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The American Journal of Orthopedics is an Index Medicus publication that is valued by orthopedic surgeons for its peer-reviewed, practice-oriented clinical information. Most articles are written by specialists at leading teaching institutions and help incorporate the latest technology into everyday practice.
Giant Solitary Synovial Chondromatosis Mimicking Chondrosarcoma: Report of a Rare Histologic Presentation and Literature Review
Synovial chondromatosis (SCM) is a relatively rare benign lesion of the synovium.1 Its pathogenesis has been thought to be a chondral metaplasia of the subintimal layer of the intra- or extra-articular synovium.2 However, evidence supporting a neoplastic cause of the disease is emerging.3 When intra-articular, any joint can be affected, though large joints are more prone to the disease; the knee, hip, and elbow are the most common locations.4 The synovial layer of tendons or bursae can be the origin of extra-articular SCM.5
Synovial chondrosarcoma (SCS), an even rarer pathology, can be caused by malignant transformation of SCM or can appear de novo on a synovial background.6 Histologic differentiation from SCM might be difficult because of the high incidence of hypercellularity, cellular atypia, and binucleated cells.6 Some features, such as presence of a very large mass or erosion of the surrounding bones, have been indicated as possible signs of malignancy.3 An unusual presentation of SCM, giant solitary synovial chondromatosis (GSSCM), can be hard to distinguish from SCS because of the large volume and possible aggressive radiologic findings.7 Some histologic features, such as presence of necrosis and mitotic cells, have been suggested as distinctive criteria for malignancy.8
In this article, we present a case of benign GSSCM with a histologic feature that has not been considered typical for benign SCM. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
An 18-year-old woman presented with a large mass over the right hip. The mass had been growing slowly for 2 years. One year before presentation, a radiograph showed a large hip mass with fluffy calcification (Figure 1), and magnetic resonance imaging (MRI) showed a large nonhomogeneous mass anterior to the hip capsule and extending into the hip joint back to the posterior part of the joint (Figures 2A, 2B). Open incisional biopsy was performed in a local hospital at the time, and the histologic analysis revealed presence of atypical binucleated cells and pleomorphism, in addition to some mitotic activity (0 to 1 per high-power field) (Figure 3). These findings suggested malignancy. The patient declined surgery up until the time she presented to our hospital, 1 year later.
Clinical examination findings on admission to our hospital were striking. The patient had a large mass in the groin region. It was fairly tender and firm to palpation, immobile, and close to the skin. Hip motion was mildly painful but obviously restricted.
The mass was restaged. New radiographs and MRI did not show any significant changes since the previous year, computed tomography (CT) did not show any bone erosion (Figure 4), and chest radiograph, CT, and whole-body bone scan did not demonstrate any signs of metastasis.
Given the clinical presentation and previous histopathologic findings, a diagnosis of GSSCM with possible malignant transformation was made. The patient was scheduled for surgery. During surgery, the tumor was exposed through the Smith-Petersen approach. The mass was extruding under the fascia between the femoral neurovascular bundle medially and iliopsoas muscle laterally. There was no adhesion of the surrounding structures, including the femoral neurovascular bundle, to the mass. The muscle was sitting on the anterolateral surface of the mass, which was considered located in the iliopsoas bursa but extending to the joint. In the vertical plane, the mass extended down to the subtrochanteric area. The entire solid extra-articular mass was excised en bloc, and hip capsulotomy was performed inferior to the area of emergence of the mass. The joint was occupied by a single solid cartilaginous mass molding around the femoral neck, filling the piriformis fossa and propagating to the posterior joint space. Obtaining enough exposure to the back of the joint required surgical hip dislocation. The visualized acetabular fossa revealed chondral fragments, which were excised. Bone erosion or significant osteoarthritis was not detected in any part of the joint. A nearly total synovectomy was performed, leaving the ascending retinacular vessels intact. Meticulous technique was used to avoid contaminating the extra-articular tissues. The wound was closed in the routine way after hip relocation.
The 16×9.5×9-cm mass (Figure 5A) had a conglomerated internal structure (Figure 5B). Multiple specimens from the intra- and extra-articular portions of the mass were sent for histopathologic analysis, which revealed clusters of mature chondrocytes arranged in a lobular pattern and separated by thin fibrous bands. Areas of calcification and ossification were appreciated as well (Figures 6A-6C). No necrosis, mitosis, or bone permeation was detected. These findings were compatible with typical SCM. Given these pathologic findings and the lack of clinical deterioration over the previous year, a diagnosis of GSSCM with extension along the iliopsoas and obturator externus bursae was made. The already-performed marginal excision was deemed sufficient treatment. At most recent follow-up, 38 months after surgery, the patient was pain-free and had good hip range of motion and no indication of recurrence.
Discussion
SCM is a benign disorder emerging from the synovium as a result of proliferative changes in the synovial membrane of the joints, tendon sheaths, or bursae, leading to the formation of numerous cartilaginous nodules, usually a few millimeters in diameter.8 In a rare presentation of the disease, the nodules may coalesce to form a large mass, or a single cartilaginous nodule may enlarge to form a mass. Edeiken and colleagues7 named this previously unrecognized SCM feature as GSSCM when there was a major single mass larger than 1 cm in diameter. There have been other SCM cases with multiple giant masses.9,10 In the English-language literature, we found 15 GSSCM cases, which include the first reported, by Edeiken and colleagues7 (Table). However, earlier SCM cases would be reclassified GSSCM according to their definition.11
The present case brings the total to 16. Nine of the 16 patients were male. Mean age at presentation was 41 years (range, 10-80 years). The knee was the most common GSSCM site (6 cases), followed by the temporomandibular and hip joints (3 each). Regarding gross pathology, 10 lesions were solid, and 6 (including the present one) were formed by conglomeration of the chondromatosis nodules. Lesions varied in size (16-200 mm), and 2 were primarily extra-articular (foot). One common issue with most of the cases was the initial diagnosis of chondrosarcoma. The exact surgical technique used was described for 6 cases (cases 11-16); the technique was marginal excision. In no case was recurrence 14 to 60 months after surgery reported.
This chondroproliferative process is potentially a diagnostic challenge, as distinguishing it from a chondrosarcoma, a more common lesion, could be difficult based on clinical and imaging findings, and, as is true for other chondral lesions, even histologic differentiation of the conditions might not be conclusive.12,13 Confusion in diagnosis was almost universal in this series of patients.
One important differentiating feature of benign and malignant skeletal lesions is the time course of the disease. Malignant tumors are expected to demonstrate rapid enlargement and local or systemic spread. Unfortunately, often SCS cannot be distinguished by this characteristic, as grade I or II chondrosarcoma is usually a slow-growing tumor and does not metastasize early.14 Although lack of recurrence is assuring, recurrence is not necessarily a sign of malignancy, as a considerable percentage of benign chondromatosis lesions recur.8
Radiologic differentiation between SCM and SCS is another challenge. Although bone erosion caused by a lesion not originating from bone is usually considered a sign of malignancy, GSSCM was reported as causing bone erosion in 5 of the 16 cases in our literature review.7,15 Our patient did not experience any bone erosion. However, lack of bone erosion is not a reliable criterion for excluding SCS, and bone erosion was noted in only 3 of the 9 SCS cases in the series reported by Bertoni and colleagues.6 Moreover, tumor size and propagation of tumor to surrounding tissue could be surprising in GSSCM. Large size (up to 20 cm) and extra-articular spread of a lesion originating in a joint are common findings.6,16 Our case was an obvious extension of a hip GSSCM to the iliopsoas and obturator externus bursa, which is the most common pattern of extracapsular spread of hip SCM.17 An interesting feature of the present case, however, was the relatively superficial location of the mass immediately under the fascia.
Calcified matrix is key in diagnosing a chondral lesion on imaging studies, but, in some cases, SCM does not demonstrate any radiographically detectable calcification at time of diagnosis.18 However, all the GSSCM cases reported to date had obvious calcified matrix.
The hypercellularity, cellular atypia, binucleated cells, and pleomorphism in the histologic examination of the present case are not features of malignancy in SCM.8 On the contrary, several other characteristics, including qualitative differences in the arrangement of chondrocytes (sheets rather than clusters), myxoid matrix, hypercellularity with crowding and spindling of the nuclei at the periphery, necrosis, and, most important, permeation of the trabecular bone with the filling up of marrow spaces, have been assumed to be indicative of malignancy.8 Furthermore, Davis and colleagues8 found no mitotic activity in the histopathologic investigation of 53 SCM cases. Even in 3 cases that developed malignant transformation to SCS, mitosis was not found in the initial biopsy specimens before transformation. This was compatible with the common opinion that SCM is not a neoplastic, but a metaplastic, process. Histopathologic data were available for only 8 of the previous 15 GSSCM cases. There were no reports of mitosis, and necrosis was found in only 1 case.16 In our patient’s case, however, the first biopsy did show remarkable mitotic activity. This was not the case for the second biopsy, when mature chondrocytes associated with marked calcification and ossification were prominent features (Figures 6A, 6B). We presume that, within a limited period during earlier stages of tissue maturation in SCM, mitotic activity might be a possible finding. Of note, none of the other aforementioned histologic criteria for malignancy was seen in the first or second biopsy in the present case (Figures 3, 6C).
The original idea that SCM originates from a metaplasia in the subintimal layer of the synovium, where the synovium is in direct contact with the articular cartilage, has been challenged. The high incidence of hypercellularity, binucleated cells, and cellular atypia was always an argument against a metaplastic origin for the disease. Evidence of clonal chromosomal changes, like translocation of chromosome 1218 and chromosome 5 and 6 abnormalities,19,20 in addition to other alterations,19,21 provide some evidence supporting a neoplastic rather than a metaplastic origin for SCM. Given the presence of mitosis in the present case, the lack of mitotic activity in SCM, as stated by other authors,22 is not a universal feature and cannot be used as an argument against a neoplastic origin for SCM.
Although mitotic activity is uncommon in SCM, the present case illustrates the possible presence of mitotic activity in GSSCM. The simple presence of mitotic activity, a common finding in some other chondral tumors,23,24 does not preclude the diagnosis of benign SCM, as suggested before,8 and correlation of the clinical and radiologic manifestations with histopathologic findings is crucial for a correct diagnosis.
1. Milgram JW. Synovial osteochondromatosis: a histopathological study of thirty cases. J Bone Joint Surg Am. 1977;59(6):792-801.
2. Trias A, Quintana O. Synovial chondrometaplasia: review of world literature and a study of 18 Canadian cases. Can J Surg. 1976;19(2):151-158.
3. Murphey MD, Vidal JA, Fanburg-Smith JC, Gajewski DA. Imaging of synovial chondromatosis with radiologic-pathologic correlation. Radiographics. 2007;27(5):1465-1488.
4. Milgram JW. Synovial osteochondromatosis in association with Legg-Calve-Perthes disease. Clin Orthop Relat Res. 1979;(145):179-182.
5. Sim FH, Dahlin DC, Ivins JC. Extra-articular synovial chondromatosis. J Bone Joint Surg Am. 1977;59(4):492-495.
6. Bertoni F, Unni KK, Beabout JW, Sim FH. Chondrosarcomas of the synovium. Cancer. 1991;67(1):155-162.
7. Edeiken J, Edeiken BS, Ayala AG, Raymond AK, Murray JA, Guo SQ. Giant solitary synovial chondromatosis. Skeletal Radiol. 1994;23(1):23-29.
8. Davis RI, Hamilton A, Biggart JD. Primary synovial chondromatosis: a clinicopathologic review and assessment of malignant potential. Hum Pathol. 1998;29(7):683-688.
9. Goel A, Cullen C, Paul AS, Freemont AJ. Multiple giant synovial chondromatosis of the knee. Knee. 2001;8(3):243-245.
10. Dogan A, Harman M, Uslu M, Bayram I, Akpinar F. Rocky form giant synovial chondromatosis: a case report. Knee Surg Sports Traumatol Arthrosc. 2006;14(5):465-468.
11. Eisenberg KS, Johnston JO. Synovial chondromatosis of the hip joint presenting as an intrapelvic mass: a case report. J Bone Joint Surg Am. 1972;54(1):176-178.
12. Lohmann CH, Köster G, Klinger HM, Kunze E. Giant synovial osteochondromatosis of the acromio-clavicular joint in a child. A case report and review of the literature. J Pediatr Orthop B. 2005;14(2):126-128.
13. Cai XY, Yang C, Chen MJ, Jiang B, Wang BL. Arthroscopically guided removal of large solitary synovial chondromatosis from the temporomandibular joint. Int J Oral Maxillofac Surg. 2010;39(12):1236-1239.
14. Gil-Salu JL, Lazaro R, Aldasoro J, Gonzalez-Darder JM. Giant solitary synovial chondromatosis of the temporomandibular joint with intracranial extension. Skull Base Surg. 1998;8(2):99-104.
15. Kang CH, Park JH, Lee DH, Kim CH, Park JM, Lee WS. Giant synovial chondromatosis of the knee mimicking a parosteal osteosarcoma: a case report. J Korean Bone Joint Tumor Soc. 2010;16(2):95-98.
16. Nihal A, Read CJ, Henderson DC, Malcolm AJ. Extra-articular giant solitary synovial chondromatosis of the foot: a case report and literature review. Foot Ankle Surg. 1999;5(1):29-32.
17. Robinson P, White LM, Kandel R, Bell RS, Wunder JS. Primary synovial osteochondromatosis of the hip: extracapsular patterns of spread. Skeletal Radiol. 2004;33(4):210-215.
18. Tallini G, Dorfman H, Brys P, et al. Correlation between clinicopathological features and karyotype in 100 cartilaginous and chordoid tumours. A report from the Chromosomes and Morphology (CHAMP) Collaborative Study Group. J Pathol. 2002;196(2):194-203.
19. Sah AP, Geller DS, Mankin HJ, et al. Malignant transformation of synovial chondromatosis of the shoulder to chondrosarcoma. A case report. J Bone Joint Surg Am. 2007;89(6):1321-1328.
20. Buddingh EP, Krallman P, Neff JR, Nelson M, Liu J, Bridge JA. Chromosome 6 abnormalities are recurrent in synovial chondromatosis. Cancer Genet Cytogenet. 2003;140(1):18-22.
21. Rizzo M, Ghert MA, Harrelson JM, Scully SP. Chondrosarcoma of bone: analysis of 108 cases and evaluation for predictors of outcome. Clin Orthop Relat Res. 2001;(391):224-233.
22. Davis RI, Foster H, Arthur K, Trewin S, Hamilton PW, Biggart DJ. Cell proliferation studies in primary synovial chondromatosis. J Pathol. 1998;184(1):18-23.
23. Ishikawa E, Tsuboi K, Onizawa K, et al. Chondroblastoma of the temporal base with high mitotic activity. Neurol Med Chir (Tokyo). 2002;42(11):516-520.
24. Kirin I, Jurisic D, Mokrovic H, Stanec Z, Stalekar H. Chondromyxoid fibroma of the second metacarpal bone—a case report. Coll Antropol. 2011;35(3):929-931.
Synovial chondromatosis (SCM) is a relatively rare benign lesion of the synovium.1 Its pathogenesis has been thought to be a chondral metaplasia of the subintimal layer of the intra- or extra-articular synovium.2 However, evidence supporting a neoplastic cause of the disease is emerging.3 When intra-articular, any joint can be affected, though large joints are more prone to the disease; the knee, hip, and elbow are the most common locations.4 The synovial layer of tendons or bursae can be the origin of extra-articular SCM.5
Synovial chondrosarcoma (SCS), an even rarer pathology, can be caused by malignant transformation of SCM or can appear de novo on a synovial background.6 Histologic differentiation from SCM might be difficult because of the high incidence of hypercellularity, cellular atypia, and binucleated cells.6 Some features, such as presence of a very large mass or erosion of the surrounding bones, have been indicated as possible signs of malignancy.3 An unusual presentation of SCM, giant solitary synovial chondromatosis (GSSCM), can be hard to distinguish from SCS because of the large volume and possible aggressive radiologic findings.7 Some histologic features, such as presence of necrosis and mitotic cells, have been suggested as distinctive criteria for malignancy.8
In this article, we present a case of benign GSSCM with a histologic feature that has not been considered typical for benign SCM. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
An 18-year-old woman presented with a large mass over the right hip. The mass had been growing slowly for 2 years. One year before presentation, a radiograph showed a large hip mass with fluffy calcification (Figure 1), and magnetic resonance imaging (MRI) showed a large nonhomogeneous mass anterior to the hip capsule and extending into the hip joint back to the posterior part of the joint (Figures 2A, 2B). Open incisional biopsy was performed in a local hospital at the time, and the histologic analysis revealed presence of atypical binucleated cells and pleomorphism, in addition to some mitotic activity (0 to 1 per high-power field) (Figure 3). These findings suggested malignancy. The patient declined surgery up until the time she presented to our hospital, 1 year later.
Clinical examination findings on admission to our hospital were striking. The patient had a large mass in the groin region. It was fairly tender and firm to palpation, immobile, and close to the skin. Hip motion was mildly painful but obviously restricted.
The mass was restaged. New radiographs and MRI did not show any significant changes since the previous year, computed tomography (CT) did not show any bone erosion (Figure 4), and chest radiograph, CT, and whole-body bone scan did not demonstrate any signs of metastasis.
Given the clinical presentation and previous histopathologic findings, a diagnosis of GSSCM with possible malignant transformation was made. The patient was scheduled for surgery. During surgery, the tumor was exposed through the Smith-Petersen approach. The mass was extruding under the fascia between the femoral neurovascular bundle medially and iliopsoas muscle laterally. There was no adhesion of the surrounding structures, including the femoral neurovascular bundle, to the mass. The muscle was sitting on the anterolateral surface of the mass, which was considered located in the iliopsoas bursa but extending to the joint. In the vertical plane, the mass extended down to the subtrochanteric area. The entire solid extra-articular mass was excised en bloc, and hip capsulotomy was performed inferior to the area of emergence of the mass. The joint was occupied by a single solid cartilaginous mass molding around the femoral neck, filling the piriformis fossa and propagating to the posterior joint space. Obtaining enough exposure to the back of the joint required surgical hip dislocation. The visualized acetabular fossa revealed chondral fragments, which were excised. Bone erosion or significant osteoarthritis was not detected in any part of the joint. A nearly total synovectomy was performed, leaving the ascending retinacular vessels intact. Meticulous technique was used to avoid contaminating the extra-articular tissues. The wound was closed in the routine way after hip relocation.
The 16×9.5×9-cm mass (Figure 5A) had a conglomerated internal structure (Figure 5B). Multiple specimens from the intra- and extra-articular portions of the mass were sent for histopathologic analysis, which revealed clusters of mature chondrocytes arranged in a lobular pattern and separated by thin fibrous bands. Areas of calcification and ossification were appreciated as well (Figures 6A-6C). No necrosis, mitosis, or bone permeation was detected. These findings were compatible with typical SCM. Given these pathologic findings and the lack of clinical deterioration over the previous year, a diagnosis of GSSCM with extension along the iliopsoas and obturator externus bursae was made. The already-performed marginal excision was deemed sufficient treatment. At most recent follow-up, 38 months after surgery, the patient was pain-free and had good hip range of motion and no indication of recurrence.
Discussion
SCM is a benign disorder emerging from the synovium as a result of proliferative changes in the synovial membrane of the joints, tendon sheaths, or bursae, leading to the formation of numerous cartilaginous nodules, usually a few millimeters in diameter.8 In a rare presentation of the disease, the nodules may coalesce to form a large mass, or a single cartilaginous nodule may enlarge to form a mass. Edeiken and colleagues7 named this previously unrecognized SCM feature as GSSCM when there was a major single mass larger than 1 cm in diameter. There have been other SCM cases with multiple giant masses.9,10 In the English-language literature, we found 15 GSSCM cases, which include the first reported, by Edeiken and colleagues7 (Table). However, earlier SCM cases would be reclassified GSSCM according to their definition.11
The present case brings the total to 16. Nine of the 16 patients were male. Mean age at presentation was 41 years (range, 10-80 years). The knee was the most common GSSCM site (6 cases), followed by the temporomandibular and hip joints (3 each). Regarding gross pathology, 10 lesions were solid, and 6 (including the present one) were formed by conglomeration of the chondromatosis nodules. Lesions varied in size (16-200 mm), and 2 were primarily extra-articular (foot). One common issue with most of the cases was the initial diagnosis of chondrosarcoma. The exact surgical technique used was described for 6 cases (cases 11-16); the technique was marginal excision. In no case was recurrence 14 to 60 months after surgery reported.
This chondroproliferative process is potentially a diagnostic challenge, as distinguishing it from a chondrosarcoma, a more common lesion, could be difficult based on clinical and imaging findings, and, as is true for other chondral lesions, even histologic differentiation of the conditions might not be conclusive.12,13 Confusion in diagnosis was almost universal in this series of patients.
One important differentiating feature of benign and malignant skeletal lesions is the time course of the disease. Malignant tumors are expected to demonstrate rapid enlargement and local or systemic spread. Unfortunately, often SCS cannot be distinguished by this characteristic, as grade I or II chondrosarcoma is usually a slow-growing tumor and does not metastasize early.14 Although lack of recurrence is assuring, recurrence is not necessarily a sign of malignancy, as a considerable percentage of benign chondromatosis lesions recur.8
Radiologic differentiation between SCM and SCS is another challenge. Although bone erosion caused by a lesion not originating from bone is usually considered a sign of malignancy, GSSCM was reported as causing bone erosion in 5 of the 16 cases in our literature review.7,15 Our patient did not experience any bone erosion. However, lack of bone erosion is not a reliable criterion for excluding SCS, and bone erosion was noted in only 3 of the 9 SCS cases in the series reported by Bertoni and colleagues.6 Moreover, tumor size and propagation of tumor to surrounding tissue could be surprising in GSSCM. Large size (up to 20 cm) and extra-articular spread of a lesion originating in a joint are common findings.6,16 Our case was an obvious extension of a hip GSSCM to the iliopsoas and obturator externus bursa, which is the most common pattern of extracapsular spread of hip SCM.17 An interesting feature of the present case, however, was the relatively superficial location of the mass immediately under the fascia.
Calcified matrix is key in diagnosing a chondral lesion on imaging studies, but, in some cases, SCM does not demonstrate any radiographically detectable calcification at time of diagnosis.18 However, all the GSSCM cases reported to date had obvious calcified matrix.
The hypercellularity, cellular atypia, binucleated cells, and pleomorphism in the histologic examination of the present case are not features of malignancy in SCM.8 On the contrary, several other characteristics, including qualitative differences in the arrangement of chondrocytes (sheets rather than clusters), myxoid matrix, hypercellularity with crowding and spindling of the nuclei at the periphery, necrosis, and, most important, permeation of the trabecular bone with the filling up of marrow spaces, have been assumed to be indicative of malignancy.8 Furthermore, Davis and colleagues8 found no mitotic activity in the histopathologic investigation of 53 SCM cases. Even in 3 cases that developed malignant transformation to SCS, mitosis was not found in the initial biopsy specimens before transformation. This was compatible with the common opinion that SCM is not a neoplastic, but a metaplastic, process. Histopathologic data were available for only 8 of the previous 15 GSSCM cases. There were no reports of mitosis, and necrosis was found in only 1 case.16 In our patient’s case, however, the first biopsy did show remarkable mitotic activity. This was not the case for the second biopsy, when mature chondrocytes associated with marked calcification and ossification were prominent features (Figures 6A, 6B). We presume that, within a limited period during earlier stages of tissue maturation in SCM, mitotic activity might be a possible finding. Of note, none of the other aforementioned histologic criteria for malignancy was seen in the first or second biopsy in the present case (Figures 3, 6C).
The original idea that SCM originates from a metaplasia in the subintimal layer of the synovium, where the synovium is in direct contact with the articular cartilage, has been challenged. The high incidence of hypercellularity, binucleated cells, and cellular atypia was always an argument against a metaplastic origin for the disease. Evidence of clonal chromosomal changes, like translocation of chromosome 1218 and chromosome 5 and 6 abnormalities,19,20 in addition to other alterations,19,21 provide some evidence supporting a neoplastic rather than a metaplastic origin for SCM. Given the presence of mitosis in the present case, the lack of mitotic activity in SCM, as stated by other authors,22 is not a universal feature and cannot be used as an argument against a neoplastic origin for SCM.
Although mitotic activity is uncommon in SCM, the present case illustrates the possible presence of mitotic activity in GSSCM. The simple presence of mitotic activity, a common finding in some other chondral tumors,23,24 does not preclude the diagnosis of benign SCM, as suggested before,8 and correlation of the clinical and radiologic manifestations with histopathologic findings is crucial for a correct diagnosis.
Synovial chondromatosis (SCM) is a relatively rare benign lesion of the synovium.1 Its pathogenesis has been thought to be a chondral metaplasia of the subintimal layer of the intra- or extra-articular synovium.2 However, evidence supporting a neoplastic cause of the disease is emerging.3 When intra-articular, any joint can be affected, though large joints are more prone to the disease; the knee, hip, and elbow are the most common locations.4 The synovial layer of tendons or bursae can be the origin of extra-articular SCM.5
Synovial chondrosarcoma (SCS), an even rarer pathology, can be caused by malignant transformation of SCM or can appear de novo on a synovial background.6 Histologic differentiation from SCM might be difficult because of the high incidence of hypercellularity, cellular atypia, and binucleated cells.6 Some features, such as presence of a very large mass or erosion of the surrounding bones, have been indicated as possible signs of malignancy.3 An unusual presentation of SCM, giant solitary synovial chondromatosis (GSSCM), can be hard to distinguish from SCS because of the large volume and possible aggressive radiologic findings.7 Some histologic features, such as presence of necrosis and mitotic cells, have been suggested as distinctive criteria for malignancy.8
In this article, we present a case of benign GSSCM with a histologic feature that has not been considered typical for benign SCM. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
An 18-year-old woman presented with a large mass over the right hip. The mass had been growing slowly for 2 years. One year before presentation, a radiograph showed a large hip mass with fluffy calcification (Figure 1), and magnetic resonance imaging (MRI) showed a large nonhomogeneous mass anterior to the hip capsule and extending into the hip joint back to the posterior part of the joint (Figures 2A, 2B). Open incisional biopsy was performed in a local hospital at the time, and the histologic analysis revealed presence of atypical binucleated cells and pleomorphism, in addition to some mitotic activity (0 to 1 per high-power field) (Figure 3). These findings suggested malignancy. The patient declined surgery up until the time she presented to our hospital, 1 year later.
Clinical examination findings on admission to our hospital were striking. The patient had a large mass in the groin region. It was fairly tender and firm to palpation, immobile, and close to the skin. Hip motion was mildly painful but obviously restricted.
The mass was restaged. New radiographs and MRI did not show any significant changes since the previous year, computed tomography (CT) did not show any bone erosion (Figure 4), and chest radiograph, CT, and whole-body bone scan did not demonstrate any signs of metastasis.
Given the clinical presentation and previous histopathologic findings, a diagnosis of GSSCM with possible malignant transformation was made. The patient was scheduled for surgery. During surgery, the tumor was exposed through the Smith-Petersen approach. The mass was extruding under the fascia between the femoral neurovascular bundle medially and iliopsoas muscle laterally. There was no adhesion of the surrounding structures, including the femoral neurovascular bundle, to the mass. The muscle was sitting on the anterolateral surface of the mass, which was considered located in the iliopsoas bursa but extending to the joint. In the vertical plane, the mass extended down to the subtrochanteric area. The entire solid extra-articular mass was excised en bloc, and hip capsulotomy was performed inferior to the area of emergence of the mass. The joint was occupied by a single solid cartilaginous mass molding around the femoral neck, filling the piriformis fossa and propagating to the posterior joint space. Obtaining enough exposure to the back of the joint required surgical hip dislocation. The visualized acetabular fossa revealed chondral fragments, which were excised. Bone erosion or significant osteoarthritis was not detected in any part of the joint. A nearly total synovectomy was performed, leaving the ascending retinacular vessels intact. Meticulous technique was used to avoid contaminating the extra-articular tissues. The wound was closed in the routine way after hip relocation.
The 16×9.5×9-cm mass (Figure 5A) had a conglomerated internal structure (Figure 5B). Multiple specimens from the intra- and extra-articular portions of the mass were sent for histopathologic analysis, which revealed clusters of mature chondrocytes arranged in a lobular pattern and separated by thin fibrous bands. Areas of calcification and ossification were appreciated as well (Figures 6A-6C). No necrosis, mitosis, or bone permeation was detected. These findings were compatible with typical SCM. Given these pathologic findings and the lack of clinical deterioration over the previous year, a diagnosis of GSSCM with extension along the iliopsoas and obturator externus bursae was made. The already-performed marginal excision was deemed sufficient treatment. At most recent follow-up, 38 months after surgery, the patient was pain-free and had good hip range of motion and no indication of recurrence.
Discussion
SCM is a benign disorder emerging from the synovium as a result of proliferative changes in the synovial membrane of the joints, tendon sheaths, or bursae, leading to the formation of numerous cartilaginous nodules, usually a few millimeters in diameter.8 In a rare presentation of the disease, the nodules may coalesce to form a large mass, or a single cartilaginous nodule may enlarge to form a mass. Edeiken and colleagues7 named this previously unrecognized SCM feature as GSSCM when there was a major single mass larger than 1 cm in diameter. There have been other SCM cases with multiple giant masses.9,10 In the English-language literature, we found 15 GSSCM cases, which include the first reported, by Edeiken and colleagues7 (Table). However, earlier SCM cases would be reclassified GSSCM according to their definition.11
The present case brings the total to 16. Nine of the 16 patients were male. Mean age at presentation was 41 years (range, 10-80 years). The knee was the most common GSSCM site (6 cases), followed by the temporomandibular and hip joints (3 each). Regarding gross pathology, 10 lesions were solid, and 6 (including the present one) were formed by conglomeration of the chondromatosis nodules. Lesions varied in size (16-200 mm), and 2 were primarily extra-articular (foot). One common issue with most of the cases was the initial diagnosis of chondrosarcoma. The exact surgical technique used was described for 6 cases (cases 11-16); the technique was marginal excision. In no case was recurrence 14 to 60 months after surgery reported.
This chondroproliferative process is potentially a diagnostic challenge, as distinguishing it from a chondrosarcoma, a more common lesion, could be difficult based on clinical and imaging findings, and, as is true for other chondral lesions, even histologic differentiation of the conditions might not be conclusive.12,13 Confusion in diagnosis was almost universal in this series of patients.
One important differentiating feature of benign and malignant skeletal lesions is the time course of the disease. Malignant tumors are expected to demonstrate rapid enlargement and local or systemic spread. Unfortunately, often SCS cannot be distinguished by this characteristic, as grade I or II chondrosarcoma is usually a slow-growing tumor and does not metastasize early.14 Although lack of recurrence is assuring, recurrence is not necessarily a sign of malignancy, as a considerable percentage of benign chondromatosis lesions recur.8
Radiologic differentiation between SCM and SCS is another challenge. Although bone erosion caused by a lesion not originating from bone is usually considered a sign of malignancy, GSSCM was reported as causing bone erosion in 5 of the 16 cases in our literature review.7,15 Our patient did not experience any bone erosion. However, lack of bone erosion is not a reliable criterion for excluding SCS, and bone erosion was noted in only 3 of the 9 SCS cases in the series reported by Bertoni and colleagues.6 Moreover, tumor size and propagation of tumor to surrounding tissue could be surprising in GSSCM. Large size (up to 20 cm) and extra-articular spread of a lesion originating in a joint are common findings.6,16 Our case was an obvious extension of a hip GSSCM to the iliopsoas and obturator externus bursa, which is the most common pattern of extracapsular spread of hip SCM.17 An interesting feature of the present case, however, was the relatively superficial location of the mass immediately under the fascia.
Calcified matrix is key in diagnosing a chondral lesion on imaging studies, but, in some cases, SCM does not demonstrate any radiographically detectable calcification at time of diagnosis.18 However, all the GSSCM cases reported to date had obvious calcified matrix.
The hypercellularity, cellular atypia, binucleated cells, and pleomorphism in the histologic examination of the present case are not features of malignancy in SCM.8 On the contrary, several other characteristics, including qualitative differences in the arrangement of chondrocytes (sheets rather than clusters), myxoid matrix, hypercellularity with crowding and spindling of the nuclei at the periphery, necrosis, and, most important, permeation of the trabecular bone with the filling up of marrow spaces, have been assumed to be indicative of malignancy.8 Furthermore, Davis and colleagues8 found no mitotic activity in the histopathologic investigation of 53 SCM cases. Even in 3 cases that developed malignant transformation to SCS, mitosis was not found in the initial biopsy specimens before transformation. This was compatible with the common opinion that SCM is not a neoplastic, but a metaplastic, process. Histopathologic data were available for only 8 of the previous 15 GSSCM cases. There were no reports of mitosis, and necrosis was found in only 1 case.16 In our patient’s case, however, the first biopsy did show remarkable mitotic activity. This was not the case for the second biopsy, when mature chondrocytes associated with marked calcification and ossification were prominent features (Figures 6A, 6B). We presume that, within a limited period during earlier stages of tissue maturation in SCM, mitotic activity might be a possible finding. Of note, none of the other aforementioned histologic criteria for malignancy was seen in the first or second biopsy in the present case (Figures 3, 6C).
The original idea that SCM originates from a metaplasia in the subintimal layer of the synovium, where the synovium is in direct contact with the articular cartilage, has been challenged. The high incidence of hypercellularity, binucleated cells, and cellular atypia was always an argument against a metaplastic origin for the disease. Evidence of clonal chromosomal changes, like translocation of chromosome 1218 and chromosome 5 and 6 abnormalities,19,20 in addition to other alterations,19,21 provide some evidence supporting a neoplastic rather than a metaplastic origin for SCM. Given the presence of mitosis in the present case, the lack of mitotic activity in SCM, as stated by other authors,22 is not a universal feature and cannot be used as an argument against a neoplastic origin for SCM.
Although mitotic activity is uncommon in SCM, the present case illustrates the possible presence of mitotic activity in GSSCM. The simple presence of mitotic activity, a common finding in some other chondral tumors,23,24 does not preclude the diagnosis of benign SCM, as suggested before,8 and correlation of the clinical and radiologic manifestations with histopathologic findings is crucial for a correct diagnosis.
1. Milgram JW. Synovial osteochondromatosis: a histopathological study of thirty cases. J Bone Joint Surg Am. 1977;59(6):792-801.
2. Trias A, Quintana O. Synovial chondrometaplasia: review of world literature and a study of 18 Canadian cases. Can J Surg. 1976;19(2):151-158.
3. Murphey MD, Vidal JA, Fanburg-Smith JC, Gajewski DA. Imaging of synovial chondromatosis with radiologic-pathologic correlation. Radiographics. 2007;27(5):1465-1488.
4. Milgram JW. Synovial osteochondromatosis in association with Legg-Calve-Perthes disease. Clin Orthop Relat Res. 1979;(145):179-182.
