bell AD, Conaway D. Corticosteroid injections for painful shoulders. Int J Clin Pract. 2005;59(10):1178-1186.

3. Michener LA, McClure PW, Karduna AR. Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech. 2003;18(5):369-379.

4. Akgün K, Birtane M, Akarirmak U. Is local subacromial corticosteroid injection beneficial in subacromial impingement syndrome? Clin Rheumatol. 2004;23(6):496-500.

5. Bhagra A, Syed H, Reed DA, et al. Efficacy of musculoskeletal injections by primary care providers in the office: a retrospective cohort study. Int J Gen Med. 2013;6:237-243.

6. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am. 1996;78(11):1685-1689.

7. Cummins CA, Sasso LM, Nicholson D. Impingement syndrome: temporal outcomes of nonoperative treatment.
J Shoulder Elbow Surg. 2009;18(2):172-177.

8. Yu C, Chen CH, Liu HT, Dai MH, Wang IC, Wang KC. Subacromial injections of corticosteroids and Xylocaine for painful subacromial impingement syndrome. Chang Gung Med J. 2006;29(5):474-478.

9. Codsi MJ. The painful shoulder: when to inject and when to refer. Cleve Clin J Med. 2007;74(7):473-474, 477-478, 480-482 passim.

10. Henkus HE, Cobben LP, Coerkamp EG, Nelissen RG, van Arkel ER. The accuracy of subacromial injections: a prospective randomized magnetic resonance imaging study. Arthroscopy. 2006;22(3):277-282.

11. Kang MN, Rizio L, Prybicien M, Middlemas DA, Blacksin MF. The accuracy of subacromial corticosteroid injections: a comparison of multiple methods. J Shoulder Elbow Surg. 2008;17(15):61S-66S.

12. Marder RA, Kim SH, Labson JD, Hunter JC. Injection of the subacromial bursa in patients with rotator cuff syndrome: a prospective, randomized study comparing the effectiveness of different routes. J Bone Joint Surg Am. 2012;94(16):
1442-1447.

13. Gruson, KI, Ruchelsman DE, Zuckerman JD. Subacromial corticosteroid injections. J Shoulder Elbow Surg. 2008;17(1 suppl):118S-130S.

14. Kuhn JE. Exercise in the treatment of rotator cuff impingement: a systematic review and a synthesized evidence-based rehabilitation protocol. J Shoulder Elbow Surg. 2009;18(1):138-160.

15. Williams GN, Gangel TJ, Arciero RA, Uhorchak JM, Taylor DC. Comparison of the Single Assessment Numeric Evaluation method and two shoulder rating scales. Outcomes measures after shoulder surgery. Am J Sports Med. 1999;27(2):214-221.

16. Tashjian RZ, Deloach J, Porucznik CA, Powell AP. Minimal clinically important differences (MCID) and patient acceptable symptomatic state (PASS) for visual analog scales (VAS) measuring pain in patients treated for rotator cuff disease.
J Shoulder Elbow Surg. 2009;88(6):927-932.

17. Eustace JA, Brophy DP, Gibney RP, Bresnihan B, FitzGerald O. Comparison of the accuracy of steroid placement with clinical outcome in patients with shoulder symptoms. Ann Rheum Dis. 1997;56(1):59-63.

18. Esenyel CZ, Esenyel M, Yeiltepe R, et al. The correlation between the accuracy of steroid injections and subsequent shoulder pain and function in subacromial impingement
syndrome [in Turkish]. Acta Orthop Traumatol Turc. 2003;37(1):
41-45.

19. Powell SE, Davis SM, Lee EH, et al. Accuracy of palpation-directed intra-articular glenohumeral injection confirmed by magnetic resonance arthrography. Arthroscopy. 2015;31(2):205-208.

20. Rutten MJ, Maresch BJ, Jager GJ, de Waal Malefijt MC. Injection of the subacromial-subdeltoid bursa: blind or ultrasound-guided? Acta Orthop. 2007;78(2):254-257.

21. Desmeules F, Côté CH, Frémont P. Therapeutic exercise and orthopedic manual therapy for impingement syndrome: a systematic review. Clin J Sport Med. 2003;13(3):176-182.

22. Winters JC, Sobel JS, Groenier KH, Arendzen HJ, Meyboom-de Jong B. Comparison of physiotherapy, manipulation, and corticosteroid injection for treating shoulder complaints in general practice: randomised, single blind study. BMJ. 1997;314(7090):1320-1325.

23. Chen MJ, Lew HL, Hsu TC, et al. Ultrasound-guided shoulder injections in the treatment of subacromial bursitis. Am J Phys Med Rehabil. 2006;85(1):31-35.

24. Hsieh LF, Hsu WC, Lin YJ, Wu SH, Chang KC, Chang HL. Is ultrasound-guided injection more effective in chronic subacromial bursitis? Med Sci Sports Exerc. 2013;45(12):
2205-2213.

25. Naredo E, Cabero F, Beneyto P, et al. A randomized comparative study of short term response to blind injection versus sonographic-guided injection of local corticosteroids in patients with painful shoulder. J Rheumatol. 2004;31(2):308-314.

26. Hall S, Buchbinder R. Do imaging methods that guide needle placement improve outcome? Ann Rheum Dis. 2004;63(9):1007-1008.

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Take-Home Points

  • When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.

  • Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months

  • CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used.

  • Clinical response to CSI may not depend on injection accuracy.

  • Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

Shoulder pain, a common clinical problem, occurs in 7% to 34% of the general population and in 21% of people older than 70 years.1 Subacromial impingement refers to shoulder pain resulting from mechanical impingement of the rotator cuff underneath the coracoacromial arch between the acromion and the humeral head.2,3 Subacromial impingement syndrome (SIS) is the most common cause of shoulder pain, resulting in significant functional deficits and disability.3

Treatment options for SIS include conservative modalities such as use of nonsteroidal anti-inflammatory drugs, physical therapy (PT), and subacromial corticosteroid injections (CSIs). Studies have found short- and long-term improvement in pain, function, and range of motion after CSI.4-8 Subacromial CSI can be administered through an anterior or a posterior route.4,9 There have been several studies of the accuracy of anterior and posterior CSIs,10-12 with 2 studies finding similar accuracy for these routes.10,11 However, there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12

Although the accuracy of anterior and posterior routes has been studied, their effect on clinical outcomes has not. We conducted a study to understand the effects of anterior and posterior CSIs on SIS. As one of the accuracy studies suggested anterior CSI is more accurate—the anterior route was theorized to provide easier access to the subacromial space12—we hypothesized patients treated with anterior CSI would have superior clinical outcomes 6 months after injection.12,13

Materials and Methods

Study Participants and Randomization

After this study received Institutional Review Board approval, patients with shoulder pain of more than 3 months’ duration and consistent with SIS were screened for inclusion. Eligible patients had pain in the anterior biceps and over the top of the shoulder with overhead activities as well as one or more clinical findings on physical examination: Hawkins-Kennedy sign, Neer sign, painful arc, and infraspinatus pain (pain with external rotation).

Patients were excluded if their history included prior subacromial CSI, adhesive capsulitis (inability to passively abduct shoulder to 90° with scapular stabilization), calcific tendonitis, radiographic evidence of os acromiale, cervical radiculopathy, Spurling sign, neck pain, radiating arm pain or numbness, sensory deficits, or neck and upper extremity motor dysfunction. Also excluded were patients with full-thickness rotator cuff tear, weakness on arm elevation, positive "drop arm sign," or high-riding humerus on standing shoulder radiograph. Patients who had work-related injuries or who were involved in worker compensation were excluded as well.

Enrolled patients were randomly assigned (with use of a computer-based random number generator) to receive either anterior CSI or posterior CSI.

Injection Procedures

All patients were administered 5 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone by 2 board-certified orthopedic surgeons using a 22-gauge 1½-inch needle. For patients who received their subacromial CSI by the anterior route, the arm was held in 0° of abduction and 20° of external rotation. The needle was inserted medial to the humeral head, lateral to the coracoid process, beginning 1 cm inferior to the clavicle with the needle directed posteriorly and laterally toward the acromion.10 For patients who received their CSI by the posterior route, the arm was held in 0° of abduction, the posterolateral corner of the acromion was identified by palpation, and the needle was inserted 1 cm inferior and medial to this point with the needle directed anteriorly and laterally toward the acromion.10,12 In both groups, the subacromial space was identified when a drop in pressure was felt during needle insertion. Accuracy was assessed post hoc by asking patients to grade their response to the injection on a visual analog scale (VAS); VAS score was used as a surrogate for improvement. All patients had a positive Neer test: Pain decreased with impingement maneuvers immediately after injection.

All patients were referred for PT provided according to an evidence-based rehabilitation protocol.14 This program emphasized range of motion with shoulder shrugs, scapular retraction, and pendulum exercises; flexibility with stretching exercises targeting the anterior and posterior aspects of the shoulder and cane stretching for forward elevation and external rotation; and strength with strengthening exercises involving the rotator cuff and scapular stabilizers.

Outcome Measures

Pain was measured with VAS scores and function with Single Assessment Numeric Evaluation (SANE) scores. The VAS is a validated outcome measure of pain intensity. A numeric version of the VAS was used: Patients selected the whole number, from 0 (no pain) to 10 (worst possible pain), that best reflected their pain intensity. On SANE, another validated outcome measure, patients rated their shoulder function as a percentage of normal, from 0% (no function possible) to 100% (perfect).15 Before injection, all patients were administered the VAS and SANE questionnaires to establish their baseline pain level and opinion of shoulder function. These measures were repeated 1, 3, and 6 months after injection. Telephone interviews were conducted at 1 month and 6 months. Patients were asked to return to clinic 3 months after injection as part of the standard of care. At 3 months, 47 (86%) of the 55 patients returned for follow-up and were administered the VAS and SANE questionnaires; the other 8 completed the questionnaires by telephone. At each time point, patients were asked to report on their participation in PT and/or adherence to their home exercise program.

Statistical Analysis

Power analysis performed with Student t test and a 2-sided level of P = .05 compared VAS pain scores between the anterior and posterior injection routes and found a mean (SD) difference of 1.4 (1.7).16 Power calculations made with nQuery Advisor Version 7.0 (Statistical Solutions) indicated a total sample size of 60 patients (30/group) would provide 80% power for detecting a significant difference assuming a 20% dropout rate.

Two-way mixed-model analysis of variance (ANOVA) was used to compare the anterior and posterior routes for statistical differences in both VAS pain scores and SANE function scores at baseline and 1, 3, and 6 months after injection. Likewise, time at baseline (just before injection)was compared with follow-up (1, 3, 6 months) with 2-way mixed-model ANOVA adjusting for anterior or posterior route. Multivariate analysis was performed to evaluate differences between baseline and 6-month follow-up with respect to anterior and posterior injection routes, controlling for age, sex, and body mass index (BMI) for VAS and SANE scores. Parametric testing methods were used for statistical analysis, which was performed with IBM SPSS Statistics Version 21.0 (IBM Corp). Significance was set at P < .05.

Results

Patient Characteristics

Of the 55 patients enrolled, 25 (46%) received anterior subacromial CSI and 30 (54%) received posterior CSI. All enrolled patients had a positive Neer impingement test immediately after injection. Mean (SD) age was 48 (9.3) years for anterior group patients and 48 (9.0) years for posterior group patients. There was no significant difference in age or BMI between the 2 groups (Table).

Table.

Five patients (9%) were excluded from the study after randomization and CSI: 2 for a full-thickness rotator cuff tear, 1 for a Bankart lesion, 1 for adhesive capsulitis, and 1 for a worker compensation claim.

One month after injection, 41 patients (75%) reported having engaged in PT as prescribed. Of the 47 patients (86%) who returned for the 3-month follow-up, 25 (46%) reported having engaged in PT between 1 month and 3 months after injection. Fourteen patients (26%) reported attending PT between 3 and 6 months post-injection.

Outcome Measures

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in VAS scores between the anterior and posterior groups at any time point (P = .45). Both groups had highly significant pain reductions (anterior, F = 9.71, P < .001; posterior, F = 13.46, P < .001). Figure 1 shows mean VAS scores and significant reductions in pain 1, 3, and 6 months after injection (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of pain reduction over time, as indicated by a nonsignificant (P = .50) difference in slopes. These pain score reductions were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 1.