5. Sim FH, Dahlin DC, Ivins JC. Extra-articular synovial chondromatosis. J Bone Joint Surg Am. 1977;59(4):492-495.
6. Bertoni F, Unni KK, Beabout JW, Sim FH. Chondrosarcomas of the synovium. Cancer. 1991;67(1):155-162.
7. Edeiken J, Edeiken BS, Ayala AG, Raymond AK, Murray JA, Guo SQ. Giant solitary synovial chondromatosis. Skeletal Radiol. 1994;23(1):23-29.
8. Davis RI, Hamilton A, Biggart JD. Primary synovial chondromatosis: a clinicopathologic review and assessment of malignant potential. Hum Pathol. 1998;29(7):683-688.
9. Goel A, Cullen C, Paul AS, Freemont AJ. Multiple giant synovial chondromatosis of the knee. Knee. 2001;8(3):243-245.
10. Dogan A, Harman M, Uslu M, Bayram I, Akpinar F. Rocky form giant synovial chondromatosis: a case report. Knee Surg Sports Traumatol Arthrosc. 2006;14(5):465-468.
11. Eisenberg KS, Johnston JO. Synovial chondromatosis of the hip joint presenting as an intrapelvic mass: a case report. J Bone Joint Surg Am. 1972;54(1):176-178.
12. Lohmann CH, Köster G, Klinger HM, Kunze E. Giant synovial osteochondromatosis of the acromio-clavicular joint in a child. A case report and review of the literature. J Pediatr Orthop B. 2005;14(2):126-128.
13. Cai XY, Yang C, Chen MJ, Jiang B, Wang BL. Arthroscopically guided removal of large solitary synovial chondromatosis from the temporomandibular joint. Int J Oral Maxillofac Surg. 2010;39(12):1236-1239.
14. Gil-Salu JL, Lazaro R, Aldasoro J, Gonzalez-Darder JM. Giant solitary synovial chondromatosis of the temporomandibular joint with intracranial extension. Skull Base Surg. 1998;8(2):99-104.
15. Kang CH, Park JH, Lee DH, Kim CH, Park JM, Lee WS. Giant synovial chondromatosis of the knee mimicking a parosteal osteosarcoma: a case report. J Korean Bone Joint Tumor Soc. 2010;16(2):95-98.
16. Nihal A, Read CJ, Henderson DC, Malcolm AJ. Extra-articular giant solitary synovial chondromatosis of the foot: a case report and literature review. Foot Ankle Surg. 1999;5(1):29-32.
17. Robinson P, White LM, Kandel R, Bell RS, Wunder JS. Primary synovial osteochondromatosis of the hip: extracapsular patterns of spread. Skeletal Radiol. 2004;33(4):210-215.
18. Tallini G, Dorfman H, Brys P, et al. Correlation between clinicopathological features and karyotype in 100 cartilaginous and chordoid tumours. A report from the Chromosomes and Morphology (CHAMP) Collaborative Study Group. J Pathol. 2002;196(2):194-203.
19. Sah AP, Geller DS, Mankin HJ, et al. Malignant transformation of synovial chondromatosis of the shoulder to chondrosarcoma. A case report. J Bone Joint Surg Am. 2007;89(6):1321-1328.
20. Buddingh EP, Krallman P, Neff JR, Nelson M, Liu J, Bridge JA. Chromosome 6 abnormalities are recurrent in synovial chondromatosis. Cancer Genet Cytogenet. 2003;140(1):18-22.
21. Rizzo M, Ghert MA, Harrelson JM, Scully SP. Chondrosarcoma of bone: analysis of 108 cases and evaluation for predictors of outcome. Clin Orthop Relat Res. 2001;(391):224-233.
22. Davis RI, Foster H, Arthur K, Trewin S, Hamilton PW, Biggart DJ. Cell proliferation studies in primary synovial chondromatosis. J Pathol. 1998;184(1):18-23.
23. Ishikawa E, Tsuboi K, Onizawa K, et al. Chondroblastoma of the temporal base with high mitotic activity. Neurol Med Chir (Tokyo). 2002;42(11):516-520.
24. Kirin I, Jurisic D, Mokrovic H, Stanec Z, Stalekar H. Chondromyxoid fibroma of the second metacarpal bone—a case report. Coll Antropol. 2011;35(3):929-931.
1. Milgram JW. Synovial osteochondromatosis: a histopathological study of thirty cases. J Bone Joint Surg Am. 1977;59(6):792-801.
2. Trias A, Quintana O. Synovial chondrometaplasia: review of world literature and a study of 18 Canadian cases. Can J Surg. 1976;19(2):151-158.
3. Murphey MD, Vidal JA, Fanburg-Smith JC, Gajewski DA. Imaging of synovial chondromatosis with radiologic-pathologic correlation. Radiographics. 2007;27(5):1465-1488.
4. Milgram JW. Synovial osteochondromatosis in association with Legg-Calve-Perthes disease. Clin Orthop Relat Res. 1979;(145):179-182.
5. Sim FH, Dahlin DC, Ivins JC. Extra-articular synovial chondromatosis. J Bone Joint Surg Am. 1977;59(4):492-495.
6. Bertoni F, Unni KK, Beabout JW, Sim FH. Chondrosarcomas of the synovium. Cancer. 1991;67(1):155-162.
7. Edeiken J, Edeiken BS, Ayala AG, Raymond AK, Murray JA, Guo SQ. Giant solitary synovial chondromatosis. Skeletal Radiol. 1994;23(1):23-29.
8. Davis RI, Hamilton A, Biggart JD. Primary synovial chondromatosis: a clinicopathologic review and assessment of malignant potential. Hum Pathol. 1998;29(7):683-688.
9. Goel A, Cullen C, Paul AS, Freemont AJ. Multiple giant synovial chondromatosis of the knee. Knee. 2001;8(3):243-245.
10. Dogan A, Harman M, Uslu M, Bayram I, Akpinar F. Rocky form giant synovial chondromatosis: a case report. Knee Surg Sports Traumatol Arthrosc. 2006;14(5):465-468.
11. Eisenberg KS, Johnston JO. Synovial chondromatosis of the hip joint presenting as an intrapelvic mass: a case report. J Bone Joint Surg Am. 1972;54(1):176-178.
12. Lohmann CH, Köster G, Klinger HM, Kunze E. Giant synovial osteochondromatosis of the acromio-clavicular joint in a child. A case report and review of the literature. J Pediatr Orthop B. 2005;14(2):126-128.
13. Cai XY, Yang C, Chen MJ, Jiang B, Wang BL. Arthroscopically guided removal of large solitary synovial chondromatosis from the temporomandibular joint. Int J Oral Maxillofac Surg. 2010;39(12):1236-1239.
14. Gil-Salu JL, Lazaro R, Aldasoro J, Gonzalez-Darder JM. Giant solitary synovial chondromatosis of the temporomandibular joint with intracranial extension. Skull Base Surg. 1998;8(2):99-104.
15. Kang CH, Park JH, Lee DH, Kim CH, Park JM, Lee WS. Giant synovial chondromatosis of the knee mimicking a parosteal osteosarcoma: a case report. J Korean Bone Joint Tumor Soc. 2010;16(2):95-98.
16. Nihal A, Read CJ, Henderson DC, Malcolm AJ. Extra-articular giant solitary synovial chondromatosis of the foot: a case report and literature review. Foot Ankle Surg. 1999;5(1):29-32.
17. Robinson P, White LM, Kandel R, Bell RS, Wunder JS. Primary synovial osteochondromatosis of the hip: extracapsular patterns of spread. Skeletal Radiol. 2004;33(4):210-215.
18. Tallini G, Dorfman H, Brys P, et al. Correlation between clinicopathological features and karyotype in 100 cartilaginous and chordoid tumours. A report from the Chromosomes and Morphology (CHAMP) Collaborative Study Group. J Pathol. 2002;196(2):194-203.
19. Sah AP, Geller DS, Mankin HJ, et al. Malignant transformation of synovial chondromatosis of the shoulder to chondrosarcoma. A case report. J Bone Joint Surg Am. 2007;89(6):1321-1328.
20. Buddingh EP, Krallman P, Neff JR, Nelson M, Liu J, Bridge JA. Chromosome 6 abnormalities are recurrent in synovial chondromatosis. Cancer Genet Cytogenet. 2003;140(1):18-22.
21. Rizzo M, Ghert MA, Harrelson JM, Scully SP. Chondrosarcoma of bone: analysis of 108 cases and evaluation for predictors of outcome. Clin Orthop Relat Res. 2001;(391):224-233.
22. Davis RI, Foster H, Arthur K, Trewin S, Hamilton PW, Biggart DJ. Cell proliferation studies in primary synovial chondromatosis. J Pathol. 1998;184(1):18-23.
23. Ishikawa E, Tsuboi K, Onizawa K, et al. Chondroblastoma of the temporal base with high mitotic activity. Neurol Med Chir (Tokyo). 2002;42(11):516-520.
24. Kirin I, Jurisic D, Mokrovic H, Stanec Z, Stalekar H. Chondromyxoid fibroma of the second metacarpal bone—a case report. Coll Antropol. 2011;35(3):929-931.
Congenital Absence of the Anterior Cruciate Ligament
Congenital absence of the anterior cruciate ligament (ACL) is a rare occurrence and has been seen most often in conjunction with conditions such as knee dislocation, knee dysplasia, proximal focal femoral deficiency, and fibular hemimelia.
We report on the incidental finding of ACL aplasia in a patient with a medial meniscal tear and history of leg-length discrepancy. Similar to earlier cases, this patient had hypertrophy of the meniscofemoral ligament of Humphrey, which likely provided stability. This case report emphasizes the importance of distinguishing between a stable and an unstable knee in congenital absence of the ACL. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 20-year-old woman presented for orthopedic evaluation with worsening medial left knee pain. Her pain was intermittent in nature, occurring about every 1 to 2 months and of 1 to 2 days’ duration. Onset was while using the elliptical machine, walking on uneven ground, or navigating stairs. She denied any buckling, catching, locking, instability, or swelling.
Her history was significant for a breech delivery and leg anisomelia, for which she had a contralateral distal femoral and proximal tibial percutaneous epiphysiodesis performed at age 10 years. Family history was negative for limb deformities.
Physical examination was notable for absence of global ligamentous laxity, overall valgus alignment of the left lower extremity, minimally decreased motion, trace effusion, positive medial joint line tenderness, positive McMurray test, and 1+ Lachman test with guarding on pivot shift testing.
Plain films showed valgus alignment with narrowing of the lateral compartment, narrow intercondylar notch, and hypoplasia of the tibial eminences and lateral femoral condyle (Figure 1). Magnetic resonance imaging showed a large tear in the posterior horn of the medial meniscus, hypertrophy of the meniscofemoral ligament of Humphrey (Figure 2A), and nonvisualization of the ACL with a small remnant (Figure 2B).
Arthroscopy showed complete absence of fibers of the ACL, hypertrophy of the meniscofemoral ligament of Humphrey, and a large posterior horn medial meniscal tear. A partial medial meniscectomy was performed. More than 2 years after surgery, the patient was doing very well without pain or instability, and was exercising regularly without difficulty.
Discussion
Our patient had left-sided congenital absence of the ACL with associated limb-length discrepancy of more than 2.5 cm. Isolated absence of the ACL has been described in a few case reports in the literature. Congenital ACL absence has most often been found in association with conditions such as knee dislocation (occurring with a frequency of .017/1000 births),1 knee dysplasia,2,3 fibular hemimelia,4 and proximal focal femoral deficiency.5 Johansson and Aparisi5,6 linked the finding of ACL absence with instability in those patients with known limb-length discrepancy and symptomatic instability. This report presents a patient who has congenital absence of the ACL in a foreshortened limb and torn medial meniscus. The classification of the patient’s cruciate dysplasia would be type I, as described by Manner and colleagues.7 The incidence of meniscal tears in association with congenital ACL absence is unknown. There have been reports of absence of the ACL associated with a ring meniscus,8 absence of both cruciate ligaments and menisci,9 and a bucket-handle tear of the medial meniscus.10
Gabos and colleagues4 recommend reconstructive surgery for patients with congenital absence of the ACL and symptomatic knee instability. Limb lengthening/shortening and realignment procedures have allowed patients such as ours to have functionally anatomic limbs and high activity levels. Surgical treatment is pursued to restore mechanical alignment and stability. Our patient had no symptoms of instability.
Similar to 3 of the 4 patients presented by Gabos and colleagues,4 our patient had marked hypertrophy of the meniscofemoral ligament of Humphrey. The report by Gabos and colleagues4 of this finding was the first in the literature. The hypertrophy of this ligament suggests it has a role in stabilizing the knee with a congenitally absent ACL. Our patient had no instability in her left knee but presented because of episodes of pain.
Of significant concern is the long-term outcome of patients with congenital ACL aplasia. Crawford and colleagues11 reported 11 patients with ACL deficiency and fibular hemimelia at a mean age of 37 years, showing similar functional outcomes to age-matched controls. However, there was no radiographic follow-up reported in regard to the development of osteoarthritis. To our knowledge, there have been no series published comparing surgical and nonsurgical treatment of congenital absence of the ACL. In the study by Gabos and colleagues,4 all patients were treated with reconstruction because these patients had symptomatic instability.
Conclusion
This report presents a patient whose symptoms improved after resection of her medial meniscal tear. This patient will be followed long-term to delineate her clinical course and to monitor for instability and/or development of osteoarthritis. Future studies should compare the treatment of congenital absence of the ACL with reconstruction and with conservative management.
1. Tachdjian MO. Pediatric Orthopedics. 2nd ed. Philadelphia: Saunders; 1990.
2. Thomas NP, Jackson AM, Aichroth PM. Congenital absence of the anterior cruciate ligament: A common component of knee dysplasia. J Bone Joint Surg Br. 1985;67(4):572-575.
3. Hejgaard N, Kjaerulff H. Congenital aplasia of the anterior cruciate ligament. Report of a case in a seven-year-old girl. Int Orthop. 1987;11(3):223-225.
4. Gabos PG, El Rassi G, Pahys J. Knee reconstruction in syndromes with congenital absence of the anterior cruciate ligament. J Pediatr Orthop. 2005;25(2):210-214.
5. Johansson E, Aparisi T. Missing cruciate ligament in congenital short femur. J Bone Joint Surg Am. 1983;65(8):1109-1115.
6. Johannson E, Aparisi T. Congenital absence of the cruciate ligaments. A case report and review of the literature. Clin Orthop Relat Res. 1982;162:108-111.
7. Manner HM, Radler C, Ganger R, Grill F. Dysplasia of the cruciate ligaments: radiographic assessment and classification. J Bone Joint Surg Am. 2006;88(1):130-137.
8. Noble J. Congenital absence of the anterior cruciate ligament associated with a ring meniscus. J Bone Joint Surg Am. 1975;57(8):1165-1166.
9. Tolo VT. Congenital absence of the menisci and cruciate ligaments of the knee. A case report. J Bone Joint Surg Am. 1981;63(6):1022-1024.
10. Kaelin A, Hulin PH, Carlioz H. Congenital aplasia of the cruciate ligaments. A report of six cases. J Bone Joint Surg Br. 1986;68(5):827-828.
11. Crawford DA, Tompkins BJ, Baird GO, Caskey PM. The long term function of the knee in patients with fibular hemimelia and anterior cruciate ligament deficiency. J Bone Joint Surg Br. 2012;94(3):328-333.
Congenital absence of the anterior cruciate ligament (ACL) is a rare occurrence and has been seen most often in conjunction with conditions such as knee dislocation, knee dysplasia, proximal focal femoral deficiency, and fibular hemimelia.
We report on the incidental finding of ACL aplasia in a patient with a medial meniscal tear and history of leg-length discrepancy. Similar to earlier cases, this patient had hypertrophy of the meniscofemoral ligament of Humphrey, which likely provided stability. This case report emphasizes the importance of distinguishing between a stable and an unstable knee in congenital absence of the ACL. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 20-year-old woman presented for orthopedic evaluation with worsening medial left knee pain. Her pain was intermittent in nature, occurring about every 1 to 2 months and of 1 to 2 days’ duration. Onset was while using the elliptical machine, walking on uneven ground, or navigating stairs. She denied any buckling, catching, locking, instability, or swelling.
Her history was significant for a breech delivery and leg anisomelia, for which she had a contralateral distal femoral and proximal tibial percutaneous epiphysiodesis performed at age 10 years. Family history was negative for limb deformities.
Physical examination was notable for absence of global ligamentous laxity, overall valgus alignment of the left lower extremity, minimally decreased motion, trace effusion, positive medial joint line tenderness, positive McMurray test, and 1+ Lachman test with guarding on pivot shift testing.
Plain films showed valgus alignment with narrowing of the lateral compartment, narrow intercondylar notch, and hypoplasia of the tibial eminences and lateral femoral condyle (Figure 1). Magnetic resonance imaging showed a large tear in the posterior horn of the medial meniscus, hypertrophy of the meniscofemoral ligament of Humphrey (Figure 2A), and nonvisualization of the ACL with a small remnant (Figure 2B).
Arthroscopy showed complete absence of fibers of the ACL, hypertrophy of the meniscofemoral ligament of Humphrey, and a large posterior horn medial meniscal tear. A partial medial meniscectomy was performed. More than 2 years after surgery, the patient was doing very well without pain or instability, and was exercising regularly without difficulty.
Discussion
Our patient had left-sided congenital absence of the ACL with associated limb-length discrepancy of more than 2.5 cm. Isolated absence of the ACL has been described in a few case reports in the literature. Congenital ACL absence has most often been found in association with conditions such as knee dislocation (occurring with a frequency of .017/1000 births),1 knee dysplasia,2,3 fibular hemimelia,4 and proximal focal femoral deficiency.5 Johansson and Aparisi5,6 linked the finding of ACL absence with instability in those patients with known limb-length discrepancy and symptomatic instability. This report presents a patient who has congenital absence of the ACL in a foreshortened limb and torn medial meniscus. The classification of the patient’s cruciate dysplasia would be type I, as described by Manner and colleagues.7 The incidence of meniscal tears in association with congenital ACL absence is unknown. There have been reports of absence of the ACL associated with a ring meniscus,8 absence of both cruciate ligaments and menisci,9 and a bucket-handle tear of the medial meniscus.10
Gabos and colleagues4 recommend reconstructive surgery for patients with congenital absence of the ACL and symptomatic knee instability. Limb lengthening/shortening and realignment procedures have allowed patients such as ours to have functionally anatomic limbs and high activity levels. Surgical treatment is pursued to restore mechanical alignment and stability. Our patient had no symptoms of instability.
Similar to 3 of the 4 patients presented by Gabos and colleagues,4 our patient had marked hypertrophy of the meniscofemoral ligament of Humphrey. The report by Gabos and colleagues4 of this finding was the first in the literature. The hypertrophy of this ligament suggests it has a role in stabilizing the knee with a congenitally absent ACL. Our patient had no instability in her left knee but presented because of episodes of pain.
Of significant concern is the long-term outcome of patients with congenital ACL aplasia. Crawford and colleagues11 reported 11 patients with ACL deficiency and fibular hemimelia at a mean age of 37 years, showing similar functional outcomes to age-matched controls. However, there was no radiographic follow-up reported in regard to the development of osteoarthritis. To our knowledge, there have been no series published comparing surgical and nonsurgical treatment of congenital absence of the ACL. In the study by Gabos and colleagues,4 all patients were treated with reconstruction because these patients had symptomatic instability.
Conclusion
This report presents a patient whose symptoms improved after resection of her medial meniscal tear. This patient will be followed long-term to delineate her clinical course and to monitor for instability and/or development of osteoarthritis. Future studies should compare the treatment of congenital absence of the ACL with reconstruction and with conservative management.
Congenital absence of the anterior cruciate ligament (ACL) is a rare occurrence and has been seen most often in conjunction with conditions such as knee dislocation, knee dysplasia, proximal focal femoral deficiency, and fibular hemimelia.
We report on the incidental finding of ACL aplasia in a patient with a medial meniscal tear and history of leg-length discrepancy. Similar to earlier cases, this patient had hypertrophy of the meniscofemoral ligament of Humphrey, which likely provided stability. This case report emphasizes the importance of distinguishing between a stable and an unstable knee in congenital absence of the ACL. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 20-year-old woman presented for orthopedic evaluation with worsening medial left knee pain. Her pain was intermittent in nature, occurring about every 1 to 2 months and of 1 to 2 days’ duration. Onset was while using the elliptical machine, walking on uneven ground, or navigating stairs. She denied any buckling, catching, locking, instability, or swelling.
Her history was significant for a breech delivery and leg anisomelia, for which she had a contralateral distal femoral and proximal tibial percutaneous epiphysiodesis performed at age 10 years. Family history was negative for limb deformities.
Physical examination was notable for absence of global ligamentous laxity, overall valgus alignment of the left lower extremity, minimally decreased motion, trace effusion, positive medial joint line tenderness, positive McMurray test, and 1+ Lachman test with guarding on pivot shift testing.
Plain films showed valgus alignment with narrowing of the lateral compartment, narrow intercondylar notch, and hypoplasia of the tibial eminences and lateral femoral condyle (Figure 1). Magnetic resonance imaging showed a large tear in the posterior horn of the medial meniscus, hypertrophy of the meniscofemoral ligament of Humphrey (Figure 2A), and nonvisualization of the ACL with a small remnant (Figure 2B).
Arthroscopy showed complete absence of fibers of the ACL, hypertrophy of the meniscofemoral ligament of Humphrey, and a large posterior horn medial meniscal tear. A partial medial meniscectomy was performed. More than 2 years after surgery, the patient was doing very well without pain or instability, and was exercising regularly without difficulty.
Discussion
Our patient had left-sided congenital absence of the ACL with associated limb-length discrepancy of more than 2.5 cm. Isolated absence of the ACL has been described in a few case reports in the literature. Congenital ACL absence has most often been found in association with conditions such as knee dislocation (occurring with a frequency of .017/1000 births),1 knee dysplasia,2,3 fibular hemimelia,4 and proximal focal femoral deficiency.5 Johansson and Aparisi5,6 linked the finding of ACL absence with instability in those patients with known limb-length discrepancy and symptomatic instability. This report presents a patient who has congenital absence of the ACL in a foreshortened limb and torn medial meniscus. The classification of the patient’s cruciate dysplasia would be type I, as described by Manner and colleagues.7 The incidence of meniscal tears in association with congenital ACL absence is unknown. There have been reports of absence of the ACL associated with a ring meniscus,8 absence of both cruciate ligaments and menisci,9 and a bucket-handle tear of the medial meniscus.10
Gabos and colleagues4 recommend reconstructive surgery for patients with congenital absence of the ACL and symptomatic knee instability. Limb lengthening/shortening and realignment procedures have allowed patients such as ours to have functionally anatomic limbs and high activity levels. Surgical treatment is pursued to restore mechanical alignment and stability. Our patient had no symptoms of instability.
Similar to 3 of the 4 patients presented by Gabos and colleagues,4 our patient had marked hypertrophy of the meniscofemoral ligament of Humphrey. The report by Gabos and colleagues4 of this finding was the first in the literature. The hypertrophy of this ligament suggests it has a role in stabilizing the knee with a congenitally absent ACL. Our patient had no instability in her left knee but presented because of episodes of pain.
Of significant concern is the long-term outcome of patients with congenital ACL aplasia. Crawford and colleagues11 reported 11 patients with ACL deficiency and fibular hemimelia at a mean age of 37 years, showing similar functional outcomes to age-matched controls. However, there was no radiographic follow-up reported in regard to the development of osteoarthritis. To our knowledge, there have been no series published comparing surgical and nonsurgical treatment of congenital absence of the ACL. In the study by Gabos and colleagues,4 all patients were treated with reconstruction because these patients had symptomatic instability.
Conclusion
This report presents a patient whose symptoms improved after resection of her medial meniscal tear. This patient will be followed long-term to delineate her clinical course and to monitor for instability and/or development of osteoarthritis. Future studies should compare the treatment of congenital absence of the ACL with reconstruction and with conservative management.
1. Tachdjian MO. Pediatric Orthopedics. 2nd ed. Philadelphia: Saunders; 1990.
2. Thomas NP, Jackson AM, Aichroth PM. Congenital absence of the anterior cruciate ligament: A common component of knee dysplasia. J Bone Joint Surg Br. 1985;67(4):572-575.
3. Hejgaard N, Kjaerulff H. Congenital aplasia of the anterior cruciate ligament. Report of a case in a seven-year-old girl. Int Orthop. 1987;11(3):223-225.
4. Gabos PG, El Rassi G, Pahys J. Knee reconstruction in syndromes with congenital absence of the anterior cruciate ligament. J Pediatr Orthop. 2005;25(2):210-214.
5. Johansson E, Aparisi T. Missing cruciate ligament in congenital short femur. J Bone Joint Surg Am. 1983;65(8):1109-1115.
6. Johannson E, Aparisi T. Congenital absence of the cruciate ligaments. A case report and review of the literature. Clin Orthop Relat Res. 1982;162:108-111.
7. Manner HM, Radler C, Ganger R, Grill F. Dysplasia of the cruciate ligaments: radiographic assessment and classification. J Bone Joint Surg Am. 2006;88(1):130-137.
8. Noble J. Congenital absence of the anterior cruciate ligament associated with a ring meniscus. J Bone Joint Surg Am. 1975;57(8):1165-1166.
9. Tolo VT. Congenital absence of the menisci and cruciate ligaments of the knee. A case report. J Bone Joint Surg Am. 1981;63(6):1022-1024.
10. Kaelin A, Hulin PH, Carlioz H. Congenital aplasia of the cruciate ligaments. A report of six cases. J Bone Joint Surg Br. 1986;68(5):827-828.
11. Crawford DA, Tompkins BJ, Baird GO, Caskey PM. The long term function of the knee in patients with fibular hemimelia and anterior cruciate ligament deficiency. J Bone Joint Surg Br. 2012;94(3):328-333.
1. Tachdjian MO. Pediatric Orthopedics. 2nd ed. Philadelphia: Saunders; 1990.
2. Thomas NP, Jackson AM, Aichroth PM. Congenital absence of the anterior cruciate ligament: A common component of knee dysplasia. J Bone Joint Surg Br. 1985;67(4):572-575.
3. Hejgaard N, Kjaerulff H. Congenital aplasia of the anterior cruciate ligament. Report of a case in a seven-year-old girl. Int Orthop. 1987;11(3):223-225.
4. Gabos PG, El Rassi G, Pahys J. Knee reconstruction in syndromes with congenital absence of the anterior cruciate ligament. J Pediatr Orthop. 2005;25(2):210-214.
5. Johansson E, Aparisi T. Missing cruciate ligament in congenital short femur. J Bone Joint Surg Am. 1983;65(8):1109-1115.
6. Johannson E, Aparisi T. Congenital absence of the cruciate ligaments. A case report and review of the literature. Clin Orthop Relat Res. 1982;162:108-111.
7. Manner HM, Radler C, Ganger R, Grill F. Dysplasia of the cruciate ligaments: radiographic assessment and classification. J Bone Joint Surg Am. 2006;88(1):130-137.
8. Noble J. Congenital absence of the anterior cruciate ligament associated with a ring meniscus. J Bone Joint Surg Am. 1975;57(8):1165-1166.
9. Tolo VT. Congenital absence of the menisci and cruciate ligaments of the knee. A case report. J Bone Joint Surg Am. 1981;63(6):1022-1024.
10. Kaelin A, Hulin PH, Carlioz H. Congenital aplasia of the cruciate ligaments. A report of six cases. J Bone Joint Surg Br. 1986;68(5):827-828.
11. Crawford DA, Tompkins BJ, Baird GO, Caskey PM. The long term function of the knee in patients with fibular hemimelia and anterior cruciate ligament deficiency. J Bone Joint Surg Br. 2012;94(3):328-333.
Iatrogenic Femoral Neck Fracture After Closed Reduction of Anterior Hip Dislocation in the Emergency Department
Anterior hip dislocations have been reported to account for approximately 5% to 10% of all hip dislocations.1 Epstein and Wiss2 originally divided anterior hip dislocations into superior (type I, including pubic or subspinous) and inferior (type II, including obturator and perineal) dislocations. This classification was further subdivided based on the presence of either no associated fracture (type A), fracture of the femoral head or neck (FNF; type B), or fracture of the acetabulum (type C).3 Of all anterior hip dislocations, it has been reported that the inferior or obturator type of dislocation is more common, constituting approximately 70% of all anterior dislocations.4 In 1943, Pringle5 described the mechanism of obturator dislocation as simultaneous abduction, flexion, and external rotation of the hip. Our literature search found only 2 case reports in non-English-language journals of a complete FNF associated with an attempted reduction of an anterior hip dislocation.6,7 Indentation fractures of the femoral head have been more commonly reported than FNFs, with a reported incidence of 35% to 55% after anterior dislocation.4,8 DeLee and colleagues8 also found that those patients with indentation fractures were at a higher risk for developing avascular necrosis of the femoral head in addition to being more likely to report poor or fair function of the hip 2 years after reduction.
There have been a number of different reduction maneuvers for anterior dislocation of hips published in the literature. Epstein and Harvey9 advocated reduction by traction in the line of the femur with the hip flexed and in gentle internal rotation and abduction while the patient was under general anesthesia. Toms and Williams,10 however, recommended adduction with gradual release of the longitudinal traction. Polesky and Polesky11 described a reduction method involving sharp internal rotation, which was found to be associated with FNF. The patient provided written informed consent for print and electronic publication of this case report, and approval was obtained from the Emory University Institutional Review Board.
Case Report
The patient was a 73-year-old woman, an independent ambulator with minimal antecedent hip pain, who, as a pedestrian, was struck by a heavy-duty pickup truck at low velocity. She was flown to our level I trauma center from an outside hospital. The patient arrived hemodynamically stable, with a Glasgow Coma Scale score of 15 and with major complaints of right shoulder and right hip pain. She had a positive Focused Assessment with Sonography for Trauma (FAST), and underwent a subsequent urgent chest, abdomen, and pelvis computed tomography (CT) scan for further investigation. CT showed a grade 1 liver laceration. Her anteroposterior (AP) pelvic radiograph and pelvic CT scan showed an anterior hip dislocation with the femoral head located adjacent to the obturator foramen (Figures 1, 2). The AP pelvic radiograph and pelvic CT scan were scrutinized extensively before reduction to rule out a possible FNF. Comparing the right and left femoral necks through multiple axial CT images showed no obvious differences between the 2 sides (Figures 3, 4). Her only other orthopedic injury was an inferior shoulder dislocation. It is not routine for the general surgery trauma team to obtain a pelvic CT scan prior to involvement of the orthopedic service and prompt reduction of a hip dislocation. Upon initial examination of her right hip, it was fixed in slight flexion and external rotation; she was neurovascularly intact.
After being cleared by the trauma service, the patient provided informed consent for closed reduction of the hip and shoulder under conscious sedation, performed by the emergency department (ED) staff. She received intravenous fentanyl and midazolam, and the reduction was attempted. The reduction maneuver was performed with gentle inline traction, adduction, and internal rotation and extension. There was an audible clunk, and the hip was thought to be reduced and stable. The right leg lower extremity was placed into a knee immobilizer and she remained neurovascularly intact. The shoulder was reduced. After the procedure, the patient had an episode of hypoxia requiring oxygenation via a bag valve mask by the ED staff. Postreduction radiographs confirmed reduction of the right shoulder; however, they also showed a FNF with the femoral head retained near the obturator foramen (Figures 5, 6). The patient and her family were informed of the fracture, and a total hip arthroplasty (THA) was recommended, given her pre-injury mild symptomatic osteoarthritis in the hip and her age. The patient was admitted to the intensive care unit for cardiopulmonary monitoring and was found to have a troponin leak on hospital day 1. She was evaluated by the cardiology service; serial electrocardiograms and troponins ruled out acute myocardial infarction. The patient was cleared for surgery on hospital day 4.
On hospital day 5, she underwent a right THA via a Kocher-Langenbeck approach. The patient’s femoral head was found to be anterior and laterally adjacent to her ischial tuberosity with an indentation fracture. The sciatic nerve was identified and found to be intact. A metal-on-polyethylene Stryker Accolade femoral component and Trident acetabular shell were implanted, and a posterior capsular repair was performed (Figure 7).
The patient tolerated the procedure well, and her postoperative course was uneventful. She was discharged to a subacute rehabilitation facility on postoperative day 3. The patient returned for her 2-week postoperative visit ambulating without assistance. At her last follow-up visit, approximately 6 weeks after surgery, she was a functionally independent community ambulator. Phone conversations with her private orthopedist at 6 months confirmed continued ambulation without problems.
Discussion
This case report of a complication that occurred in our institution has resulted in a change in our protocol for treatment of geriatric anterior hip dislocations. Our institution is a level I trauma center, and traumatic hip dislocations are relatively common, occurring usually in young patients with high-energy trauma. Although somewhat controversial, it is generally assumed that the incidence of avascular necrosis of the femoral head after dislocation of the hip is correlated with the time interval from dislocation to reduction of the hip. Therefore, our protocol for hip dislocations of the hip in young trauma patients is urgent reduction in the ED under appropriate analgesia and muscle relaxation.
In this case report, the patient was older than 65 years with radiographic evidence of possible impingement and postsurgical evidence of impingement of the femoral head in the obturator foremen (Figures 1, 2, 8). In addition, the patient was significantly osteopenic radiographically. An attempted reduction in the ED resulted in FNF requiring THA (Figures 5, 6, 9). After discussion of this complication in our institution’s morbidity and mortality conference, we have developed a protocol for the geriatric patient (older than 65 years) with a traumatic hip dislocation. These patients will undergo attempted reduction under controlled analgesia and muscle relaxation in the operating room (OR) with an attending surgeon present, ideally, an attending surgeon comfortable with arthroplasty in a terminally cleaned OR room. Our institution’s surgical site infection rate after total joint arthroplasty has significantly decreased with improved patient selection and the use of terminally cleaned OR rooms. Because our policy is to perform closed reduction of dislocated hips in an urgent manner, if there is not a terminally clean room or an arthroplasty-trained attending orthopedic surgeon available, then informed consent with discussion of the possibility of fracture requiring a subsequent arthroplasty should be obtained from the patient before the attempted reduction.
After review of the available literature, we believe that this case highlights some of the important treatment principles when treating anterior hip dislocations in the ED. The relatively high incidence of indentation fractures of the femoral head with obturator dislocations puts these fractures at higher risk for possible impingement around the obturator ring. This impingement, coupled with preexisting osteopenia, can predispose these dislocations to FNF, if appropriate analgesia and sedation are not obtained and gentle reduction is not performed. In addition, while it may not be time- or cost-effective to perform closed reduction on every hip dislocation, we bring geriatric patients with radiographic osteopenia to the OR for more controlled reductions. In the informed consent discussion, the possibility of FNF is mentioned, and the patient and family are told that an elective total hip replacement will be performed if this complication occurs.
We consider the following to be risk factors for closed reductions of anterior hip dislocations: (1) preexisting osteopenia on plain films, (2) age greater than 65 years, and (3) radiographic femoral head impingement on the surrounding bony pelvis. We continue to consider closed reduction of both anterior and posterior hip dislocations as urgent (within 6 hours from time of dislocation). This case adds to the existing literature on the risk of FNF with closed reduction of obturator hip dislocations, and we hope that it will encourage further study into the safest and most cost-effective reduction protocol.
1. Amihood, S. Anterior dislocation of the hip. Injury. 1975;7(2):107-110.
2. Epstein HC, Wiss DA. Traumatic anterior dislocation of the hip. Orthopedics. 1985;8(1):130, 132-134.
3. Epstein HC. Traumatic dislocations of the hip. Clin Orthop Relat Res. 1973(92):116-142.
4. Erb RE, Steele JR, Nance EP Jr, Edwards JR. Traumatic anterior dislocation of the hip: spectrum of plain film and CT findings. AJR Am J Roentgenol. 1995;165(5):1215-1219.
5. Pringle JH. Traumatic dislocation at the hip joint. An experimental study in the cadaver. Glasgow Med J. 1943;21:25-40.
6. Esenkaya I, Görgeç M. Traumatic anterior dislocation of the hip associated with ipsilateral femoral neck fracture: a case report. Acta Orthop Traumatol Turc. 2002;36(4):366-368.
7. Sadler AH, DiStefano M. Anterior dislocation of the hip with ipsilateral basicervical fracture. A case report. J Bone Joint Surg Am. 1985;67(2):326-329.
8. DeLee JC, Evans JA, Thomas J. Anterior dislocation of the hip and associated femoral-head fractures. J Bone Joint Surg Am. 1980;62(6):960-964.
9. Epstein HC, Harvey JP Jr. Traumatic anterior dislocations of the hip: management and results. An analysis of fifty-five cases. J Bone Joint Surg Am. 1972;54(7):1561-1562.
10. Toms AD, Williams S, White SH. Obturator dislocation of the hip. J Bone Joint Surg Br. 2001;83(1):113-115.
11. Polesky RE, Polesky FA. Intrapelvic dislocation of the femoral head following anterior dislocation of the hip. A case report. J Bone Joint Surg Am. 1972;54(5):1097-1098.
Anterior hip dislocations have been reported to account for approximately 5% to 10% of all hip dislocations.1 Epstein and Wiss2 originally divided anterior hip dislocations into superior (type I, including pubic or subspinous) and inferior (type II, including obturator and perineal) dislocations. This classification was further subdivided based on the presence of either no associated fracture (type A), fracture of the femoral head or neck (FNF; type B), or fracture of the acetabulum (type C).3 Of all anterior hip dislocations, it has been reported that the inferior or obturator type of dislocation is more common, constituting approximately 70% of all anterior dislocations.4 In 1943, Pringle5 described the mechanism of obturator dislocation as simultaneous abduction, flexion, and external rotation of the hip. Our literature search found only 2 case reports in non-English-language journals of a complete FNF associated with an attempted reduction of an anterior hip dislocation.6,7 Indentation fractures of the femoral head have been more commonly reported than FNFs, with a reported incidence of 35% to 55% after anterior dislocation.4,8 DeLee and colleagues8 also found that those patients with indentation fractures were at a higher risk for developing avascular necrosis of the femoral head in addition to being more likely to report poor or fair function of the hip 2 years after reduction.
There have been a number of different reduction maneuvers for anterior dislocation of hips published in the literature. Epstein and Harvey9 advocated reduction by traction in the line of the femur with the hip flexed and in gentle internal rotation and abduction while the patient was under general anesthesia. Toms and Williams,10 however, recommended adduction with gradual release of the longitudinal traction. Polesky and Polesky11 described a reduction method involving sharp internal rotation, which was found to be associated with FNF. The patient provided written informed consent for print and electronic publication of this case report, and approval was obtained from the Emory University Institutional Review Board.
Case Report
The patient was a 73-year-old woman, an independent ambulator with minimal antecedent hip pain, who, as a pedestrian, was struck by a heavy-duty pickup truck at low velocity. She was flown to our level I trauma center from an outside hospital. The patient arrived hemodynamically stable, with a Glasgow Coma Scale score of 15 and with major complaints of right shoulder and right hip pain. She had a positive Focused Assessment with Sonography for Trauma (FAST), and underwent a subsequent urgent chest, abdomen, and pelvis computed tomography (CT) scan for further investigation. CT showed a grade 1 liver laceration. Her anteroposterior (AP) pelvic radiograph and pelvic CT scan showed an anterior hip dislocation with the femoral head located adjacent to the obturator foramen (Figures 1, 2). The AP pelvic radiograph and pelvic CT scan were scrutinized extensively before reduction to rule out a possible FNF. Comparing the right and left femoral necks through multiple axial CT images showed no obvious differences between the 2 sides (Figures 3, 4). Her only other orthopedic injury was an inferior shoulder dislocation. It is not routine for the general surgery trauma team to obtain a pelvic CT scan prior to involvement of the orthopedic service and prompt reduction of a hip dislocation. Upon initial examination of her right hip, it was fixed in slight flexion and external rotation; she was neurovascularly intact.
After being cleared by the trauma service, the patient provided informed consent for closed reduction of the hip and shoulder under conscious sedation, performed by the emergency department (ED) staff. She received intravenous fentanyl and midazolam, and the reduction was attempted. The reduction maneuver was performed with gentle inline traction, adduction, and internal rotation and extension. There was an audible clunk, and the hip was thought to be reduced and stable. The right leg lower extremity was placed into a knee immobilizer and she remained neurovascularly intact. The shoulder was reduced. After the procedure, the patient had an episode of hypoxia requiring oxygenation via a bag valve mask by the ED staff. Postreduction radiographs confirmed reduction of the right shoulder; however, they also showed a FNF with the femoral head retained near the obturator foramen (Figures 5, 6). The patient and her family were informed of the fracture, and a total hip arthroplasty (THA) was recommended, given her pre-injury mild symptomatic osteoarthritis in the hip and her age. The patient was admitted to the intensive care unit for cardiopulmonary monitoring and was found to have a troponin leak on hospital day 1. She was evaluated by the cardiology service; serial electrocardiograms and troponins ruled out acute myocardial infarction. The patient was cleared for surgery on hospital day 4.
On hospital day 5, she underwent a right THA via a Kocher-Langenbeck approach. The patient’s femoral head was found to be anterior and laterally adjacent to her ischial tuberosity with an indentation fracture. The sciatic nerve was identified and found to be intact. A metal-on-polyethylene Stryker Accolade femoral component and Trident acetabular shell were implanted, and a posterior capsular repair was performed (Figure 7).
The patient tolerated the procedure well, and her postoperative course was uneventful. She was discharged to a subacute rehabilitation facility on postoperative day 3. The patient returned for her 2-week postoperative visit ambulating without assistance. At her last follow-up visit, approximately 6 weeks after surgery, she was a functionally independent community ambulator. Phone conversations with her private orthopedist at 6 months confirmed continued ambulation without problems.
Discussion
This case report of a complication that occurred in our institution has resulted in a change in our protocol for treatment of geriatric anterior hip dislocations. Our institution is a level I trauma center, and traumatic hip dislocations are relatively common, occurring usually in young patients with high-energy trauma. Although somewhat controversial, it is generally assumed that the incidence of avascular necrosis of the femoral head after dislocation of the hip is correlated with the time interval from dislocation to reduction of the hip. Therefore, our protocol for hip dislocations of the hip in young trauma patients is urgent reduction in the ED under appropriate analgesia and muscle relaxation.
In this case report, the patient was older than 65 years with radiographic evidence of possible impingement and postsurgical evidence of impingement of the femoral head in the obturator foremen (Figures 1, 2, 8). In addition, the patient was significantly osteopenic radiographically. An attempted reduction in the ED resulted in FNF requiring THA (Figures 5, 6, 9). After discussion of this complication in our institution’s morbidity and mortality conference, we have developed a protocol for the geriatric patient (older than 65 years) with a traumatic hip dislocation. These patients will undergo attempted reduction under controlled analgesia and muscle relaxation in the operating room (OR) with an attending surgeon present, ideally, an attending surgeon comfortable with arthroplasty in a terminally cleaned OR room. Our institution’s surgical site infection rate after total joint arthroplasty has significantly decreased with improved patient selection and the use of terminally cleaned OR rooms. Because our policy is to perform closed reduction of dislocated hips in an urgent manner, if there is not a terminally clean room or an arthroplasty-trained attending orthopedic surgeon available, then informed consent with discussion of the possibility of fracture requiring a subsequent arthroplasty should be obtained from the patient before the attempted reduction.
After review of the available literature, we believe that this case highlights some of the important treatment principles when treating anterior hip dislocations in the ED. The relatively high incidence of indentation fractures of the femoral head with obturator dislocations puts these fractures at higher risk for possible impingement around the obturator ring. This impingement, coupled with preexisting osteopenia, can predispose these dislocations to FNF, if appropriate analgesia and sedation are not obtained and gentle reduction is not performed. In addition, while it may not be time- or cost-effective to perform closed reduction on every hip dislocation, we bring geriatric patients with radiographic osteopenia to the OR for more controlled reductions. In the informed consent discussion, the possibility of FNF is mentioned, and the patient and family are told that an elective total hip replacement will be performed if this complication occurs.
We consider the following to be risk factors for closed reductions of anterior hip dislocations: (1) preexisting osteopenia on plain films, (2) age greater than 65 years, and (3) radiographic femoral head impingement on the surrounding bony pelvis. We continue to consider closed reduction of both anterior and posterior hip dislocations as urgent (within 6 hours from time of dislocation). This case adds to the existing literature on the risk of FNF with closed reduction of obturator hip dislocations, and we hope that it will encourage further study into the safest and most cost-effective reduction protocol.
Anterior hip dislocations have been reported to account for approximately 5% to 10% of all hip dislocations.1 Epstein and Wiss2 originally divided anterior hip dislocations into superior (type I, including pubic or subspinous) and inferior (type II, including obturator and perineal) dislocations. This classification was further subdivided based on the presence of either no associated fracture (type A), fracture of the femoral head or neck (FNF; type B), or fracture of the acetabulum (type C).3 Of all anterior hip dislocations, it has been reported that the inferior or obturator type of dislocation is more common, constituting approximately 70% of all anterior dislocations.4 In 1943, Pringle5 described the mechanism of obturator dislocation as simultaneous abduction, flexion, and external rotation of the hip. Our literature search found only 2 case reports in non-English-language journals of a complete FNF associated with an attempted reduction of an anterior hip dislocation.6,7 Indentation fractures of the femoral head have been more commonly reported than FNFs, with a reported incidence of 35% to 55% after anterior dislocation.4,8 DeLee and colleagues8 also found that those patients with indentation fractures were at a higher risk for developing avascular necrosis of the femoral head in addition to being more likely to report poor or fair function of the hip 2 years after reduction.
There have been a number of different reduction maneuvers for anterior dislocation of hips published in the literature. Epstein and Harvey9 advocated reduction by traction in the line of the femur with the hip flexed and in gentle internal rotation and abduction while the patient was under general anesthesia. Toms and Williams,10 however, recommended adduction with gradual release of the longitudinal traction. Polesky and Polesky11 described a reduction method involving sharp internal rotation, which was found to be associated with FNF. The patient provided written informed consent for print and electronic publication of this case report, and approval was obtained from the Emory University Institutional Review Board.
Case Report
The patient was a 73-year-old woman, an independent ambulator with minimal antecedent hip pain, who, as a pedestrian, was struck by a heavy-duty pickup truck at low velocity. She was flown to our level I trauma center from an outside hospital. The patient arrived hemodynamically stable, with a Glasgow Coma Scale score of 15 and with major complaints of right shoulder and right hip pain. She had a positive Focused Assessment with Sonography for Trauma (FAST), and underwent a subsequent urgent chest, abdomen, and pelvis computed tomography (CT) scan for further investigation. CT showed a grade 1 liver laceration. Her anteroposterior (AP) pelvic radiograph and pelvic CT scan showed an anterior hip dislocation with the femoral head located adjacent to the obturator foramen (Figures 1, 2). The AP pelvic radiograph and pelvic CT scan were scrutinized extensively before reduction to rule out a possible FNF. Comparing the right and left femoral necks through multiple axial CT images showed no obvious differences between the 2 sides (Figures 3, 4). Her only other orthopedic injury was an inferior shoulder dislocation. It is not routine for the general surgery trauma team to obtain a pelvic CT scan prior to involvement of the orthopedic service and prompt reduction of a hip dislocation. Upon initial examination of her right hip, it was fixed in slight flexion and external rotation; she was neurovascularly intact.
After being cleared by the trauma service, the patient provided informed consent for closed reduction of the hip and shoulder under conscious sedation, performed by the emergency department (ED) staff. She received intravenous fentanyl and midazolam, and the reduction was attempted. The reduction maneuver was performed with gentle inline traction, adduction, and internal rotation and extension. There was an audible clunk, and the hip was thought to be reduced and stable. The right leg lower extremity was placed into a knee immobilizer and she remained neurovascularly intact. The shoulder was reduced. After the procedure, the patient had an episode of hypoxia requiring oxygenation via a bag valve mask by the ED staff. Postreduction radiographs confirmed reduction of the right shoulder; however, they also showed a FNF with the femoral head retained near the obturator foramen (Figures 5, 6). The patient and her family were informed of the fracture, and a total hip arthroplasty (THA) was recommended, given her pre-injury mild symptomatic osteoarthritis in the hip and her age. The patient was admitted to the intensive care unit for cardiopulmonary monitoring and was found to have a troponin leak on hospital day 1. She was evaluated by the cardiology service; serial electrocardiograms and troponins ruled out acute myocardial infarction. The patient was cleared for surgery on hospital day 4.
On hospital day 5, she underwent a right THA via a Kocher-Langenbeck approach. The patient’s femoral head was found to be anterior and laterally adjacent to her ischial tuberosity with an indentation fracture. The sciatic nerve was identified and found to be intact. A metal-on-polyethylene Stryker Accolade femoral component and Trident acetabular shell were implanted, and a posterior capsular repair was performed (Figure 7).
The patient tolerated the procedure well, and her postoperative course was uneventful. She was discharged to a subacute rehabilitation facility on postoperative day 3. The patient returned for her 2-week postoperative visit ambulating without assistance. At her last follow-up visit, approximately 6 weeks after surgery, she was a functionally independent community ambulator. Phone conversations with her private orthopedist at 6 months confirmed continued ambulation without problems.
Discussion
This case report of a complication that occurred in our institution has resulted in a change in our protocol for treatment of geriatric anterior hip dislocations. Our institution is a level I trauma center, and traumatic hip dislocations are relatively common, occurring usually in young patients with high-energy trauma. Although somewhat controversial, it is generally assumed that the incidence of avascular necrosis of the femoral head after dislocation of the hip is correlated with the time interval from dislocation to reduction of the hip. Therefore, our protocol for hip dislocations of the hip in young trauma patients is urgent reduction in the ED under appropriate analgesia and muscle relaxation.
In this case report, the patient was older than 65 years with radiographic evidence of possible impingement and postsurgical evidence of impingement of the femoral head in the obturator foremen (Figures 1, 2, 8). In addition, the patient was significantly osteopenic radiographically. An attempted reduction in the ED resulted in FNF requiring THA (Figures 5, 6, 9). After discussion of this complication in our institution’s morbidity and mortality conference, we have developed a protocol for the geriatric patient (older than 65 years) with a traumatic hip dislocation. These patients will undergo attempted reduction under controlled analgesia and muscle relaxation in the operating room (OR) with an attending surgeon present, ideally, an attending surgeon comfortable with arthroplasty in a terminally cleaned OR room. Our institution’s surgical site infection rate after total joint arthroplasty has significantly decreased with improved patient selection and the use of terminally cleaned OR rooms. Because our policy is to perform closed reduction of dislocated hips in an urgent manner, if there is not a terminally clean room or an arthroplasty-trained attending orthopedic surgeon available, then informed consent with discussion of the possibility of fracture requiring a subsequent arthroplasty should be obtained from the patient before the attempted reduction.
After review of the available literature, we believe that this case highlights some of the important treatment principles when treating anterior hip dislocations in the ED. The relatively high incidence of indentation fractures of the femoral head with obturator dislocations puts these fractures at higher risk for possible impingement around the obturator ring. This impingement, coupled with preexisting osteopenia, can predispose these dislocations to FNF, if appropriate analgesia and sedation are not obtained and gentle reduction is not performed. In addition, while it may not be time- or cost-effective to perform closed reduction on every hip dislocation, we bring geriatric patients with radiographic osteopenia to the OR for more controlled reductions. In the informed consent discussion, the possibility of FNF is mentioned, and the patient and family are told that an elective total hip replacement will be performed if this complication occurs.
We consider the following to be risk factors for closed reductions of anterior hip dislocations: (1) preexisting osteopenia on plain films, (2) age greater than 65 years, and (3) radiographic femoral head impingement on the surrounding bony pelvis. We continue to consider closed reduction of both anterior and posterior hip dislocations as urgent (within 6 hours from time of dislocation). This case adds to the existing literature on the risk of FNF with closed reduction of obturator hip dislocations, and we hope that it will encourage further study into the safest and most cost-effective reduction protocol.
1. Amihood, S. Anterior dislocation of the hip. Injury. 1975;7(2):107-110.
2. Epstein HC, Wiss DA. Traumatic anterior dislocation of the hip. Orthopedics. 1985;8(1):130, 132-134.
3. Epstein HC. Traumatic dislocations of the hip. Clin Orthop Relat Res. 1973(92):116-142.
4. Erb RE, Steele JR, Nance EP Jr, Edwards JR. Traumatic anterior dislocation of the hip: spectrum of plain film and CT findings. AJR Am J Roentgenol. 1995;165(5):1215-1219.
5. Pringle JH. Traumatic dislocation at the hip joint. An experimental study in the cadaver. Glasgow Med J. 1943;21:25-40.
6. Esenkaya I, Görgeç M. Traumatic anterior dislocation of the hip associated with ipsilateral femoral neck fracture: a case report. Acta Orthop Traumatol Turc. 2002;36(4):366-368.
7. Sadler AH, DiStefano M. Anterior dislocation of the hip with ipsilateral basicervical fracture. A case report. J Bone Joint Surg Am. 1985;67(2):326-329.
8. DeLee JC, Evans JA, Thomas J. Anterior dislocation of the hip and associated femoral-head fractures. J Bone Joint Surg Am. 1980;62(6):960-964.
9. Epstein HC, Harvey JP Jr. Traumatic anterior dislocations of the hip: management and results. An analysis of fifty-five cases. J Bone Joint Surg Am. 1972;54(7):1561-1562.
10. Toms AD, Williams S, White SH. Obturator dislocation of the hip. J Bone Joint Surg Br. 2001;83(1):113-115.
11. Polesky RE, Polesky FA. Intrapelvic dislocation of the femoral head following anterior dislocation of the hip. A case report. J Bone Joint Surg Am. 1972;54(5):1097-1098.
1. Amihood, S. Anterior dislocation of the hip. Injury. 1975;7(2):107-110.
2. Epstein HC, Wiss DA. Traumatic anterior dislocation of the hip. Orthopedics. 1985;8(1):130, 132-134.
3. Epstein HC. Traumatic dislocations of the hip. Clin Orthop Relat Res. 1973(92):116-142.
4. Erb RE, Steele JR, Nance EP Jr, Edwards JR. Traumatic anterior dislocation of the hip: spectrum of plain film and CT findings. AJR Am J Roentgenol. 1995;165(5):1215-1219.
5. Pringle JH. Traumatic dislocation at the hip joint. An experimental study in the cadaver. Glasgow Med J. 1943;21:25-40.
6. Esenkaya I, Görgeç M. Traumatic anterior dislocation of the hip associated with ipsilateral femoral neck fracture: a case report. Acta Orthop Traumatol Turc. 2002;36(4):366-368.
7. Sadler AH, DiStefano M. Anterior dislocation of the hip with ipsilateral basicervical fracture. A case report. J Bone Joint Surg Am. 1985;67(2):326-329.
8. DeLee JC, Evans JA, Thomas J. Anterior dislocation of the hip and associated femoral-head fractures. J Bone Joint Surg Am. 1980;62(6):960-964.
9. Epstein HC, Harvey JP Jr. Traumatic anterior dislocations of the hip: management and results. An analysis of fifty-five cases. J Bone Joint Surg Am. 1972;54(7):1561-1562.
10. Toms AD, Williams S, White SH. Obturator dislocation of the hip. J Bone Joint Surg Br. 2001;83(1):113-115.
11. Polesky RE, Polesky FA. Intrapelvic dislocation of the femoral head following anterior dislocation of the hip. A case report. J Bone Joint Surg Am. 1972;54(5):1097-1098.
Bilateral Superior Labrum Anterior to Posterior (SLAP) Tears With Abnormal Anatomy of Biceps Tendon
The biceps brachii derives its name from the 2 heads of the muscle. The short head originates from the coracoid apex, with the coracobrachialis muscle. The long head of the biceps tendon (LHBT) starts within the capsule of the shoulder joint, running from the supraglenoid tubercle or labrum.1 The tendon typically runs free along its intra-articular course, but it is also extrasynovial and ensheathed by a continuation of the synovial lining of the articular capsule that extends to the inferior-most extent of the bicipital groove.2 Congenital anomalies of the LHBT are uncommon, although several atypical forms have been described. A literature search for anomalous LHBT identified several variations in anatomic descriptions, including Y-shaped variant, complete absence of tendon, extra-articular attachment, and a variety of intracapsular attachments. In all, 8 case reports of aberrant intracapsular attachment of LHBT3-12 were identified. These cases presented with a variety of clinical manifestations and pathologic changes. Often, these anatomic variations are considered innocuous, yet some present with pathologic findings.
We present the clinical, magnetic resonance imaging (MRI), and arthroscopic findings of a relatively young athletic patient who was experiencing symptoms of bilateral superior labrum anterior to posterior (SLAP) tears that were unresponsive to conservative management. A unique anatomic variant of the LHBT that involved confluence of the LHBT with the undersurface of the anterosuperior capsule at the rotator interval, as well as a Buford complex anteriorly, was identified and treated. We believe that the tethering of the biceps tendon to the capsule combined with the Buford complex created increased stress on the superior labrum and biceps anchor variant, leading to the development of bilateral symptomatic type II SLAP tears. Knowledge of this variant, though perhaps rare, may be relevant for diagnostic recognition of young athletic patients who present with recalcitrant shoulder symptoms. The patient and the patient’s parents provided written informed consent for print and electronic publication of this case report.
Case Report
A 15-year-old healthy and active athletic boy presented with pain in the right shoulder without history of trauma. He was active in both swimming and baseball. He complained of pain that was present with activities, such as lifting weights, swimming, and throwing. His treatment prior to the office visit consisted of nonsteroidal anti-inflammatory medication, rest, and a therapy program initiated by his high school athletic trainer.
Physical examination demonstrated tenderness to palpation over the posterior capsule and biceps. Motion was full, cuff strength was normal, and SLAP signs (O’Brien, Speed, and Jobe relocation) were positive. A radiograph showed no sign of fracture or dislocation, and no evidence of bony abnormality.
The patient was sent for an MRI arthrogram, which showed a SLAP tear extending from 1 o’clock anteriorly to 10 o’clock posteriorly without intra-articular displacement. No rotator cuff tear was noted. The biceps tendon was noted to be unremarkable and located within the bicipital groove, although retrospective review of the MRI showed that the intra-articular biceps tendon was somewhat confluent with the adjacent tissues.
The patient underwent right shoulder arthroscopy. The shoulder was stable to ligamentous examination under anesthesia. Arthroscopic evaluation revealed that there was a type II SLAP tear extending from the 11-o’clock to the 2-o’clock positions. The superior glenohumeral ligament was identified as it arose from the upper pole of the glenoid labrum and then ran parallel and inferior to the tendon of the biceps towards the lesser tubercle. Surprisingly, there was a very unusual attachment of the intracapsular LHBT to the undersurface of the rotator interval, which restricted biceps excursion in relation to the rotator cuff. Additionally, there was a thick cord-like middle glenohumeral ligament anteriorly that lacked the normal glenoid attachments, thus representing a Buford complex. Interestingly, the labral tear could not only be displaced with a probe, but placing the shoulder through a range of motion also led to increased displacement of the labrum from the glenoid, likely because the biceps tendon was tethered to the undersurface of the capsule.
At the time of arthroscopy, the LHBT was released from its attachment to the capsule at the rotator interval with a radiofrequency wand and shaver. A labral repair was performed using three 2.9-mm bioabsorbable suture anchors, placing 2 posterior and 1 anterior to the biceps tendon. The integrity of the labral repair was observed while placing the shoulder through range of motion.
Postoperatively, the patient was kept in a sling for 5 weeks. Home exercises were initiated at 2 weeks, and outpatient physical therapy was implemented at 4 weeks. The patient resumed swimming, throwing, and other activities—with minimal discomfort—at 6 months postoperatively.
Three years after his initial visit, the patient returned to the office with a similar complaint of pain and limitation of function in his left shoulder after returning to full athletic competition. Once again, there was no history of injury, and history, physical examination, and MRI arthrogram (Figures 1A, 1B) evaluation proved to be very similar to this young athlete’s right shoulder work-up.
The patient once again underwent shoulder arthroscopy and treatment. Although this was now the left shoulder, the findings were essentially identical to the right shoulder. Once again, the labrum was detached from the 11-o’clock to 2-o’clock positions, and a Buford complex was present anteriorly (Figure 2A). The labral tear was easily displaceable from the glenoid with a probe, and placing the shoulder through a range of motion led to increased displacement of the labrum from the glenoid. There was also confluence of the intra-articular LHBT with the undersurface of the capsule within the rotator interval (Figure 2B). A radiofrequency wand, shaver, and elevator were used to define the biceps tendon and separate it from the undersurface of the capsule. The SLAP repair was performed using three 2.9-mm absorbable suture anchors with 2 posterior and 1 anterior to the biceps tendon insertion. The labral repair was observed while placing the shoulder through range of motion and the shoulder was seen to be free of any undue tension on the labrum.
Postoperatively, the patient’s sling and rehabilitation protocol was identical to that of the right shoulder. The patient progressed well, was released to full activity at 6 months, and has not returned with any further complaints of left or right shoulder pain. Approximately 3 years after treatment the patient was contacted via phone and asked about symptoms, pain, and activity. He denies current symptoms of clicking or instability and has no pain that he can identify as being related to previous pathology or treatment. Since the surgery, he has ceased competitive sports and weight lifting, which he attributes to deconditioning associated with postsurgical immobilization and lack of motivation.
Discussion
Of the 8 case reports in the literature that identified variable intra-articular biceps insertional anatomy, only 2 reports represented confluence of the biceps within the rotator interval.7 Interestingly, of the cases identified, the single case that presented a patient with similar pathology of a type II SLAP lesion had an almost identical anatomical variant presentation consisting of both the anomalous insertion of the LHBT into the undersurface of the rotator interval and a Buford variant of the anterosuperior glenohumeral ligament complex. To our knowledge, our bilateral case of an altered intra-articular biceps insertion and a concomitant SLAP tear supports the theory that this pattern of anomalous insertion may very well have altered the biomechanics of the tendon, resulting in acquired pathology to the superior labrum.
The literature reviewed showed the prevalence of anatomic variations of the LHBT ranged from 1.9% to 7.4%.13,14 These variations are generally considered benign; however, in some cases—as in the cases of the young athletes presented by Wahl and MacGillivray7 and in this report—anatomic variation may play an important role in pathogenesis of different injury patterns. The primary function of the LHBT is the stabilization of the glenohumeral joint during abduction and external rotation.15 When the insertion diverges from normal (eg, when the tendon is tethered to the undersurface of the rotator cuff), the biomechanical stresses on the tendon likely change. As a result of the anomalous position of the LHBT origin, there may be a change in the shoulder joint’s biomechanics, with increased strain on the glenohumeral ligament and its attachment onto the glenoid.16
This case report differs from publications on variable superior glenohumeral ligament attachments because a discrete superior glenohumeral ligament structure was isolated from the biceps tendon. Although a larger case series or patient cohort, as well as more involved biomechanical analysis, would certainly be necessary to prove our hypothesis, we believe that this case suggests certain anatomic LHBT and labral variations can contribute to the develop of SLAP tears in younger individuals.
1. Vangsness CT Jr, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br. 1994;76(6):951-954.
2. Burkhead WZ Jr. The biceps tendon. In: Rockwood CA Jr, Matsen FA III, eds. The Shoulder. Vol. 2. Philadelphia: WB Saunders; 1990:791-836.
3. Parikh SN, Bonnaig N, Zbojniewicz A. Intracapsular origin of the long head biceps tendon with glenoid avulsion of the glenohumeral ligaments. Orthopedics. 2011;34(11):781-784.
4. Gaskin CM, Golish SR, Blount KJ, Diduch DR. Anomalies of the long head of the biceps brachii tendon: clinical significance, MR arthrographic findings, and arthroscopic correlation in two patients. Skeletal Radiol. 2007;36(8):785-789.
5. Yeh L, Pedowitz R, Kwak S, et al. Intracapsular origin of the long head of the biceps tendon. Skeletal Radiol. 1999;28(3):178-181.
6. Richards DP, Schwartz M. Anomalous intraarticular origin of the long head of the biceps brachii. Clin J Sport Med. 2003;13(2):122-124.
7. Wahl CJ, MacGillivray JD. Three congenital variations in the long head of the biceps tendon: a review of the pathoanatomic considerations and case reports. J Shoulder Elbow Surg. 2007;16(6):e25-e30.I
8. Egea JM, Melguizo C, Prados J, Aránega A. Capsular origin of the long head of the biceps tendon: a clinical case. Rom J Morphol Embryol. 2010;51(2):375-377.
9. Hyman JL, Warren RF. Extra-articular origin of biceps brachii. Arthroscopy. 2001;17(7): E29.
10. Enad JG. Bifurcate origin of the long head of the biceps tendon. Arthroscopy. 2004;20(10):1081-1083.
11. Mariani PP, Bellelli A, Botticella C. Arthroscopic absence of the long head of the biceps tendon. Arthroscopy. 1997;13(4):499-501.
12. Koplas MC, Winalski CS, Ulmer WH Jr, Recht M. Bilateral congenital absence of the long head of the biceps tendon. Skeletal Radiol. 2009;38(7):715-719.
13. Kanatli U, Ozturk BY, Eisen E, Bolukbasi S. Intra-articular variations of the long head of the biceps tendon. Knee Surg Sports Traumatol Arthrosc. 2011;19(9):1576-1581.
14. Dierickx C, Ceccarelli E, Conti M, Vanlommel J, Castagna A. Variations of the intra-articular portion of the long head of the biceps tendon: a classification of embryologically explained variations. J Shoulder Elbow Surg. 2009;18(4):556-565.
15. Rodosky MW, Harner CD, Fu FH. The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med. 1994;22(1):121-130.
16. Bigliani LU, Kelkar R, Flatow EL, Pollock RG, Mow VC. Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res. 1996;(330):13-30.
The biceps brachii derives its name from the 2 heads of the muscle. The short head originates from the coracoid apex, with the coracobrachialis muscle. The long head of the biceps tendon (LHBT) starts within the capsule of the shoulder joint, running from the supraglenoid tubercle or labrum.1 The tendon typically runs free along its intra-articular course, but it is also extrasynovial and ensheathed by a continuation of the synovial lining of the articular capsule that extends to the inferior-most extent of the bicipital groove.2 Congenital anomalies of the LHBT are uncommon, although several atypical forms have been described. A literature search for anomalous LHBT identified several variations in anatomic descriptions, including Y-shaped variant, complete absence of tendon, extra-articular attachment, and a variety of intracapsular attachments. In all, 8 case reports of aberrant intracapsular attachment of LHBT3-12 were identified. These cases presented with a variety of clinical manifestations and pathologic changes. Often, these anatomic variations are considered innocuous, yet some present with pathologic findings.
We present the clinical, magnetic resonance imaging (MRI), and arthroscopic findings of a relatively young athletic patient who was experiencing symptoms of bilateral superior labrum anterior to posterior (SLAP) tears that were unresponsive to conservative management. A unique anatomic variant of the LHBT that involved confluence of the LHBT with the undersurface of the anterosuperior capsule at the rotator interval, as well as a Buford complex anteriorly, was identified and treated. We believe that the tethering of the biceps tendon to the capsule combined with the Buford complex created increased stress on the superior labrum and biceps anchor variant, leading to the development of bilateral symptomatic type II SLAP tears. Knowledge of this variant, though perhaps rare, may be relevant for diagnostic recognition of young athletic patients who present with recalcitrant shoulder symptoms. The patient and the patient’s parents provided written informed consent for print and electronic publication of this case report.
Case Report
A 15-year-old healthy and active athletic boy presented with pain in the right shoulder without history of trauma. He was active in both swimming and baseball. He complained of pain that was present with activities, such as lifting weights, swimming, and throwing. His treatment prior to the office visit consisted of nonsteroidal anti-inflammatory medication, rest, and a therapy program initiated by his high school athletic trainer.
Physical examination demonstrated tenderness to palpation over the posterior capsule and biceps. Motion was full, cuff strength was normal, and SLAP signs (O’Brien, Speed, and Jobe relocation) were positive. A radiograph showed no sign of fracture or dislocation, and no evidence of bony abnormality.
The patient was sent for an MRI arthrogram, which showed a SLAP tear extending from 1 o’clock anteriorly to 10 o’clock posteriorly without intra-articular displacement. No rotator cuff tear was noted. The biceps tendon was noted to be unremarkable and located within the bicipital groove, although retrospective review of the MRI showed that the intra-articular biceps tendon was somewhat confluent with the adjacent tissues.
The patient underwent right shoulder arthroscopy. The shoulder was stable to ligamentous examination under anesthesia. Arthroscopic evaluation revealed that there was a type II SLAP tear extending from the 11-o’clock to the 2-o’clock positions. The superior glenohumeral ligament was identified as it arose from the upper pole of the glenoid labrum and then ran parallel and inferior to the tendon of the biceps towards the lesser tubercle. Surprisingly, there was a very unusual attachment of the intracapsular LHBT to the undersurface of the rotator interval, which restricted biceps excursion in relation to the rotator cuff. Additionally, there was a thick cord-like middle glenohumeral ligament anteriorly that lacked the normal glenoid attachments, thus representing a Buford complex. Interestingly, the labral tear could not only be displaced with a probe, but placing the shoulder through a range of motion also led to increased displacement of the labrum from the glenoid, likely because the biceps tendon was tethered to the undersurface of the capsule.
At the time of arthroscopy, the LHBT was released from its attachment to the capsule at the rotator interval with a radiofrequency wand and shaver. A labral repair was performed using three 2.9-mm bioabsorbable suture anchors, placing 2 posterior and 1 anterior to the biceps tendon. The integrity of the labral repair was observed while placing the shoulder through range of motion.
Postoperatively, the patient was kept in a sling for 5 weeks. Home exercises were initiated at 2 weeks, and outpatient physical therapy was implemented at 4 weeks. The patient resumed swimming, throwing, and other activities—with minimal discomfort—at 6 months postoperatively.
Three years after his initial visit, the patient returned to the office with a similar complaint of pain and limitation of function in his left shoulder after returning to full athletic competition. Once again, there was no history of injury, and history, physical examination, and MRI arthrogram (Figures 1A, 1B) evaluation proved to be very similar to this young athlete’s right shoulder work-up.