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in SANE scores between the anterior and posterior groups, except for a higher mean score in the anterior group at 3 months
(P = .02). There were no other group differences (P > .10 for all). Both groups had highly significant improvements in function (anterior, F = 17.34,
P < .001; posterior, F = 13.57, P < .001). Figure 2 shows mean SANE scores and significant improvement at 1, 3, and 6 months (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of improved function over time, as indicated by a nonsignificant (P = .51) difference in slopes. These function score improvements were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 2.

From the results of this prospective randomized study, we concluded subacromial CSI significantly reduces pain and improves function regardless of route used. In addition, age, sex, and BMI do not significantly affect the efficacy of either anterior CSI or posterior CSI.

Discussion

In patients with SIS, anterior CSI and posterior CSI provided significant improvements in pain and function 1, 3, and 6 months after injection. These effects were independent of age, sex, BMI, and PT participation. There were no significant differences in outcomes between injection routes.

When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.4-8 Although clinical outcomes are inconsistent, CSI can be used to address SIS symptoms in appropriate patients. Specifically, Blair and colleagues6 found that, CSI consisting of 4 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone was effective in alleviating shoulder pain and improving shoulder range of motion. Other authors have similarly reported improved outcomes after subacromial injection and short-term follow-up with PT.4,7,8 Our findings are consistent with these reports: CSI coupled with a structured rehabilitation program is effective in alleviating symptoms associated with acute or subacute SIS.

Numerous studies have found improved clinical outcomes after anterior CSI and after posterior CSI,6-8 but no study has directly compared the clinical impact of anterior CSI with that of posterior CSI—which suggests injection route may not affect ultimate clinical outcomes.

CSI accuracy has been studied extensively.10-12,17-20 Although 2 studies found similar accuracy for anterior and posterior routes,10,11 there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12 Collectively, these studies expose the inherent difficulty in treating shoulder pain with localized subacromial injection. Therapy may fail because of errant needle positioning. Two prospective studies found improved clinical outcomes with successful delivery of medication into the subacromial space.17,18 Poor clinical outcomes may result from inaccurate CSI.

In contrast to other clinical studies, our study found that injection route was not associated with differences in clinical response. In a prospective randomized clinical trial in which 75 patients received a subacromial injection, Marder and colleagues12 found anterior routes 84% accurate and posterior routes 56% accurate; they concluded acromion anatomy and subacromial bursa anatomy make posterior injections more difficult. As theorized by Gruson and colleagues,13 with use of an anterior route, the needle enters inferior to the concavity of the acromion and provides easier access to the subacromial space. This idea is in line with Marder and colleagues’12 conclusion that subacromial bursa anatomy provides a favorable environment for accurate CSI.

If accuracy is positively correlated with clinical improvement and anterior routes are more accurate, there should be a difference in response to posterior injections. Our results provide evidence that clinical response to CSI may not depend on injection accuracy. Perhaps merely placing the corticosteroid near the bursa is adequate for improving symptoms or perhaps some of the clinical improvement is due to the systemic effect of corticosteroids. These possibilities require further analysis.

Establishing the efficacy of CSI in SIS is difficult. The literature includes various study designs, different CSI indications and medication formulations, and varying emphasis on the role of organized PT. Rehabilitation has been found to alleviate joint pain by reducing inflammation,14 but data do not universally support this finding.21,22 Nevertheless, use of PT might explain the divergence in clinical outcomes reported by Marder and colleagues,12 who found anterior CSI more accurate than posterior CSI. In our practice, PT is recommended for all SIS patients, not only those who have CSI. Thus, our findings are framed within the context of successful CSI but may include patients who improved with PT alone. This issue raises the question of whether subacromial CSI should be guided by ultrasound. Ultrasound guidance can improve CSI accuracy and clinical outcomes,23-25 though the value of this benefit is debated.26

This study had several limitations. First, pain relief was patient reported. Second, the treatment plan involved CSI with PT but did not control for CSI used alone. PT, which is part of the standard of care for patients with SIS, added another degree of complexity to the study. Third, there may have been some variability in SIS severity (stage 1, 2, or 3). Fourth, although the study design controlled for various shoulder pathologies, advanced imaging, which could have provided diagnosis confirmation, was not available for all patients. Therefore, concurrent conditions may have confounded results. However, randomization was used to try to minimize this effect. Fifth, although injection routes were randomly assigned, the trial was not blinded. Sixth, the study was underpowered by 1 patient, as there was an estimated 20% dropout rate over 3 and 6 months of follow-up. However, we do not think our results were significantly affected.

Although more research is needed to fully describe the role of subacromial CSI in SIS, our study findings suggested that CSI using either an anterior or a posterior route creates a window of symptomatic relief in which patients may be able to engage in PT.

Conclusion

Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months. No differences were found between anterior and posterior CSIs. In the context of this study, CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used. Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

Take-Home Points

  • When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.

  • Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months

  • CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used.

  • Clinical response to CSI may not depend on injection accuracy.

  • Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

Shoulder pain, a common clinical problem, occurs in 7% to 34% of the general population and in 21% of people older than 70 years.1 Subacromial impingement refers to shoulder pain resulting from mechanical impingement of the rotator cuff underneath the coracoacromial arch between the acromion and the humeral head.2,3 Subacromial impingement syndrome (SIS) is the most common cause of shoulder pain, resulting in significant functional deficits and disability.3

Treatment options for SIS include conservative modalities such as use of nonsteroidal anti-inflammatory drugs, physical therapy (PT), and subacromial corticosteroid injections (CSIs). Studies have found short- and long-term improvement in pain, function, and range of motion after CSI.4-8 Subacromial CSI can be administered through an anterior or a posterior route.4,9 There have been several studies of the accuracy of anterior and posterior CSIs,10-12 with 2 studies finding similar accuracy for these routes.10,11 However, there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12

Although the accuracy of anterior and posterior routes has been studied, their effect on clinical outcomes has not. We conducted a study to understand the effects of anterior and posterior CSIs on SIS. As one of the accuracy studies suggested anterior CSI is more accurate—the anterior route was theorized to provide easier access to the subacromial space12—we hypothesized patients treated with anterior CSI would have superior clinical outcomes 6 months after injection.12,13

Materials and Methods

Study Participants and Randomization

After this study received Institutional Review Board approval, patients with shoulder pain of more than 3 months’ duration and consistent with SIS were screened for inclusion. Eligible patients had pain in the anterior biceps and over the top of the shoulder with overhead activities as well as one or more clinical findings on physical examination: Hawkins-Kennedy sign, Neer sign, painful arc, and infraspinatus pain (pain with external rotation).

Patients were excluded if their history included prior subacromial CSI, adhesive capsulitis (inability to passively abduct shoulder to 90° with scapular stabilization), calcific tendonitis, radiographic evidence of os acromiale, cervical radiculopathy, Spurling sign, neck pain, radiating arm pain or numbness, sensory deficits, or neck and upper extremity motor dysfunction. Also excluded were patients with full-thickness rotator cuff tear, weakness on arm elevation, positive "drop arm sign," or high-riding humerus on standing shoulder radiograph. Patients who had work-related injuries or who were involved in worker compensation were excluded as well.

Enrolled patients were randomly assigned (with use of a computer-based random number generator) to receive either anterior CSI or posterior CSI.

Injection Procedures

All patients were administered 5 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone by 2 board-certified orthopedic surgeons using a 22-gauge 1½-inch needle. For patients who received their subacromial CSI by the anterior route, the arm was held in 0° of abduction and 20° of external rotation. The needle was inserted medial to the humeral head, lateral to the coracoid process, beginning 1 cm inferior to the clavicle with the needle directed posteriorly and laterally toward the acromion.10 For patients who received their CSI by the posterior route, the arm was held in 0° of abduction, the posterolateral corner of the acromion was identified by palpation, and the needle was inserted 1 cm inferior and medial to this point with the needle directed anteriorly and laterally toward the acromion.10,12 In both groups, the subacromial space was identified when a drop in pressure was felt during needle insertion. Accuracy was assessed post hoc by asking patients to grade their response to the injection on a visual analog scale (VAS); VAS score was used as a surrogate for improvement. All patients had a positive Neer test: Pain decreased with impingement maneuvers immediately after injection.

All patients were referred for PT provided according to an evidence-based rehabilitation protocol.14 This program emphasized range of motion with shoulder shrugs, scapular retraction, and pendulum exercises; flexibility with stretching exercises targeting the anterior and posterior aspects of the shoulder and cane stretching for forward elevation and external rotation; and strength with strengthening exercises involving the rotator cuff and scapular stabilizers.

Outcome Measures

Pain was measured with VAS scores and function with Single Assessment Numeric Evaluation (SANE) scores. The VAS is a validated outcome measure of pain intensity. A numeric version of the VAS was used: Patients selected the whole number, from 0 (no pain) to 10 (worst possible pain), that best reflected their pain intensity. On SANE, another validated outcome measure, patients rated their shoulder function as a percentage of normal, from 0% (no function possible) to 100% (perfect).15 Before injection, all patients were administered the VAS and SANE questionnaires to establish their baseline pain level and opinion of shoulder function. These measures were repeated 1, 3, and 6 months after injection. Telephone interviews were conducted at 1 month and 6 months. Patients were asked to return to clinic 3 months after injection as part of the standard of care. At 3 months, 47 (86%) of the 55 patients returned for follow-up and were administered the VAS and SANE questionnaires; the other 8 completed the questionnaires by telephone. At each time point, patients were asked to report on their participation in PT and/or adherence to their home exercise program.

Statistical Analysis

Power analysis performed with Student t test and a 2-sided level of P = .05 compared VAS pain scores between the anterior and posterior injection routes and found a mean (SD) difference of 1.4 (1.7).16 Power calculations made with nQuery Advisor Version 7.0 (Statistical Solutions) indicated a total sample size of 60 patients (30/group) would provide 80% power for detecting a significant difference assuming a 20% dropout rate.

Two-way mixed-model analysis of variance (ANOVA) was used to compare the anterior and posterior routes for statistical differences in both VAS pain scores and SANE function scores at baseline and 1, 3, and 6 months after injection. Likewise, time at baseline (just before injection)was compared with follow-up (1, 3, 6 months) with 2-way mixed-model ANOVA adjusting for anterior or posterior route. Multivariate analysis was performed to evaluate differences between baseline and 6-month follow-up with respect to anterior and posterior injection routes, controlling for age, sex, and body mass index (BMI) for VAS and SANE scores. Parametric testing methods were used for statistical analysis, which was performed with IBM SPSS Statistics Version 21.0 (IBM Corp). Significance was set at P < .05.

Results

Patient Characteristics

Of the 55 patients enrolled, 25 (46%) received anterior subacromial CSI and 30 (54%) received posterior CSI. All enrolled patients had a positive Neer impingement test immediately after injection. Mean (SD) age was 48 (9.3) years for anterior group patients and 48 (9.0) years for posterior group patients. There was no significant difference in age or BMI between the 2 groups (Table).

Table.

Five patients (9%) were excluded from the study after randomization and CSI: 2 for a full-thickness rotator cuff tear, 1 for a Bankart lesion, 1 for adhesive capsulitis, and 1 for a worker compensation claim.

One month after injection, 41 patients (75%) reported having engaged in PT as prescribed. Of the 47 patients (86%) who returned for the 3-month follow-up, 25 (46%) reported having engaged in PT between 1 month and 3 months after injection. Fourteen patients (26%) reported attending PT between 3 and 6 months post-injection.

Outcome Measures

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in VAS scores between the anterior and posterior groups at any time point (P = .45). Both groups had highly significant pain reductions (anterior, F = 9.71, P < .001; posterior, F = 13.46, P < .001). Figure 1 shows mean VAS scores and significant reductions in pain 1, 3, and 6 months after injection (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of pain reduction over time, as indicated by a nonsignificant (P = .50) difference in slopes. These pain score reductions were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 1.

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in SANE scores between the anterior and posterior groups, except for a higher mean score in the anterior group at 3 months
(P = .02). There were no other group differences (P > .10 for all). Both groups had highly significant improvements in function (anterior, F = 17.34,
P < .001; posterior, F = 13.57, P < .001). Figure 2 shows mean SANE scores and significant improvement at 1, 3, and 6 months (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of improved function over time, as indicated by a nonsignificant (P = .51) difference in slopes. These function score improvements were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 2.