The patient once again underwent shoulder arthroscopy and treatment. Although this was now the left shoulder, the findings were essentially identical to the right shoulder. Once again, the labrum was detached from the 11-o’clock to 2-o’clock positions, and a Buford complex was present anteriorly (Figure 2A). The labral tear was easily displaceable from the glenoid with a probe, and placing the shoulder through a range of motion led to increased displacement of the labrum from the glenoid. There was also confluence of the intra-articular LHBT with the undersurface of the capsule within the rotator interval (Figure 2B). A radiofrequency wand, shaver, and elevator were used to define the biceps tendon and separate it from the undersurface of the capsule. The SLAP repair was performed using three 2.9-mm absorbable suture anchors with 2 posterior and 1 anterior to the biceps tendon insertion. The labral repair was observed while placing the shoulder through range of motion and the shoulder was seen to be free of any undue tension on the labrum.
Postoperatively, the patient’s sling and rehabilitation protocol was identical to that of the right shoulder. The patient progressed well, was released to full activity at 6 months, and has not returned with any further complaints of left or right shoulder pain. Approximately 3 years after treatment the patient was contacted via phone and asked about symptoms, pain, and activity. He denies current symptoms of clicking or instability and has no pain that he can identify as being related to previous pathology or treatment. Since the surgery, he has ceased competitive sports and weight lifting, which he attributes to deconditioning associated with postsurgical immobilization and lack of motivation.
Discussion
Of the 8 case reports in the literature that identified variable intra-articular biceps insertional anatomy, only 2 reports represented confluence of the biceps within the rotator interval.7 Interestingly, of the cases identified, the single case that presented a patient with similar pathology of a type II SLAP lesion had an almost identical anatomical variant presentation consisting of both the anomalous insertion of the LHBT into the undersurface of the rotator interval and a Buford variant of the anterosuperior glenohumeral ligament complex. To our knowledge, our bilateral case of an altered intra-articular biceps insertion and a concomitant SLAP tear supports the theory that this pattern of anomalous insertion may very well have altered the biomechanics of the tendon, resulting in acquired pathology to the superior labrum.
The literature reviewed showed the prevalence of anatomic variations of the LHBT ranged from 1.9% to 7.4%.13,14 These variations are generally considered benign; however, in some cases—as in the cases of the young athletes presented by Wahl and MacGillivray7 and in this report—anatomic variation may play an important role in pathogenesis of different injury patterns. The primary function of the LHBT is the stabilization of the glenohumeral joint during abduction and external rotation.15 When the insertion diverges from normal (eg, when the tendon is tethered to the undersurface of the rotator cuff), the biomechanical stresses on the tendon likely change. As a result of the anomalous position of the LHBT origin, there may be a change in the shoulder joint’s biomechanics, with increased strain on the glenohumeral ligament and its attachment onto the glenoid.16
This case report differs from publications on variable superior glenohumeral ligament attachments because a discrete superior glenohumeral ligament structure was isolated from the biceps tendon. Although a larger case series or patient cohort, as well as more involved biomechanical analysis, would certainly be necessary to prove our hypothesis, we believe that this case suggests certain anatomic LHBT and labral variations can contribute to the develop of SLAP tears in younger individuals.
The biceps brachii derives its name from the 2 heads of the muscle. The short head originates from the coracoid apex, with the coracobrachialis muscle. The long head of the biceps tendon (LHBT) starts within the capsule of the shoulder joint, running from the supraglenoid tubercle or labrum.1 The tendon typically runs free along its intra-articular course, but it is also extrasynovial and ensheathed by a continuation of the synovial lining of the articular capsule that extends to the inferior-most extent of the bicipital groove.2 Congenital anomalies of the LHBT are uncommon, although several atypical forms have been described. A literature search for anomalous LHBT identified several variations in anatomic descriptions, including Y-shaped variant, complete absence of tendon, extra-articular attachment, and a variety of intracapsular attachments. In all, 8 case reports of aberrant intracapsular attachment of LHBT3-12 were identified. These cases presented with a variety of clinical manifestations and pathologic changes. Often, these anatomic variations are considered innocuous, yet some present with pathologic findings.
We present the clinical, magnetic resonance imaging (MRI), and arthroscopic findings of a relatively young athletic patient who was experiencing symptoms of bilateral superior labrum anterior to posterior (SLAP) tears that were unresponsive to conservative management. A unique anatomic variant of the LHBT that involved confluence of the LHBT with the undersurface of the anterosuperior capsule at the rotator interval, as well as a Buford complex anteriorly, was identified and treated. We believe that the tethering of the biceps tendon to the capsule combined with the Buford complex created increased stress on the superior labrum and biceps anchor variant, leading to the development of bilateral symptomatic type II SLAP tears. Knowledge of this variant, though perhaps rare, may be relevant for diagnostic recognition of young athletic patients who present with recalcitrant shoulder symptoms. The patient and the patient’s parents provided written informed consent for print and electronic publication of this case report.
Case Report
A 15-year-old healthy and active athletic boy presented with pain in the right shoulder without history of trauma. He was active in both swimming and baseball. He complained of pain that was present with activities, such as lifting weights, swimming, and throwing. His treatment prior to the office visit consisted of nonsteroidal anti-inflammatory medication, rest, and a therapy program initiated by his high school athletic trainer.
Physical examination demonstrated tenderness to palpation over the posterior capsule and biceps. Motion was full, cuff strength was normal, and SLAP signs (O’Brien, Speed, and Jobe relocation) were positive. A radiograph showed no sign of fracture or dislocation, and no evidence of bony abnormality.
The patient was sent for an MRI arthrogram, which showed a SLAP tear extending from 1 o’clock anteriorly to 10 o’clock posteriorly without intra-articular displacement. No rotator cuff tear was noted. The biceps tendon was noted to be unremarkable and located within the bicipital groove, although retrospective review of the MRI showed that the intra-articular biceps tendon was somewhat confluent with the adjacent tissues.
The patient underwent right shoulder arthroscopy. The shoulder was stable to ligamentous examination under anesthesia. Arthroscopic evaluation revealed that there was a type II SLAP tear extending from the 11-o’clock to the 2-o’clock positions. The superior glenohumeral ligament was identified as it arose from the upper pole of the glenoid labrum and then ran parallel and inferior to the tendon of the biceps towards the lesser tubercle. Surprisingly, there was a very unusual attachment of the intracapsular LHBT to the undersurface of the rotator interval, which restricted biceps excursion in relation to the rotator cuff. Additionally, there was a thick cord-like middle glenohumeral ligament anteriorly that lacked the normal glenoid attachments, thus representing a Buford complex. Interestingly, the labral tear could not only be displaced with a probe, but placing the shoulder through a range of motion also led to increased displacement of the labrum from the glenoid, likely because the biceps tendon was tethered to the undersurface of the capsule.
At the time of arthroscopy, the LHBT was released from its attachment to the capsule at the rotator interval with a radiofrequency wand and shaver. A labral repair was performed using three 2.9-mm bioabsorbable suture anchors, placing 2 posterior and 1 anterior to the biceps tendon. The integrity of the labral repair was observed while placing the shoulder through range of motion.
Postoperatively, the patient was kept in a sling for 5 weeks. Home exercises were initiated at 2 weeks, and outpatient physical therapy was implemented at 4 weeks. The patient resumed swimming, throwing, and other activities—with minimal discomfort—at 6 months postoperatively.
Three years after his initial visit, the patient returned to the office with a similar complaint of pain and limitation of function in his left shoulder after returning to full athletic competition. Once again, there was no history of injury, and history, physical examination, and MRI arthrogram (Figures 1A, 1B) evaluation proved to be very similar to this young athlete’s right shoulder work-up.
The patient once again underwent shoulder arthroscopy and treatment. Although this was now the left shoulder, the findings were essentially identical to the right shoulder. Once again, the labrum was detached from the 11-o’clock to 2-o’clock positions, and a Buford complex was present anteriorly (Figure 2A). The labral tear was easily displaceable from the glenoid with a probe, and placing the shoulder through a range of motion led to increased displacement of the labrum from the glenoid. There was also confluence of the intra-articular LHBT with the undersurface of the capsule within the rotator interval (Figure 2B). A radiofrequency wand, shaver, and elevator were used to define the biceps tendon and separate it from the undersurface of the capsule. The SLAP repair was performed using three 2.9-mm absorbable suture anchors with 2 posterior and 1 anterior to the biceps tendon insertion. The labral repair was observed while placing the shoulder through range of motion and the shoulder was seen to be free of any undue tension on the labrum.
Postoperatively, the patient’s sling and rehabilitation protocol was identical to that of the right shoulder. The patient progressed well, was released to full activity at 6 months, and has not returned with any further complaints of left or right shoulder pain. Approximately 3 years after treatment the patient was contacted via phone and asked about symptoms, pain, and activity. He denies current symptoms of clicking or instability and has no pain that he can identify as being related to previous pathology or treatment. Since the surgery, he has ceased competitive sports and weight lifting, which he attributes to deconditioning associated with postsurgical immobilization and lack of motivation.
Discussion
Of the 8 case reports in the literature that identified variable intra-articular biceps insertional anatomy, only 2 reports represented confluence of the biceps within the rotator interval.7 Interestingly, of the cases identified, the single case that presented a patient with similar pathology of a type II SLAP lesion had an almost identical anatomical variant presentation consisting of both the anomalous insertion of the LHBT into the undersurface of the rotator interval and a Buford variant of the anterosuperior glenohumeral ligament complex. To our knowledge, our bilateral case of an altered intra-articular biceps insertion and a concomitant SLAP tear supports the theory that this pattern of anomalous insertion may very well have altered the biomechanics of the tendon, resulting in acquired pathology to the superior labrum.
The literature reviewed showed the prevalence of anatomic variations of the LHBT ranged from 1.9% to 7.4%.13,14 These variations are generally considered benign; however, in some cases—as in the cases of the young athletes presented by Wahl and MacGillivray7 and in this report—anatomic variation may play an important role in pathogenesis of different injury patterns. The primary function of the LHBT is the stabilization of the glenohumeral joint during abduction and external rotation.15 When the insertion diverges from normal (eg, when the tendon is tethered to the undersurface of the rotator cuff), the biomechanical stresses on the tendon likely change. As a result of the anomalous position of the LHBT origin, there may be a change in the shoulder joint’s biomechanics, with increased strain on the glenohumeral ligament and its attachment onto the glenoid.16
This case report differs from publications on variable superior glenohumeral ligament attachments because a discrete superior glenohumeral ligament structure was isolated from the biceps tendon. Although a larger case series or patient cohort, as well as more involved biomechanical analysis, would certainly be necessary to prove our hypothesis, we believe that this case suggests certain anatomic LHBT and labral variations can contribute to the develop of SLAP tears in younger individuals.
1. Vangsness CT Jr, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br. 1994;76(6):951-954.
2. Burkhead WZ Jr. The biceps tendon. In: Rockwood CA Jr, Matsen FA III, eds. The Shoulder. Vol. 2. Philadelphia: WB Saunders; 1990:791-836.
3. Parikh SN, Bonnaig N, Zbojniewicz A. Intracapsular origin of the long head biceps tendon with glenoid avulsion of the glenohumeral ligaments. Orthopedics. 2011;34(11):781-784.
4. Gaskin CM, Golish SR, Blount KJ, Diduch DR. Anomalies of the long head of the biceps brachii tendon: clinical significance, MR arthrographic findings, and arthroscopic correlation in two patients. Skeletal Radiol. 2007;36(8):785-789.
5. Yeh L, Pedowitz R, Kwak S, et al. Intracapsular origin of the long head of the biceps tendon. Skeletal Radiol. 1999;28(3):178-181.
6. Richards DP, Schwartz M. Anomalous intraarticular origin of the long head of the biceps brachii. Clin J Sport Med. 2003;13(2):122-124.
7. Wahl CJ, MacGillivray JD. Three congenital variations in the long head of the biceps tendon: a review of the pathoanatomic considerations and case reports. J Shoulder Elbow Surg. 2007;16(6):e25-e30.I
8. Egea JM, Melguizo C, Prados J, Aránega A. Capsular origin of the long head of the biceps tendon: a clinical case. Rom J Morphol Embryol. 2010;51(2):375-377.
9. Hyman JL, Warren RF. Extra-articular origin of biceps brachii. Arthroscopy. 2001;17(7): E29.
10. Enad JG. Bifurcate origin of the long head of the biceps tendon. Arthroscopy. 2004;20(10):1081-1083.
11. Mariani PP, Bellelli A, Botticella C. Arthroscopic absence of the long head of the biceps tendon. Arthroscopy. 1997;13(4):499-501.
12. Koplas MC, Winalski CS, Ulmer WH Jr, Recht M. Bilateral congenital absence of the long head of the biceps tendon. Skeletal Radiol. 2009;38(7):715-719.
13. Kanatli U, Ozturk BY, Eisen E, Bolukbasi S. Intra-articular variations of the long head of the biceps tendon. Knee Surg Sports Traumatol Arthrosc. 2011;19(9):1576-1581.
14. Dierickx C, Ceccarelli E, Conti M, Vanlommel J, Castagna A. Variations of the intra-articular portion of the long head of the biceps tendon: a classification of embryologically explained variations. J Shoulder Elbow Surg. 2009;18(4):556-565.
15. Rodosky MW, Harner CD, Fu FH. The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med. 1994;22(1):121-130.
16. Bigliani LU, Kelkar R, Flatow EL, Pollock RG, Mow VC. Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res. 1996;(330):13-30.
1. Vangsness CT Jr, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br. 1994;76(6):951-954.
2. Burkhead WZ Jr. The biceps tendon. In: Rockwood CA Jr, Matsen FA III, eds. The Shoulder. Vol. 2. Philadelphia: WB Saunders; 1990:791-836.
3. Parikh SN, Bonnaig N, Zbojniewicz A. Intracapsular origin of the long head biceps tendon with glenoid avulsion of the glenohumeral ligaments. Orthopedics. 2011;34(11):781-784.
4. Gaskin CM, Golish SR, Blount KJ, Diduch DR. Anomalies of the long head of the biceps brachii tendon: clinical significance, MR arthrographic findings, and arthroscopic correlation in two patients. Skeletal Radiol. 2007;36(8):785-789.
5. Yeh L, Pedowitz R, Kwak S, et al. Intracapsular origin of the long head of the biceps tendon. Skeletal Radiol. 1999;28(3):178-181.
6. Richards DP, Schwartz M. Anomalous intraarticular origin of the long head of the biceps brachii. Clin J Sport Med. 2003;13(2):122-124.
7. Wahl CJ, MacGillivray JD. Three congenital variations in the long head of the biceps tendon: a review of the pathoanatomic considerations and case reports. J Shoulder Elbow Surg. 2007;16(6):e25-e30.I
8. Egea JM, Melguizo C, Prados J, Aránega A. Capsular origin of the long head of the biceps tendon: a clinical case. Rom J Morphol Embryol. 2010;51(2):375-377.
9. Hyman JL, Warren RF. Extra-articular origin of biceps brachii. Arthroscopy. 2001;17(7): E29.
10. Enad JG. Bifurcate origin of the long head of the biceps tendon. Arthroscopy. 2004;20(10):1081-1083.
11. Mariani PP, Bellelli A, Botticella C. Arthroscopic absence of the long head of the biceps tendon. Arthroscopy. 1997;13(4):499-501.
12. Koplas MC, Winalski CS, Ulmer WH Jr, Recht M. Bilateral congenital absence of the long head of the biceps tendon. Skeletal Radiol. 2009;38(7):715-719.
13. Kanatli U, Ozturk BY, Eisen E, Bolukbasi S. Intra-articular variations of the long head of the biceps tendon. Knee Surg Sports Traumatol Arthrosc. 2011;19(9):1576-1581.
14. Dierickx C, Ceccarelli E, Conti M, Vanlommel J, Castagna A. Variations of the intra-articular portion of the long head of the biceps tendon: a classification of embryologically explained variations. J Shoulder Elbow Surg. 2009;18(4):556-565.
15. Rodosky MW, Harner CD, Fu FH. The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med. 1994;22(1):121-130.
16. Bigliani LU, Kelkar R, Flatow EL, Pollock RG, Mow VC. Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res. 1996;(330):13-30.
Xanthogranulomatous Osteomyelitis of Proximal Femur Masquerading as Benign Bone Tumor
Xanthogranulomatous osteomyelitis (XO) is a type of chronic inflammatory process that is characterized by the collection of foamy macrophages along with mononuclear cells in the tissue.1 Xanthogranulomatous osteomyelitis is characterized by the presence of granular, eosinophilic, periodic acid–Schiff–positive histiocytes in the initial stages, followed by the mixture of foamy macrophages and activated plasma cells and, last, by the presence of suppurative foci and hemorrhage. This is an uncommon process best known to occur in the gallbladder, kidney, urinary bladder, fallopian tube, ovary, vagina, prostate, testis, epididymis, colon, and appendix.2-4 Very rarely, it can affect lungs, brain, or bone. Only 5 cases of XO have been reported in the literature.5-8
We report XO of the proximal femur in a 65-year-old woman who initially had a clinical and radiologic diagnosis of aneurysmal bone cyst; however, histopathologic examination confirmed the diagnosis of XO. Xanthogranulomatous osteomyelitis mimics a neoplastic pathology in gallbladder, kidney, and prostrate on gross clinical and radiologic examination.9 The pathogenesis of XO is best characterized by a delayed type of hypersensitivity reaction.10 The differential diagnosis includes chronic recurrent multifocal osteomyelitis, xanthoma, infiltrative storage disorder, malakoplakia, Langerhans cell histiocytosis, fibrohistiocytic tumor, Erdheim-Chester disease, and metastatic renal cell carcinoma.11-14 The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 65-year-old hypertensive woman presented with complaints of pain in the right hip for a duration of 6 months. Pain was radiating from the right hip region to the anteromedial aspect of the knee and progressively increasing, with a history of pain at rest suggestive of a nonmechanical pathology in the hip. There was no history of fever, weight loss, loss of appetite, pain in any other joint, or morning stiffness. The patient was mobile without support and was able to squat and sit cross-legged; however, the stance phase on the right side was less than on the left side, suggestive of an antalgic component in the gait.
On examining the patient, there was anterior hip joint tenderness with no local sign of any infective or inflammatory pathology. Trochanteric tenderness was present, but there was no irregularity, broadening, or thickening of the trochanter. There was no restriction in the range of motion, and no coronal or sagittal plane deformity in the right hip. There was no limb-length discrepancy. However, the patient was not able to raise her leg actively, probably because of pain in the right hip.
On plain radiographs of the pelvis with bilateral hips, a well-defined nonexpansile uniloculated lytic lesion with sclerotic margins was present in the neck of the right femur, extending to the intertrochanteric area (Figure 1). Ground-glass appearance was also noted. Considering the benign nature of the lesion radiologically and clinically, a differential diagnosis of hyperparathyroidism, renal osteodystrophy, multiple myeloma, and fibrous dysplasia was considered. Hematologic investigations, skeletal survey, and magnetic resonance imaging (MRI) of the bilateral hips were performed to rule out the differential diagnosis.
The patient’s hemoglobin level was 11.8 g/dL with total white blood cell count of 10,300/µL. Renal and hepatic functions were within normal limit. Serum erythrocyte sedimentation rate (ESR) was 12 mm/h and C-reactive protein level was normal. Serum parathyroid level was 32 pg/mL, which was within normal limits, with an alkaline phosphatase level of 101 U/L. The skeletal survey showed no other bony lesion in the body. T1-weighted MRI of both hips showed a well-defined hypointense lesion in the neck and intertrochanteric area of the right hip, which was hyperintense on T2-weighted MRI, suggestive of aneurysmal bone cyst (Figure 2).
Normal ESR, hemoglobin, alkaline phosphatase, and serum parathyroid levels and normal skeletal survey almost ruled out multiple myeloma and hyperparathyroidism. Normal renal profile ruled out renal osteodystrophy and the osteitis fibrosa cystica lesion associated with it. We planned for prophylactic internal fixation of the lesion to prevent a pathologic fracture. According to Mirels,15 if there is a lytic lesion covering more than two-thirds of the circumference of the bone in the peritrochanteric area, the chances of a pathologic fracture are high and such fractures should be fixed.
We planned for curettage of the lesion with bone grafting and in situ intramedullary fixation of the lesion. Curettage was done according to the plan and the sample was sent for histopathologic examination. In situ internal fixation and bone grafting were performed by using a proximal femoral intramedullary nail. To our surprise, the biopsy sample was reported as xanthogranuloma, with multiple foamy macrophages mixed with inflammatory cells and aggregates of lymphocytes (Figure 3). Mycobacterial and routine bacterial cultures were reported as negative. The patient was kept on oral antibiotics (cefixime and moxifloxacin) for 6 weeks, and she made an uneventful recovery. At 6-month follow-up, a radiograph of the right hip showed a healed lesion with proximal femoral nail in situ (Figure 4).
Discussion
To the best of our knowledge, a total of 5 cases of XO have been reported in the literature. The earliest of these reports were by Cozzutto and Carbone,1 who reported 2 cases of XO of the first rib and of the epiphysis of the tibia, respectively. The importance of these lesions to diagnosis is their confusion with a neoplastic disease, as XO is itself a benign disorder. These lesions can mimic a neoplastic lesion in clinical and radiologic presentation and the only way to differentiate the lesion from a neoplastic disease is by histopathologic examination of the tissue. Hypothetically, xanthogranulomatous disorders can be related to trauma or infection.
In 2007, Vankalakunti and colleagues6 reported XO of the ulna in a 50-year-old postmenopausal woman. In that case, progressive swelling was present on the extensor aspect of her right forearm for a period of 2 years, for which curettage and bone grafting were performed, using autograft from the ipsilateral iliac crest. The tissue culture was sterile, and XO was diagnosed as a result of the histopathologic examination. In 2009, Cennimo and colleagues7 reported XO of the index finger and wrist of a man complaining of pain and swelling for 1 year, which was unresponsive to antibiotics. The diagnosis of XO was confirmed histopathologically, when the culture of the same tissue grew Mycobacterium marinum. Radical synovectomy of the lesion was performed, after which minocycline, clarithromycin, and ethambutol were administered. In 2012, Borjian and colleagues8 reported a case of XO of the proximal humerus and proximal fibula in a 14-year-old child. The child, who presented with fever, pain, and restriction of shoulder movements, was started on oral antibiotics as the tissue culture grew Staphylococcus aureus; the patient did not complete the course of treatment in the hospital. No surgical intervention was done in this case. The diagnosis of XO was confirmed by microscopic examination of the tissue.
An association between bacterial infection and xanthogranulomatous inflammation has existed in several organs, such as the kidneys, and in the gastrointestinal system, but such an association of the 2 is yet to be determined for bone.5,10,16-19 Because of the paucity of literature on the disease, a management protocol for XO of bone has not been defined, and decisions have to be made considering the natural history of the disease in other organs. We present this case primarily because of its rarity, curability, and its close resemblance to bone tumors. While XO is benign, it can mimic a neoplastic bone lesion in its imaging and clinical manifestations, and appropriate differentiation is crucial. Currently, histopathologic examination of lesions is the most specific and is the gold standard for diagnosis.
Conclusion
Xanthogranulomatous osteomyelitis is a very rare entity, and only a few cases have been reported in the English-language literature. Though rare, XO warrants greater emphasis than it receives in the literature. It is a chronic inflammatory disease having a close resemblance to bone tumors. A high index of suspicion must be practiced to differentiate XO from tumors. Histopathologic examination is mandatory to establish definitive diagnosis and correct treatment.
1. Cozzutto C, Carbone A. The xanthogranulomatous process. Xanthogranulomatous inflammation. Pathol Res Pract. 1988;183(4):395-402.
2. Ladefoged C, Lorentzen M. Xanthogranulomatous cholecystitis. A clinicopathological study of 20 cases and review of the literature. APMIS. 1993;101(11):869-875.
3. Nistal M, Gonzalez-Peramato P, Serrano A, Regadera J. Xanthogranulomatous funiculitis and orchiepididymitis: report of 2 cases with immunohistochemical study and literature review. Arch Pathol Lab Med. 2004;128(8):911-914.
4. Oh YH, Seong SS, Jang KS, et al. Xanthogranulomatous inflammation presenting as a submucosal mass of the sigmoid colon. Pathol Int. 2005;55(7):440-444.
5. Cozzutto C. Xanthogranulomatous osteomyelitis. Arch Pathol Lab Med. 1984;108(12):973-6.
6. Vankalakunti M, Saikia UN, Mathew M, Kang M. Xanthogranulomatous osteomyelitis of ulna mimicking neoplasm. World J Surg Oncol. 2007;30(5):46.
7. Cennimo DJ, Agag R, Fleegler E, et al. Mycobacterium marinum hand infection in a “sushi chef.” Eplasty. 2009;14(9):e43.
8. Borjian A, Rezaei F, Eshaghi MA, Shemshaki H. Xanthogranulomatous osteomyelitis. J Orthop Traumatol. 2012;13(4):217-220.
9. Rafique M, Yaqoob N. Xanthogranulomatous prostatitis: a mimic of carcinoma of prostate. World J Surg Oncol. 2006;4:30.
10. Nakashiro H, Haraoka S, Fujiwara K, Harada S, Hisatsugu T, Watanabe T. Xanthogranulomatous cholecystis. Cell composition and a possible pathogenetic role of cell-mediated immunity. Pathol Res Pract. 1995;191(11):1078-1086.
11. Hamada T, Ito H, Araki Y, Fujii K, Inoue M, Ishida O. Benign fibrous histiocytoma of the femur: review of three cases. Skeletal Radiol. 1996;25(1):25-29.
12. Kossard S, Chow E, Wilkinson B, Killingsworth M. Lipid and giant cell poor necrobiotic xanthogranuloma. J Cutan Pathol. 2000;27(7):374-378.
13. Girschick HJ, Huppertz HI, Harmsen D, Krauspe R, Müller-Hermelink HK, Papadopoulos T. Chronic recurrent multifocal osteomyelitis in children: diagnostic value of histopathology and microbial testing. Hum Pathol. 1999;30(1):59-65.
14. Kayser R, Mahlfeld K, Grasshoff H. Vertebral Langerhans-cell histiocytosis in childhood – a differential diagnosis of spinal osteomyelitis. Klin Padiatr. 1999;211(5):399-402.
15. Mirels H. Metastatic disease in long bones. A proposed scoring system for diagnosing impending pathologic fractures. Clin Orthop Relat Res. 1989;249:256-264.
16. Machiz S, Gordon J, Block N, Politano VA. Salmonella typhosa urinary tract infection and xanthogranulomatous pyelonephritis. Case report and review of literature. J Fla Med Assoc. 1974;61(9):703-705.
17. Gauperaa T, Stalsberg H. Renal endometriosis. A case report. Scand J Urol Nephrol. 1977;11(2):189-191.
18. Goodman M, Curry T, Russell T. Xanthogranulomatous pyelonephritis (XGP): a local disease with systemic manifestations. Report of 23 patients and review of the literature. Medicine. 1979;58(2):171-181.
19. Guarino M, Reale D, Micoli G, Tricomi P, Cristofori E. Xanthogranulomatous gastritis: association with xanthogranulomatous cholecystitis. J Clin Pathol. 1993;46(1):88-90.
Xanthogranulomatous osteomyelitis (XO) is a type of chronic inflammatory process that is characterized by the collection of foamy macrophages along with mononuclear cells in the tissue.1 Xanthogranulomatous osteomyelitis is characterized by the presence of granular, eosinophilic, periodic acid–Schiff–positive histiocytes in the initial stages, followed by the mixture of foamy macrophages and activated plasma cells and, last, by the presence of suppurative foci and hemorrhage. This is an uncommon process best known to occur in the gallbladder, kidney, urinary bladder, fallopian tube, ovary, vagina, prostate, testis, epididymis, colon, and appendix.2-4 Very rarely, it can affect lungs, brain, or bone. Only 5 cases of XO have been reported in the literature.5-8
We report XO of the proximal femur in a 65-year-old woman who initially had a clinical and radiologic diagnosis of aneurysmal bone cyst; however, histopathologic examination confirmed the diagnosis of XO. Xanthogranulomatous osteomyelitis mimics a neoplastic pathology in gallbladder, kidney, and prostrate on gross clinical and radiologic examination.9 The pathogenesis of XO is best characterized by a delayed type of hypersensitivity reaction.10 The differential diagnosis includes chronic recurrent multifocal osteomyelitis, xanthoma, infiltrative storage disorder, malakoplakia, Langerhans cell histiocytosis, fibrohistiocytic tumor, Erdheim-Chester disease, and metastatic renal cell carcinoma.11-14 The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 65-year-old hypertensive woman presented with complaints of pain in the right hip for a duration of 6 months. Pain was radiating from the right hip region to the anteromedial aspect of the knee and progressively increasing, with a history of pain at rest suggestive of a nonmechanical pathology in the hip. There was no history of fever, weight loss, loss of appetite, pain in any other joint, or morning stiffness. The patient was mobile without support and was able to squat and sit cross-legged; however, the stance phase on the right side was less than on the left side, suggestive of an antalgic component in the gait.
On examining the patient, there was anterior hip joint tenderness with no local sign of any infective or inflammatory pathology. Trochanteric tenderness was present, but there was no irregularity, broadening, or thickening of the trochanter. There was no restriction in the range of motion, and no coronal or sagittal plane deformity in the right hip. There was no limb-length discrepancy. However, the patient was not able to raise her leg actively, probably because of pain in the right hip.
On plain radiographs of the pelvis with bilateral hips, a well-defined nonexpansile uniloculated lytic lesion with sclerotic margins was present in the neck of the right femur, extending to the intertrochanteric area (Figure 1). Ground-glass appearance was also noted. Considering the benign nature of the lesion radiologically and clinically, a differential diagnosis of hyperparathyroidism, renal osteodystrophy, multiple myeloma, and fibrous dysplasia was considered. Hematologic investigations, skeletal survey, and magnetic resonance imaging (MRI) of the bilateral hips were performed to rule out the differential diagnosis.
The patient’s hemoglobin level was 11.8 g/dL with total white blood cell count of 10,300/µL. Renal and hepatic functions were within normal limit. Serum erythrocyte sedimentation rate (ESR) was 12 mm/h and C-reactive protein level was normal. Serum parathyroid level was 32 pg/mL, which was within normal limits, with an alkaline phosphatase level of 101 U/L. The skeletal survey showed no other bony lesion in the body. T1-weighted MRI of both hips showed a well-defined hypointense lesion in the neck and intertrochanteric area of the right hip, which was hyperintense on T2-weighted MRI, suggestive of aneurysmal bone cyst (Figure 2).
Normal ESR, hemoglobin, alkaline phosphatase, and serum parathyroid levels and normal skeletal survey almost ruled out multiple myeloma and hyperparathyroidism. Normal renal profile ruled out renal osteodystrophy and the osteitis fibrosa cystica lesion associated with it. We planned for prophylactic internal fixation of the lesion to prevent a pathologic fracture. According to Mirels,15 if there is a lytic lesion covering more than two-thirds of the circumference of the bone in the peritrochanteric area, the chances of a pathologic fracture are high and such fractures should be fixed.
We planned for curettage of the lesion with bone grafting and in situ intramedullary fixation of the lesion. Curettage was done according to the plan and the sample was sent for histopathologic examination. In situ internal fixation and bone grafting were performed by using a proximal femoral intramedullary nail. To our surprise, the biopsy sample was reported as xanthogranuloma, with multiple foamy macrophages mixed with inflammatory cells and aggregates of lymphocytes (Figure 3). Mycobacterial and routine bacterial cultures were reported as negative. The patient was kept on oral antibiotics (cefixime and moxifloxacin) for 6 weeks, and she made an uneventful recovery. At 6-month follow-up, a radiograph of the right hip showed a healed lesion with proximal femoral nail in situ (Figure 4).
Discussion
To the best of our knowledge, a total of 5 cases of XO have been reported in the literature. The earliest of these reports were by Cozzutto and Carbone,1 who reported 2 cases of XO of the first rib and of the epiphysis of the tibia, respectively. The importance of these lesions to diagnosis is their confusion with a neoplastic disease, as XO is itself a benign disorder. These lesions can mimic a neoplastic lesion in clinical and radiologic presentation and the only way to differentiate the lesion from a neoplastic disease is by histopathologic examination of the tissue. Hypothetically, xanthogranulomatous disorders can be related to trauma or infection.
In 2007, Vankalakunti and colleagues6 reported XO of the ulna in a 50-year-old postmenopausal woman. In that case, progressive swelling was present on the extensor aspect of her right forearm for a period of 2 years, for which curettage and bone grafting were performed, using autograft from the ipsilateral iliac crest. The tissue culture was sterile, and XO was diagnosed as a result of the histopathologic examination. In 2009, Cennimo and colleagues7 reported XO of the index finger and wrist of a man complaining of pain and swelling for 1 year, which was unresponsive to antibiotics. The diagnosis of XO was confirmed histopathologically, when the culture of the same tissue grew Mycobacterium marinum. Radical synovectomy of the lesion was performed, after which minocycline, clarithromycin, and ethambutol were administered. In 2012, Borjian and colleagues8 reported a case of XO of the proximal humerus and proximal fibula in a 14-year-old child. The child, who presented with fever, pain, and restriction of shoulder movements, was started on oral antibiotics as the tissue culture grew Staphylococcus aureus; the patient did not complete the course of treatment in the hospital. No surgical intervention was done in this case. The diagnosis of XO was confirmed by microscopic examination of the tissue.
An association between bacterial infection and xanthogranulomatous inflammation has existed in several organs, such as the kidneys, and in the gastrointestinal system, but such an association of the 2 is yet to be determined for bone.5,10,16-19 Because of the paucity of literature on the disease, a management protocol for XO of bone has not been defined, and decisions have to be made considering the natural history of the disease in other organs. We present this case primarily because of its rarity, curability, and its close resemblance to bone tumors. While XO is benign, it can mimic a neoplastic bone lesion in its imaging and clinical manifestations, and appropriate differentiation is crucial. Currently, histopathologic examination of lesions is the most specific and is the gold standard for diagnosis.
Conclusion
Xanthogranulomatous osteomyelitis is a very rare entity, and only a few cases have been reported in the English-language literature. Though rare, XO warrants greater emphasis than it receives in the literature. It is a chronic inflammatory disease having a close resemblance to bone tumors. A high index of suspicion must be practiced to differentiate XO from tumors. Histopathologic examination is mandatory to establish definitive diagnosis and correct treatment.