From the results of this prospective randomized study, we concluded subacromial CSI significantly reduces pain and improves function regardless of route used. In addition, age, sex, and BMI do not significantly affect the efficacy of either anterior CSI or posterior CSI.

Discussion

In patients with SIS, anterior CSI and posterior CSI provided significant improvements in pain and function 1, 3, and 6 months after injection. These effects were independent of age, sex, BMI, and PT participation. There were no significant differences in outcomes between injection routes.

When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.4-8 Although clinical outcomes are inconsistent, CSI can be used to address SIS symptoms in appropriate patients. Specifically, Blair and colleagues6 found that, CSI consisting of 4 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone was effective in alleviating shoulder pain and improving shoulder range of motion. Other authors have similarly reported improved outcomes after subacromial injection and short-term follow-up with PT.4,7,8 Our findings are consistent with these reports: CSI coupled with a structured rehabilitation program is effective in alleviating symptoms associated with acute or subacute SIS.

Numerous studies have found improved clinical outcomes after anterior CSI and after posterior CSI,6-8 but no study has directly compared the clinical impact of anterior CSI with that of posterior CSI—which suggests injection route may not affect ultimate clinical outcomes.

CSI accuracy has been studied extensively.10-12,17-20 Although 2 studies found similar accuracy for anterior and posterior routes,10,11 there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12 Collectively, these studies expose the inherent difficulty in treating shoulder pain with localized subacromial injection. Therapy may fail because of errant needle positioning. Two prospective studies found improved clinical outcomes with successful delivery of medication into the subacromial space.17,18 Poor clinical outcomes may result from inaccurate CSI.

In contrast to other clinical studies, our study found that injection route was not associated with differences in clinical response. In a prospective randomized clinical trial in which 75 patients received a subacromial injection, Marder and colleagues12 found anterior routes 84% accurate and posterior routes 56% accurate; they concluded acromion anatomy and subacromial bursa anatomy make posterior injections more difficult. As theorized by Gruson and colleagues,13 with use of an anterior route, the needle enters inferior to the concavity of the acromion and provides easier access to the subacromial space. This idea is in line with Marder and colleagues’12 conclusion that subacromial bursa anatomy provides a favorable environment for accurate CSI.

If accuracy is positively correlated with clinical improvement and anterior routes are more accurate, there should be a difference in response to posterior injections. Our results provide evidence that clinical response to CSI may not depend on injection accuracy. Perhaps merely placing the corticosteroid near the bursa is adequate for improving symptoms or perhaps some of the clinical improvement is due to the systemic effect of corticosteroids. These possibilities require further analysis.

Establishing the efficacy of CSI in SIS is difficult. The literature includes various study designs, different CSI indications and medication formulations, and varying emphasis on the role of organized PT. Rehabilitation has been found to alleviate joint pain by reducing inflammation,14 but data do not universally support this finding.21,22 Nevertheless, use of PT might explain the divergence in clinical outcomes reported by Marder and colleagues,12 who found anterior CSI more accurate than posterior CSI. In our practice, PT is recommended for all SIS patients, not only those who have CSI. Thus, our findings are framed within the context of successful CSI but may include patients who improved with PT alone. This issue raises the question of whether subacromial CSI should be guided by ultrasound. Ultrasound guidance can improve CSI accuracy and clinical outcomes,23-25 though the value of this benefit is debated.26

This study had several limitations. First, pain relief was patient reported. Second, the treatment plan involved CSI with PT but did not control for CSI used alone. PT, which is part of the standard of care for patients with SIS, added another degree of complexity to the study. Third, there may have been some variability in SIS severity (stage 1, 2, or 3). Fourth, although the study design controlled for various shoulder pathologies, advanced imaging, which could have provided diagnosis confirmation, was not available for all patients. Therefore, concurrent conditions may have confounded results. However, randomization was used to try to minimize this effect. Fifth, although injection routes were randomly assigned, the trial was not blinded. Sixth, the study was underpowered by 1 patient, as there was an estimated 20% dropout rate over 3 and 6 months of follow-up. However, we do not think our results were significantly affected.

Although more research is needed to fully describe the role of subacromial CSI in SIS, our study findings suggested that CSI using either an anterior or a posterior route creates a window of symptomatic relief in which patients may be able to engage in PT.

Conclusion

Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months. No differences were found between anterior and posterior CSIs. In the context of this study, CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used. Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

References

1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain. Cochrane Database Syst Rev. 2003;(1):CD004016.

2. Bell AD, Conaway D. Corticosteroid injections for painful shoulders. Int J Clin Pract. 2005;59(10):1178-1186.

3. Michener LA, McClure PW, Karduna AR. Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech. 2003;18(5):369-379.

4. Akgün K, Birtane M, Akarirmak U. Is local subacromial corticosteroid injection beneficial in subacromial impingement syndrome? Clin Rheumatol. 2004;23(6):496-500.

5. Bhagra A, Syed H, Reed DA, et al. Efficacy of musculoskeletal injections by primary care providers in the office: a retrospective cohort study. Int J Gen Med. 2013;6:237-243.

6. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am. 1996;78(11):1685-1689.

7. Cummins CA, Sasso LM, Nicholson D. Impingement syndrome: temporal outcomes of nonoperative treatment.
J Shoulder Elbow Surg. 2009;18(2):172-177.

8. Yu C, Chen CH, Liu HT, Dai MH, Wang IC, Wang KC. Subacromial injections of corticosteroids and Xylocaine for painful subacromial impingement syndrome. Chang Gung Med J. 2006;29(5):474-478.

9. Codsi MJ. The painful shoulder: when to inject and when to refer. Cleve Clin J Med. 2007;74(7):473-474, 477-478, 480-482 passim.

10. Henkus HE, Cobben LP, Coerkamp EG, Nelissen RG, van Arkel ER. The accuracy of subacromial injections: a prospective randomized magnetic resonance imaging study. Arthroscopy. 2006;22(3):277-282.

11. Kang MN, Rizio L, Prybicien M, Middlemas DA, Blacksin MF. The accuracy of subacromial corticosteroid injections: a comparison of multiple methods. J Shoulder Elbow Surg. 2008;17(15):61S-66S.

12. Marder RA, Kim SH, Labson JD, Hunter JC. Injection of the subacromial bursa in patients with rotator cuff syndrome: a prospective, randomized study comparing the effectiveness of different routes. J Bone Joint Surg Am. 2012;94(16):
1442-1447.

13. Gruson, KI, Ruchelsman DE, Zuckerman JD. Subacromial corticosteroid injections. J Shoulder Elbow Surg. 2008;17(1 suppl):118S-130S.

14. Kuhn JE. Exercise in the treatment of rotator cuff impingement: a systematic review and a synthesized evidence-based rehabilitation protocol. J Shoulder Elbow Surg. 2009;18(1):138-160.

15. Williams GN, Gangel TJ, Arciero RA, Uhorchak JM, Taylor DC. Comparison of the Single Assessment Numeric Evaluation method and two shoulder rating scales. Outcomes measures after shoulder surgery. Am J Sports Med. 1999;27(2):214-221.

16. Tashjian RZ, Deloach J, Porucznik CA, Powell AP. Minimal clinically important differences (MCID) and patient acceptable symptomatic state (PASS) for visual analog scales (VAS) measuring pain in patients treated for rotator cuff disease.
J Shoulder Elbow Surg. 2009;88(6):927-932.

17. Eustace JA, Brophy DP, Gibney RP, Bresnihan B, FitzGerald O. Comparison of the accuracy of steroid placement with clinical outcome in patients with shoulder symptoms. Ann Rheum Dis. 1997;56(1):59-63.

18. Esenyel CZ, Esenyel M, Yeiltepe R, et al. The correlation between the accuracy of steroid injections and subsequent shoulder pain and function in subacromial impingement
syndrome [in Turkish]. Acta Orthop Traumatol Turc. 2003;37(1):
41-45.

19. Powell SE, Davis SM, Lee EH, et al. Accuracy of palpation-directed intra-articular glenohumeral injection confirmed by magnetic resonance arthrography. Arthroscopy. 2015;31(2):205-208.

20. Rutten MJ, Maresch BJ, Jager GJ, de Waal Malefijt MC. Injection of the subacromial-subdeltoid bursa: blind or ultrasound-guided? Acta Orthop. 2007;78(2):254-257.

21. Desmeules F, Côté CH, Frémont P. Therapeutic exercise and orthopedic manual therapy for impingement syndrome: a systematic review. Clin J Sport Med. 2003;13(3):176-182.

22. Winters JC, Sobel JS, Groenier KH, Arendzen HJ, Meyboom-de Jong B. Comparison of physiotherapy, manipulation, and corticosteroid injection for treating shoulder complaints in general practice: randomised, single blind study. BMJ. 1997;314(7090):1320-1325.

23. Chen MJ, Lew HL, Hsu TC, et al. Ultrasound-guided shoulder injections in the treatment of subacromial bursitis. Am J Phys Med Rehabil. 2006;85(1):31-35.

24. Hsieh LF, Hsu WC, Lin YJ, Wu SH, Chang KC, Chang HL. Is ultrasound-guided injection more effective in chronic subacromial bursitis? Med Sci Sports Exerc. 2013;45(12):
2205-2213.

25. Naredo E, Cabero F, Beneyto P, et al. A randomized comparative study of short term response to blind injection versus sonographic-guided injection of local corticosteroids in patients with painful shoulder. J Rheumatol. 2004;31(2):308-314.

26. Hall S, Buchbinder R. Do imaging methods that guide needle placement improve outcome? Ann Rheum Dis. 2004;63(9):1007-1008.

References

1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain. Cochrane Database Syst Rev. 2003;(1):CD004016.

2. Bell AD, Conaway D. Corticosteroid injections for painful shoulders. Int J Clin Pract. 2005;59(10):1178-1186.

3. Michener LA, McClure PW, Karduna AR. Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech. 2003;18(5):369-379.

4. Akgün K, Birtane M, Akarirmak U. Is local subacromial corticosteroid injection beneficial in subacromial impingement syndrome? Clin Rheumatol. 2004;23(6):496-500.

5. Bhagra A, Syed H, Reed DA, et al. Efficacy of musculoskeletal injections by primary care providers in the office: a retrospective cohort study. Int J Gen Med. 2013;6:237-243.

6. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am. 1996;78(11):1685-1689.

7. Cummins CA, Sasso LM, Nicholson D. Impingement syndrome: temporal outcomes of nonoperative treatment.
J Shoulder Elbow Surg. 2009;18(2):172-177.

8. Yu C, Chen CH, Liu HT, Dai MH, Wang IC, Wang KC. Subacromial injections of corticosteroids and Xylocaine for painful subacromial impingement syndrome. Chang Gung Med J. 2006;29(5):474-478.

9. Codsi MJ. The painful shoulder: when to inject and when to refer. Cleve Clin J Med. 2007;74(7):473-474, 477-478, 480-482 passim.

10. Henkus HE, Cobben LP, Coerkamp EG, Nelissen RG, van Arkel ER. The accuracy of subacromial injections: a prospective randomized magnetic resonance imaging study. Arthroscopy. 2006;22(3):277-282.

11. Kang MN, Rizio L, Prybicien M, Middlemas DA, Blacksin MF. The accuracy of subacromial corticosteroid injections: a comparison of multiple methods. J Shoulder Elbow Surg. 2008;17(15):61S-66S.

12. Marder RA, Kim SH, Labson JD, Hunter JC. Injection of the subacromial bursa in patients with rotator cuff syndrome: a prospective, randomized study comparing the effectiveness of different routes. J Bone Joint Surg Am. 2012;94(16):
1442-1447.

13. Gruson, KI, Ruchelsman DE, Zuckerman JD. Subacromial corticosteroid injections. J Shoulder Elbow Surg. 2008;17(1 suppl):118S-130S.

14. Kuhn JE. Exercise in the treatment of rotator cuff impingement: a systematic review and a synthesized evidence-based rehabilitation protocol. J Shoulder Elbow Surg. 2009;18(1):138-160.

15. Williams GN, Gangel TJ, Arciero RA, Uhorchak JM, Taylor DC. Comparison of the Single Assessment Numeric Evaluation method and two shoulder rating scales. Outcomes measures after shoulder surgery. Am J Sports Med. 1999;27(2):214-221.

16. Tashjian RZ, Deloach J, Porucznik CA, Powell AP. Minimal clinically important differences (MCID) and patient acceptable symptomatic state (PASS) for visual analog scales (VAS) measuring pain in patients treated for rotator cuff disease.
J Shoulder Elbow Surg. 2009;88(6):927-932.

17. Eustace JA, Brophy DP, Gibney RP, Bresnihan B, FitzGerald O. Comparison of the accuracy of steroid placement with clinical outcome in patients with shoulder symptoms. Ann Rheum Dis. 1997;56(1):59-63.

18. Esenyel CZ, Esenyel M, Yeiltepe R, et al. The correlation between the accuracy of steroid injections and subsequent shoulder pain and function in subacromial impingement
syndrome [in Turkish]. Acta Orthop Traumatol Turc. 2003;37(1):
41-45.

19. Powell SE, Davis SM, Lee EH, et al. Accuracy of palpation-directed intra-articular glenohumeral injection confirmed by magnetic resonance arthrography. Arthroscopy. 2015;31(2):205-208.

20. Rutten MJ, Maresch BJ, Jager GJ, de Waal Malefijt MC. Injection of the subacromial-subdeltoid bursa: blind or ultrasound-guided? Acta Orthop. 2007;78(2):254-257.

21. Desmeules F, Côté CH, Frémont P. Therapeutic exercise and orthopedic manual therapy for impingement syndrome: a systematic review. Clin J Sport Med. 2003;13(3):176-182.

22. Winters JC, Sobel JS, Groenier KH, Arendzen HJ, Meyboom-de Jong B. Comparison of physiotherapy, manipulation, and corticosteroid injection for treating shoulder complaints in general practice: randomised, single blind study. BMJ. 1997;314(7090):1320-1325.

23. Chen MJ, Lew HL, Hsu TC, et al. Ultrasound-guided shoulder injections in the treatment of subacromial bursitis. Am J Phys Med Rehabil. 2006;85(1):31-35.

24. Hsieh LF, Hsu WC, Lin YJ, Wu SH, Chang KC, Chang HL. Is ultrasound-guided injection more effective in chronic subacromial bursitis? Med Sci Sports Exerc. 2013;45(12):
2205-2213.

25. Naredo E, Cabero F, Beneyto P, et al. A randomized comparative study of short term response to blind injection versus sonographic-guided injection of local corticosteroids in patients with painful shoulder. J Rheumatol. 2004;31(2):308-314.

26. Hall S, Buchbinder R. Do imaging methods that guide needle placement improve outcome? Ann Rheum Dis. 2004;63(9):1007-1008.

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Referral Patterns for Chronic Groin Pain and Athletic Pubalgia/Sports Hernia: Magnetic Resonance Imaging Findings, Treatment, and Outcomes

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The past 3 decades have seen an evolution in the understanding, diagnosis, and treatment of groin pain, both chronic and acute, in athletes and non-athletes alike. Groin pain and groin injury are common. Most cases are transient, with patients returning to their activities within weeks or months. There has also been increasing awareness of a definitive population of patients who do not get better, or who improve and plateau before reaching preinjury level of performance.1-3 Several authors have brought more attention to the injury, introducing vocabulary, theories, diagnostic testing, and diagnoses, which now constitute a knowledge base.1,3-5

As stated in almost every article on groin pain and diagnosis, lack of cohesive agreement and vocabulary, and consistent protocols and procedures, has abounded, making general understanding and agreement in this area inconsistent.1,6-8In this article, members of a tertiary-care group specializing in chronic groin pain, athletic pubalgia (sports hernia), and inguinal herniorrhaphy outline their clinical examination, diagnostic algorithm, imaging protocol, treatment strategy, and outcomes for a population of patients referred by physicians and allied health professionals for a suspected diagnosis of athletic pubalgia.

Background

The pubic symphysis acts as a stabilizing central anchor with elaborate involvement of the anterior structures, including the rectus abdominis, adductor longus, and inguinal ligaments.3,7,9 Literature from Europe, Australia, and the United States has described groin pain, mostly in professional athletes, involving these pubic structures and attachments. Several publications have been addressing chronic groin pain, and each has its own diagnostic algorithm, imaging protocol, and treatment strategy.3,6,9-18

Terminology specific to groin pain in athletes is not new, and has a varied history dating to the early 20th century. Terms such as sportsman hernia19 and subsequently sports hernia20, have recently been embraced by the lay population. In 1999, Gibbon21 described shearing of the common adductor–rectus abdominis anatomical and functional unit and referenced a 1902 anatomical text that describes vertical ligamentous fibers contiguous with rectus sheath and adductor muscles, both attaching to the pubis. Injury to this region is the basis of pubalgia, a term originally used in 1984 by Brunet to describe a pain syndrome at the pubis.22

Many authors have proposed replacing sports hernia with athletic pubalgia.1,3,6,7,10,14,18,23 These terms refer to a group of musculoskeletal processes that occur in and around the pubic symphysis and that share similar mechanisms of injury and common clinical manifestations. The condition was originally described in high-performance athletes, and at one point the term sports hernia was reserved for this patient population.5 According to many authors, presence of an inguinal hernia excludes the diagnosis.1,2,5Magnetic resonance imaging (MRI) has helped to advance and define our understanding of the injury.10 As the history of the literature suggests, earlier concepts of chronic pain focused either on the medial aspect of the inguinal canal and its structures or on the pubic attachments. Many specialists in the area have concluded that the chronic groin pain injury can and often does embody both elements.3,9 Correlation with MRI findings, injury seen during surgical procedures, and cadaveric studies have directed our understanding to a structure, the pre-pubic aponeurotic complex (P-PAC), or rectus aponeurotic plate.12,24,25 Anatomically, the P-PAC, which has several fascial components, attaches posteriorly to the pubic bone and, to a degree, the pubic symphyseal cartilaginous disc. Major contributions to the P-PAC are fibers from the rectus abdominis tendon, the medial aspect of the transversalis and internal oblique muscles (the conjoint tendon, according to some), the inguinal ligament, and the adductor longus tendon.26When communicating with referring physicians, we use the term athletic pubalgia to indicate a specific injury. The athletic pubalgia injury can be defined as serial microtearing,1 or complete tearing, of the posterior attachment of the P-PAC off the anterior pubis.3,10 Complete tearing or displacement can occur unilaterally or across the midline to the other side. As athletic pubalgia is a specific anatomical injury rather than a broad category of findings, an additional pathologic diagnosis, such as inguinal hernia, does not exclude the diagnosis of athletic pubalgia. Unfortunately, the terms sports hernia and sportsman hernia, commonly used in the media and in professional communities, have largely confused the broader understanding of nuances and of the differences between the specific injuries and MRI findings.18

 

 

Our Experience

In our practice, we see groin pain patients referred by internists, physiatrists, physical therapists, trainers, general surgeons, urologists, gynecologists, and orthopedic surgeons. In many cases, patients have been through several consultations and work-ups, as their pain syndrome does not fall under a specific category. Patients without inguinal hernia, hip injury, urologic, or gynecologic issues typically are referred to a physiatrist or a physical therapist. Often, there are marginal improvements with physical therapy, but in some cases the injury never completely resolves, and the patient continues to have pain with activity or return to sports.

Most of our patients are nonprofessional athletes, men and women who range widely in age and participate casually or regularly in sporting events. Most lack the rigorous training, conditioning, and close supervision that professional athletes receive. Many other patients are nonprofessional but elite athletes who train 7 days a week for marathons, ultramarathons, triathlons, obstacle course races (“mudders”), and similar events.

Work-Up

A single algorithm is used for all patients initially referred to the surgeon’s office for pelvic or groin pain. The initial interview directs attention to injury onset and mechanism, duration of rest or physical therapy after surgery, pain quality and pain levels, and antagonistic movements and positions. Examination starts with assessment for inguinal, femoral, and umbilical hernias. Resisted sit-up, leg-raise, adduction, and hip assessment tests are performed. The P-PAC is examined with a maneuver similar to the one used for inguinal hernia, as it allows for better assessment of the transversalis fascia (over the direct space) to determine if the inguinal canal floor is attenuated and bulges forward with the Valsalva maneuver. Then, the lateral aspect of the rectus muscle is assessed for pain, usually with the head raised to contract the muscle, to determine tenderness along the lateral border. The rectus edge is traced down to the pubis at its attachment, the superolateral border of the P-PAC. Examination proceeds medially, over the rectus attachment, toward the pubic symphysis, continuing the assessment for tenderness. Laterally, the conjoint tendon and inguinal ligament medial attachments are assessed at the level of the pubic tubercle, which represents the lateral border of the P-PAC. Finally, the examination continues to the inferior border with assessment of the adductor longus attachment, which is best performed with the leg in an adducted position. In the acute or semiacute setting (pain within 1 year of injury onset), tenderness is often elicited. With long-standing injuries, pain is often not elicited, but the patient experiences pain along this axis during activity or afterward.

Patients with positive history and physical examination findings proceed through an MRI protocol designed to detect pathology of the pubic symphysis, hips, and inguinal canals (Figures 1A-1D).

Figure 1.
Imaging includes use of axial single-shot fast spin-echo with and without the Valsalva maneuver. Use of this maneuver increases sensitivity in detecting abdominal wall deficiencies, such as inguinal hernias (Figures 2A, 2B).
Figure 2.
We developed this pubalgia protocol (Table) to specifically assess each of the potential areas of concern.
Table.

Treatment

Patients who report sustaining an acute groin injury within the previous 6 months are treated nonoperatively. A combination of rest, nonsteroidal anti-inflammatory drugs, and physical therapy is generally recommended.2,10 In cases of failed nonoperative management, patients are evaluated for surgery. No single operation is recommended for all patients.1,6,14,27,28 (Larson26 recently reviewed results from several trials involving a variety of surgical repairs and found return-to-sports rates ranging from 80% to 100%.) Findings from the physical examination and from the properly protocolled MRI examination are used in planning surgery to correct any pathology that could be contributing to symptoms or destabilization of the structures attaching to the pubis. Disruption of the P-PAC from the pubis would be repaired, for example. Additional injuries, such as partial or complete detachment of the conjoint tendon or inguinal ligament, may be repaired as well. If the transversalis fascia is attenuated and bulging forward, the inguinal floor is closed. Adductor longus tendon pathology is addressed, most commonly with partial tendinolysis. Often, concomitant inguinal hernias are found, and these may be repaired in open fashion while other maneuvers are being performed, or laparoscopically.

Materials and Methods

After receiving study approval from our Institutional Review Board, we retrospectively searched for all MRIs performed by our radiology department between March 1, 2011 and March 31, 2013 on patients referred for an indication of groin pain, sports hernia, or athletic pubalgia. Patients were excluded if they were younger than 18 years any time during their care. Some patients previously or subsequently underwent computed tomography or ultrasonography. MRIs were reviewed and positive findings were compiled in a database. Charts were reviewed to identify which patients in the dataset underwent surgery, after MRI, to address their presenting chief complaint. Surgery date and procedure(s) performed were recorded. Patients were interviewed by telephone as part of the in-office postoperative follow-up.

 

 

Results

One hundred nineteen MRIs were performed on 117 patients (97 men, 83%). Mean age was 39.8 years. Seventy-nine patients (68%) had an MRI finding of athletic pubalgia, 67 (57%) had an acetabular labral tear in one or both hip joints, and 41 (35%) had a true inguinal hernia. Concomitant findings were common: 47 cases of athletic pubalgia and labral tear(s), 28 cases of athletic pubalgia and inguinal hernia, and 15 cases of all 3 (athletic pubalgia, labral tear, inguinal hernia).

Use of breath-hold axial single-shot fast spin-echo sequences with and without the Valsalva maneuver increased sensitivity in detecting pathologies—inguinal hernia and Gilmore groin in particular. On 24 of the 119 MRIs, the Valsalva maneuver either revealed the finding or made it significantly more apparent.

Of all patients referred for MRI for chronic groin pain, 48 (41%) subsequently underwent surgery. In 29 surgeries, the rectus abdominis, adductor longus, and/or pre-pubic aponeurotic plate were repaired; in 13 cases, herniorrhaphy was performed as well; in 2 cases, masses involving the spermatic cord were removed.