Xanthogranulomatous osteomyelitis (XO) is a type of chronic inflammatory process that is characterized by the collection of foamy macrophages along with mononuclear cells in the tissue.1 Xanthogranulomatous osteomyelitis is characterized by the presence of granular, eosinophilic, periodic acid–Schiff–positive histiocytes in the initial stages, followed by the mixture of foamy macrophages and activated plasma cells and, last, by the presence of suppurative foci and hemorrhage. This is an uncommon process best known to occur in the gallbladder, kidney, urinary bladder, fallopian tube, ovary, vagina, prostate, testis, epididymis, colon, and appendix.2-4 Very rarely, it can affect lungs, brain, or bone. Only 5 cases of XO have been reported in the literature.5-8
We report XO of the proximal femur in a 65-year-old woman who initially had a clinical and radiologic diagnosis of aneurysmal bone cyst; however, histopathologic examination confirmed the diagnosis of XO. Xanthogranulomatous osteomyelitis mimics a neoplastic pathology in gallbladder, kidney, and prostrate on gross clinical and radiologic examination.9 The pathogenesis of XO is best characterized by a delayed type of hypersensitivity reaction.10 The differential diagnosis includes chronic recurrent multifocal osteomyelitis, xanthoma, infiltrative storage disorder, malakoplakia, Langerhans cell histiocytosis, fibrohistiocytic tumor, Erdheim-Chester disease, and metastatic renal cell carcinoma.11-14 The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 65-year-old hypertensive woman presented with complaints of pain in the right hip for a duration of 6 months. Pain was radiating from the right hip region to the anteromedial aspect of the knee and progressively increasing, with a history of pain at rest suggestive of a nonmechanical pathology in the hip. There was no history of fever, weight loss, loss of appetite, pain in any other joint, or morning stiffness. The patient was mobile without support and was able to squat and sit cross-legged; however, the stance phase on the right side was less than on the left side, suggestive of an antalgic component in the gait.
On examining the patient, there was anterior hip joint tenderness with no local sign of any infective or inflammatory pathology. Trochanteric tenderness was present, but there was no irregularity, broadening, or thickening of the trochanter. There was no restriction in the range of motion, and no coronal or sagittal plane deformity in the right hip. There was no limb-length discrepancy. However, the patient was not able to raise her leg actively, probably because of pain in the right hip.
On plain radiographs of the pelvis with bilateral hips, a well-defined nonexpansile uniloculated lytic lesion with sclerotic margins was present in the neck of the right femur, extending to the intertrochanteric area (Figure 1). Ground-glass appearance was also noted. Considering the benign nature of the lesion radiologically and clinically, a differential diagnosis of hyperparathyroidism, renal osteodystrophy, multiple myeloma, and fibrous dysplasia was considered. Hematologic investigations, skeletal survey, and magnetic resonance imaging (MRI) of the bilateral hips were performed to rule out the differential diagnosis.
The patient’s hemoglobin level was 11.8 g/dL with total white blood cell count of 10,300/µL. Renal and hepatic functions were within normal limit. Serum erythrocyte sedimentation rate (ESR) was 12 mm/h and C-reactive protein level was normal. Serum parathyroid level was 32 pg/mL, which was within normal limits, with an alkaline phosphatase level of 101 U/L. The skeletal survey showed no other bony lesion in the body. T1-weighted MRI of both hips showed a well-defined hypointense lesion in the neck and intertrochanteric area of the right hip, which was hyperintense on T2-weighted MRI, suggestive of aneurysmal bone cyst (Figure 2).
Normal ESR, hemoglobin, alkaline phosphatase, and serum parathyroid levels and normal skeletal survey almost ruled out multiple myeloma and hyperparathyroidism. Normal renal profile ruled out renal osteodystrophy and the osteitis fibrosa cystica lesion associated with it. We planned for prophylactic internal fixation of the lesion to prevent a pathologic fracture. According to Mirels,15 if there is a lytic lesion covering more than two-thirds of the circumference of the bone in the peritrochanteric area, the chances of a pathologic fracture are high and such fractures should be fixed.
We planned for curettage of the lesion with bone grafting and in situ intramedullary fixation of the lesion. Curettage was done according to the plan and the sample was sent for histopathologic examination. In situ internal fixation and bone grafting were performed by using a proximal femoral intramedullary nail. To our surprise, the biopsy sample was reported as xanthogranuloma, with multiple foamy macrophages mixed with inflammatory cells and aggregates of lymphocytes (Figure 3). Mycobacterial and routine bacterial cultures were reported as negative. The patient was kept on oral antibiotics (cefixime and moxifloxacin) for 6 weeks, and she made an uneventful recovery. At 6-month follow-up, a radiograph of the right hip showed a healed lesion with proximal femoral nail in situ (Figure 4).
Discussion
To the best of our knowledge, a total of 5 cases of XO have been reported in the literature. The earliest of these reports were by Cozzutto and Carbone,1 who reported 2 cases of XO of the first rib and of the epiphysis of the tibia, respectively. The importance of these lesions to diagnosis is their confusion with a neoplastic disease, as XO is itself a benign disorder. These lesions can mimic a neoplastic lesion in clinical and radiologic presentation and the only way to differentiate the lesion from a neoplastic disease is by histopathologic examination of the tissue. Hypothetically, xanthogranulomatous disorders can be related to trauma or infection.
In 2007, Vankalakunti and colleagues6 reported XO of the ulna in a 50-year-old postmenopausal woman. In that case, progressive swelling was present on the extensor aspect of her right forearm for a period of 2 years, for which curettage and bone grafting were performed, using autograft from the ipsilateral iliac crest. The tissue culture was sterile, and XO was diagnosed as a result of the histopathologic examination. In 2009, Cennimo and colleagues7 reported XO of the index finger and wrist of a man complaining of pain and swelling for 1 year, which was unresponsive to antibiotics. The diagnosis of XO was confirmed histopathologically, when the culture of the same tissue grew Mycobacterium marinum. Radical synovectomy of the lesion was performed, after which minocycline, clarithromycin, and ethambutol were administered. In 2012, Borjian and colleagues8 reported a case of XO of the proximal humerus and proximal fibula in a 14-year-old child. The child, who presented with fever, pain, and restriction of shoulder movements, was started on oral antibiotics as the tissue culture grew Staphylococcus aureus; the patient did not complete the course of treatment in the hospital. No surgical intervention was done in this case. The diagnosis of XO was confirmed by microscopic examination of the tissue.
An association between bacterial infection and xanthogranulomatous inflammation has existed in several organs, such as the kidneys, and in the gastrointestinal system, but such an association of the 2 is yet to be determined for bone.5,10,16-19 Because of the paucity of literature on the disease, a management protocol for XO of bone has not been defined, and decisions have to be made considering the natural history of the disease in other organs. We present this case primarily because of its rarity, curability, and its close resemblance to bone tumors. While XO is benign, it can mimic a neoplastic bone lesion in its imaging and clinical manifestations, and appropriate differentiation is crucial. Currently, histopathologic examination of lesions is the most specific and is the gold standard for diagnosis.
Conclusion
Xanthogranulomatous osteomyelitis is a very rare entity, and only a few cases have been reported in the English-language literature. Though rare, XO warrants greater emphasis than it receives in the literature. It is a chronic inflammatory disease having a close resemblance to bone tumors. A high index of suspicion must be practiced to differentiate XO from tumors. Histopathologic examination is mandatory to establish definitive diagnosis and correct treatment.
1. Cozzutto C, Carbone A. The xanthogranulomatous process. Xanthogranulomatous inflammation. Pathol Res Pract. 1988;183(4):395-402.
2. Ladefoged C, Lorentzen M. Xanthogranulomatous cholecystitis. A clinicopathological study of 20 cases and review of the literature. APMIS. 1993;101(11):869-875.
3. Nistal M, Gonzalez-Peramato P, Serrano A, Regadera J. Xanthogranulomatous funiculitis and orchiepididymitis: report of 2 cases with immunohistochemical study and literature review. Arch Pathol Lab Med. 2004;128(8):911-914.
4. Oh YH, Seong SS, Jang KS, et al. Xanthogranulomatous inflammation presenting as a submucosal mass of the sigmoid colon. Pathol Int. 2005;55(7):440-444.
5. Cozzutto C. Xanthogranulomatous osteomyelitis. Arch Pathol Lab Med. 1984;108(12):973-6.
6. Vankalakunti M, Saikia UN, Mathew M, Kang M. Xanthogranulomatous osteomyelitis of ulna mimicking neoplasm. World J Surg Oncol. 2007;30(5):46.
7. Cennimo DJ, Agag R, Fleegler E, et al. Mycobacterium marinum hand infection in a “sushi chef.” Eplasty. 2009;14(9):e43.
8. Borjian A, Rezaei F, Eshaghi MA, Shemshaki H. Xanthogranulomatous osteomyelitis. J Orthop Traumatol. 2012;13(4):217-220.
9. Rafique M, Yaqoob N. Xanthogranulomatous prostatitis: a mimic of carcinoma of prostate. World J Surg Oncol. 2006;4:30.
10. Nakashiro H, Haraoka S, Fujiwara K, Harada S, Hisatsugu T, Watanabe T. Xanthogranulomatous cholecystis. Cell composition and a possible pathogenetic role of cell-mediated immunity. Pathol Res Pract. 1995;191(11):1078-1086.
11. Hamada T, Ito H, Araki Y, Fujii K, Inoue M, Ishida O. Benign fibrous histiocytoma of the femur: review of three cases. Skeletal Radiol. 1996;25(1):25-29.
12. Kossard S, Chow E, Wilkinson B, Killingsworth M. Lipid and giant cell poor necrobiotic xanthogranuloma. J Cutan Pathol. 2000;27(7):374-378.
13. Girschick HJ, Huppertz HI, Harmsen D, Krauspe R, Müller-Hermelink HK, Papadopoulos T. Chronic recurrent multifocal osteomyelitis in children: diagnostic value of histopathology and microbial testing. Hum Pathol. 1999;30(1):59-65.
14. Kayser R, Mahlfeld K, Grasshoff H. Vertebral Langerhans-cell histiocytosis in childhood – a differential diagnosis of spinal osteomyelitis. Klin Padiatr. 1999;211(5):399-402.
15. Mirels H. Metastatic disease in long bones. A proposed scoring system for diagnosing impending pathologic fractures. Clin Orthop Relat Res. 1989;249:256-264.
16. Machiz S, Gordon J, Block N, Politano VA. Salmonella typhosa urinary tract infection and xanthogranulomatous pyelonephritis. Case report and review of literature. J Fla Med Assoc. 1974;61(9):703-705.
17. Gauperaa T, Stalsberg H. Renal endometriosis. A case report. Scand J Urol Nephrol. 1977;11(2):189-191.
18. Goodman M, Curry T, Russell T. Xanthogranulomatous pyelonephritis (XGP): a local disease with systemic manifestations. Report of 23 patients and review of the literature. Medicine. 1979;58(2):171-181.
19. Guarino M, Reale D, Micoli G, Tricomi P, Cristofori E. Xanthogranulomatous gastritis: association with xanthogranulomatous cholecystitis. J Clin Pathol. 1993;46(1):88-90.
1. Cozzutto C, Carbone A. The xanthogranulomatous process. Xanthogranulomatous inflammation. Pathol Res Pract. 1988;183(4):395-402.
2. Ladefoged C, Lorentzen M. Xanthogranulomatous cholecystitis. A clinicopathological study of 20 cases and review of the literature. APMIS. 1993;101(11):869-875.
3. Nistal M, Gonzalez-Peramato P, Serrano A, Regadera J. Xanthogranulomatous funiculitis and orchiepididymitis: report of 2 cases with immunohistochemical study and literature review. Arch Pathol Lab Med. 2004;128(8):911-914.
4. Oh YH, Seong SS, Jang KS, et al. Xanthogranulomatous inflammation presenting as a submucosal mass of the sigmoid colon. Pathol Int. 2005;55(7):440-444.
5. Cozzutto C. Xanthogranulomatous osteomyelitis. Arch Pathol Lab Med. 1984;108(12):973-6.
6. Vankalakunti M, Saikia UN, Mathew M, Kang M. Xanthogranulomatous osteomyelitis of ulna mimicking neoplasm. World J Surg Oncol. 2007;30(5):46.
7. Cennimo DJ, Agag R, Fleegler E, et al. Mycobacterium marinum hand infection in a “sushi chef.” Eplasty. 2009;14(9):e43.
8. Borjian A, Rezaei F, Eshaghi MA, Shemshaki H. Xanthogranulomatous osteomyelitis. J Orthop Traumatol. 2012;13(4):217-220.
9. Rafique M, Yaqoob N. Xanthogranulomatous prostatitis: a mimic of carcinoma of prostate. World J Surg Oncol. 2006;4:30.
10. Nakashiro H, Haraoka S, Fujiwara K, Harada S, Hisatsugu T, Watanabe T. Xanthogranulomatous cholecystis. Cell composition and a possible pathogenetic role of cell-mediated immunity. Pathol Res Pract. 1995;191(11):1078-1086.
11. Hamada T, Ito H, Araki Y, Fujii K, Inoue M, Ishida O. Benign fibrous histiocytoma of the femur: review of three cases. Skeletal Radiol. 1996;25(1):25-29.
12. Kossard S, Chow E, Wilkinson B, Killingsworth M. Lipid and giant cell poor necrobiotic xanthogranuloma. J Cutan Pathol. 2000;27(7):374-378.
13. Girschick HJ, Huppertz HI, Harmsen D, Krauspe R, Müller-Hermelink HK, Papadopoulos T. Chronic recurrent multifocal osteomyelitis in children: diagnostic value of histopathology and microbial testing. Hum Pathol. 1999;30(1):59-65.
14. Kayser R, Mahlfeld K, Grasshoff H. Vertebral Langerhans-cell histiocytosis in childhood – a differential diagnosis of spinal osteomyelitis. Klin Padiatr. 1999;211(5):399-402.
15. Mirels H. Metastatic disease in long bones. A proposed scoring system for diagnosing impending pathologic fractures. Clin Orthop Relat Res. 1989;249:256-264.
16. Machiz S, Gordon J, Block N, Politano VA. Salmonella typhosa urinary tract infection and xanthogranulomatous pyelonephritis. Case report and review of literature. J Fla Med Assoc. 1974;61(9):703-705.
17. Gauperaa T, Stalsberg H. Renal endometriosis. A case report. Scand J Urol Nephrol. 1977;11(2):189-191.
18. Goodman M, Curry T, Russell T. Xanthogranulomatous pyelonephritis (XGP): a local disease with systemic manifestations. Report of 23 patients and review of the literature. Medicine. 1979;58(2):171-181.
19. Guarino M, Reale D, Micoli G, Tricomi P, Cristofori E. Xanthogranulomatous gastritis: association with xanthogranulomatous cholecystitis. J Clin Pathol. 1993;46(1):88-90.
Length of Stay and Readmission After Total Shoulder Arthroplasty: An Analysis of 1505 Cases
Use of total shoulder arthroplasty (TSA) and reverse TSA for shoulder conditions has increased dramatically in recent years.1 Approximately 27,000 standard TSAs were performed in the United States in 2008, and this number is expected to double by 2015.2 TSA provides excellent pain relief, restoration of function, and patient satisfaction.3 The evolution of implant design over the past 25 years has contributed to excellent long-term implant survival, with rates comparable to those of total knee and hip arthroplasty.4 Similarly, compared with previous designs, contemporary designs and techniques have resulted in fewer complications.5
Several studies have investigated the long-term complications of TSA. These complications include prosthetic loosening, instability, periprosthetic fracture, rotator cuff tears, nerve injury, and deltoid dysfunction.6-11 In addition, Waterman and colleagues11 very recently assessed the influence of risk factors on short-term postoperative complications of TSA. However, none of these studies has assessed the influence of multiple risk factors on postoperative length of stay (LOS) after TSA. Only 1 study, using data from 2005 and earlier, has analyzed the potential effect of multiple patient characteristics on readmission after TSA12; other studies have been only descriptive.13-16
We conducted a retrospective cohort study to characterize the risk factors for extended LOS and readmission after TSA in a large sample of patients drawn from a national database. We hypothesized that patient factors, including age, sex, and obesity, would be significantly associated with postoperative LOS and readmission after TSA. National databases have been increasingly used in orthopedic research, as they offer particular advantages. Large sample sizes allow for powerful analyses of associations—analyses previously not possible in single-surgeon and single-institution studies. In addition, use of a large, national patient sample allows us to draw generalizable conclusions to better define patients’ and physicians’ postoperative expectations.
Methods
We conducted a retrospective cohort study using the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database. ACS-NSQIP collects 150 patient variables from 374 participating US hospitals.17 Patients are prospectively identified, and information is collected from operative reports, medical records, and patient interviews by trained clinical reviewers.17,18 Routine auditing by the program ensures high-quality data, with reported interrater disagreement below 2% for all variables. Data are collected through the 30th postoperative day, including after discharge.
This study was granted an exemption from our institutional review board, as we used a deidentified and publicly available database. Patients who were 60 years or older and underwent TSA between 2011 and 2012 were identified in the ACS-NSQIP database. TSA patients were identified using Current Procedural Terminology (CPT) code 23472, which includes TSA and reverse TSA procedures.
Patients were divided into groups based on surgical indications, which were available as International Classification of Diseases, Ninth Revision (ICD-9) diagnosis codes. Patients with postoperative ICD-9 codes 714.0 (rheumatoid arthritis), 715.0-9 (osteoarthritis), 716.61/716.81/716.91 (unspecified arthropathy), 718.01 (articular cartilage disorder), 718.31 (recurrent dislocation of shoulder), 718.81 (other joint derangement of shoulder), 719.41/719.91 (unspecified shoulder pain/disorder), 726.0-2 (disorder of shoulder tendons and bursa), 727.61 (rotator cuff rupture), and 840.3-9 (rotator cuff sprain) were classified as having a nonfracture indication. Patients with postoperative ICD-9 codes 716.11 (traumatic arthropathy), 833.80-89 (malunion/nonunion of fracture), and 812.00-20 (fracture of proximal humerus) were classified as having a fracture-associated indication. Patients with incomplete perioperative data were excluded from the study, leaving 1505 patients for the study (out of an initial 1726).
Patient characteristics, including sex, age, height, weight, and history of smoking, were collected from the ACS-NSQIP database. Body mass index (BMI) was calculated from each patient’s height and weight. Information about medical comorbidities was also collected from the ACS-NSQIP database. History of pulmonary disease was defined as a history of dyspnea, severe chronic obstructive pulmonary disease, ventilator-assisted respiration within 48 hours before surgery, or current pneumonia. History of heart disease was defined as a history of congestive heart failure or angina within 1 month before admission, myocardial infarction within 6 months before admission, cardiac surgery, or percutaneous coronary intervention. American Society of Anesthesiologists (ASA) class 3 or higher indicates severe systemic disease. Steroid use was defined as regular administration of corticosteroid medications within 30 days before surgery. Functional status was defined as the ability to perform activities of daily living (ADLs) within 30 days before surgery, with the patient’s best functional status during this period recorded. Similar to how other variables were collected from the database, this information was obtained through medical record abstraction and patient interviews by trained personnel. ADLs are defined in the ACS-NSQIP as “activities usually performed in the course of a normal day in a person’s life” and include bathing, feeding, dressing, toileting, and mobility. An independent patient does not require assistance for any ADLs, a partially dependent patient requires assistance for some ADLs, and a totally dependent patient requires assistance in completing all ADLs. Partially and totally dependent patients were grouped for analysis. Information about a patient’s discharge destination (to home or a facility) was also available in the database.17
Extended Length of Stay
Extended LOS was defined as a binary variable that was positive when the postoperative LOS exceeded the 90th percentile LOS. The 90th percentile LOS was chosen as a cutoff to account for normal variations in LOS and differing practices of surgeons while still capturing patients with abnormally extended LOS.
Readmission
Readmission was defined as a binary variable that was positive when a patient had an unplanned readmission 1 or more times after the initial postoperative discharge.
Patient Demographics
Table 1 summarizes the demographics and comorbidities of the 1505 TSA patients who met our study inclusion criteria. Mean age was 72.8 years (range, 60-90 years). Mean BMI was 30.3 kg/m2 (range, 15.7-63.9 kg/m2); 46.7% of patients were classified as obese (BMI, ≥30 kg/m2). The cohort was 58.9% female. Four percent of patients underwent TSA for a fracture-associated indication.
Statistical Analyses
Statistical analyses were performed with Stata 11.2 (StataCorp). Bivariate and multivariate analyses were used to test patient characteristics for association with extended LOS and readmission. Discharge destination and LOS were included in the readmission analysis because this information would be available at time of discharge and would be useful to include in a model that predicts odds of readmission.
Final multivariate models were constructed using a backward stepwise process that initially included all potential variables and sequentially excluded variables with the highest P value until only those with P < .20 remained. Variables with .05 < P < .20 were left in the model to control for potential confounding but were not considered significantly associated with the outcome. All tests were 2-tailed, and the statistical difference was established at a 2-sided α level of 0.05 (P < .05).
Results
Median LOS after TSA was 2 days (interquartile range, 1-3 days), and extended LOS was defined as LOS of more than 3 days (90th percentile LOS). The distribution of LOS is depicted in the Figure. Results of the bivariate and multivariate analyses are reported in Table 2 and Table 3, respectively. Bivariate analysis revealed an association between extended LOS and increased age, ASA class 3 or higher, and history of diabetes, pulmonary disease, and heart disease. On multivariate analysis, extended LOS was associated with age 70 to 79 years (odds ratio [OR], 1.71; 95% confidence interval [CI], 1.01-2.95; P = .049), age 80 years or older (OR, 3.38; 95% CI, 1.94-5.91; P < .001), and history of diabetes (OR, 2.37; 95% CI, 1.53-3.66; P < .001).
Forty-nine patients (3.3%) were readmitted within the first 30 postoperative days. Bivariate analysis revealed an association between readmission and ASA class 3 or higher, history of heart disease, and history of hypertension. On multivariate analysis, readmission was associated only with history of heart disease (OR, 2.94; 95% CI, 1.45-5.96; P = .003) and history of hypertension (OR, 3.93; 95% CI, 1.40-11.04; P = .010).
Discussion
In the United States, TSA has become increasingly popular because of its favorable outcomes and continued implant development.1-5 However, there is a shortage of information about risk factors for short-term outcomes after TSA. In this study, we used multivariate analyses to identify patient-related factors associated with extended LOS and readmission after discharge. By identifying these factors, we can improve the preoperative discussion and postoperative planning for this procedure.
In the present study, extended LOS (>3 days) was found to be associated with older age and history of diabetes. The TSA literature has little information that can be used to compare these results, though age over 80 years was previously described as a risk factor for extended LOS after TSA.19 Uncontrolled diabetes has been identified as a risk factor for extended LOS in hip and knee arthroplasty,20 and management of diabetes may similarly complicate postoperative care, leading to extended LOS and increased costs in TSA patients. Patients with the identified risk factors for extended LOS should be counseled before surgery. In addition, this is important information for health care organizations and providers.
Readmission within 30 days after TSA was found to be independently associated with history of heart disease and history of hypertension. Similar to factors affecting LOS, patient-related risk factors for readmission are also poorly defined in the TSA literature. In total hip arthroplasty patients, heart disease has been found to be associated with readmission.21,22 Hypertension has also been associated with readmission for other orthopedic procedures.23 Results of the present study indicate these comorbidities may increase the risk for complications after discharge. It is important to note, however, that LOS did not correlate with readmission rates, indicating patients are likely being discharged at the most clinically appropriate time.
Waterman and colleagues11 very recently identified (in the ACS-NSQIP database) a patient population that underwent TSA between 2006 and 2011 to describe risk factors for postoperative complications within 30 days. They found that comorbid cardiac disease and older age were independently associated with mortality. Interestingly, the present study identified older age as associated with extended LOS, and cardiac disease as associated with readmission. Together with the results from the previous study, age and cardiac disease seem to be important patient factors to consider when planning TSA, as they are associated with a significantly worse postoperative course.
This study had several limitations. First, given the nature of the ACS-NSQIP database, readmissions are recorded only up to 30 days after surgery, including after discharge. Second, though the ACS-NSQIP tries to collect as many patient variables as possible, some information is not captured. Additional variables that could potentially affect LOS and readmission (eg, insurance status, hospital volume) were not available for analysis. However, we think the high-quality data collection process used by the ACS-NSQIP outweighs the lack of certain variables. Third, original operative notes are not available in the ACS-NSQIP database, and the only way to identify operative procedures is to check CPT codes. Unfortunately, CPT code 23472 is used for both TSA and reverse TSA, so these procedures could not be separated for analysis, and the results of this study can be used to comment only on the risks of both procedures. Another limitation is that there were not enough patients to further analyze the data by each indication.
Conclusion
With the increasing popularity of TSA for an expanding set of indications, it is important to understand the factors that can affect the postoperative course. In this study, we found several patient-related risk factors for extended LOS and readmission. Although the identified factors are generally not modifiable, this information can be used to better define the expectations of patients, providers, and organizations for this increasingly common procedure.
1. Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254.
2. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120.
3. Adams JE, Sperling JW, Hoskin TL, Melton LJ 3rd, Cofield RH. Shoulder arthroplasty in Olmsted County, Minnesota, 1976–2000: a population-based study. J Shoulder Elbow Surg. 2006;15(1):50-55.
4. Farmer KW, Hammond JW, Queale WS, Keyurapan E, McFarland EG. Shoulder arthroplasty versus hip and knee arthroplasties: a comparison of outcomes. Clin Orthop Relat Res. 2007;(455):183-189.
5. Chin PY, Sperling JW, Cofield RH, Schleck C. Complications of total shoulder arthroplasty: are they fewer or different? J Shoulder Elbow Surg. 2006;15(1):19-22.
6. Bohsali KI, Wirth MA, Rockwood CA Jr. Complications of total shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(10):2279-2292.
7. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
8. Sneppen O, Fruensgaard S, Johannsen HV, Olsen BS, Søjbjerg JO, Andersen NH. Total shoulder replacement in rheumatoid arthritis: proximal migration and loosening. J Shoulder Elbow Surg. 1996;5(1):47-52.
9. Søjbjerg JO, Frich LH, Johannsen HV, Sneppen O. Late results of total shoulder replacement in patients with rheumatoid arthritis. Clin Orthop Relat Res. 1999;(366):39-45.
10. Raiss P, Bruckner T, Rickert M, Walch G. Longitudinal observational study of total shoulder replacements with cement: fifteen to twenty-year follow-up. J Bone Joint Surg Am. 2014;96(3):198-205.
11. Waterman BR, Dunn JC, Bader J, Urrea L, Schoenfeld AJ, Belmont PJ Jr. Thirty-day morbidity and mortality after elective total shoulder arthroplasty: patient-based and surgical risk factors. J Shoulder Elbow Surg. 2015;24(1):24-30.
12. Farng E, Zingmond D, Krenek L, Soohoo NF. Factors predicting complication rates after primary shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(4):557-563.
13. Streubel PN, Simone JP, Sperling JW, Cofield R. Thirty and ninety-day reoperation rates after shoulder arthroplasty. J Bone Joint Surg Am. 2014;96(3):e17.
14. Mahoney A, Bosco JA 3rd, Zuckerman JD. Readmission after shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(3):377-381.
15. Gay DM, Lyman S, Do H, Hotchkiss RN, Marx RG, Daluiski A. Indications and reoperation rates for total elbow arthroplasty: an analysis of trends in New York state. J Bone Joint Surg Am. 2012;94(2):110-117.
16. Zumstein MA, Pinedo M, Old J, Boileau P. Problems, complications, reoperations, and revisions in reverse total shoulder arthroplasty: a systematic review. J Shoulder Elbow Surg. 2011;20(1):146-157.
17. American College of Surgeons. User Guide for the 2012 ACS NSQIP Participant Use Data File. https://www.facs.org/~/media/files/quality%20programs/nsqip/ug12.ashx. Published October 2013. Accessed June 21, 2015.
18. Khuri SF, Henderson WG, Daley J, et al; Principal Investigators of Patient Safety in Surgery Study. Successful implementation of the Department of Veterans Affairs’ National Surgical Quality Improvement Program in the private sector: the Patient Safety in Surgery study. Ann Surg. 2008;248(2):329-336.
19. Ricchetti ET, Abboud JA, Kuntz AF, Ramsey ML, Glaser DL, Williams GR Jr. Total shoulder arthroplasty in older patients: increased perioperative morbidity? Clin Orthop Relat Res. 2011;469(4):1042-1049.
20. Marchant MH Jr, Viens NA, Cook C, Vail TP, Bolognesi MP. The impact of glycemic control and diabetes mellitus on perioperative outcomes after total joint arthroplasty. J Bone Joint Surg Am. 2009;91(7):1621-1629.
21. Schairer WW, Sing DC, Vail TP, Bozic KJ. Causes and frequency of unplanned hospital readmission after total hip arthroplasty. Clin Orthop Relat Res. 2014;472(2):464-470.
22. Vorhies JS, Wang Y, Herndon J, Maloney WJ, Huddleston JI. Readmission and length of stay after total hip arthroplasty in a national Medicare sample. J Arthroplasty. 2011;26(6 suppl):119-123.
23. Lovecchio F, Hsu WK, Smith TR, Cybulski G, Kim B, Kim JY. Predictors of thirty-day readmission after anterior cervical fusion. Spine. 2014;39(2):127-133.
Use of total shoulder arthroplasty (TSA) and reverse TSA for shoulder conditions has increased dramatically in recent years.1 Approximately 27,000 standard TSAs were performed in the United States in 2008, and this number is expected to double by 2015.2 TSA provides excellent pain relief, restoration of function, and patient satisfaction.3 The evolution of implant design over the past 25 years has contributed to excellent long-term implant survival, with rates comparable to those of total knee and hip arthroplasty.4 Similarly, compared with previous designs, contemporary designs and techniques have resulted in fewer complications.5
Several studies have investigated the long-term complications of TSA. These complications include prosthetic loosening, instability, periprosthetic fracture, rotator cuff tears, nerve injury, and deltoid dysfunction.6-11 In addition, Waterman and colleagues11 very recently assessed the influence of risk factors on short-term postoperative complications of TSA. However, none of these studies has assessed the influence of multiple risk factors on postoperative length of stay (LOS) after TSA. Only 1 study, using data from 2005 and earlier, has analyzed the potential effect of multiple patient characteristics on readmission after TSA12; other studies have been only descriptive.13-16
We conducted a retrospective cohort study to characterize the risk factors for extended LOS and readmission after TSA in a large sample of patients drawn from a national database. We hypothesized that patient factors, including age, sex, and obesity, would be significantly associated with postoperative LOS and readmission after TSA. National databases have been increasingly used in orthopedic research, as they offer particular advantages. Large sample sizes allow for powerful analyses of associations—analyses previously not possible in single-surgeon and single-institution studies. In addition, use of a large, national patient sample allows us to draw generalizable conclusions to better define patients’ and physicians’ postoperative expectations.
Methods
We conducted a retrospective cohort study using the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database. ACS-NSQIP collects 150 patient variables from 374 participating US hospitals.17 Patients are prospectively identified, and information is collected from operative reports, medical records, and patient interviews by trained clinical reviewers.17,18 Routine auditing by the program ensures high-quality data, with reported interrater disagreement below 2% for all variables. Data are collected through the 30th postoperative day, including after discharge.
This study was granted an exemption from our institutional review board, as we used a deidentified and publicly available database. Patients who were 60 years or older and underwent TSA between 2011 and 2012 were identified in the ACS-NSQIP database. TSA patients were identified using Current Procedural Terminology (CPT) code 23472, which includes TSA and reverse TSA procedures.
Patients were divided into groups based on surgical indications, which were available as International Classification of Diseases, Ninth Revision (ICD-9) diagnosis codes. Patients with postoperative ICD-9 codes 714.0 (rheumatoid arthritis), 715.0-9 (osteoarthritis), 716.61/716.81/716.91 (unspecified arthropathy), 718.01 (articular cartilage disorder), 718.31 (recurrent dislocation of shoulder), 718.81 (other joint derangement of shoulder), 719.41/719.91 (unspecified shoulder pain/disorder), 726.0-2 (disorder of shoulder tendons and bursa), 727.61 (rotator cuff rupture), and 840.3-9 (rotator cuff sprain) were classified as having a nonfracture indication. Patients with postoperative ICD-9 codes 716.11 (traumatic arthropathy), 833.80-89 (malunion/nonunion of fracture), and 812.00-20 (fracture of proximal humerus) were classified as having a fracture-associated indication. Patients with incomplete perioperative data were excluded from the study, leaving 1505 patients for the study (out of an initial 1726).
Patient characteristics, including sex, age, height, weight, and history of smoking, were collected from the ACS-NSQIP database. Body mass index (BMI) was calculated from each patient’s height and weight. Information about medical comorbidities was also collected from the ACS-NSQIP database. History of pulmonary disease was defined as a history of dyspnea, severe chronic obstructive pulmonary disease, ventilator-assisted respiration within 48 hours before surgery, or current pneumonia. History of heart disease was defined as a history of congestive heart failure or angina within 1 month before admission, myocardial infarction within 6 months before admission, cardiac surgery, or percutaneous coronary intervention. American Society of Anesthesiologists (ASA) class 3 or higher indicates severe systemic disease. Steroid use was defined as regular administration of corticosteroid medications within 30 days before surgery. Functional status was defined as the ability to perform activities of daily living (ADLs) within 30 days before surgery, with the patient’s best functional status during this period recorded. Similar to how other variables were collected from the database, this information was obtained through medical record abstraction and patient interviews by trained personnel. ADLs are defined in the ACS-NSQIP as “activities usually performed in the course of a normal day in a person’s life” and include bathing, feeding, dressing, toileting, and mobility. An independent patient does not require assistance for any ADLs, a partially dependent patient requires assistance for some ADLs, and a totally dependent patient requires assistance in completing all ADLs. Partially and totally dependent patients were grouped for analysis. Information about a patient’s discharge destination (to home or a facility) was also available in the database.17
Extended Length of Stay
Extended LOS was defined as a binary variable that was positive when the postoperative LOS exceeded the 90th percentile LOS. The 90th percentile LOS was chosen as a cutoff to account for normal variations in LOS and differing practices of surgeons while still capturing patients with abnormally extended LOS.
Readmission
Readmission was defined as a binary variable that was positive when a patient had an unplanned readmission 1 or more times after the initial postoperative discharge.
Patient Demographics
Table 1 summarizes the demographics and comorbidities of the 1505 TSA patients who met our study inclusion criteria. Mean age was 72.8 years (range, 60-90 years). Mean BMI was 30.3 kg/m2 (range, 15.7-63.9 kg/m2); 46.7% of patients were classified as obese (BMI, ≥30 kg/m2). The cohort was 58.9% female. Four percent of patients underwent TSA for a fracture-associated indication.
Statistical Analyses
Statistical analyses were performed with Stata 11.2 (StataCorp). Bivariate and multivariate analyses were used to test patient characteristics for association with extended LOS and readmission. Discharge destination and LOS were included in the readmission analysis because this information would be available at time of discharge and would be useful to include in a model that predicts odds of readmission.
Final multivariate models were constructed using a backward stepwise process that initially included all potential variables and sequentially excluded variables with the highest P value until only those with P < .20 remained. Variables with .05 < P < .20 were left in the model to control for potential confounding but were not considered significantly associated with the outcome. All tests were 2-tailed, and the statistical difference was established at a 2-sided α level of 0.05 (P < .05).
Results
Median LOS after TSA was 2 days (interquartile range, 1-3 days), and extended LOS was defined as LOS of more than 3 days (90th percentile LOS). The distribution of LOS is depicted in the Figure. Results of the bivariate and multivariate analyses are reported in Table 2 and Table 3, respectively. Bivariate analysis revealed an association between extended LOS and increased age, ASA class 3 or higher, and history of diabetes, pulmonary disease, and heart disease. On multivariate analysis, extended LOS was associated with age 70 to 79 years (odds ratio [OR], 1.71; 95% confidence interval [CI], 1.01-2.95; P = .049), age 80 years or older (OR, 3.38; 95% CI, 1.94-5.91; P < .001), and history of diabetes (OR, 2.37; 95% CI, 1.53-3.66; P < .001).
Forty-nine patients (3.3%) were readmitted within the first 30 postoperative days. Bivariate analysis revealed an association between readmission and ASA class 3 or higher, history of heart disease, and history of hypertension. On multivariate analysis, readmission was associated only with history of heart disease (OR, 2.94; 95% CI, 1.45-5.96; P = .003) and history of hypertension (OR, 3.93; 95% CI, 1.40-11.04; P = .010).
Discussion
In the United States, TSA has become increasingly popular because of its favorable outcomes and continued implant development.1-5 However, there is a shortage of information about risk factors for short-term outcomes after TSA. In this study, we used multivariate analyses to identify patient-related factors associated with extended LOS and readmission after discharge. By identifying these factors, we can improve the preoperative discussion and postoperative planning for this procedure.
In the present study, extended LOS (>3 days) was found to be associated with older age and history of diabetes. The TSA literature has little information that can be used to compare these results, though age over 80 years was previously described as a risk factor for extended LOS after TSA.19 Uncontrolled diabetes has been identified as a risk factor for extended LOS in hip and knee arthroplasty,20 and management of diabetes may similarly complicate postoperative care, leading to extended LOS and increased costs in TSA patients. Patients with the identified risk factors for extended LOS should be counseled before surgery. In addition, this is important information for health care organizations and providers.
Readmission within 30 days after TSA was found to be independently associated with history of heart disease and history of hypertension. Similar to factors affecting LOS, patient-related risk factors for readmission are also poorly defined in the TSA literature. In total hip arthroplasty patients, heart disease has been found to be associated with readmission.21,22 Hypertension has also been associated with readmission for other orthopedic procedures.23 Results of the present study indicate these comorbidities may increase the risk for complications after discharge. It is important to note, however, that LOS did not correlate with readmission rates, indicating patients are likely being discharged at the most clinically appropriate time.
Waterman and colleagues11 very recently identified (in the ACS-NSQIP database) a patient population that underwent TSA between 2006 and 2011 to describe risk factors for postoperative complications within 30 days. They found that comorbid cardiac disease and older age were independently associated with mortality. Interestingly, the present study identified older age as associated with extended LOS, and cardiac disease as associated with readmission. Together with the results from the previous study, age and cardiac disease seem to be important patient factors to consider when planning TSA, as they are associated with a significantly worse postoperative course.
This study had several limitations. First, given the nature of the ACS-NSQIP database, readmissions are recorded only up to 30 days after surgery, including after discharge. Second, though the ACS-NSQIP tries to collect as many patient variables as possible, some information is not captured. Additional variables that could potentially affect LOS and readmission (eg, insurance status, hospital volume) were not available for analysis. However, we think the high-quality data collection process used by the ACS-NSQIP outweighs the lack of certain variables. Third, original operative notes are not available in the ACS-NSQIP database, and the only way to identify operative procedures is to check CPT codes. Unfortunately, CPT code 23472 is used for both TSA and reverse TSA, so these procedures could not be separated for analysis, and the results of this study can be used to comment only on the risks of both procedures. Another limitation is that there were not enough patients to further analyze the data by each indication.
Conclusion
With the increasing popularity of TSA for an expanding set of indications, it is important to understand the factors that can affect the postoperative course. In this study, we found several patient-related risk factors for extended LOS and readmission. Although the identified factors are generally not modifiable, this information can be used to better define the expectations of patients, providers, and organizations for this increasingly common procedure.
Use of total shoulder arthroplasty (TSA) and reverse TSA for shoulder conditions has increased dramatically in recent years.1 Approximately 27,000 standard TSAs were performed in the United States in 2008, and this number is expected to double by 2015.2 TSA provides excellent pain relief, restoration of function, and patient satisfaction.3 The evolution of implant design over the past 25 years has contributed to excellent long-term implant survival, with rates comparable to those of total knee and hip arthroplasty.4 Similarly, compared with previous designs, contemporary designs and techniques have resulted in fewer complications.5
Several studies have investigated the long-term complications of TSA. These complications include prosthetic loosening, instability, periprosthetic fracture, rotator cuff tears, nerve injury, and deltoid dysfunction.6-11 In addition, Waterman and colleagues11 very recently assessed the influence of risk factors on short-term postoperative complications of TSA. However, none of these studies has assessed the influence of multiple risk factors on postoperative length of stay (LOS) after TSA. Only 1 study, using data from 2005 and earlier, has analyzed the potential effect of multiple patient characteristics on readmission after TSA12; other studies have been only descriptive.13-16
We conducted a retrospective cohort study to characterize the risk factors for extended LOS and readmission after TSA in a large sample of patients drawn from a national database. We hypothesized that patient factors, including age, sex, and obesity, would be significantly associated with postoperative LOS and readmission after TSA. National databases have been increasingly used in orthopedic research, as they offer particular advantages. Large sample sizes allow for powerful analyses of associations—analyses previously not possible in single-surgeon and single-institution studies. In addition, use of a large, national patient sample allows us to draw generalizable conclusions to better define patients’ and physicians’ postoperative expectations.
Methods
We conducted a retrospective cohort study using the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database. ACS-NSQIP collects 150 patient variables from 374 participating US hospitals.17 Patients are prospectively identified, and information is collected from operative reports, medical records, and patient interviews by trained clinical reviewers.17,18 Routine auditing by the program ensures high-quality data, with reported interrater disagreement below 2% for all variables. Data are collected through the 30th postoperative day, including after discharge.
This study was granted an exemption from our institutional review board, as we used a deidentified and publicly available database. Patients who were 60 years or older and underwent TSA between 2011 and 2012 were identified in the ACS-NSQIP database. TSA patients were identified using Current Procedural Terminology (CPT) code 23472, which includes TSA and reverse TSA procedures.
Patients were divided into groups based on surgical indications, which were available as International Classification of Diseases, Ninth Revision (ICD-9) diagnosis codes. Patients with postoperative ICD-9 codes 714.0 (rheumatoid arthritis), 715.0-9 (osteoarthritis), 716.61/716.81/716.91 (unspecified arthropathy), 718.01 (articular cartilage disorder), 718.31 (recurrent dislocation of shoulder), 718.81 (other joint derangement of shoulder), 719.41/719.91 (unspecified shoulder pain/disorder), 726.0-2 (disorder of shoulder tendons and bursa), 727.61 (rotator cuff rupture), and 840.3-9 (rotator cuff sprain) were classified as having a nonfracture indication. Patients with postoperative ICD-9 codes 716.11 (traumatic arthropathy), 833.80-89 (malunion/nonunion of fracture), and 812.00-20 (fracture of proximal humerus) were classified as having a fracture-associated indication. Patients with incomplete perioperative data were excluded from the study, leaving 1505 patients for the study (out of an initial 1726).
Patient characteristics, including sex, age, height, weight, and history of smoking, were collected from the ACS-NSQIP database. Body mass index (BMI) was calculated from each patient’s height and weight. Information about medical comorbidities was also collected from the ACS-NSQIP database. History of pulmonary disease was defined as a history of dyspnea, severe chronic obstructive pulmonary disease, ventilator-assisted respiration within 48 hours before surgery, or current pneumonia. History of heart disease was defined as a history of congestive heart failure or angina within 1 month before admission, myocardial infarction within 6 months before admission, cardiac surgery, or percutaneous coronary intervention. American Society of Anesthesiologists (ASA) class 3 or higher indicates severe systemic disease. Steroid use was defined as regular administration of corticosteroid medications within 30 days before surgery. Functional status was defined as the ability to perform activities of daily living (ADLs) within 30 days before surgery, with the patient’s best functional status during this period recorded. Similar to how other variables were collected from the database, this information was obtained through medical record abstraction and patient interviews by trained personnel. ADLs are defined in the ACS-NSQIP as “activities usually performed in the course of a normal day in a person’s life” and include bathing, feeding, dressing, toileting, and mobility. An independent patient does not require assistance for any ADLs, a partially dependent patient requires assistance for some ADLs, and a totally dependent patient requires assistance in completing all ADLs. Partially and totally dependent patients were grouped for analysis. Information about a patient’s discharge destination (to home or a facility) was also available in the database.17
Extended Length of Stay
Extended LOS was defined as a binary variable that was positive when the postoperative LOS exceeded the 90th percentile LOS. The 90th percentile LOS was chosen as a cutoff to account for normal variations in LOS and differing practices of surgeons while still capturing patients with abnormally extended LOS.
Readmission
Readmission was defined as a binary variable that was positive when a patient had an unplanned readmission 1 or more times after the initial postoperative discharge.
Patient Demographics
Table 1 summarizes the demographics and comorbidities of the 1505 TSA patients who met our study inclusion criteria. Mean age was 72.8 years (range, 60-90 years). Mean BMI was 30.3 kg/m2 (range, 15.7-63.9 kg/m2); 46.7% of patients were classified as obese (BMI, ≥30 kg/m2). The cohort was 58.9% female. Four percent of patients underwent TSA for a fracture-associated indication.
Statistical Analyses
Statistical analyses were performed with Stata 11.2 (StataCorp). Bivariate and multivariate analyses were used to test patient characteristics for association with extended LOS and readmission. Discharge destination and LOS were included in the readmission analysis because this information would be available at time of discharge and would be useful to include in a model that predicts odds of readmission.
Final multivariate models were constructed using a backward stepwise process that initially included all potential variables and sequentially excluded variables with the highest P value until only those with P < .20 remained. Variables with .05 < P < .20 were left in the model to control for potential confounding but were not considered significantly associated with the outcome. All tests were 2-tailed, and the statistical difference was established at a 2-sided α level of 0.05 (P < .05).
Results
Median LOS after TSA was 2 days (interquartile range, 1-3 days), and extended LOS was defined as LOS of more than 3 days (90th percentile LOS). The distribution of LOS is depicted in the Figure. Results of the bivariate and multivariate analyses are reported in Table 2 and Table 3, respectively. Bivariate analysis revealed an association between extended LOS and increased age, ASA class 3 or higher, and history of diabetes, pulmonary disease, and heart disease. On multivariate analysis, extended LOS was associated with age 70 to 79 years (odds ratio [OR], 1.71; 95% confidence interval [CI], 1.01-2.95; P = .049), age 80 years or older (OR, 3.38; 95% CI, 1.94-5.91; P < .001), and history of diabetes (OR, 2.37; 95% CI, 1.53-3.66; P < .001).
Forty-nine patients (3.3%) were readmitted within the first 30 postoperative days. Bivariate analysis revealed an association between readmission and ASA class 3 or higher, history of heart disease, and history of hypertension. On multivariate analysis, readmission was associated only with history of heart disease (OR, 2.94; 95% CI, 1.45-5.96; P = .003) and history of hypertension (OR, 3.93; 95% CI, 1.40-11.04; P = .010).
Discussion
In the United States, TSA has become increasingly popular because of its favorable outcomes and continued implant development.1-5 However, there is a shortage of information about risk factors for short-term outcomes after TSA. In this study, we used multivariate analyses to identify patient-related factors associated with extended LOS and readmission after discharge. By identifying these factors, we can improve the preoperative discussion and postoperative planning for this procedure.
In the present study, extended LOS (>3 days) was found to be associated with older age and history of diabetes. The TSA literature has little information that can be used to compare these results, though age over 80 years was previously described as a risk factor for extended LOS after TSA.19 Uncontrolled diabetes has been identified as a risk factor for extended LOS in hip and knee arthroplasty,20 and management of diabetes may similarly complicate postoperative care, leading to extended LOS and increased costs in TSA patients. Patients with the identified risk factors for extended LOS should be counseled before surgery. In addition, this is important information for health care organizations and providers.
Readmission within 30 days after TSA was found to be independently associated with history of heart disease and history of hypertension. Similar to factors affecting LOS, patient-related risk factors for readmission are also poorly defined in the TSA literature. In total hip arthroplasty patients, heart disease has been found to be associated with readmission.21,22 Hypertension has also been associated with readmission for other orthopedic procedures.23 Results of the present study indicate these comorbidities may increase the risk for complications after discharge. It is important to note, however, that LOS did not correlate with readmission rates, indicating patients are likely being discharged at the most clinically appropriate time.
Waterman and colleagues11 very recently identified (in the ACS-NSQIP database) a patient population that underwent TSA between 2006 and 2011 to describe risk factors for postoperative complications within 30 days. They found that comorbid cardiac disease and older age were independently associated with mortality. Interestingly, the present study identified older age as associated with extended LOS, and cardiac disease as associated with readmission. Together with the results from the previous study, age and cardiac disease seem to be important patient factors to consider when planning TSA, as they are associated with a significantly worse postoperative course.
This study had several limitations. First, given the nature of the ACS-NSQIP database, readmissions are recorded only up to 30 days after surgery, including after discharge. Second, though the ACS-NSQIP tries to collect as many patient variables as possible, some information is not captured. Additional variables that could potentially affect LOS and readmission (eg, insurance status, hospital volume) were not available for analysis. However, we think the high-quality data collection process used by the ACS-NSQIP outweighs the lack of certain variables. Third, original operative notes are not available in the ACS-NSQIP database, and the only way to identify operative procedures is to check CPT codes. Unfortunately, CPT code 23472 is used for both TSA and reverse TSA, so these procedures could not be separated for analysis, and the results of this study can be used to comment only on the risks of both procedures. Another limitation is that there were not enough patients to further analyze the data by each indication.
Conclusion
With the increasing popularity of TSA for an expanding set of indications, it is important to understand the factors that can affect the postoperative course. In this study, we found several patient-related risk factors for extended LOS and readmission. Although the identified factors are generally not modifiable, this information can be used to better define the expectations of patients, providers, and organizations for this increasingly common procedure.
1. Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254.
2. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120.
3. Adams JE, Sperling JW, Hoskin TL, Melton LJ 3rd, Cofield RH. Shoulder arthroplasty in Olmsted County, Minnesota, 1976–2000: a population-based study. J Shoulder Elbow Surg. 2006;15(1):50-55.
4. Farmer KW, Hammond JW, Queale WS, Keyurapan E, McFarland EG. Shoulder arthroplasty versus hip and knee arthroplasties: a comparison of outcomes. Clin Orthop Relat Res. 2007;(455):183-189.
5. Chin PY, Sperling JW, Cofield RH, Schleck C. Complications of total shoulder arthroplasty: are they fewer or different? J Shoulder Elbow Surg. 2006;15(1):19-22.
6. Bohsali KI, Wirth MA, Rockwood CA Jr. Complications of total shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(10):2279-2292.
7. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
8. Sneppen O, Fruensgaard S, Johannsen HV, Olsen BS, Søjbjerg JO, Andersen NH. Total shoulder replacement in rheumatoid arthritis: proximal migration and loosening. J Shoulder Elbow Surg. 1996;5(1):47-52.
9. Søjbjerg JO, Frich LH, Johannsen HV, Sneppen O. Late results of total shoulder replacement in patients with rheumatoid arthritis. Clin Orthop Relat Res. 1999;(366):39-45.
10. Raiss P, Bruckner T, Rickert M, Walch G. Longitudinal observational study of total shoulder replacements with cement: fifteen to twenty-year follow-up. J Bone Joint Surg Am. 2014;96(3):198-205.
11. Waterman BR, Dunn JC, Bader J, Urrea L, Schoenfeld AJ, Belmont PJ Jr. Thirty-day morbidity and mortality after elective total shoulder arthroplasty: patient-based and surgical risk factors. J Shoulder Elbow Surg. 2015;24(1):24-30.
12. Farng E, Zingmond D, Krenek L, Soohoo NF. Factors predicting complication rates after primary shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(4):557-563.
13. Streubel PN, Simone JP, Sperling JW, Cofield R. Thirty and ninety-day reoperation rates after shoulder arthroplasty. J Bone Joint Surg Am. 2014;96(3):e17.
14. Mahoney A, Bosco JA 3rd, Zuckerman JD. Readmission after shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(3):377-381.
15. Gay DM, Lyman S, Do H, Hotchkiss RN, Marx RG, Daluiski A. Indications and reoperation rates for total elbow arthroplasty: an analysis of trends in New York state. J Bone Joint Surg Am. 2012;94(2):110-117.
16. Zumstein MA, Pinedo M, Old J, Boileau P. Problems, complications, reoperations, and revisions in reverse total shoulder arthroplasty: a systematic review. J Shoulder Elbow Surg. 2011;20(1):146-157.
17. American College of Surgeons. User Guide for the 2012 ACS NSQIP Participant Use Data File. https://www.facs.org/~/media/files/quality%20programs/nsqip/ug12.ashx. Published October 2013. Accessed June 21, 2015.
18. Khuri SF, Henderson WG, Daley J, et al; Principal Investigators of Patient Safety in Surgery Study. Successful implementation of the Department of Veterans Affairs’ National Surgical Quality Improvement Program in the private sector: the Patient Safety in Surgery study. Ann Surg. 2008;248(2):329-336.
19. Ricchetti ET, Abboud JA, Kuntz AF, Ramsey ML, Glaser DL, Williams GR Jr. Total shoulder arthroplasty in older patients: increased perioperative morbidity? Clin Orthop Relat Res. 2011;469(4):1042-1049.
20. Marchant MH Jr, Viens NA, Cook C, Vail TP, Bolognesi MP. The impact of glycemic control and diabetes mellitus on perioperative outcomes after total joint arthroplasty. J Bone Joint Surg Am. 2009;91(7):1621-1629.
21. Schairer WW, Sing DC, Vail TP, Bozic KJ. Causes and frequency of unplanned hospital readmission after total hip arthroplasty. Clin Orthop Relat Res. 2014;472(2):464-470.
22. Vorhies JS, Wang Y, Herndon J, Maloney WJ, Huddleston JI. Readmission and length of stay after total hip arthroplasty in a national Medicare sample. J Arthroplasty. 2011;26(6 suppl):119-123.
23. Lovecchio F, Hsu WK, Smith TR, Cybulski G, Kim B, Kim JY. Predictors of thirty-day readmission after anterior cervical fusion. Spine. 2014;39(2):127-133.
1. Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254.
2. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120.
3. Adams JE, Sperling JW, Hoskin TL, Melton LJ 3rd, Cofield RH. Shoulder arthroplasty in Olmsted County, Minnesota, 1976–2000: a population-based study. J Shoulder Elbow Surg. 2006;15(1):50-55.
4. Farmer KW, Hammond JW, Queale WS, Keyurapan E, McFarland EG. Shoulder arthroplasty versus hip and knee arthroplasties: a comparison of outcomes. Clin Orthop Relat Res. 2007;(455):183-189.
5. Chin PY, Sperling JW, Cofield RH, Schleck C. Complications of total shoulder arthroplasty: are they fewer or different? J Shoulder Elbow Surg. 2006;15(1):19-22.
6. Bohsali KI, Wirth MA, Rockwood CA Jr. Complications of total shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(10):2279-2292.
7. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
8. Sneppen O, Fruensgaard S, Johannsen HV, Olsen BS, Søjbjerg JO, Andersen NH. Total shoulder replacement in rheumatoid arthritis: proximal migration and loosening. J Shoulder Elbow Surg. 1996;5(1):47-52.
9. Søjbjerg JO, Frich LH, Johannsen HV, Sneppen O. Late results of total shoulder replacement in patients with rheumatoid arthritis. Clin Orthop Relat Res. 1999;(366):39-45.
10. Raiss P, Bruckner T, Rickert M, Walch G. Longitudinal observational study of total shoulder replacements with cement: fifteen to twenty-year follow-up. J Bone Joint Surg Am. 2014;96(3):198-205.
11. Waterman BR, Dunn JC, Bader J, Urrea L, Schoenfeld AJ, Belmont PJ Jr. Thirty-day morbidity and mortality after elective total shoulder arthroplasty: patient-based and surgical risk factors. J Shoulder Elbow Surg. 2015;24(1):24-30.
12. Farng E, Zingmond D, Krenek L, Soohoo NF. Factors predicting complication rates after primary shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(4):557-563.
13. Streubel PN, Simone JP, Sperling JW, Cofield R. Thirty and ninety-day reoperation rates after shoulder arthroplasty. J Bone Joint Surg Am. 2014;96(3):e17.
14. Mahoney A, Bosco JA 3rd, Zuckerman JD. Readmission after shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(3):377-381.
15. Gay DM, Lyman S, Do H, Hotchkiss RN, Marx RG, Daluiski A. Indications and reoperation rates for total elbow arthroplasty: an analysis of trends in New York state. J Bone Joint Surg Am. 2012;94(2):110-117.
16. Zumstein MA, Pinedo M, Old J, Boileau P. Problems, complications, reoperations, and revisions in reverse total shoulder arthroplasty: a systematic review. J Shoulder Elbow Surg. 2011;20(1):146-157.
17. American College of Surgeons. User Guide for the 2012 ACS NSQIP Participant Use Data File. https://www.facs.org/~/media/files/quality%20programs/nsqip/ug12.ashx. Published October 2013. Accessed June 21, 2015.
18. Khuri SF, Henderson WG, Daley J, et al; Principal Investigators of Patient Safety in Surgery Study. Successful implementation of the Department of Veterans Affairs’ National Surgical Quality Improvement Program in the private sector: the Patient Safety in Surgery study. Ann Surg. 2008;248(2):329-336.
19. Ricchetti ET, Abboud JA, Kuntz AF, Ramsey ML, Glaser DL, Williams GR Jr. Total shoulder arthroplasty in older patients: increased perioperative morbidity? Clin Orthop Relat Res. 2011;469(4):1042-1049.
20. Marchant MH Jr, Viens NA, Cook C, Vail TP, Bolognesi MP. The impact of glycemic control and diabetes mellitus on perioperative outcomes after total joint arthroplasty. J Bone Joint Surg Am. 2009;91(7):1621-1629.
21. Schairer WW, Sing DC, Vail TP, Bozic KJ. Causes and frequency of unplanned hospital readmission after total hip arthroplasty. Clin Orthop Relat Res. 2014;472(2):464-470.
22. Vorhies JS, Wang Y, Herndon J, Maloney WJ, Huddleston JI. Readmission and length of stay after total hip arthroplasty in a national Medicare sample. J Arthroplasty. 2011;26(6 suppl):119-123.
23. Lovecchio F, Hsu WK, Smith TR, Cybulski G, Kim B, Kim JY. Predictors of thirty-day readmission after anterior cervical fusion. Spine. 2014;39(2):127-133.
Use of a Topical Thrombin-Based Hemostatic Agent in Shoulder Arthroplasty
Shoulder arthroplasty can be associated with significant perioperative blood loss, with the overall rate of postoperative allogeneic blood transfusion ranging from 7.4% to 43%.1-6 Blood transfusions are associated with a range of health risks.7 Soft-tissue dissection and cutting and reaming of bone surfaces can be sources of significant blood loss. Directly visualized sources of bleeding can be addressed using standard surgical hemostasis, including electrocautery, suture ligation, compression, and careful avoidance of vascular structures. However, difficult-to-visualize areas and bony sources of bleeding are more difficult to manage.
Numerous products for mitigating perioperative blood loss are commercially available. Topical hemostatic agents have been used in many surgical specialties, including orthopedic surgery, cardiothoracic surgery, neurosurgery, vascular surgery, and general surgery.8-10 In orthopedic surgery, use of topical thrombin- and fibrin-based products as hemostatic agents has been studied in knee and hip arthroplasty, with varying results.11-14 Early studies have shown reduced blood loss and postoperative transfusion rates with use of a fibrin sealant or fibrin tissue adhesive,11,12,15 whereas others have shown no significant benefit of using these hemostatic agents. Massin and colleagues14 found no difference in blood loss in the setting of total knee arthroplasty (TKA) with use of a fibrin sealant. In a 2012 prospective study, Kim and colleagues13 also showed no significant reduction in blood loss in patients treated with a topical thrombin-based hemostatic agent in TKA.
Surgiflo (Ethicon) is a hemostatic matrix that is combined with a topical human thrombin solution before sterile application. The matrix consists of an absorbable porcine gelatin powder that provides a structure for platelet adhesion and aggregation.16 When used in combination with thrombin, it aids in fibrin clot formation, leading to hemostasis of oozing blood and minor bleeding from small capillaries and venules. According to the manufacturer’s data, it can halt bleeding in less than 2 minutes and retains its efficacy for up to 8 hours.
To our knowledge, there are no reports of studies on use of topical fibrin- or thrombin-based hemostatic agents in shoulder arthroplasty. We conducted a study to investigate perioperative blood loss, transfusion rates, and complications during the hospital stays of patients who underwent shoulder arthroplasty and were treated with or without the Surgiflo topical hemostatic agent. Our hypothesis was that patients intraoperatively treated with this agent would have significantly less perioperative blood loss and lower transfusion rates without increased rates of in-hospital complications.
Patients and Methods
We retrospectively reviewed data from 211 consecutive shoulder arthroplasties performed by Dr. J. Michael Wiater between December 2012 and August 2013. All primary and revision anatomical and reverse total shoulder arthroplasty (TSA) procedures were included. Patients with a preoperative diagnosis of acute fracture, and patients with a diagnosis of any type of blood diathesis, including anemia and platelet disorders that lead to excessive clotting or bleeding, were excluded. Patients treated between May 2013 and August 2013 had the hemostatic matrix applied to the soft tissues before final wound closure. Chart review for any exclusion criteria left 102 patients in the experimental (hemostatic agent) group and 98 patients in the control group.
For all patients, any anticoagulation or anti-inflammatory medication was discontinued 1 week before the elective arthroplasty. An interscalene regional block combined with general anesthesia was used in all cases. All procedures were performed through a standard anterior deltopectoral approach. Patients in the experimental group had 10 mL of the hemostatic agent topically applied to the soft tissues of the wound before closure. Half the mixture (5 mL) was applied to the deep tissues of the axillary recess, subacromial, and joint spaces, and the other half was applied superficially after closure of the deltopectoral interval. A medium Hemovac (Zimmer) drain was used in all cases, with 1 tubing placed in the deep space and another between the deltoid and the skin, both draining to a single drain evacuator.
After surgery, all patients received deep venous thrombosis (DVT) prophylaxis consisting of 5000 units of subcutaneous unfractionated heparin every 8 hours until discharge, and then aspirin 325 mg twice daily for 2 weeks after discharge unless contraindicated. Any long-term anticoagulation therapy discontinued before surgery was resumed on postoperative day 2 (POD 2). All drains were removed on POD 2 unless they had more than 50 mL of output over an 8-hour period. Complete blood cell counts were collected for all patients before surgery and on PODs 1 and 2. Whether to transfuse blood was based on clinical judgment of severe or symptomatic acute blood loss anemia; however, no strict predetermined criteria were followed.
Patient electronic medical records were reviewed for demographic information, including age, sex, height, weight, comorbidities, American Society of Anesthesiologists (ASA) physical status, and preoperative anticoagulation use. Anesthesia records were reviewed for intraoperative estimated blood loss (EBL) and intraoperative autologous blood return (Cell Saver, Haemonetics). Patient laboratory results were reviewed for preoperative and postoperative hemoglobin (Hb) and hematocrit levels. Electronic medical records were also reviewed for incidence of transfusion and any major or minor complications occurring within 90 days of the procedure. All data were collected and reviewed under the approval of the human investigations committee at our institution.
Hemoglobin loss and hidden blood loss (HBL) were calculated as described by Good and colleagues.17 Total Hb loss was estimated using the total blood volume formula described by Nadler and colleagues.18 Difference between preoperative Hb level and final Hb level recorded during hospital stay was corrected for units of blood transfused (estimate, 52 g of Hb per unit). Hemoglobin loss was then used to calculate total blood loss, and total drain output was added to total blood loss to determine HBL. These formulas were used:
Hbloss = Blood Volume (L) × [Hbinitial (g/L) – Hbfinal (g/L)] + Hbtransfused
Total Blood Loss (mL) = 1000 × Hbloss/Hbinitial
HBL (mL) = Total Blood Loss (mL) + Total Drain Output (mL)
All statistical analyses were performed using SPSS Statistics Version 20 (IBM). A Shapiro-Wilk test was used to test for normality. All variables collected were compared between the experimental and control cohorts. For continuous variables, independent t test was used to compare normal data, and the Mann-Whitney rank sum test was used for non-normal data. Categorical variables were compared with the Fisher exact test for 2×2 tables and with the χ2 test for larger tables. In all tests, P < .05 was considered statistically significant.
Results
The experimental and control cohorts were demographically similar with respect to age, sex, body mass index (BMI), ASA status, and home anticoagulation treatment (Table 1). Patients who received preoperative anticoagulation therapy were evenly distributed between the 2 patient groups (P = .745). Thirty-five patients in the experimental group and 39 in the control group were taking aspirin. In addition, in the experimental group, 5 patients were taking warfarin, 4 clopidogrel, 1 dabigatran, and 1 prasugrel. In the control group, 6 patients were taking warfarin, 3 clopidogrel, 2 dabigatran, and 1 rivaroxaban. Type of arthroplasty (primary anatomical, primary reverse, revision shoulder arthroplasty) was also evenly distributed (P = .256), and operative time did not vary significantly between cohorts (P = .518).
Markers of operative blood loss were also compared between patient groups (Table 2). There was no significant difference in intraoperative EBL or cell saver volume between cohorts (Ps = .301 and .800). Drain output on PODs 1 and 2 did not differ between cohorts (Ps = .789 and .777); the same was true for total postoperative drain output (P = .906). Hemoglobin levels did vary significantly between groups before surgery (P = .002) and on PODs 1 and 2 (Ps = .027 and .005), with the experimental group having a lower mean Hb level at each time point. Mean Hb loss, however, did not vary significantly (P = .253). There was also no difference in HBL between cohorts (P = .601), the calculation of which accounts for patient height and weight, Hb loss, and transfusions. The incidence of transfusion was 25% in the experimental group and 20% in the control group—not a statistically significant difference (P = .407). Mean (SD) number of transfused units of packed red blood cells was 0.54 (1.05) in the experimental group and 0.40 (0.91) in the control group—again, not a statistically significant difference (P = .377).
Preoperative Hb level under 13 g/dL has been reported as a risk factor for transfusion after surgery.19 To account for the significantly lower Hb level in the experimental group, we examined the incidence of transfusion in patients with preoperative Hb levels above and below this cutoff. Among patients with preoperative Hb levels under 13 g/dL, transfusion incidence was 45.8% (experimental group) and 42.9% (control group) (P > .99); among those with preoperative Hb levels above 13 g/dL, transfusion incidence was 7.7% (experimental) and 11.1% (control) (P = .760).
To account for reportedly higher blood loss and transfusion rates in revision cases,1,2,20 we stratified our data by primary and revision cases, comparing them within the entire patient cohort and comparing the experimental and control groups within these subsets. Tables 3 and 4 list the results. Revision cases had more EBL (P < .001), autologous blood return (P < .001), drain output on POD 1 (P = .025), and total drain output (P = .002). There was no significant difference in transfusion rate between primary (22.2%) and revision (27.3%) cases (P = .505) or when the experimental and control groups were compared within primary and revision subsets. Among primary cases, transfusion rates were 23% (experimental) and 21.2% (control) (P = .853); among revision cases, rates were 35% (experimental) and 15% (control) (P = .263). Revisions showed a significant (P = .043) difference in HBL between the experimental and control groups, with more blood loss in the experimental group. EBL and autologous blood return were equivocal. Hb levels and drain outputs were statistically different only for POD 2, but there was no difference between overall Hb loss or total drain outputs. Among primary cases, no parameters of blood loss were statistically significantly different. The significantly lower preoperative and postoperative Hb levels were again seen in the experimental group.
The groups’ complication rates were comparable, and there was no significant risk associated with use of the hemostatic agent (P = .764). In each group, there were no complications that would be of particular concern with use of this agent. These complications included wound complications, deep prosthesis infection, and systemic thromboembolic disease (eg, myocardial infarction, stroke, DVT, pulmonary embolus). Nine patients (5 control, 4 experimental) had minor medical complications, and 2 (1 control, 1 experimental) had major medical complications. The control group’s 5 minor medical complications were acute kidney infection treated with antibiotics (1 patient), persistent urinary retention requiring Foley catheter for short period after discharge (1), minor upper gastrointestinal bleed treated medically (1), recalcitrant tachycardia in setting of chronic atrial fibrillation (1), and vasovagal syncope with no identified cardiovascular cause or periprosthetic complication (1); the control patient with the major medical complication died 2 weeks after surgery, after discharge to the inpatient rehabilitation unit. This death was secondary to pneumonia, sepsis, and eventual multisystem organ failure. The experimental group’s 4 minor medical complications were urinary retention requiring catheterization for short period (1 patient), urinary tract infections diagnosed 2 weeks after surgery and treated with antibiotics (2), and new-onset atrial fibrillation treated medically (1); the experimental patient with the major medical complication developed Takotsubo cardiomyopathy, a nonischemic stress-induced weakening of the myocardium requiring medical management. An experimental patient also had reverse TSA shoulder dislocation 12 days after surgery—thought to be caused by inadequate soft-tissue tension and unrelated to hemostatic agent use. The patient was returned to the operating room for polyethylene liner exchange and metallic spacer implantation.
Discussion
Reported rates of transfusion after shoulder arthroplasty have ranged from 7.4% to 43%, when including revision and reverse TSAs.2,3 In the present study, the overall transfusion rate was 23% (includes patients who underwent primary or revision shoulder arthroplasties with anatomical or reverse prostheses). Although the risk for complications is low, serious issues may arise with blood transfusions. Allogeneic blood transfusions can cause fluid overload, allergic reactions, fever, acute immune hemolytic reaction, transfusion-related acute lung injury (TRALI), bloodborne infections, and formation of antibodies complicating any future need for transfusions.7 According to the National Heart, Lung, and Blood Institute, the chances of becoming infected from transfusion are 1 in 2 million for the hepatitis C and human immunodeficiency viruses and 1 in 205,000 for the hepatitis B virus.7 Some studies have also found higher rates of infection after hip or knee arthroplasty in patients who received allogeneic blood transfusions.21,22 In addition, for hospitals, transfusion costs are significant. One study showed that direct and indirect overhead costs amounted to $522 to $1183 per red blood cell unit.23 Given the risks and costs associated with blood transfusions, use of an effective intraoperative blood loss management agent could be beneficial in the setting of shoulder arthroplasty.