The most common surgery (30 cases) was herniorrhaphy, which was performed as a single procedure, multiple procedures, or in combination with procedures not related to a true hernia. Eighteen patients underwent surgery only for hernia repair.

Of the 79 patients with MRI-positive athletic pubalgia, 39 subsequently underwent surgery, and 31 (79%) of these were followed up by telephone. Mean duration of rest after surgery was 6.2 weeks. Twelve patients (39%) had physical therapy after surgery, some as early as 4 weeks, and some have continued their therapy since surgery. Of the 31 patients who were followed up after surgery, 23 (74%) resumed previous activity levels. Return to previous activity level took these patients a mean of 17.9 weeks. When asked if outcomes satisfied their expectations, 28 patients (90%) said yes, and 3 said no.

Forty patients with MRI-positive athletic pubalgia were nonoperatively treated, and 28 (70%) of these patients were followed up. In this group, mean duration of rest after surgery was 6.9 weeks. Thirteen patients (46%) participated in physical therapy, for a mean duration of 10.8 weeks. Of the patients followed up, 19 (68%) returned to previous activity level. Twenty-one patients (75%) were satisfied with their outcome.

Discussion

Diagnosis and treatment of chronic groin pain have had a long, confusing, and frustrating history for both patients and the medical professionals who provide them with care.3,6,7,10 Historically, the problem has been, in part, the lack of diagnostic capabilities. Currently, however, pubalgia MRI protocol allows the exact pathology to be demonstrated.3 As already noted, concomitant hip pathology or inguinal hernia is not unusual8; any structural abnormality in the area is a potential destabilizer of the structures attached to the pubis.18 Solving only one of these issues may offer only partial resolution of symptoms and thereby reduce the rate of successful treatment of groin pain.

Diagnostic algorithms are being developed. In addition, nonoperative treatments are being tried for some of the issues. Physicians are giving diagnostic and therapeutic steroid injections in the pubic cleft, along the rectus abdominis/adductor longus complex, or posterior to the P-PAC. Platelet-rich plasma injection therapy has had limited success.29This article provides a snapshot of what a tertiary-care group of physicians specializing in chronic groin pain sees in an unfiltered setting. We think this is instructive for several reasons.

First, many patients in our population have visited a multitude of specialists without receiving a diagnosis or being referred appropriately. Simply, many specialists do not know the next step in treating groin pain and thus do not make the appropriate referral. Until recently, the literature has not been helpful. It has poorly described the constellation of injuries comprising chronic groin pain. More significantly, groin injuries have been presented as ambiguous injuries lacking effective treatment. Over the past decade, however, abundant literature on the correlation of these injuries with specific MRI findings has made the case otherwise.

Second, a specific MRI pubalgia protocol is needed. Inability to make a correct diagnosis, because of improper MRI, continues to add to the confusion surrounding the injury and undoubtedly prolongs the general medical community’s thinking that diagnosis and treatment of chronic groin pain are elusive. Our data support this point in many ways. Although all patients in this study were seen by a medical professional before coming to our office, none had received a diagnosis of occult hernia or attenuated transversalis fascia; nevertheless, we identified inguinal hernia, Gilmore groin, or both in 44% of these patients. These findings are not surprising, as MRI was the crucial link in diagnosis. In addition, the point made by other groin pain specialists—that a hernia precludes a pubalgia diagnosis1,2,5—is not supported by our data. Inguinal hernia can and does exist in conjunction with pubalgia. More than half the patients in our study had a combined diagnosis. We contend that, much as hip labral pathology occurs concomitantly with pubalgia,23 inguinal hernia may be a predisposing factor as well. A defect in the direct or indirect space can destabilize the area and place additional strain on the pubic attachments.

In our experience, the dynamic Valsalva sequence improves detection of true hernias and anterior abdominal wall deficiencies and should be included in each protocol for the evaluation of acute or chronic groin pain.

Shear forces and injury at the pubis can occur outside professional athletics. Our patient population is nonprofessional athletes, teenagers to retirees, and all can develop athletic pubalgia. Ninety percent of surveyed patients who received a diagnosis and were treated surgically were satisfied with their outcomes.


Am J Orthop. 2017;46(4):E251-E256. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Meyers WC, Lanfranco A, Castellanos A. Surgical management of chronic lower abdominal and groin pain in high-performance athletes. Curr Sports Med Rep. 2002;1(5):301-305.

2. Ahumada LA, Ashruf S, Espinosa-de-los-Monteros A, et al. Athletic pubalgia: definition and surgical treatment. Ann Plast Surg. 2005;55(4):393-396.

3. Omar IM, Zoga AC, Kavanagh EC, et al. Athletic pubalgia and “sports hernia”: optimal MR imaging technique and findings. Radiographics. 2008;28(5):1415-1438.

4. Gilmore OJA. Gilmore’s groin: ten years experience of groin disruption—a previously unsolved problem in sportsmen. Sports Med Soft Tissue Trauma. 1991;3:12-14.

5. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.

6. Kavanagh EC, Koulouris G, Ford S, McMahon P, Johnson C, Eustace SJ. MR imaging of groin pain in the athlete. Semin Musculoskelet Radiol. 2006;10(3):197-207.

7. Cunningham PM, Brennan D, O’Connell M, MacMahon P, O’Neill P, Eustace S. Patterns of bone and soft-tissue injury at the symphysis pubis in soccer players: observations at MRI. AJR Am J Roentgenol. 2007;188(3):W291-W296.

8. Zoga AC, Kavanagh EC, Omar IM, et al. Athletic pubalgia and the “sports hernia”: MR imaging findings. Radiology. 2008;247(3):797-807.

9. Koulouris G. Imaging review of groin pain in elite athletes: an anatomic approach to imaging findings. AJR Am J Roentgenol. 2008;191(4):962-972.

10. Albers SL, Spritzer CE, Garrett WE Jr, Meyers WC. MR findings in athletes with pubalgia. Skeletal Radiol. 2001;30(5):270-277.

11. Brennan D, O’Connell MJ, Ryan M, et al. Secondary cleft sign as a marker of injury in athletes with groin pain: MR image appearance and interpretation. Radiology. 2005;235(1):162-167.

12. Robinson P, Salehi F, Grainger A, et al. Cadaveric and MRI study of the musculotendinous contributions to the capsule of the symphysis pubis. AJR Am J Roentgenol. 2007;188(5):W440-W445.

13. Schilders E, Talbot JC, Robinson P, Dimitrakopoulou A, Gibbon WW, Bismil Q. Adductor-related groin pain in recreational athletes. J Bone Joint Surg Am. 2009;91(10):2455-2460.

14. Davies AG, Clarke AW, Gilmore J, Wotherspoon M, Connell DA. Review: imaging of groin pain in the athlete. Skeletal Radiol. 2010;39(7):629-644.

15. Mullens FE, Zoga AC, Morrison WB, Meyers WC. Review of MRI technique and imaging findings in athletic pubalgia and the “sports hernia.” Eur J Radiol. 2012;81(12):3780-3792.

16. Zoga AC, Meyers WC. Magnetic resonance imaging for pain after surgical treatment for athletic pubalgia and the “sports hernia.” Semin Musculoskelet Radiol. 2011;15(4):372-382.

17. Beer E. Periostitis of symphysis and descending rami of pubes following suprapubic operations. Int J Med Surg. 1924;37(5):224-225.

18. MacMahon PJ, Hogan BA, Shelly MJ, Eustace SJ, Kavanagh EC. Imaging of groin pain. Magn Reson Imaging Clin N Am. 2009;17(4):655-666.

19. Malycha P, Lovell G. Inguinal surgery in athletes with chronic groin pain: the ‘sportsman’s’ hernia. Aust N Z J Surg. 1992;62(2):123-125.

20. Hackney RG. The sports hernia: a cause of chronic groin pain. Br J Sports Med. 1993;27(1):58-62.

21. Gibbon WW. Groin pain in athletes. Lancet. 1999;353(9162):1444-1445.

22. Brunet B, Brunet-Geudj E, Genety J. La pubalgie: syndrome “fourre-tout” pur une plus grande riguer diagnostique et therapeutique. Intantanes Medicaux. 1984;55:25-30.

23. Lischuk AW, Dorantes TM, Wong W, Haims AH. Imaging of sports-related hip and groin injuries. Sports Health. 2010;2(3):252-261.

24. Gibbon WW, Hession PR. Diseases of the pubis and pubic symphysis: MR imaging appearances. AJR Am J Roentgenol. 1997;169(3):849-853.

25. Gamble JG, Simmons SC, Freedman M. The symphysis pubis. Anatomic and pathologic considerations. Clin Orthop Relat Res. 1986;(203):261-272.

26. Larson CM. Sports hernia/athletic pubalgia: evaluation and management. Sports Health. 2014;6(2):139-144.

27. Maffulli N, Loppini M, Longo UG, Denaro V. Bilateral mini-invasive adductor tenotomy for the management of chronic unilateral adductor longus tendinopathy in athletes. Am J Sports Med. 2012;40(8):1880-1886.

28. Schilders E, Dimitrakopoulou A, Cooke M, Bismil Q, Cooke C. Effectiveness of a selective partial adductor release for chronic adductor-related groin pain in professional athletes. Am J Sports Med. 2013;41(3):603-607.

29. Scholten PM, Massimi S, Dahmen N, Diamond J, Wyss J. Successful treatment of athletic pubalgia in a lacrosse player with ultrasound-guided needle tenotomy and platelet-rich plasma injection: a case report. PM R. 2015;7(1):79-83.

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The past 3 decades have seen an evolution in the understanding, diagnosis, and treatment of groin pain, both chronic and acute, in athletes and non-athletes alike. Groin pain and groin injury are common. Most cases are transient, with patients returning to their activities within weeks or months. There has also been increasing awareness of a definitive population of patients who do not get better, or who improve and plateau before reaching preinjury level of performance.1-3 Several authors have brought more attention to the injury, introducing vocabulary, theories, diagnostic testing, and diagnoses, which now constitute a knowledge base.1,3-5

As stated in almost every article on groin pain and diagnosis, lack of cohesive agreement and vocabulary, and consistent protocols and procedures, has abounded, making general understanding and agreement in this area inconsistent.1,6-8In this article, members of a tertiary-care group specializing in chronic groin pain, athletic pubalgia (sports hernia), and inguinal herniorrhaphy outline their clinical examination, diagnostic algorithm, imaging protocol, treatment strategy, and outcomes for a population of patients referred by physicians and allied health professionals for a suspected diagnosis of athletic pubalgia.

Background

The pubic symphysis acts as a stabilizing central anchor with elaborate involvement of the anterior structures, including the rectus abdominis, adductor longus, and inguinal ligaments.3,7,9 Literature from Europe, Australia, and the United States has described groin pain, mostly in professional athletes, involving these pubic structures and attachments. Several publications have been addressing chronic groin pain, and each has its own diagnostic algorithm, imaging protocol, and treatment strategy.3,6,9-18

Terminology specific to groin pain in athletes is not new, and has a varied history dating to the early 20th century. Terms such as sportsman hernia19 and subsequently sports hernia20, have recently been embraced by the lay population. In 1999, Gibbon21 described shearing of the common adductor–rectus abdominis anatomical and functional unit and referenced a 1902 anatomical text that describes vertical ligamentous fibers contiguous with rectus sheath and adductor muscles, both attaching to the pubis. Injury to this region is the basis of pubalgia, a term originally used in 1984 by Brunet to describe a pain syndrome at the pubis.22

Many authors have proposed replacing sports hernia with athletic pubalgia.1,3,6,7,10,14,18,23 These terms refer to a group of musculoskeletal processes that occur in and around the pubic symphysis and that share similar mechanisms of injury and common clinical manifestations. The condition was originally described in high-performance athletes, and at one point the term sports hernia was reserved for this patient population.5 According to many authors, presence of an inguinal hernia excludes the diagnosis.1,2,5Magnetic resonance imaging (MRI) has helped to advance and define our understanding of the injury.10 As the history of the literature suggests, earlier concepts of chronic pain focused either on the medial aspect of the inguinal canal and its structures or on the pubic attachments. Many specialists in the area have concluded that the chronic groin pain injury can and often does embody both elements.3,9 Correlation with MRI findings, injury seen during surgical procedures, and cadaveric studies have directed our understanding to a structure, the pre-pubic aponeurotic complex (P-PAC), or rectus aponeurotic plate.12,24,25 Anatomically, the P-PAC, which has several fascial components, attaches posteriorly to the pubic bone and, to a degree, the pubic symphyseal cartilaginous disc. Major contributions to the P-PAC are fibers from the rectus abdominis tendon, the medial aspect of the transversalis and internal oblique muscles (the conjoint tendon, according to some), the inguinal ligament, and the adductor longus tendon.26When communicating with referring physicians, we use the term athletic pubalgia to indicate a specific injury. The athletic pubalgia injury can be defined as serial microtearing,1 or complete tearing, of the posterior attachment of the P-PAC off the anterior pubis.3,10 Complete tearing or displacement can occur unilaterally or across the midline to the other side. As athletic pubalgia is a specific anatomical injury rather than a broad category of findings, an additional pathologic diagnosis, such as inguinal hernia, does not exclude the diagnosis of athletic pubalgia. Unfortunately, the terms sports hernia and sportsman hernia, commonly used in the media and in professional communities, have largely confused the broader understanding of nuances and of the differences between the specific injuries and MRI findings.18

 

 

Our Experience

In our practice, we see groin pain patients referred by internists, physiatrists, physical therapists, trainers, general surgeons, urologists, gynecologists, and orthopedic surgeons. In many cases, patients have been through several consultations and work-ups, as their pain syndrome does not fall under a specific category. Patients without inguinal hernia, hip injury, urologic, or gynecologic issues typically are referred to a physiatrist or a physical therapist. Often, there are marginal improvements with physical therapy, but in some cases the injury never completely resolves, and the patient continues to have pain with activity or return to sports.

Most of our patients are nonprofessional athletes, men and women who range widely in age and participate casually or regularly in sporting events. Most lack the rigorous training, conditioning, and close supervision that professional athletes receive. Many other patients are nonprofessional but elite athletes who train 7 days a week for marathons, ultramarathons, triathlons, obstacle course races (“mudders”), and similar events.

Work-Up

A single algorithm is used for all patients initially referred to the surgeon’s office for pelvic or groin pain. The initial interview directs attention to injury onset and mechanism, duration of rest or physical therapy after surgery, pain quality and pain levels, and antagonistic movements and positions. Examination starts with assessment for inguinal, femoral, and umbilical hernias. Resisted sit-up, leg-raise, adduction, and hip assessment tests are performed. The P-PAC is examined with a maneuver similar to the one used for inguinal hernia, as it allows for better assessment of the transversalis fascia (over the direct space) to determine if the inguinal canal floor is attenuated and bulges forward with the Valsalva maneuver. Then, the lateral aspect of the rectus muscle is assessed for pain, usually with the head raised to contract the muscle, to determine tenderness along the lateral border. The rectus edge is traced down to the pubis at its attachment, the superolateral border of the P-PAC. Examination proceeds medially, over the rectus attachment, toward the pubic symphysis, continuing the assessment for tenderness. Laterally, the conjoint tendon and inguinal ligament medial attachments are assessed at the level of the pubic tubercle, which represents the lateral border of the P-PAC. Finally, the examination continues to the inferior border with assessment of the adductor longus attachment, which is best performed with the leg in an adducted position. In the acute or semiacute setting (pain within 1 year of injury onset), tenderness is often elicited. With long-standing injuries, pain is often not elicited, but the patient experiences pain along this axis during activity or afterward.

Patients with positive history and physical examination findings proceed through an MRI protocol designed to detect pathology of the pubic symphysis, hips, and inguinal canals (Figures 1A-1D).

Figure 1.
Imaging includes use of axial single-shot fast spin-echo with and without the Valsalva maneuver. Use of this maneuver increases sensitivity in detecting abdominal wall deficiencies, such as inguinal hernias (Figures 2A, 2B).
Figure 2.
We developed this pubalgia protocol (Table) to specifically assess each of the potential areas of concern.
Table.

Treatment

Patients who report sustaining an acute groin injury within the previous 6 months are treated nonoperatively. A combination of rest, nonsteroidal anti-inflammatory drugs, and physical therapy is generally recommended.2,10 In cases of failed nonoperative management, patients are evaluated for surgery. No single operation is recommended for all patients.1,6,14,27,28 (Larson26 recently reviewed results from several trials involving a variety of surgical repairs and found return-to-sports rates ranging from 80% to 100%.) Findings from the physical examination and from the properly protocolled MRI examination are used in planning surgery to correct any pathology that could be contributing to symptoms or destabilization of the structures attaching to the pubis. Disruption of the P-PAC from the pubis would be repaired, for example. Additional injuries, such as partial or complete detachment of the conjoint tendon or inguinal ligament, may be repaired as well. If the transversalis fascia is attenuated and bulging forward, the inguinal floor is closed. Adductor longus tendon pathology is addressed, most commonly with partial tendinolysis. Often, concomitant inguinal hernias are found, and these may be repaired in open fashion while other maneuvers are being performed, or laparoscopically.

Materials and Methods

After receiving study approval from our Institutional Review Board, we retrospectively searched for all MRIs performed by our radiology department between March 1, 2011 and March 31, 2013 on patients referred for an indication of groin pain, sports hernia, or athletic pubalgia. Patients were excluded if they were younger than 18 years any time during their care. Some patients previously or subsequently underwent computed tomography or ultrasonography. MRIs were reviewed and positive findings were compiled in a database. Charts were reviewed to identify which patients in the dataset underwent surgery, after MRI, to address their presenting chief complaint. Surgery date and procedure(s) performed were recorded. Patients were interviewed by telephone as part of the in-office postoperative follow-up.

 

 

Results

One hundred nineteen MRIs were performed on 117 patients (97 men, 83%). Mean age was 39.8 years. Seventy-nine patients (68%) had an MRI finding of athletic pubalgia, 67 (57%) had an acetabular labral tear in one or both hip joints, and 41 (35%) had a true inguinal hernia. Concomitant findings were common: 47 cases of athletic pubalgia and labral tear(s), 28 cases of athletic pubalgia and inguinal hernia, and 15 cases of all 3 (athletic pubalgia, labral tear, inguinal hernia).

Use of breath-hold axial single-shot fast spin-echo sequences with and without the Valsalva maneuver increased sensitivity in detecting pathologies—inguinal hernia and Gilmore groin in particular. On 24 of the 119 MRIs, the Valsalva maneuver either revealed the finding or made it significantly more apparent.

Of all patients referred for MRI for chronic groin pain, 48 (41%) subsequently underwent surgery. In 29 surgeries, the rectus abdominis, adductor longus, and/or pre-pubic aponeurotic plate were repaired; in 13 cases, herniorrhaphy was performed as well; in 2 cases, masses involving the spermatic cord were removed.

The most common surgery (30 cases) was herniorrhaphy, which was performed as a single procedure, multiple procedures, or in combination with procedures not related to a true hernia. Eighteen patients underwent surgery only for hernia repair.

Of the 79 patients with MRI-positive athletic pubalgia, 39 subsequently underwent surgery, and 31 (79%) of these were followed up by telephone. Mean duration of rest after surgery was 6.2 weeks. Twelve patients (39%) had physical therapy after surgery, some as early as 4 weeks, and some have continued their therapy since surgery. Of the 31 patients who were followed up after surgery, 23 (74%) resumed previous activity levels. Return to previous activity level took these patients a mean of 17.9 weeks. When asked if outcomes satisfied their expectations, 28 patients (90%) said yes, and 3 said no.

Forty patients with MRI-positive athletic pubalgia were nonoperatively treated, and 28 (70%) of these patients were followed up. In this group, mean duration of rest after surgery was 6.9 weeks. Thirteen patients (46%) participated in physical therapy, for a mean duration of 10.8 weeks. Of the patients followed up, 19 (68%) returned to previous activity level. Twenty-one patients (75%) were satisfied with their outcome.

Discussion

Diagnosis and treatment of chronic groin pain have had a long, confusing, and frustrating history for both patients and the medical professionals who provide them with care.3,6,7,10 Historically, the problem has been, in part, the lack of diagnostic capabilities. Currently, however, pubalgia MRI protocol allows the exact pathology to be demonstrated.3 As already noted, concomitant hip pathology or inguinal hernia is not unusual8; any structural abnormality in the area is a potential destabilizer of the structures attached to the pubis.18 Solving only one of these issues may offer only partial resolution of symptoms and thereby reduce the rate of successful treatment of groin pain.

Diagnostic algorithms are being developed. In addition, nonoperative treatments are being tried for some of the issues. Physicians are giving diagnostic and therapeutic steroid injections in the pubic cleft, along the rectus abdominis/adductor longus complex, or posterior to the P-PAC. Platelet-rich plasma injection therapy has had limited success.29This article provides a snapshot of what a tertiary-care group of physicians specializing in chronic groin pain sees in an unfiltered setting. We think this is instructive for several reasons.

First, many patients in our population have visited a multitude of specialists without receiving a diagnosis or being referred appropriately. Simply, many specialists do not know the next step in treating groin pain and thus do not make the appropriate referral. Until recently, the literature has not been helpful. It has poorly described the constellation of injuries comprising chronic groin pain. More significantly, groin injuries have been presented as ambiguous injuries lacking effective treatment. Over the past decade, however, abundant literature on the correlation of these injuries with specific MRI findings has made the case otherwise.

Second, a specific MRI pubalgia protocol is needed. Inability to make a correct diagnosis, because of improper MRI, continues to add to the confusion surrounding the injury and undoubtedly prolongs the general medical community’s thinking that diagnosis and treatment of chronic groin pain are elusive. Our data support this point in many ways. Although all patients in this study were seen by a medical professional before coming to our office, none had received a diagnosis of occult hernia or attenuated transversalis fascia; nevertheless, we identified inguinal hernia, Gilmore groin, or both in 44% of these patients. These findings are not surprising, as MRI was the crucial link in diagnosis. In addition, the point made by other groin pain specialists—that a hernia precludes a pubalgia diagnosis1,2,5—is not supported by our data. Inguinal hernia can and does exist in conjunction with pubalgia. More than half the patients in our study had a combined diagnosis. We contend that, much as hip labral pathology occurs concomitantly with pubalgia,23 inguinal hernia may be a predisposing factor as well. A defect in the direct or indirect space can destabilize the area and place additional strain on the pubic attachments.

In our experience, the dynamic Valsalva sequence improves detection of true hernias and anterior abdominal wall deficiencies and should be included in each protocol for the evaluation of acute or chronic groin pain.

Shear forces and injury at the pubis can occur outside professional athletics. Our patient population is nonprofessional athletes, teenagers to retirees, and all can develop athletic pubalgia. Ninety percent of surveyed patients who received a diagnosis and were treated surgically were satisfied with their outcomes.


Am J Orthop. 2017;46(4):E251-E256. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

The past 3 decades have seen an evolution in the understanding, diagnosis, and treatment of groin pain, both chronic and acute, in athletes and non-athletes alike. Groin pain and groin injury are common. Most cases are transient, with patients returning to their activities within weeks or months. There has also been increasing awareness of a definitive population of patients who do not get better, or who improve and plateau before reaching preinjury level of performance.1-3 Several authors have brought more attention to the injury, introducing vocabulary, theories, diagnostic testing, and diagnoses, which now constitute a knowledge base.1,3-5

As stated in almost every article on groin pain and diagnosis, lack of cohesive agreement and vocabulary, and consistent protocols and procedures, has abounded, making general understanding and agreement in this area inconsistent.1,6-8In this article, members of a tertiary-care group specializing in chronic groin pain, athletic pubalgia (sports hernia), and inguinal herniorrhaphy outline their clinical examination, diagnostic algorithm, imaging protocol, treatment strategy, and outcomes for a population of patients referred by physicians and allied health professionals for a suspected diagnosis of athletic pubalgia.