The use and efficacy of intraoperative blood management agents remain controversial. Numerous agents for managing perioperative blood loss are commercially available. Previous clinical studies have shown variable results with use of topical hemostatic agents, but not in the setting of shoulder arthroplasty.24 In 1999, Levy and colleagues11 showed that use of fibrin tissue adhesive reduced blood loss and postoperative transfusion rates in patients who underwent TKA. In 2001, Wang and colleagues15 showed that using a fibrin sealant in TKA reduced bloody drainage and maintained higher Hb levels. In 2003, the same group showed that use of fibrin sealant also reduced perioperative blood loss in total hip arthroplasty.12 More recent studies have had contradicting results,13,14 similar to ours. A 2012 prospective study failed to show any significant difference in blood loss after TKA in patients treated with a topical thrombin-based hemostatic agent.13 The authors did find significantly higher Hb values in the treated group on PODs 1 and 2, though the drain outputs and transfusion rates did not differ.
To our knowledge, the present study is the first to evaluate use of a topical hemostatic agent during shoulder arthroplasty. We did not find a significant difference in perioperative blood loss with application of Surgiflo, a topical thrombin-based hemostatic agent. Interestingly, we found that Hb levels both before surgery and on PODs 1 and 2 were significantly lower in the experimental group. However, the difference was about 0.7 g/dL, which would not be clinically significant. The lower Hb levels on PODs 1 and 2 likely resulted from lower preoperative levels.
Other studies have found higher transfusion rates for revision versus primary shoulder arthroplasty.1,2,20 In our series, EBL, autologous blood return, and drain output were higher overall for revision versus primary cases. When we stratified by primary and revision cases, we could not detect a difference in transfusion rates between the experimental and control groups. The lack of significant difference in the revision group could be caused by low statistical power, as the control group had only 13 revision cases. Having more patients in the study may have revealed a larger difference in blood loss with use of the hemostatic agent in revision cases.
We also found no significant increase in adverse events related to use of the hemostatic agent. Complications of particular concern would include wound complications, deep prosthesis infection, and systemic thromboembolic disease (eg, myocardial infarction, stroke, DVT, pulmonary embolus). There were no statistical differences in major and minor complications between the groups and no identifiable complications related to the hemostatic agent used.
Our results should be viewed in light of study limitations. First, with this retrospective study, we relied heavily on the accuracy of computer-based patient documentation. In addition, blood loss estimates are imperfect regardless of measurement technique. Intraoperative EBL is often determined by the surgeon and is highly variable, and autologous blood collection does not account for blood lost in operative sponges, instruments, and irrigation. To minimize this issue, we tried to assess perioperative blood loss through multiple data points, including intraoperative EBL, autologous blood returned during surgery, drain output, transfusion rates, and HBL calculations. Also, blood transfusion criteria depend on the physician’s clinical assessment and decision making, as well as patient condition, which could certainly add variability to the transfusion rate between groups. Another limitation is that the procedures studied were not homogeneous, and including primary and revision anatomical and reverse shoulder arthroplasties may have added variability to the results. In this single-surgeon study, however, we were able to ensure that the same standard techniques and hemostasis were applied in all procedures. Last, given the relatively small sample used, more patients may be needed to reveal a significant and clinically relevant difference in blood loss.
Conclusion
Perioperative blood loss poses serious risks to patient health. In light of the varying findings in the literature and the cost of transfusions and blood loss management products, use of these hemostatic agents remains controversial. In the present study, we found no significant difference in perioperative blood loss or transfusion rates with use of a hemostatic agent during shoulder arthroplasty. Therefore, we cannot conclude that this agent is effective for blood loss management in shoulder arthroplasty. Highly powered prospective studies are needed to confirm our findings.
1. Millett PJ, Porramatikul M, Chen N, Zurakowski D, Warner JJ. Analysis of transfusion predictors in shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(6):1223-1230.
2. Hardy JC, Hung M, Snow BJ, et al. Blood transfusion associated with shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(2):233-239.
3. Gruson KI, Accousti KJ, Parsons BO, Pillai G, Flatow EL. Transfusion after shoulder arthroplasty: an analysis of rates and risk factors. J Shoulder Elbow Surg. 2009;18(2):225-230.
4. Schumer RA, Chae JS, Markert RJ, Sprott D, Crosby LA. Predicting transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):91-96.
5. Sperling JW, Duncan SF, Cofield RH, Schleck CD, Harmsen WS. Incidence and risk factors for blood transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(6):599-601.
6. Ahmadi S, Lawrence TM, Sahota S, et al. The incidence and risk factors for blood transfusion in revision shoulder arthroplasty: our institution’s experience and review of the literature. J Shoulder Elbow Surg. 2014;23(1):43-48.
7. National Heart, Lung, and Blood Institute. What are the risks of a blood transfusion? http://www.nhlbi.nih.gov/health/health-topics/topics/bt/risks.html. Published January 30, 2012. Accessed June 24, 2015.
8. Bracale U, Rovani M, Picardo A, et al. Beneficial effects of fibrin glue (Quixil) versus Lichtenstein conventional technique in inguinal hernia repair: a randomized clinical trial. Hernia. 2014;18(2):185-192.
9. Gazzeri R, Galarza M, Alfier A. Safety biocompatibility of gelatin hemostatic matrix (Floseal and Surgiflo) in neurosurgical procedures. Surg Technol Int. 2012;22:49-54.
10. Krishnan S, Conner TM, Leslie R, Stemkowski S, Shander A. Choice of hemostatic agent and hospital length of stay in cardiovascular surgery. Semin Cardiothorac Vasc Anesth. 2009;13(4):225-230.
11. Levy O, Martinowitz U, Oran A, Tauber C, Horoszowski H. The use of fibrin tissue adhesive to reduce blood loss and the need for blood transfusion after total knee arthroplasty. A prospective, randomized, multicenter study. J Bone Joint Surg Am. 1999;81(11):1580-1588.
12. Wang GJ, Goldthwaite CA Jr, Burks S, Crawford R, Spotnitz WD; Orthopaedic Investigators Group. Fibrin sealant reduces perioperative blood loss in total hip replacement. J Long Term Eff Med Implants. 2003;13(5):399-411.
13. Kim HJ, Fraser MR, Kahn B, Lyman S, Figgie MP. The efficacy of a thrombin-based hemostatic agent in unilateral total knee arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2012;94(13):1160-1165.
14. Massin P, Scemama C, Jeanrot C, Boyer P. Does fibrin sealant use in total knee replacement reduce transfusion rates? A non-randomised comparative study. Orthop Traumatol Surg Res. 2012;98(2):180-185.
15. Wang GJ, Hungerford DS, Savory CG, et al. Use of fibrin sealant to reduce bloody drainage and hemoglobin loss after total knee arthroplasty: a brief note on a randomized prospective trial. J Bone Joint Surg Am. 2001;83(10):1503-1505.
16. Surgiflo Hemostatic Matrix Kit [package insert]. Somerville, NJ: Ethicon; 2012.
17. Good L, Peterson E, Lisander B. Tranexamic acid decreases external blood loss but not hidden blood loss in total knee replacement. Br J Anaesth. 2003;90(5):596-599.
18. Nadler SB, Hidalgo JH, Bloch T. Prediction of blood volume in normal human adults. Surgery. 1962;51(2):224-232.
19. Faris PM, Spence RK, Larholt KM, Sampson AR, Frei D. The predictive power of baseline hemoglobin for transfusion risk in surgery patients. Orthopedics. 1999;22(1 suppl):s135-s140.
20. Saltzman BM, Chalmers PN, Gupta AK, Romeo AA, Nicholson GP. Complication rates comparing primary with revision reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(11):1647-1654.
21. Murphy P, Heal JM, Blumberg N. Infection or suspected infection after hip replacement surgery with autologous or homologous blood transfusions. Transfusion. 1991;31(3):212-217.
22. Thomas D, Wareham K, Cohen D, Hutchings H. Autologous blood transfusion in total knee replacement surgery. Br J Anaesth. 2001;86(5):669-673.
23. Shander A, Hofmann A, Ozawa S, Theusinger OM, Gombotz H, Spahn DR. Activity-based costs of blood transfusions in surgical patients at four hospitals. Transfusion. 2010;50(4):753-765.
24. Thoms RJ, Marwin SE. The role of fibrin sealants in orthopaedic surgery. J Am Acad Orthop Surg. 2009;17(12):727-736.
Shoulder arthroplasty can be associated with significant perioperative blood loss, with the overall rate of postoperative allogeneic blood transfusion ranging from 7.4% to 43%.1-6 Blood transfusions are associated with a range of health risks.7 Soft-tissue dissection and cutting and reaming of bone surfaces can be sources of significant blood loss. Directly visualized sources of bleeding can be addressed using standard surgical hemostasis, including electrocautery, suture ligation, compression, and careful avoidance of vascular structures. However, difficult-to-visualize areas and bony sources of bleeding are more difficult to manage.
Numerous products for mitigating perioperative blood loss are commercially available. Topical hemostatic agents have been used in many surgical specialties, including orthopedic surgery, cardiothoracic surgery, neurosurgery, vascular surgery, and general surgery.8-10 In orthopedic surgery, use of topical thrombin- and fibrin-based products as hemostatic agents has been studied in knee and hip arthroplasty, with varying results.11-14 Early studies have shown reduced blood loss and postoperative transfusion rates with use of a fibrin sealant or fibrin tissue adhesive,11,12,15 whereas others have shown no significant benefit of using these hemostatic agents. Massin and colleagues14 found no difference in blood loss in the setting of total knee arthroplasty (TKA) with use of a fibrin sealant. In a 2012 prospective study, Kim and colleagues13 also showed no significant reduction in blood loss in patients treated with a topical thrombin-based hemostatic agent in TKA.
Surgiflo (Ethicon) is a hemostatic matrix that is combined with a topical human thrombin solution before sterile application. The matrix consists of an absorbable porcine gelatin powder that provides a structure for platelet adhesion and aggregation.16 When used in combination with thrombin, it aids in fibrin clot formation, leading to hemostasis of oozing blood and minor bleeding from small capillaries and venules. According to the manufacturer’s data, it can halt bleeding in less than 2 minutes and retains its efficacy for up to 8 hours.
To our knowledge, there are no reports of studies on use of topical fibrin- or thrombin-based hemostatic agents in shoulder arthroplasty. We conducted a study to investigate perioperative blood loss, transfusion rates, and complications during the hospital stays of patients who underwent shoulder arthroplasty and were treated with or without the Surgiflo topical hemostatic agent. Our hypothesis was that patients intraoperatively treated with this agent would have significantly less perioperative blood loss and lower transfusion rates without increased rates of in-hospital complications.
Patients and Methods
We retrospectively reviewed data from 211 consecutive shoulder arthroplasties performed by Dr. J. Michael Wiater between December 2012 and August 2013. All primary and revision anatomical and reverse total shoulder arthroplasty (TSA) procedures were included. Patients with a preoperative diagnosis of acute fracture, and patients with a diagnosis of any type of blood diathesis, including anemia and platelet disorders that lead to excessive clotting or bleeding, were excluded. Patients treated between May 2013 and August 2013 had the hemostatic matrix applied to the soft tissues before final wound closure. Chart review for any exclusion criteria left 102 patients in the experimental (hemostatic agent) group and 98 patients in the control group.
For all patients, any anticoagulation or anti-inflammatory medication was discontinued 1 week before the elective arthroplasty. An interscalene regional block combined with general anesthesia was used in all cases. All procedures were performed through a standard anterior deltopectoral approach. Patients in the experimental group had 10 mL of the hemostatic agent topically applied to the soft tissues of the wound before closure. Half the mixture (5 mL) was applied to the deep tissues of the axillary recess, subacromial, and joint spaces, and the other half was applied superficially after closure of the deltopectoral interval. A medium Hemovac (Zimmer) drain was used in all cases, with 1 tubing placed in the deep space and another between the deltoid and the skin, both draining to a single drain evacuator.
After surgery, all patients received deep venous thrombosis (DVT) prophylaxis consisting of 5000 units of subcutaneous unfractionated heparin every 8 hours until discharge, and then aspirin 325 mg twice daily for 2 weeks after discharge unless contraindicated. Any long-term anticoagulation therapy discontinued before surgery was resumed on postoperative day 2 (POD 2). All drains were removed on POD 2 unless they had more than 50 mL of output over an 8-hour period. Complete blood cell counts were collected for all patients before surgery and on PODs 1 and 2. Whether to transfuse blood was based on clinical judgment of severe or symptomatic acute blood loss anemia; however, no strict predetermined criteria were followed.
Patient electronic medical records were reviewed for demographic information, including age, sex, height, weight, comorbidities, American Society of Anesthesiologists (ASA) physical status, and preoperative anticoagulation use. Anesthesia records were reviewed for intraoperative estimated blood loss (EBL) and intraoperative autologous blood return (Cell Saver, Haemonetics). Patient laboratory results were reviewed for preoperative and postoperative hemoglobin (Hb) and hematocrit levels. Electronic medical records were also reviewed for incidence of transfusion and any major or minor complications occurring within 90 days of the procedure. All data were collected and reviewed under the approval of the human investigations committee at our institution.
Hemoglobin loss and hidden blood loss (HBL) were calculated as described by Good and colleagues.17 Total Hb loss was estimated using the total blood volume formula described by Nadler and colleagues.18 Difference between preoperative Hb level and final Hb level recorded during hospital stay was corrected for units of blood transfused (estimate, 52 g of Hb per unit). Hemoglobin loss was then used to calculate total blood loss, and total drain output was added to total blood loss to determine HBL. These formulas were used:
Hbloss = Blood Volume (L) × [Hbinitial (g/L) – Hbfinal (g/L)] + Hbtransfused
Total Blood Loss (mL) = 1000 × Hbloss/Hbinitial
HBL (mL) = Total Blood Loss (mL) + Total Drain Output (mL)
All statistical analyses were performed using SPSS Statistics Version 20 (IBM). A Shapiro-Wilk test was used to test for normality. All variables collected were compared between the experimental and control cohorts. For continuous variables, independent t test was used to compare normal data, and the Mann-Whitney rank sum test was used for non-normal data. Categorical variables were compared with the Fisher exact test for 2×2 tables and with the χ2 test for larger tables. In all tests, P < .05 was considered statistically significant.
Results
The experimental and control cohorts were demographically similar with respect to age, sex, body mass index (BMI), ASA status, and home anticoagulation treatment (Table 1). Patients who received preoperative anticoagulation therapy were evenly distributed between the 2 patient groups (P = .745). Thirty-five patients in the experimental group and 39 in the control group were taking aspirin. In addition, in the experimental group, 5 patients were taking warfarin, 4 clopidogrel, 1 dabigatran, and 1 prasugrel. In the control group, 6 patients were taking warfarin, 3 clopidogrel, 2 dabigatran, and 1 rivaroxaban. Type of arthroplasty (primary anatomical, primary reverse, revision shoulder arthroplasty) was also evenly distributed (P = .256), and operative time did not vary significantly between cohorts (P = .518).
Markers of operative blood loss were also compared between patient groups (Table 2). There was no significant difference in intraoperative EBL or cell saver volume between cohorts (Ps = .301 and .800). Drain output on PODs 1 and 2 did not differ between cohorts (Ps = .789 and .777); the same was true for total postoperative drain output (P = .906). Hemoglobin levels did vary significantly between groups before surgery (P = .002) and on PODs 1 and 2 (Ps = .027 and .005), with the experimental group having a lower mean Hb level at each time point. Mean Hb loss, however, did not vary significantly (P = .253). There was also no difference in HBL between cohorts (P = .601), the calculation of which accounts for patient height and weight, Hb loss, and transfusions. The incidence of transfusion was 25% in the experimental group and 20% in the control group—not a statistically significant difference (P = .407). Mean (SD) number of transfused units of packed red blood cells was 0.54 (1.05) in the experimental group and 0.40 (0.91) in the control group—again, not a statistically significant difference (P = .377).
Preoperative Hb level under 13 g/dL has been reported as a risk factor for transfusion after surgery.19 To account for the significantly lower Hb level in the experimental group, we examined the incidence of transfusion in patients with preoperative Hb levels above and below this cutoff. Among patients with preoperative Hb levels under 13 g/dL, transfusion incidence was 45.8% (experimental group) and 42.9% (control group) (P > .99); among those with preoperative Hb levels above 13 g/dL, transfusion incidence was 7.7% (experimental) and 11.1% (control) (P = .760).
To account for reportedly higher blood loss and transfusion rates in revision cases,1,2,20 we stratified our data by primary and revision cases, comparing them within the entire patient cohort and comparing the experimental and control groups within these subsets. Tables 3 and 4 list the results. Revision cases had more EBL (P < .001), autologous blood return (P < .001), drain output on POD 1 (P = .025), and total drain output (P = .002). There was no significant difference in transfusion rate between primary (22.2%) and revision (27.3%) cases (P = .505) or when the experimental and control groups were compared within primary and revision subsets. Among primary cases, transfusion rates were 23% (experimental) and 21.2% (control) (P = .853); among revision cases, rates were 35% (experimental) and 15% (control) (P = .263). Revisions showed a significant (P = .043) difference in HBL between the experimental and control groups, with more blood loss in the experimental group. EBL and autologous blood return were equivocal. Hb levels and drain outputs were statistically different only for POD 2, but there was no difference between overall Hb loss or total drain outputs. Among primary cases, no parameters of blood loss were statistically significantly different. The significantly lower preoperative and postoperative Hb levels were again seen in the experimental group.
The groups’ complication rates were comparable, and there was no significant risk associated with use of the hemostatic agent (P = .764). In each group, there were no complications that would be of particular concern with use of this agent. These complications included wound complications, deep prosthesis infection, and systemic thromboembolic disease (eg, myocardial infarction, stroke, DVT, pulmonary embolus). Nine patients (5 control, 4 experimental) had minor medical complications, and 2 (1 control, 1 experimental) had major medical complications. The control group’s 5 minor medical complications were acute kidney infection treated with antibiotics (1 patient), persistent urinary retention requiring Foley catheter for short period after discharge (1), minor upper gastrointestinal bleed treated medically (1), recalcitrant tachycardia in setting of chronic atrial fibrillation (1), and vasovagal syncope with no identified cardiovascular cause or periprosthetic complication (1); the control patient with the major medical complication died 2 weeks after surgery, after discharge to the inpatient rehabilitation unit. This death was secondary to pneumonia, sepsis, and eventual multisystem organ failure. The experimental group’s 4 minor medical complications were urinary retention requiring catheterization for short period (1 patient), urinary tract infections diagnosed 2 weeks after surgery and treated with antibiotics (2), and new-onset atrial fibrillation treated medically (1); the experimental patient with the major medical complication developed Takotsubo cardiomyopathy, a nonischemic stress-induced weakening of the myocardium requiring medical management. An experimental patient also had reverse TSA shoulder dislocation 12 days after surgery—thought to be caused by inadequate soft-tissue tension and unrelated to hemostatic agent use. The patient was returned to the operating room for polyethylene liner exchange and metallic spacer implantation.
Discussion
Reported rates of transfusion after shoulder arthroplasty have ranged from 7.4% to 43%, when including revision and reverse TSAs.2,3 In the present study, the overall transfusion rate was 23% (includes patients who underwent primary or revision shoulder arthroplasties with anatomical or reverse prostheses). Although the risk for complications is low, serious issues may arise with blood transfusions. Allogeneic blood transfusions can cause fluid overload, allergic reactions, fever, acute immune hemolytic reaction, transfusion-related acute lung injury (TRALI), bloodborne infections, and formation of antibodies complicating any future need for transfusions.7 According to the National Heart, Lung, and Blood Institute, the chances of becoming infected from transfusion are 1 in 2 million for the hepatitis C and human immunodeficiency viruses and 1 in 205,000 for the hepatitis B virus.7 Some studies have also found higher rates of infection after hip or knee arthroplasty in patients who received allogeneic blood transfusions.21,22 In addition, for hospitals, transfusion costs are significant. One study showed that direct and indirect overhead costs amounted to $522 to $1183 per red blood cell unit.23 Given the risks and costs associated with blood transfusions, use of an effective intraoperative blood loss management agent could be beneficial in the setting of shoulder arthroplasty.
The use and efficacy of intraoperative blood management agents remain controversial. Numerous agents for managing perioperative blood loss are commercially available. Previous clinical studies have shown variable results with use of topical hemostatic agents, but not in the setting of shoulder arthroplasty.24 In 1999, Levy and colleagues11 showed that use of fibrin tissue adhesive reduced blood loss and postoperative transfusion rates in patients who underwent TKA. In 2001, Wang and colleagues15 showed that using a fibrin sealant in TKA reduced bloody drainage and maintained higher Hb levels. In 2003, the same group showed that use of fibrin sealant also reduced perioperative blood loss in total hip arthroplasty.12 More recent studies have had contradicting results,13,14 similar to ours. A 2012 prospective study failed to show any significant difference in blood loss after TKA in patients treated with a topical thrombin-based hemostatic agent.13 The authors did find significantly higher Hb values in the treated group on PODs 1 and 2, though the drain outputs and transfusion rates did not differ.
To our knowledge, the present study is the first to evaluate use of a topical hemostatic agent during shoulder arthroplasty. We did not find a significant difference in perioperative blood loss with application of Surgiflo, a topical thrombin-based hemostatic agent. Interestingly, we found that Hb levels both before surgery and on PODs 1 and 2 were significantly lower in the experimental group. However, the difference was about 0.7 g/dL, which would not be clinically significant. The lower Hb levels on PODs 1 and 2 likely resulted from lower preoperative levels.
Other studies have found higher transfusion rates for revision versus primary shoulder arthroplasty.1,2,20 In our series, EBL, autologous blood return, and drain output were higher overall for revision versus primary cases. When we stratified by primary and revision cases, we could not detect a difference in transfusion rates between the experimental and control groups. The lack of significant difference in the revision group could be caused by low statistical power, as the control group had only 13 revision cases. Having more patients in the study may have revealed a larger difference in blood loss with use of the hemostatic agent in revision cases.
We also found no significant increase in adverse events related to use of the hemostatic agent. Complications of particular concern would include wound complications, deep prosthesis infection, and systemic thromboembolic disease (eg, myocardial infarction, stroke, DVT, pulmonary embolus). There were no statistical differences in major and minor complications between the groups and no identifiable complications related to the hemostatic agent used.
Our results should be viewed in light of study limitations. First, with this retrospective study, we relied heavily on the accuracy of computer-based patient documentation. In addition, blood loss estimates are imperfect regardless of measurement technique. Intraoperative EBL is often determined by the surgeon and is highly variable, and autologous blood collection does not account for blood lost in operative sponges, instruments, and irrigation. To minimize this issue, we tried to assess perioperative blood loss through multiple data points, including intraoperative EBL, autologous blood returned during surgery, drain output, transfusion rates, and HBL calculations. Also, blood transfusion criteria depend on the physician’s clinical assessment and decision making, as well as patient condition, which could certainly add variability to the transfusion rate between groups. Another limitation is that the procedures studied were not homogeneous, and including primary and revision anatomical and reverse shoulder arthroplasties may have added variability to the results. In this single-surgeon study, however, we were able to ensure that the same standard techniques and hemostasis were applied in all procedures. Last, given the relatively small sample used, more patients may be needed to reveal a significant and clinically relevant difference in blood loss.
Conclusion
Perioperative blood loss poses serious risks to patient health. In light of the varying findings in the literature and the cost of transfusions and blood loss management products, use of these hemostatic agents remains controversial. In the present study, we found no significant difference in perioperative blood loss or transfusion rates with use of a hemostatic agent during shoulder arthroplasty. Therefore, we cannot conclude that this agent is effective for blood loss management in shoulder arthroplasty. Highly powered prospective studies are needed to confirm our findings.
Shoulder arthroplasty can be associated with significant perioperative blood loss, with the overall rate of postoperative allogeneic blood transfusion ranging from 7.4% to 43%.1-6 Blood transfusions are associated with a range of health risks.7 Soft-tissue dissection and cutting and reaming of bone surfaces can be sources of significant blood loss. Directly visualized sources of bleeding can be addressed using standard surgical hemostasis, including electrocautery, suture ligation, compression, and careful avoidance of vascular structures. However, difficult-to-visualize areas and bony sources of bleeding are more difficult to manage.
Numerous products for mitigating perioperative blood loss are commercially available. Topical hemostatic agents have been used in many surgical specialties, including orthopedic surgery, cardiothoracic surgery, neurosurgery, vascular surgery, and general surgery.8-10 In orthopedic surgery, use of topical thrombin- and fibrin-based products as hemostatic agents has been studied in knee and hip arthroplasty, with varying results.11-14 Early studies have shown reduced blood loss and postoperative transfusion rates with use of a fibrin sealant or fibrin tissue adhesive,11,12,15 whereas others have shown no significant benefit of using these hemostatic agents. Massin and colleagues14 found no difference in blood loss in the setting of total knee arthroplasty (TKA) with use of a fibrin sealant. In a 2012 prospective study, Kim and colleagues13 also showed no significant reduction in blood loss in patients treated with a topical thrombin-based hemostatic agent in TKA.
Surgiflo (Ethicon) is a hemostatic matrix that is combined with a topical human thrombin solution before sterile application. The matrix consists of an absorbable porcine gelatin powder that provides a structure for platelet adhesion and aggregation.16 When used in combination with thrombin, it aids in fibrin clot formation, leading to hemostasis of oozing blood and minor bleeding from small capillaries and venules. According to the manufacturer’s data, it can halt bleeding in less than 2 minutes and retains its efficacy for up to 8 hours.
To our knowledge, there are no reports of studies on use of topical fibrin- or thrombin-based hemostatic agents in shoulder arthroplasty. We conducted a study to investigate perioperative blood loss, transfusion rates, and complications during the hospital stays of patients who underwent shoulder arthroplasty and were treated with or without the Surgiflo topical hemostatic agent. Our hypothesis was that patients intraoperatively treated with this agent would have significantly less perioperative blood loss and lower transfusion rates without increased rates of in-hospital complications.
Patients and Methods
We retrospectively reviewed data from 211 consecutive shoulder arthroplasties performed by Dr. J. Michael Wiater between December 2012 and August 2013. All primary and revision anatomical and reverse total shoulder arthroplasty (TSA) procedures were included. Patients with a preoperative diagnosis of acute fracture, and patients with a diagnosis of any type of blood diathesis, including anemia and platelet disorders that lead to excessive clotting or bleeding, were excluded. Patients treated between May 2013 and August 2013 had the hemostatic matrix applied to the soft tissues before final wound closure. Chart review for any exclusion criteria left 102 patients in the experimental (hemostatic agent) group and 98 patients in the control group.
For all patients, any anticoagulation or anti-inflammatory medication was discontinued 1 week before the elective arthroplasty. An interscalene regional block combined with general anesthesia was used in all cases. All procedures were performed through a standard anterior deltopectoral approach. Patients in the experimental group had 10 mL of the hemostatic agent topically applied to the soft tissues of the wound before closure. Half the mixture (5 mL) was applied to the deep tissues of the axillary recess, subacromial, and joint spaces, and the other half was applied superficially after closure of the deltopectoral interval. A medium Hemovac (Zimmer) drain was used in all cases, with 1 tubing placed in the deep space and another between the deltoid and the skin, both draining to a single drain evacuator.
After surgery, all patients received deep venous thrombosis (DVT) prophylaxis consisting of 5000 units of subcutaneous unfractionated heparin every 8 hours until discharge, and then aspirin 325 mg twice daily for 2 weeks after discharge unless contraindicated. Any long-term anticoagulation therapy discontinued before surgery was resumed on postoperative day 2 (POD 2). All drains were removed on POD 2 unless they had more than 50 mL of output over an 8-hour period. Complete blood cell counts were collected for all patients before surgery and on PODs 1 and 2. Whether to transfuse blood was based on clinical judgment of severe or symptomatic acute blood loss anemia; however, no strict predetermined criteria were followed.
Patient electronic medical records were reviewed for demographic information, including age, sex, height, weight, comorbidities, American Society of Anesthesiologists (ASA) physical status, and preoperative anticoagulation use. Anesthesia records were reviewed for intraoperative estimated blood loss (EBL) and intraoperative autologous blood return (Cell Saver, Haemonetics). Patient laboratory results were reviewed for preoperative and postoperative hemoglobin (Hb) and hematocrit levels. Electronic medical records were also reviewed for incidence of transfusion and any major or minor complications occurring within 90 days of the procedure. All data were collected and reviewed under the approval of the human investigations committee at our institution.
Hemoglobin loss and hidden blood loss (HBL) were calculated as described by Good and colleagues.17 Total Hb loss was estimated using the total blood volume formula described by Nadler and colleagues.18 Difference between preoperative Hb level and final Hb level recorded during hospital stay was corrected for units of blood transfused (estimate, 52 g of Hb per unit). Hemoglobin loss was then used to calculate total blood loss, and total drain output was added to total blood loss to determine HBL. These formulas were used:
Hbloss = Blood Volume (L) × [Hbinitial (g/L) – Hbfinal (g/L)] + Hbtransfused
Total Blood Loss (mL) = 1000 × Hbloss/Hbinitial
HBL (mL) = Total Blood Loss (mL) + Total Drain Output (mL)
All statistical analyses were performed using SPSS Statistics Version 20 (IBM). A Shapiro-Wilk test was used to test for normality. All variables collected were compared between the experimental and control cohorts. For continuous variables, independent t test was used to compare normal data, and the Mann-Whitney rank sum test was used for non-normal data. Categorical variables were compared with the Fisher exact test for 2×2 tables and with the χ2 test for larger tables. In all tests, P < .05 was considered statistically significant.
Results
The experimental and control cohorts were demographically similar with respect to age, sex, body mass index (BMI), ASA status, and home anticoagulation treatment (Table 1). Patients who received preoperative anticoagulation therapy were evenly distributed between the 2 patient groups (P = .745). Thirty-five patients in the experimental group and 39 in the control group were taking aspirin. In addition, in the experimental group, 5 patients were taking warfarin, 4 clopidogrel, 1 dabigatran, and 1 prasugrel. In the control group, 6 patients were taking warfarin, 3 clopidogrel, 2 dabigatran, and 1 rivaroxaban. Type of arthroplasty (primary anatomical, primary reverse, revision shoulder arthroplasty) was also evenly distributed (P = .256), and operative time did not vary significantly between cohorts (P = .518).
Markers of operative blood loss were also compared between patient groups (Table 2). There was no significant difference in intraoperative EBL or cell saver volume between cohorts (Ps = .301 and .800). Drain output on PODs 1 and 2 did not differ between cohorts (Ps = .789 and .777); the same was true for total postoperative drain output (P = .906). Hemoglobin levels did vary significantly between groups before surgery (P = .002) and on PODs 1 and 2 (Ps = .027 and .005), with the experimental group having a lower mean Hb level at each time point. Mean Hb loss, however, did not vary significantly (P = .253). There was also no difference in HBL between cohorts (P = .601), the calculation of which accounts for patient height and weight, Hb loss, and transfusions. The incidence of transfusion was 25% in the experimental group and 20% in the control group—not a statistically significant difference (P = .407). Mean (SD) number of transfused units of packed red blood cells was 0.54 (1.05) in the experimental group and 0.40 (0.91) in the control group—again, not a statistically significant difference (P = .377).
Preoperative Hb level under 13 g/dL has been reported as a risk factor for transfusion after surgery.19 To account for the significantly lower Hb level in the experimental group, we examined the incidence of transfusion in patients with preoperative Hb levels above and below this cutoff. Among patients with preoperative Hb levels under 13 g/dL, transfusion incidence was 45.8% (experimental group) and 42.9% (control group) (P > .99); among those with preoperative Hb levels above 13 g/dL, transfusion incidence was 7.7% (experimental) and 11.1% (control) (P = .760).
To account for reportedly higher blood loss and transfusion rates in revision cases,1,2,20 we stratified our data by primary and revision cases, comparing them within the entire patient cohort and comparing the experimental and control groups within these subsets. Tables 3 and 4 list the results. Revision cases had more EBL (P < .001), autologous blood return (P < .001), drain output on POD 1 (P = .025), and total drain output (P = .002). There was no significant difference in transfusion rate between primary (22.2%) and revision (27.3%) cases (P = .505) or when the experimental and control groups were compared within primary and revision subsets. Among primary cases, transfusion rates were 23% (experimental) and 21.2% (control) (P = .853); among revision cases, rates were 35% (experimental) and 15% (control) (P = .263). Revisions showed a significant (P = .043) difference in HBL between the experimental and control groups, with more blood loss in the experimental group. EBL and autologous blood return were equivocal. Hb levels and drain outputs were statistically different only for POD 2, but there was no difference between overall Hb loss or total drain outputs. Among primary cases, no parameters of blood loss were statistically significantly different. The significantly lower preoperative and postoperative Hb levels were again seen in the experimental group.
The groups’ complication rates were comparable, and there was no significant risk associated with use of the hemostatic agent (P = .764). In each group, there were no complications that would be of particular concern with use of this agent. These complications included wound complications, deep prosthesis infection, and systemic thromboembolic disease (eg, myocardial infarction, stroke, DVT, pulmonary embolus). Nine patients (5 control, 4 experimental) had minor medical complications, and 2 (1 control, 1 experimental) had major medical complications. The control group’s 5 minor medical complications were acute kidney infection treated with antibiotics (1 patient), persistent urinary retention requiring Foley catheter for short period after discharge (1), minor upper gastrointestinal bleed treated medically (1), recalcitrant tachycardia in setting of chronic atrial fibrillation (1), and vasovagal syncope with no identified cardiovascular cause or periprosthetic complication (1); the control patient with the major medical complication died 2 weeks after surgery, after discharge to the inpatient rehabilitation unit. This death was secondary to pneumonia, sepsis, and eventual multisystem organ failure. The experimental group’s 4 minor medical complications were urinary retention requiring catheterization for short period (1 patient), urinary tract infections diagnosed 2 weeks after surgery and treated with antibiotics (2), and new-onset atrial fibrillation treated medically (1); the experimental patient with the major medical complication developed Takotsubo cardiomyopathy, a nonischemic stress-induced weakening of the myocardium requiring medical management. An experimental patient also had reverse TSA shoulder dislocation 12 days after surgery—thought to be caused by inadequate soft-tissue tension and unrelated to hemostatic agent use. The patient was returned to the operating room for polyethylene liner exchange and metallic spacer implantation.
Discussion
Reported rates of transfusion after shoulder arthroplasty have ranged from 7.4% to 43%, when including revision and reverse TSAs.2,3 In the present study, the overall transfusion rate was 23% (includes patients who underwent primary or revision shoulder arthroplasties with anatomical or reverse prostheses). Although the risk for complications is low, serious issues may arise with blood transfusions. Allogeneic blood transfusions can cause fluid overload, allergic reactions, fever, acute immune hemolytic reaction, transfusion-related acute lung injury (TRALI), bloodborne infections, and formation of antibodies complicating any future need for transfusions.7 According to the National Heart, Lung, and Blood Institute, the chances of becoming infected from transfusion are 1 in 2 million for the hepatitis C and human immunodeficiency viruses and 1 in 205,000 for the hepatitis B virus.7 Some studies have also found higher rates of infection after hip or knee arthroplasty in patients who received allogeneic blood transfusions.21,22 In addition, for hospitals, transfusion costs are significant. One study showed that direct and indirect overhead costs amounted to $522 to $1183 per red blood cell unit.23 Given the risks and costs associated with blood transfusions, use of an effective intraoperative blood loss management agent could be beneficial in the setting of shoulder arthroplasty.