Background

The pubic symphysis acts as a stabilizing central anchor with elaborate involvement of the anterior structures, including the rectus abdominis, adductor longus, and inguinal ligaments.3,7,9 Literature from Europe, Australia, and the United States has described groin pain, mostly in professional athletes, involving these pubic structures and attachments. Several publications have been addressing chronic groin pain, and each has its own diagnostic algorithm, imaging protocol, and treatment strategy.3,6,9-18

Terminology specific to groin pain in athletes is not new, and has a varied history dating to the early 20th century. Terms such as sportsman hernia19 and subsequently sports hernia20, have recently been embraced by the lay population. In 1999, Gibbon21 described shearing of the common adductor–rectus abdominis anatomical and functional unit and referenced a 1902 anatomical text that describes vertical ligamentous fibers contiguous with rectus sheath and adductor muscles, both attaching to the pubis. Injury to this region is the basis of pubalgia, a term originally used in 1984 by Brunet to describe a pain syndrome at the pubis.22

Many authors have proposed replacing sports hernia with athletic pubalgia.1,3,6,7,10,14,18,23 These terms refer to a group of musculoskeletal processes that occur in and around the pubic symphysis and that share similar mechanisms of injury and common clinical manifestations. The condition was originally described in high-performance athletes, and at one point the term sports hernia was reserved for this patient population.5 According to many authors, presence of an inguinal hernia excludes the diagnosis.1,2,5Magnetic resonance imaging (MRI) has helped to advance and define our understanding of the injury.10 As the history of the literature suggests, earlier concepts of chronic pain focused either on the medial aspect of the inguinal canal and its structures or on the pubic attachments. Many specialists in the area have concluded that the chronic groin pain injury can and often does embody both elements.3,9 Correlation with MRI findings, injury seen during surgical procedures, and cadaveric studies have directed our understanding to a structure, the pre-pubic aponeurotic complex (P-PAC), or rectus aponeurotic plate.12,24,25 Anatomically, the P-PAC, which has several fascial components, attaches posteriorly to the pubic bone and, to a degree, the pubic symphyseal cartilaginous disc. Major contributions to the P-PAC are fibers from the rectus abdominis tendon, the medial aspect of the transversalis and internal oblique muscles (the conjoint tendon, according to some), the inguinal ligament, and the adductor longus tendon.26When communicating with referring physicians, we use the term athletic pubalgia to indicate a specific injury. The athletic pubalgia injury can be defined as serial microtearing,1 or complete tearing, of the posterior attachment of the P-PAC off the anterior pubis.3,10 Complete tearing or displacement can occur unilaterally or across the midline to the other side. As athletic pubalgia is a specific anatomical injury rather than a broad category of findings, an additional pathologic diagnosis, such as inguinal hernia, does not exclude the diagnosis of athletic pubalgia. Unfortunately, the terms sports hernia and sportsman hernia, commonly used in the media and in professional communities, have largely confused the broader understanding of nuances and of the differences between the specific injuries and MRI findings.18

 

 

Our Experience

In our practice, we see groin pain patients referred by internists, physiatrists, physical therapists, trainers, general surgeons, urologists, gynecologists, and orthopedic surgeons. In many cases, patients have been through several consultations and work-ups, as their pain syndrome does not fall under a specific category. Patients without inguinal hernia, hip injury, urologic, or gynecologic issues typically are referred to a physiatrist or a physical therapist. Often, there are marginal improvements with physical therapy, but in some cases the injury never completely resolves, and the patient continues to have pain with activity or return to sports.

Most of our patients are nonprofessional athletes, men and women who range widely in age and participate casually or regularly in sporting events. Most lack the rigorous training, conditioning, and close supervision that professional athletes receive. Many other patients are nonprofessional but elite athletes who train 7 days a week for marathons, ultramarathons, triathlons, obstacle course races (“mudders”), and similar events.

Work-Up

A single algorithm is used for all patients initially referred to the surgeon’s office for pelvic or groin pain. The initial interview directs attention to injury onset and mechanism, duration of rest or physical therapy after surgery, pain quality and pain levels, and antagonistic movements and positions. Examination starts with assessment for inguinal, femoral, and umbilical hernias. Resisted sit-up, leg-raise, adduction, and hip assessment tests are performed. The P-PAC is examined with a maneuver similar to the one used for inguinal hernia, as it allows for better assessment of the transversalis fascia (over the direct space) to determine if the inguinal canal floor is attenuated and bulges forward with the Valsalva maneuver. Then, the lateral aspect of the rectus muscle is assessed for pain, usually with the head raised to contract the muscle, to determine tenderness along the lateral border. The rectus edge is traced down to the pubis at its attachment, the superolateral border of the P-PAC. Examination proceeds medially, over the rectus attachment, toward the pubic symphysis, continuing the assessment for tenderness. Laterally, the conjoint tendon and inguinal ligament medial attachments are assessed at the level of the pubic tubercle, which represents the lateral border of the P-PAC. Finally, the examination continues to the inferior border with assessment of the adductor longus attachment, which is best performed with the leg in an adducted position. In the acute or semiacute setting (pain within 1 year of injury onset), tenderness is often elicited. With long-standing injuries, pain is often not elicited, but the patient experiences pain along this axis during activity or afterward.

Patients with positive history and physical examination findings proceed through an MRI protocol designed to detect pathology of the pubic symphysis, hips, and inguinal canals (Figures 1A-1D).

Figure 1.
Imaging includes use of axial single-shot fast spin-echo with and without the Valsalva maneuver. Use of this maneuver increases sensitivity in detecting abdominal wall deficiencies, such as inguinal hernias (Figures 2A, 2B).
Figure 2.
We developed this pubalgia protocol (Table) to specifically assess each of the potential areas of concern.
Table.

Treatment

Patients who report sustaining an acute groin injury within the previous 6 months are treated nonoperatively. A combination of rest, nonsteroidal anti-inflammatory drugs, and physical therapy is generally recommended.2,10 In cases of failed nonoperative management, patients are evaluated for surgery. No single operation is recommended for all patients.1,6,14,27,28 (Larson26 recently reviewed results from several trials involving a variety of surgical repairs and found return-to-sports rates ranging from 80% to 100%.) Findings from the physical examination and from the properly protocolled MRI examination are used in planning surgery to correct any pathology that could be contributing to symptoms or destabilization of the structures attaching to the pubis. Disruption of the P-PAC from the pubis would be repaired, for example. Additional injuries, such as partial or complete detachment of the conjoint tendon or inguinal ligament, may be repaired as well. If the transversalis fascia is attenuated and bulging forward, the inguinal floor is closed. Adductor longus tendon pathology is addressed, most commonly with partial tendinolysis. Often, concomitant inguinal hernias are found, and these may be repaired in open fashion while other maneuvers are being performed, or laparoscopically.

Materials and Methods

After receiving study approval from our Institutional Review Board, we retrospectively searched for all MRIs performed by our radiology department between March 1, 2011 and March 31, 2013 on patients referred for an indication of groin pain, sports hernia, or athletic pubalgia. Patients were excluded if they were younger than 18 years any time during their care. Some patients previously or subsequently underwent computed tomography or ultrasonography. MRIs were reviewed and positive findings were compiled in a database. Charts were reviewed to identify which patients in the dataset underwent surgery, after MRI, to address their presenting chief complaint. Surgery date and procedure(s) performed were recorded. Patients were interviewed by telephone as part of the in-office postoperative follow-up.

 

 

Results

One hundred nineteen MRIs were performed on 117 patients (97 men, 83%). Mean age was 39.8 years. Seventy-nine patients (68%) had an MRI finding of athletic pubalgia, 67 (57%) had an acetabular labral tear in one or both hip joints, and 41 (35%) had a true inguinal hernia. Concomitant findings were common: 47 cases of athletic pubalgia and labral tear(s), 28 cases of athletic pubalgia and inguinal hernia, and 15 cases of all 3 (athletic pubalgia, labral tear, inguinal hernia).

Use of breath-hold axial single-shot fast spin-echo sequences with and without the Valsalva maneuver increased sensitivity in detecting pathologies—inguinal hernia and Gilmore groin in particular. On 24 of the 119 MRIs, the Valsalva maneuver either revealed the finding or made it significantly more apparent.

Of all patients referred for MRI for chronic groin pain, 48 (41%) subsequently underwent surgery. In 29 surgeries, the rectus abdominis, adductor longus, and/or pre-pubic aponeurotic plate were repaired; in 13 cases, herniorrhaphy was performed as well; in 2 cases, masses involving the spermatic cord were removed.

The most common surgery (30 cases) was herniorrhaphy, which was performed as a single procedure, multiple procedures, or in combination with procedures not related to a true hernia. Eighteen patients underwent surgery only for hernia repair.

Of the 79 patients with MRI-positive athletic pubalgia, 39 subsequently underwent surgery, and 31 (79%) of these were followed up by telephone. Mean duration of rest after surgery was 6.2 weeks. Twelve patients (39%) had physical therapy after surgery, some as early as 4 weeks, and some have continued their therapy since surgery. Of the 31 patients who were followed up after surgery, 23 (74%) resumed previous activity levels. Return to previous activity level took these patients a mean of 17.9 weeks. When asked if outcomes satisfied their expectations, 28 patients (90%) said yes, and 3 said no.

Forty patients with MRI-positive athletic pubalgia were nonoperatively treated, and 28 (70%) of these patients were followed up. In this group, mean duration of rest after surgery was 6.9 weeks. Thirteen patients (46%) participated in physical therapy, for a mean duration of 10.8 weeks. Of the patients followed up, 19 (68%) returned to previous activity level. Twenty-one patients (75%) were satisfied with their outcome.

Discussion

Diagnosis and treatment of chronic groin pain have had a long, confusing, and frustrating history for both patients and the medical professionals who provide them with care.3,6,7,10 Historically, the problem has been, in part, the lack of diagnostic capabilities. Currently, however, pubalgia MRI protocol allows the exact pathology to be demonstrated.3 As already noted, concomitant hip pathology or inguinal hernia is not unusual8; any structural abnormality in the area is a potential destabilizer of the structures attached to the pubis.18 Solving only one of these issues may offer only partial resolution of symptoms and thereby reduce the rate of successful treatment of groin pain.

Diagnostic algorithms are being developed. In addition, nonoperative treatments are being tried for some of the issues. Physicians are giving diagnostic and therapeutic steroid injections in the pubic cleft, along the rectus abdominis/adductor longus complex, or posterior to the P-PAC. Platelet-rich plasma injection therapy has had limited success.29This article provides a snapshot of what a tertiary-care group of physicians specializing in chronic groin pain sees in an unfiltered setting. We think this is instructive for several reasons.

First, many patients in our population have visited a multitude of specialists without receiving a diagnosis or being referred appropriately. Simply, many specialists do not know the next step in treating groin pain and thus do not make the appropriate referral. Until recently, the literature has not been helpful. It has poorly described the constellation of injuries comprising chronic groin pain. More significantly, groin injuries have been presented as ambiguous injuries lacking effective treatment. Over the past decade, however, abundant literature on the correlation of these injuries with specific MRI findings has made the case otherwise.

Second, a specific MRI pubalgia protocol is needed. Inability to make a correct diagnosis, because of improper MRI, continues to add to the confusion surrounding the injury and undoubtedly prolongs the general medical community’s thinking that diagnosis and treatment of chronic groin pain are elusive. Our data support this point in many ways. Although all patients in this study were seen by a medical professional before coming to our office, none had received a diagnosis of occult hernia or attenuated transversalis fascia; nevertheless, we identified inguinal hernia, Gilmore groin, or both in 44% of these patients. These findings are not surprising, as MRI was the crucial link in diagnosis. In addition, the point made by other groin pain specialists—that a hernia precludes a pubalgia diagnosis1,2,5—is not supported by our data. Inguinal hernia can and does exist in conjunction with pubalgia. More than half the patients in our study had a combined diagnosis. We contend that, much as hip labral pathology occurs concomitantly with pubalgia,23 inguinal hernia may be a predisposing factor as well. A defect in the direct or indirect space can destabilize the area and place additional strain on the pubic attachments.

In our experience, the dynamic Valsalva sequence improves detection of true hernias and anterior abdominal wall deficiencies and should be included in each protocol for the evaluation of acute or chronic groin pain.

Shear forces and injury at the pubis can occur outside professional athletics. Our patient population is nonprofessional athletes, teenagers to retirees, and all can develop athletic pubalgia. Ninety percent of surveyed patients who received a diagnosis and were treated surgically were satisfied with their outcomes.


Am J Orthop. 2017;46(4):E251-E256. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Meyers WC, Lanfranco A, Castellanos A. Surgical management of chronic lower abdominal and groin pain in high-performance athletes. Curr Sports Med Rep. 2002;1(5):301-305.

2. Ahumada LA, Ashruf S, Espinosa-de-los-Monteros A, et al. Athletic pubalgia: definition and surgical treatment. Ann Plast Surg. 2005;55(4):393-396.

3. Omar IM, Zoga AC, Kavanagh EC, et al. Athletic pubalgia and “sports hernia”: optimal MR imaging technique and findings. Radiographics. 2008;28(5):1415-1438.

4. Gilmore OJA. Gilmore’s groin: ten years experience of groin disruption—a previously unsolved problem in sportsmen. Sports Med Soft Tissue Trauma. 1991;3:12-14.

5. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.

6. Kavanagh EC, Koulouris G, Ford S, McMahon P, Johnson C, Eustace SJ. MR imaging of groin pain in the athlete. Semin Musculoskelet Radiol. 2006;10(3):197-207.

7. Cunningham PM, Brennan D, O’Connell M, MacMahon P, O’Neill P, Eustace S. Patterns of bone and soft-tissue injury at the symphysis pubis in soccer players: observations at MRI. AJR Am J Roentgenol. 2007;188(3):W291-W296.

8. Zoga AC, Kavanagh EC, Omar IM, et al. Athletic pubalgia and the “sports hernia”: MR imaging findings. Radiology. 2008;247(3):797-807.

9. Koulouris G. Imaging review of groin pain in elite athletes: an anatomic approach to imaging findings. AJR Am J Roentgenol. 2008;191(4):962-972.

10. Albers SL, Spritzer CE, Garrett WE Jr, Meyers WC. MR findings in athletes with pubalgia. Skeletal Radiol. 2001;30(5):270-277.

11. Brennan D, O’Connell MJ, Ryan M, et al. Secondary cleft sign as a marker of injury in athletes with groin pain: MR image appearance and interpretation. Radiology. 2005;235(1):162-167.

12. Robinson P, Salehi F, Grainger A, et al. Cadaveric and MRI study of the musculotendinous contributions to the capsule of the symphysis pubis. AJR Am J Roentgenol. 2007;188(5):W440-W445.

13. Schilders E, Talbot JC, Robinson P, Dimitrakopoulou A, Gibbon WW, Bismil Q. Adductor-related groin pain in recreational athletes. J Bone Joint Surg Am. 2009;91(10):2455-2460.

14. Davies AG, Clarke AW, Gilmore J, Wotherspoon M, Connell DA. Review: imaging of groin pain in the athlete. Skeletal Radiol. 2010;39(7):629-644.

15. Mullens FE, Zoga AC, Morrison WB, Meyers WC. Review of MRI technique and imaging findings in athletic pubalgia and the “sports hernia.” Eur J Radiol. 2012;81(12):3780-3792.

16. Zoga AC, Meyers WC. Magnetic resonance imaging for pain after surgical treatment for athletic pubalgia and the “sports hernia.” Semin Musculoskelet Radiol. 2011;15(4):372-382.

17. Beer E. Periostitis of symphysis and descending rami of pubes following suprapubic operations. Int J Med Surg. 1924;37(5):224-225.

18. MacMahon PJ, Hogan BA, Shelly MJ, Eustace SJ, Kavanagh EC. Imaging of groin pain. Magn Reson Imaging Clin N Am. 2009;17(4):655-666.

19. Malycha P, Lovell G. Inguinal surgery in athletes with chronic groin pain: the ‘sportsman’s’ hernia. Aust N Z J Surg. 1992;62(2):123-125.

20. Hackney RG. The sports hernia: a cause of chronic groin pain. Br J Sports Med. 1993;27(1):58-62.

21. Gibbon WW. Groin pain in athletes. Lancet. 1999;353(9162):1444-1445.

22. Brunet B, Brunet-Geudj E, Genety J. La pubalgie: syndrome “fourre-tout” pur une plus grande riguer diagnostique et therapeutique. Intantanes Medicaux. 1984;55:25-30.

23. Lischuk AW, Dorantes TM, Wong W, Haims AH. Imaging of sports-related hip and groin injuries. Sports Health. 2010;2(3):252-261.

24. Gibbon WW, Hession PR. Diseases of the pubis and pubic symphysis: MR imaging appearances. AJR Am J Roentgenol. 1997;169(3):849-853.

25. Gamble JG, Simmons SC, Freedman M. The symphysis pubis. Anatomic and pathologic considerations. Clin Orthop Relat Res. 1986;(203):261-272.

26. Larson CM. Sports hernia/athletic pubalgia: evaluation and management. Sports Health. 2014;6(2):139-144.

27. Maffulli N, Loppini M, Longo UG, Denaro V. Bilateral mini-invasive adductor tenotomy for the management of chronic unilateral adductor longus tendinopathy in athletes. Am J Sports Med. 2012;40(8):1880-1886.

28. Schilders E, Dimitrakopoulou A, Cooke M, Bismil Q, Cooke C. Effectiveness of a selective partial adductor release for chronic adductor-related groin pain in professional athletes. Am J Sports Med. 2013;41(3):603-607.

29. Scholten PM, Massimi S, Dahmen N, Diamond J, Wyss J. Successful treatment of athletic pubalgia in a lacrosse player with ultrasound-guided needle tenotomy and platelet-rich plasma injection: a case report. PM R. 2015;7(1):79-83.

References

1. Meyers WC, Lanfranco A, Castellanos A. Surgical management of chronic lower abdominal and groin pain in high-performance athletes. Curr Sports Med Rep. 2002;1(5):301-305.

2. Ahumada LA, Ashruf S, Espinosa-de-los-Monteros A, et al. Athletic pubalgia: definition and surgical treatment. Ann Plast Surg. 2005;55(4):393-396.

3. Omar IM, Zoga AC, Kavanagh EC, et al. Athletic pubalgia and “sports hernia”: optimal MR imaging technique and findings. Radiographics. 2008;28(5):1415-1438.

4. Gilmore OJA. Gilmore’s groin: ten years experience of groin disruption—a previously unsolved problem in sportsmen. Sports Med Soft Tissue Trauma. 1991;3:12-14.

5. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.

6. Kavanagh EC, Koulouris G, Ford S, McMahon P, Johnson C, Eustace SJ. MR imaging of groin pain in the athlete. Semin Musculoskelet Radiol. 2006;10(3):197-207.

7. Cunningham PM, Brennan D, O’Connell M, MacMahon P, O’Neill P, Eustace S. Patterns of bone and soft-tissue injury at the symphysis pubis in soccer players: observations at MRI. AJR Am J Roentgenol. 2007;188(3):W291-W296.

8. Zoga AC, Kavanagh EC, Omar IM, et al. Athletic pubalgia and the “sports hernia”: MR imaging findings. Radiology. 2008;247(3):797-807.

9. Koulouris G. Imaging review of groin pain in elite athletes: an anatomic approach to imaging findings. AJR Am J Roentgenol. 2008;191(4):962-972.

10. Albers SL, Spritzer CE, Garrett WE Jr, Meyers WC. MR findings in athletes with pubalgia. Skeletal Radiol. 2001;30(5):270-277.

11. Brennan D, O’Connell MJ, Ryan M, et al. Secondary cleft sign as a marker of injury in athletes with groin pain: MR image appearance and interpretation. Radiology. 2005;235(1):162-167.

12. Robinson P, Salehi F, Grainger A, et al. Cadaveric and MRI study of the musculotendinous contributions to the capsule of the symphysis pubis. AJR Am J Roentgenol. 2007;188(5):W440-W445.

13. Schilders E, Talbot JC, Robinson P, Dimitrakopoulou A, Gibbon WW, Bismil Q. Adductor-related groin pain in recreational athletes. J Bone Joint Surg Am. 2009;91(10):2455-2460.

14. Davies AG, Clarke AW, Gilmore J, Wotherspoon M, Connell DA. Review: imaging of groin pain in the athlete. Skeletal Radiol. 2010;39(7):629-644.

15. Mullens FE, Zoga AC, Morrison WB, Meyers WC. Review of MRI technique and imaging findings in athletic pubalgia and the “sports hernia.” Eur J Radiol. 2012;81(12):3780-3792.

16. Zoga AC, Meyers WC. Magnetic resonance imaging for pain after surgical treatment for athletic pubalgia and the “sports hernia.” Semin Musculoskelet Radiol. 2011;15(4):372-382.

17. Beer E. Periostitis of symphysis and descending rami of pubes following suprapubic operations. Int J Med Surg. 1924;37(5):224-225.

18. MacMahon PJ, Hogan BA, Shelly MJ, Eustace SJ, Kavanagh EC. Imaging of groin pain. Magn Reson Imaging Clin N Am. 2009;17(4):655-666.

19. Malycha P, Lovell G. Inguinal surgery in athletes with chronic groin pain: the ‘sportsman’s’ hernia. Aust N Z J Surg. 1992;62(2):123-125.

20. Hackney RG. The sports hernia: a cause of chronic groin pain. Br J Sports Med. 1993;27(1):58-62.

21. Gibbon WW. Groin pain in athletes. Lancet. 1999;353(9162):1444-1445.

22. Brunet B, Brunet-Geudj E, Genety J. La pubalgie: syndrome “fourre-tout” pur une plus grande riguer diagnostique et therapeutique. Intantanes Medicaux. 1984;55:25-30.

23. Lischuk AW, Dorantes TM, Wong W, Haims AH. Imaging of sports-related hip and groin injuries. Sports Health. 2010;2(3):252-261.

24. Gibbon WW, Hession PR. Diseases of the pubis and pubic symphysis: MR imaging appearances. AJR Am J Roentgenol. 1997;169(3):849-853.

25. Gamble JG, Simmons SC, Freedman M. The symphysis pubis. Anatomic and pathologic considerations. Clin Orthop Relat Res. 1986;(203):261-272.

26. Larson CM. Sports hernia/athletic pubalgia: evaluation and management. Sports Health. 2014;6(2):139-144.

27. Maffulli N, Loppini M, Longo UG, Denaro V. Bilateral mini-invasive adductor tenotomy for the management of chronic unilateral adductor longus tendinopathy in athletes. Am J Sports Med. 2012;40(8):1880-1886.

28. Schilders E, Dimitrakopoulou A, Cooke M, Bismil Q, Cooke C. Effectiveness of a selective partial adductor release for chronic adductor-related groin pain in professional athletes. Am J Sports Med. 2013;41(3):603-607.

29. Scholten PM, Massimi S, Dahmen N, Diamond J, Wyss J. Successful treatment of athletic pubalgia in a lacrosse player with ultrasound-guided needle tenotomy and platelet-rich plasma injection: a case report. PM R. 2015;7(1):79-83.

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The radiograph shows that the patient is intubated. The lungs are clear overall. There is a fractured, slightly displaced left clavicle. Of concern, though, is the widened appearance of the mediastinum. In patients with blunt chest trauma, there should be a high index of suspicion for a great vessel injury, warranting a chest CT with contrast for further evaluation. Fortunately, in this patient's case, CT was negative.

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The radiograph shows that the patient is intubated. The lungs are clear overall. There is a fractured, slightly displaced left clavicle. Of concern, though, is the widened appearance of the mediastinum. In patients with blunt chest trauma, there should be a high index of suspicion for a great vessel injury, warranting a chest CT with contrast for further evaluation. Fortunately, in this patient's case, CT was negative.

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The radiograph shows that the patient is intubated. The lungs are clear overall. There is a fractured, slightly displaced left clavicle. Of concern, though, is the widened appearance of the mediastinum. In patients with blunt chest trauma, there should be a high index of suspicion for a great vessel injury, warranting a chest CT with contrast for further evaluation. Fortunately, in this patient's case, CT was negative.

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A 40-year-old construction worker was remodeling a home when the roof collapsed. The patient’s head, face, and chest were reportedly struck by a large metal support beam. He was taken to a local facility, where he was found to have decreased level of consciousness and was combative. He was intubated for airway protection and sent to your facility for tertiary level of care.

History is limited. On arrival, you note a male patient who is intubated and sedated. His blood pressure is 90/60 mm Hg and his heart rate, 130 beats/min. A large laceration on his forehead and scalp has been primarily closed. His pupils are unequal, but both react. Neurologic exam is limited secondary to sedation.

As you complete your primary and secondary surveys, a portable chest radiograph is obtained (shown). What is your impression?

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