The use and efficacy of intraoperative blood management agents remain controversial. Numerous agents for managing perioperative blood loss are commercially available. Previous clinical studies have shown variable results with use of topical hemostatic agents, but not in the setting of shoulder arthroplasty.24 In 1999, Levy and colleagues11 showed that use of fibrin tissue adhesive reduced blood loss and postoperative transfusion rates in patients who underwent TKA. In 2001, Wang and colleagues15 showed that using a fibrin sealant in TKA reduced bloody drainage and maintained higher Hb levels. In 2003, the same group showed that use of fibrin sealant also reduced perioperative blood loss in total hip arthroplasty.12 More recent studies have had contradicting results,13,14 similar to ours. A 2012 prospective study failed to show any significant difference in blood loss after TKA in patients treated with a topical thrombin-based hemostatic agent.13 The authors did find significantly higher Hb values in the treated group on PODs 1 and 2, though the drain outputs and transfusion rates did not differ.
To our knowledge, the present study is the first to evaluate use of a topical hemostatic agent during shoulder arthroplasty. We did not find a significant difference in perioperative blood loss with application of Surgiflo, a topical thrombin-based hemostatic agent. Interestingly, we found that Hb levels both before surgery and on PODs 1 and 2 were significantly lower in the experimental group. However, the difference was about 0.7 g/dL, which would not be clinically significant. The lower Hb levels on PODs 1 and 2 likely resulted from lower preoperative levels.
Other studies have found higher transfusion rates for revision versus primary shoulder arthroplasty.1,2,20 In our series, EBL, autologous blood return, and drain output were higher overall for revision versus primary cases. When we stratified by primary and revision cases, we could not detect a difference in transfusion rates between the experimental and control groups. The lack of significant difference in the revision group could be caused by low statistical power, as the control group had only 13 revision cases. Having more patients in the study may have revealed a larger difference in blood loss with use of the hemostatic agent in revision cases.
We also found no significant increase in adverse events related to use of the hemostatic agent. Complications of particular concern would include wound complications, deep prosthesis infection, and systemic thromboembolic disease (eg, myocardial infarction, stroke, DVT, pulmonary embolus). There were no statistical differences in major and minor complications between the groups and no identifiable complications related to the hemostatic agent used.
Our results should be viewed in light of study limitations. First, with this retrospective study, we relied heavily on the accuracy of computer-based patient documentation. In addition, blood loss estimates are imperfect regardless of measurement technique. Intraoperative EBL is often determined by the surgeon and is highly variable, and autologous blood collection does not account for blood lost in operative sponges, instruments, and irrigation. To minimize this issue, we tried to assess perioperative blood loss through multiple data points, including intraoperative EBL, autologous blood returned during surgery, drain output, transfusion rates, and HBL calculations. Also, blood transfusion criteria depend on the physician’s clinical assessment and decision making, as well as patient condition, which could certainly add variability to the transfusion rate between groups. Another limitation is that the procedures studied were not homogeneous, and including primary and revision anatomical and reverse shoulder arthroplasties may have added variability to the results. In this single-surgeon study, however, we were able to ensure that the same standard techniques and hemostasis were applied in all procedures. Last, given the relatively small sample used, more patients may be needed to reveal a significant and clinically relevant difference in blood loss.
Conclusion
Perioperative blood loss poses serious risks to patient health. In light of the varying findings in the literature and the cost of transfusions and blood loss management products, use of these hemostatic agents remains controversial. In the present study, we found no significant difference in perioperative blood loss or transfusion rates with use of a hemostatic agent during shoulder arthroplasty. Therefore, we cannot conclude that this agent is effective for blood loss management in shoulder arthroplasty. Highly powered prospective studies are needed to confirm our findings.
1. Millett PJ, Porramatikul M, Chen N, Zurakowski D, Warner JJ. Analysis of transfusion predictors in shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(6):1223-1230.
2. Hardy JC, Hung M, Snow BJ, et al. Blood transfusion associated with shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(2):233-239.
3. Gruson KI, Accousti KJ, Parsons BO, Pillai G, Flatow EL. Transfusion after shoulder arthroplasty: an analysis of rates and risk factors. J Shoulder Elbow Surg. 2009;18(2):225-230.
4. Schumer RA, Chae JS, Markert RJ, Sprott D, Crosby LA. Predicting transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):91-96.
5. Sperling JW, Duncan SF, Cofield RH, Schleck CD, Harmsen WS. Incidence and risk factors for blood transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(6):599-601.
6. Ahmadi S, Lawrence TM, Sahota S, et al. The incidence and risk factors for blood transfusion in revision shoulder arthroplasty: our institution’s experience and review of the literature. J Shoulder Elbow Surg. 2014;23(1):43-48.
7. National Heart, Lung, and Blood Institute. What are the risks of a blood transfusion? http://www.nhlbi.nih.gov/health/health-topics/topics/bt/risks.html. Published January 30, 2012. Accessed June 24, 2015.
8. Bracale U, Rovani M, Picardo A, et al. Beneficial effects of fibrin glue (Quixil) versus Lichtenstein conventional technique in inguinal hernia repair: a randomized clinical trial. Hernia. 2014;18(2):185-192.
9. Gazzeri R, Galarza M, Alfier A. Safety biocompatibility of gelatin hemostatic matrix (Floseal and Surgiflo) in neurosurgical procedures. Surg Technol Int. 2012;22:49-54.
10. Krishnan S, Conner TM, Leslie R, Stemkowski S, Shander A. Choice of hemostatic agent and hospital length of stay in cardiovascular surgery. Semin Cardiothorac Vasc Anesth. 2009;13(4):225-230.
11. Levy O, Martinowitz U, Oran A, Tauber C, Horoszowski H. The use of fibrin tissue adhesive to reduce blood loss and the need for blood transfusion after total knee arthroplasty. A prospective, randomized, multicenter study. J Bone Joint Surg Am. 1999;81(11):1580-1588.
12. Wang GJ, Goldthwaite CA Jr, Burks S, Crawford R, Spotnitz WD; Orthopaedic Investigators Group. Fibrin sealant reduces perioperative blood loss in total hip replacement. J Long Term Eff Med Implants. 2003;13(5):399-411.
13. Kim HJ, Fraser MR, Kahn B, Lyman S, Figgie MP. The efficacy of a thrombin-based hemostatic agent in unilateral total knee arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2012;94(13):1160-1165.
14. Massin P, Scemama C, Jeanrot C, Boyer P. Does fibrin sealant use in total knee replacement reduce transfusion rates? A non-randomised comparative study. Orthop Traumatol Surg Res. 2012;98(2):180-185.
15. Wang GJ, Hungerford DS, Savory CG, et al. Use of fibrin sealant to reduce bloody drainage and hemoglobin loss after total knee arthroplasty: a brief note on a randomized prospective trial. J Bone Joint Surg Am. 2001;83(10):1503-1505.
16. Surgiflo Hemostatic Matrix Kit [package insert]. Somerville, NJ: Ethicon; 2012.
17. Good L, Peterson E, Lisander B. Tranexamic acid decreases external blood loss but not hidden blood loss in total knee replacement. Br J Anaesth. 2003;90(5):596-599.
18. Nadler SB, Hidalgo JH, Bloch T. Prediction of blood volume in normal human adults. Surgery. 1962;51(2):224-232.
19. Faris PM, Spence RK, Larholt KM, Sampson AR, Frei D. The predictive power of baseline hemoglobin for transfusion risk in surgery patients. Orthopedics. 1999;22(1 suppl):s135-s140.
20. Saltzman BM, Chalmers PN, Gupta AK, Romeo AA, Nicholson GP. Complication rates comparing primary with revision reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(11):1647-1654.
21. Murphy P, Heal JM, Blumberg N. Infection or suspected infection after hip replacement surgery with autologous or homologous blood transfusions. Transfusion. 1991;31(3):212-217.
22. Thomas D, Wareham K, Cohen D, Hutchings H. Autologous blood transfusion in total knee replacement surgery. Br J Anaesth. 2001;86(5):669-673.
23. Shander A, Hofmann A, Ozawa S, Theusinger OM, Gombotz H, Spahn DR. Activity-based costs of blood transfusions in surgical patients at four hospitals. Transfusion. 2010;50(4):753-765.
24. Thoms RJ, Marwin SE. The role of fibrin sealants in orthopaedic surgery. J Am Acad Orthop Surg. 2009;17(12):727-736.
1. Millett PJ, Porramatikul M, Chen N, Zurakowski D, Warner JJ. Analysis of transfusion predictors in shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(6):1223-1230.
2. Hardy JC, Hung M, Snow BJ, et al. Blood transfusion associated with shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(2):233-239.
3. Gruson KI, Accousti KJ, Parsons BO, Pillai G, Flatow EL. Transfusion after shoulder arthroplasty: an analysis of rates and risk factors. J Shoulder Elbow Surg. 2009;18(2):225-230.
4. Schumer RA, Chae JS, Markert RJ, Sprott D, Crosby LA. Predicting transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):91-96.
5. Sperling JW, Duncan SF, Cofield RH, Schleck CD, Harmsen WS. Incidence and risk factors for blood transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(6):599-601.
6. Ahmadi S, Lawrence TM, Sahota S, et al. The incidence and risk factors for blood transfusion in revision shoulder arthroplasty: our institution’s experience and review of the literature. J Shoulder Elbow Surg. 2014;23(1):43-48.
7. National Heart, Lung, and Blood Institute. What are the risks of a blood transfusion? http://www.nhlbi.nih.gov/health/health-topics/topics/bt/risks.html. Published January 30, 2012. Accessed June 24, 2015.
8. Bracale U, Rovani M, Picardo A, et al. Beneficial effects of fibrin glue (Quixil) versus Lichtenstein conventional technique in inguinal hernia repair: a randomized clinical trial. Hernia. 2014;18(2):185-192.
9. Gazzeri R, Galarza M, Alfier A. Safety biocompatibility of gelatin hemostatic matrix (Floseal and Surgiflo) in neurosurgical procedures. Surg Technol Int. 2012;22:49-54.
10. Krishnan S, Conner TM, Leslie R, Stemkowski S, Shander A. Choice of hemostatic agent and hospital length of stay in cardiovascular surgery. Semin Cardiothorac Vasc Anesth. 2009;13(4):225-230.
11. Levy O, Martinowitz U, Oran A, Tauber C, Horoszowski H. The use of fibrin tissue adhesive to reduce blood loss and the need for blood transfusion after total knee arthroplasty. A prospective, randomized, multicenter study. J Bone Joint Surg Am. 1999;81(11):1580-1588.
12. Wang GJ, Goldthwaite CA Jr, Burks S, Crawford R, Spotnitz WD; Orthopaedic Investigators Group. Fibrin sealant reduces perioperative blood loss in total hip replacement. J Long Term Eff Med Implants. 2003;13(5):399-411.
13. Kim HJ, Fraser MR, Kahn B, Lyman S, Figgie MP. The efficacy of a thrombin-based hemostatic agent in unilateral total knee arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2012;94(13):1160-1165.
14. Massin P, Scemama C, Jeanrot C, Boyer P. Does fibrin sealant use in total knee replacement reduce transfusion rates? A non-randomised comparative study. Orthop Traumatol Surg Res. 2012;98(2):180-185.
15. Wang GJ, Hungerford DS, Savory CG, et al. Use of fibrin sealant to reduce bloody drainage and hemoglobin loss after total knee arthroplasty: a brief note on a randomized prospective trial. J Bone Joint Surg Am. 2001;83(10):1503-1505.
16. Surgiflo Hemostatic Matrix Kit [package insert]. Somerville, NJ: Ethicon; 2012.
17. Good L, Peterson E, Lisander B. Tranexamic acid decreases external blood loss but not hidden blood loss in total knee replacement. Br J Anaesth. 2003;90(5):596-599.
18. Nadler SB, Hidalgo JH, Bloch T. Prediction of blood volume in normal human adults. Surgery. 1962;51(2):224-232.
19. Faris PM, Spence RK, Larholt KM, Sampson AR, Frei D. The predictive power of baseline hemoglobin for transfusion risk in surgery patients. Orthopedics. 1999;22(1 suppl):s135-s140.
20. Saltzman BM, Chalmers PN, Gupta AK, Romeo AA, Nicholson GP. Complication rates comparing primary with revision reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(11):1647-1654.
21. Murphy P, Heal JM, Blumberg N. Infection or suspected infection after hip replacement surgery with autologous or homologous blood transfusions. Transfusion. 1991;31(3):212-217.
22. Thomas D, Wareham K, Cohen D, Hutchings H. Autologous blood transfusion in total knee replacement surgery. Br J Anaesth. 2001;86(5):669-673.
23. Shander A, Hofmann A, Ozawa S, Theusinger OM, Gombotz H, Spahn DR. Activity-based costs of blood transfusions in surgical patients at four hospitals. Transfusion. 2010;50(4):753-765.
24. Thoms RJ, Marwin SE. The role of fibrin sealants in orthopaedic surgery. J Am Acad Orthop Surg. 2009;17(12):727-736.
The Top 100 Cited Articles in Clinical Orthopedic Sports Medicine
Orthopedics and the sports medicine subspecialty are continually evolving fields that depend on research investigation and publication to further knowledge and advance practice. Research has produced new findings that have changed the way we practice sports medicine. In this review, we identify the most widely referenced sports medicine topics and articles, which we believe by their permeative presence in the literature have made lasting contributions to the field.
Many factors can be used to quantify the influence of an academic article on the practice of medicine. Citation analysis is one method that reflects the impact of a publication on the academic medical community.1-3 Total citations record the number of times a journal article has been credited by another study. Therefore, citation count indirectly highlights the articles that are widespread, relevant, and that form the foundation for other investigations on the topic. Related to the impact of the article is the impact of the journal that published the study. We examined journals by impact factor, a score based on the mean number of citations a published article received during the preceding 2 years.
Similar analyses have been performed of publication history in orthopedics and other medical fields. Investigators have examined which historical articles were the most influential in orthopedics as a whole,4 pediatric orthopedics,5,6 shoulder surgery,7 and arthroscopy.8 This influence has also been studied in general surgery,9 otolaryngology,10 plastic surgery,11 dermatology,12 critical care,13 and other disciplines. To our knowledge, the present study is the first bibliometric analysis of the highest-impact articles in orthopedic sports medicine.
Our goal was to identify the 100 articles that have had the highest impact on the clinical orthopedic sports medicine literature. We hypothesized that the most widely recognized articles would be from the highest-impact journals and may also have earlier publication dates. We describe the topics and objectives of these articles to highlight the sports medicine areas on which most research has focused during the past century.
Materials and Methods
Our bibliometric analysis used the Thomson Reuters Web of Knowledge, which consists of all publications from 1900 to the present. This research modality ranks journal articles by frequency of citation. Similar analyses have identified the most often cited articles in pediatric orthopedics,5 shoulder surgery,7 and arthroscopy.8 In our analysis, we included the top 25 journals by impact factor in the field of sports medicine, as rated by the Journal Citation Reports database. Within the highest-impact journals, we sorted all articles by those most often cited, and read them all to identify which ones discuss conditions commonly encountered in the clinical practice of sports medicine. We focused on clinical articles only and therefore excluded related basic science and cadaveric biomechanical studies. The 100 most cited articles were then further evaluated by primary author, journal of publication, institution, country of origin, year of publication, topic, and total number of citations. One-way analysis of variance (ANOVA) and linear regression analyses were used to determine if publication date correlated with mean number of citations.
Results
Eighty authors wrote the top 100 articles in sports medicine, and each publication garnered several hundred citations, ranging from 229 to 1629 with a mean of 408 (Table 114-113). Most of these articles were written in the past 3 decades, with equal distribution from the 1980s, 1990s, and 2000s (Figure 1A). We ran a linear regression to determine if publication date correlated with higher number of citations by virtue of longer time available for citation. The analysis poorly modeled the variability (R2 = 0.05), revealing no correlation between number of citations and publication date. Further, 1-way ANOVA found no significant difference between the number of citations per decade, F(5, 93) = 1.60, P = .17 (Figure 1B). Despite this finding, the oldest cited article, written by Fairbank39 in 1948, ranked high (position 7). Of these top 100 publications, the most recent, written by Knutsen and colleagues69 in 2007, ranked in the second half at position 66.
Seven journals published the top 100 articles, with the American volume of the Journal of Bone and Joint Surgery publishing nearly half (44%) (Table 2). In second place, with 28 articles, was the American Journal of Sports Medicine, followed by the British volume of the Journal of Bone and Joint Surgery, with 10 articles.
Thirty different topics were investigated in this collection of articles, encompassing nearly every major research area of sports medicine. There was a heavy emphasis on anterior cruciate ligament (ACL) injury and reconstruction, knee rating systems, rotator cuff reconstruction, and chondrocyte transplantation (Table 3).
In several cases, an author contributed more than 1 classic article. In fact, 31 of the top 100 articles were by an individual who had coauthored 2 or more of the publications on this list. The researchers with the largest number of first-authored articles were Noyes88-92 (5 articles), Neer81-84 (4 articles), and Rowe,102-104 Daniel,35-37 Peterson,97-99 and Hewett52-54 (3 articles each) (Table 417,19,21-24,29-31,35-37,42,44,45,52-54,58,61-65,69,70,72,74,80-84,87-92,97-99,101-105,107,109,110,113). Articles from authors with multiple publications had a common topic.
Last, these articles originated from a number of different countries and institutions. Of the 15 source countries (Figure 2), the United States contributed the most (61 articles). Other countries had prominent representation: Sweden and Switzerland (8 each), United Kingdom (5), and Canada, France, and Norway (3 each). These articles originated from 69 universities, hospitals, and clinics; 21 institutions had 2 or more articles (Table 5). The 5 institutions with the highest number of articles were Hospital for Special Surgery, University of Bern, Columbia College of Physicians and Surgeons/Columbia-Presbyterian Medical Center, Cincinnati Sports Medicine and Orthopaedic Center, and Massachusetts General Hospital.
Discussion
Several trends can be ascertained from analyzing the top 100 clinical articles cited in sports medicine. The 5 most frequent topics discussed were ACL injury and reconstruction, knee rating systems for injury and function, rotator cuff reconstruction, chondrocyte transplantation, and femoroacetabular impingement (Table 3). Of those 5 topics, only ACL injury and reconstruction falls within the top 10 most common orthopedic surgical procedures performed in the United States reported by one analysis.114 The most common orthopedic surgical procedure, knee arthroscopy, ranks 10th of all topics covered by the top 100 articles, whereas the second most common procedure, shoulder arthroscopy, was not discussed by any of those 100 articles. Also notable is the high frequency of knee rating system studies, which correlates well with the fact that 4 of the most common orthopedic surgical procedures are knee procedures. The prevalence of rating system articles reflects the importance of and need for accurate methods in the diagnosis of injuries in sports medicine.
The most cited sports medicine article was written by Insall and colleagues62 in 1989, more than 2 decades ago. In this article, “Rationale of the Knee Society Clinical Rating System,” they reported on a rigorous system that rates knee function and ability to walk and climb stairs. The second most cited article, “A Clinical Method of Functional Assessment of the Shoulder,” was written in 1987 by Constant and Murley.32 This article discusses another rating system but offers a functional assessment of the shoulder that is highly reproducible and time-efficient. “Rating Systems in the Evaluation of Knee Ligament Injuries,” the third most cited article, was written in 1985 by Tegner and Lysholm.113 This article details the complexities and variable uses of different knee ligament injury rating systems. These top 3 articles were all published in Clinical Orthopaedics and Related Research. In addition, all 3 discussed rating systems, reinforcing the need for accurate scoring systems to standardize the diagnosis of injury across the field of orthopedics and qualify outcomes after injury.
A number of studies have introduced physical examination findings, clinical tests, and rating systems used in the clinical setting of sports medicine (and named after the contributing authors). For example, the Neer sign82 and the Hawkins-Kennedy test51 are used to determine shoulder impingement. In knee ligament injuries, the Tegner knee activity score113 complements other functional scores (eg, Lysholm knee score74). For grading joint cartilage breakdown, the Outerbridge classification system96 is commonly used. The Fairbank test39 is used to gauge knee instability. In evaluating fatty degeneration of rotator cuff muscles through computed tomography scans, the Goutallier classification47 is used. Other metrics, such as the Knee Injury and Osteoarthritis Outcome Score, introduced by Roos and colleagues,101 measure knee injury and osteoarthritis. In other scenarios, studies have improved on surgical techniques—for example, the Neer open modification84 of the Bankart procedure. Many of these rating systems and named clinical findings are so ingrained in the practice and vernacular of orthopedics that it is possible they are in fact undercited in the literature.
As in other bibliometric analyses, one concession made here was to credit the first author listed for making the primary contribution to an article. As a result of journal variability and inconsistency, we were precluded from analyzing senior authors. When analyzed for authorship at any position, 3 of the top authors (Table 4) showed contributions to additional articles in the top 100 list. Noyes was listed as last author on 2 other articles,52,54 raising his total to 7. Daniel was listed as second author on 1 additional article,105 and Beck was listed as third author on 1 other article,42 raising their totals to 4 and 3, respectively.
A criticism of bibliometric analysis is its use of number of citations as an accurate measure of academic contribution. However, other methods for measuring the productivity and impact of researchers (eg, the recently developed Hirsch Index) have their own drawbacks,115,116 including being able to compare authors only at the same point in their careers and self-citation. It is important to note that our analyses focused strictly on publications related to clinical sports medicine, with the exclusion of basic science and cadaveric biomechanical studies.
Through bibliometric citation analysis, we have identified the authors who have made lasting contributions to the field of sports medicine, and we have highlighted the publications that have been cited by hundreds to thousands of authors. This list identifies trends within the articles that have become “classic,” by nature of their deep permeation into subsequent sports medicine literature, and offers guidance for trainees interested in studying the most high-yield sports medicine literature. Given that 69 institutions in 15 countries conducted these studies, we have also shown that orthopedic research can be readily disseminated internationally. Last, our study provides a thorough overview of the sports medicine literature over the past century and provides a strong framework for future research in our field.
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3. Cheek J, Garnham B, Quan J. What’s in a number? Issues in providing evidence of impact and quality of research(ers). Qual Health Res. 2006;16(3):423-435.
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13. Baltussen A, Kindler CH. Citation classics in critical care medicine. Intensive Care Med. 2004;30(5):902-910.
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78. Matsusue Y, Yamamuro T, Hama H. Arthroscopic multiple osteochondral transplantation to the chondral defect in the knee associated with anterior cruciate ligament disruption. Arthroscopy. 1993;9(3):318-321.
79. McDaniel WJ Jr, Dameron TB Jr. Untreated ruptures of the anterior cruciate ligament. A follow-up study. J Bone Joint Surg Am. 1980;62(5):696-705.
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81. Neer CS 2nd. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am. 1972;54(1):41-50.
82. Neer CS 2nd. Impingement lesions. Clin Orthop Relat Res. 1983;(173):70-77.
83. Neer CS 2nd, Craig EV, Fukuda H. Cuff-tear arthropathy. J Bone Joint Surg Am. 1983;65(9):1232-1244.
84. Neer CS 2nd, Foster CR. Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am. 1980;62(6):897-908.
85. Nirschl RP, Pettrone FA. Tennis elbow. The surgical treatment of lateral epicondylitis. J Bone Joint Surg Am. 1979;61(6):832-839.
86. Nistor L. Surgical and non-surgical treatment of Achilles tendon rupture. J Bone Joint Surg Am. 1981;63(3):394-399.
87. Notzli HP, Wyss TF, Stoecklin CH, Schmid MR, Treiber K, Hodler J. The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg Br. 2002;84(4):556-560.
88. Noyes FR, Barber SD, Mangine RE. Abnormal lower limb symmetry determined by function hop tests after anterior cruciate ligament rupture. Am J Sports Med. 1991;19(5):513-518.
89. Noyes FR, Bassett RW, Grood ES, Butler DL. Arthroscopy in acute traumatic hemarthrosis of the knee. Incidence of anterior cruciate tears and other injuries. J Bone Joint Surg Am. 1980;62(5):687-695, 757.
90. Noyes FR, Matthews DS, Mooar PA, Grood ES. The symptomatic anterior cruciate–deficient knee. Part II: the results of rehabilitation, activity modification, and counseling on functional disability. J Bone Joint Surg Am. 1983;65(2):163-174.
91. Noyes FR, Mooar PA, Matthews DS, Butler DL. The symptomatic anterior cruciate–deficient knee. Part I: the long-term functional disability in athletically active individuals. J Bone Joint Surg Am. 1983;65(2):154-162.
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Orthopedics and the sports medicine subspecialty are continually evolving fields that depend on research investigation and publication to further knowledge and advance practice. Research has produced new findings that have changed the way we practice sports medicine. In this review, we identify the most widely referenced sports medicine topics and articles, which we believe by their permeative presence in the literature have made lasting contributions to the field.
Many factors can be used to quantify the influence of an academic article on the practice of medicine. Citation analysis is one method that reflects the impact of a publication on the academic medical community.1-3 Total citations record the number of times a journal article has been credited by another study. Therefore, citation count indirectly highlights the articles that are widespread, relevant, and that form the foundation for other investigations on the topic. Related to the impact of the article is the impact of the journal that published the study. We examined journals by impact factor, a score based on the mean number of citations a published article received during the preceding 2 years.
Similar analyses have been performed of publication history in orthopedics and other medical fields. Investigators have examined which historical articles were the most influential in orthopedics as a whole,4 pediatric orthopedics,5,6 shoulder surgery,7 and arthroscopy.8 This influence has also been studied in general surgery,9 otolaryngology,10 plastic surgery,11 dermatology,12 critical care,13 and other disciplines. To our knowledge, the present study is the first bibliometric analysis of the highest-impact articles in orthopedic sports medicine.
Our goal was to identify the 100 articles that have had the highest impact on the clinical orthopedic sports medicine literature. We hypothesized that the most widely recognized articles would be from the highest-impact journals and may also have earlier publication dates. We describe the topics and objectives of these articles to highlight the sports medicine areas on which most research has focused during the past century.
Materials and Methods
Our bibliometric analysis used the Thomson Reuters Web of Knowledge, which consists of all publications from 1900 to the present. This research modality ranks journal articles by frequency of citation. Similar analyses have identified the most often cited articles in pediatric orthopedics,5 shoulder surgery,7 and arthroscopy.8 In our analysis, we included the top 25 journals by impact factor in the field of sports medicine, as rated by the Journal Citation Reports database. Within the highest-impact journals, we sorted all articles by those most often cited, and read them all to identify which ones discuss conditions commonly encountered in the clinical practice of sports medicine. We focused on clinical articles only and therefore excluded related basic science and cadaveric biomechanical studies. The 100 most cited articles were then further evaluated by primary author, journal of publication, institution, country of origin, year of publication, topic, and total number of citations. One-way analysis of variance (ANOVA) and linear regression analyses were used to determine if publication date correlated with mean number of citations.
Results
Eighty authors wrote the top 100 articles in sports medicine, and each publication garnered several hundred citations, ranging from 229 to 1629 with a mean of 408 (Table 114-113). Most of these articles were written in the past 3 decades, with equal distribution from the 1980s, 1990s, and 2000s (Figure 1A). We ran a linear regression to determine if publication date correlated with higher number of citations by virtue of longer time available for citation. The analysis poorly modeled the variability (R2 = 0.05), revealing no correlation between number of citations and publication date. Further, 1-way ANOVA found no significant difference between the number of citations per decade, F(5, 93) = 1.60, P = .17 (Figure 1B). Despite this finding, the oldest cited article, written by Fairbank39 in 1948, ranked high (position 7). Of these top 100 publications, the most recent, written by Knutsen and colleagues69 in 2007, ranked in the second half at position 66.
Seven journals published the top 100 articles, with the American volume of the Journal of Bone and Joint Surgery publishing nearly half (44%) (Table 2). In second place, with 28 articles, was the American Journal of Sports Medicine, followed by the British volume of the Journal of Bone and Joint Surgery, with 10 articles.
Thirty different topics were investigated in this collection of articles, encompassing nearly every major research area of sports medicine. There was a heavy emphasis on anterior cruciate ligament (ACL) injury and reconstruction, knee rating systems, rotator cuff reconstruction, and chondrocyte transplantation (Table 3).
In several cases, an author contributed more than 1 classic article. In fact, 31 of the top 100 articles were by an individual who had coauthored 2 or more of the publications on this list. The researchers with the largest number of first-authored articles were Noyes88-92 (5 articles), Neer81-84 (4 articles), and Rowe,102-104 Daniel,35-37 Peterson,97-99 and Hewett52-54 (3 articles each) (Table 417,19,21-24,29-31,35-37,42,44,45,52-54,58,61-65,69,70,72,74,80-84,87-92,97-99,101-105,107,109,110,113). Articles from authors with multiple publications had a common topic.
Last, these articles originated from a number of different countries and institutions. Of the 15 source countries (Figure 2), the United States contributed the most (61 articles). Other countries had prominent representation: Sweden and Switzerland (8 each), United Kingdom (5), and Canada, France, and Norway (3 each). These articles originated from 69 universities, hospitals, and clinics; 21 institutions had 2 or more articles (Table 5). The 5 institutions with the highest number of articles were Hospital for Special Surgery, University of Bern, Columbia College of Physicians and Surgeons/Columbia-Presbyterian Medical Center, Cincinnati Sports Medicine and Orthopaedic Center, and Massachusetts General Hospital.
Discussion
Several trends can be ascertained from analyzing the top 100 clinical articles cited in sports medicine. The 5 most frequent topics discussed were ACL injury and reconstruction, knee rating systems for injury and function, rotator cuff reconstruction, chondrocyte transplantation, and femoroacetabular impingement (Table 3). Of those 5 topics, only ACL injury and reconstruction falls within the top 10 most common orthopedic surgical procedures performed in the United States reported by one analysis.114 The most common orthopedic surgical procedure, knee arthroscopy, ranks 10th of all topics covered by the top 100 articles, whereas the second most common procedure, shoulder arthroscopy, was not discussed by any of those 100 articles. Also notable is the high frequency of knee rating system studies, which correlates well with the fact that 4 of the most common orthopedic surgical procedures are knee procedures. The prevalence of rating system articles reflects the importance of and need for accurate methods in the diagnosis of injuries in sports medicine.
The most cited sports medicine article was written by Insall and colleagues62 in 1989, more than 2 decades ago. In this article, “Rationale of the Knee Society Clinical Rating System,” they reported on a rigorous system that rates knee function and ability to walk and climb stairs. The second most cited article, “A Clinical Method of Functional Assessment of the Shoulder,” was written in 1987 by Constant and Murley.32 This article discusses another rating system but offers a functional assessment of the shoulder that is highly reproducible and time-efficient. “Rating Systems in the Evaluation of Knee Ligament Injuries,” the third most cited article, was written in 1985 by Tegner and Lysholm.113 This article details the complexities and variable uses of different knee ligament injury rating systems. These top 3 articles were all published in Clinical Orthopaedics and Related Research. In addition, all 3 discussed rating systems, reinforcing the need for accurate scoring systems to standardize the diagnosis of injury across the field of orthopedics and qualify outcomes after injury.
A number of studies have introduced physical examination findings, clinical tests, and rating systems used in the clinical setting of sports medicine (and named after the contributing authors). For example, the Neer sign82 and the Hawkins-Kennedy test51 are used to determine shoulder impingement. In knee ligament injuries, the Tegner knee activity score113 complements other functional scores (eg, Lysholm knee score74). For grading joint cartilage breakdown, the Outerbridge classification system96 is commonly used. The Fairbank test39 is used to gauge knee instability. In evaluating fatty degeneration of rotator cuff muscles through computed tomography scans, the Goutallier classification47 is used. Other metrics, such as the Knee Injury and Osteoarthritis Outcome Score, introduced by Roos and colleagues,101 measure knee injury and osteoarthritis. In other scenarios, studies have improved on surgical techniques—for example, the Neer open modification84 of the Bankart procedure. Many of these rating systems and named clinical findings are so ingrained in the practice and vernacular of orthopedics that it is possible they are in fact undercited in the literature.
As in other bibliometric analyses, one concession made here was to credit the first author listed for making the primary contribution to an article. As a result of journal variability and inconsistency, we were precluded from analyzing senior authors. When analyzed for authorship at any position, 3 of the top authors (Table 4) showed contributions to additional articles in the top 100 list. Noyes was listed as last author on 2 other articles,52,54 raising his total to 7. Daniel was listed as second author on 1 additional article,105 and Beck was listed as third author on 1 other article,42 raising their totals to 4 and 3, respectively.
A criticism of bibliometric analysis is its use of number of citations as an accurate measure of academic contribution. However, other methods for measuring the productivity and impact of researchers (eg, the recently developed Hirsch Index) have their own drawbacks,115,116 including being able to compare authors only at the same point in their careers and self-citation. It is important to note that our analyses focused strictly on publications related to clinical sports medicine, with the exclusion of basic science and cadaveric biomechanical studies.
Through bibliometric citation analysis, we have identified the authors who have made lasting contributions to the field of sports medicine, and we have highlighted the publications that have been cited by hundreds to thousands of authors. This list identifies trends within the articles that have become “classic,” by nature of their deep permeation into subsequent sports medicine literature, and offers guidance for trainees interested in studying the most high-yield sports medicine literature. Given that 69 institutions in 15 countries conducted these studies, we have also shown that orthopedic research can be readily disseminated internationally. Last, our study provides a thorough overview of the sports medicine literature over the past century and provides a strong framework for future research in our field.
Orthopedics and the sports medicine subspecialty are continually evolving fields that depend on research investigation and publication to further knowledge and advance practice. Research has produced new findings that have changed the way we practice sports medicine. In this review, we identify the most widely referenced sports medicine topics and articles, which we believe by their permeative presence in the literature have made lasting contributions to the field.
Many factors can be used to quantify the influence of an academic article on the practice of medicine. Citation analysis is one method that reflects the impact of a publication on the academic medical community.1-3 Total citations record the number of times a journal article has been credited by another study. Therefore, citation count indirectly highlights the articles that are widespread, relevant, and that form the foundation for other investigations on the topic. Related to the impact of the article is the impact of the journal that published the study. We examined journals by impact factor, a score based on the mean number of citations a published article received during the preceding 2 years.
Similar analyses have been performed of publication history in orthopedics and other medical fields. Investigators have examined which historical articles were the most influential in orthopedics as a whole,4 pediatric orthopedics,5,6 shoulder surgery,7 and arthroscopy.8 This influence has also been studied in general surgery,9 otolaryngology,10 plastic surgery,11 dermatology,12 critical care,13 and other disciplines. To our knowledge, the present study is the first bibliometric analysis of the highest-impact articles in orthopedic sports medicine.
Our goal was to identify the 100 articles that have had the highest impact on the clinical orthopedic sports medicine literature. We hypothesized that the most widely recognized articles would be from the highest-impact journals and may also have earlier publication dates. We describe the topics and objectives of these articles to highlight the sports medicine areas on which most research has focused during the past century.
Materials and Methods
Our bibliometric analysis used the Thomson Reuters Web of Knowledge, which consists of all publications from 1900 to the present. This research modality ranks journal articles by frequency of citation. Similar analyses have identified the most often cited articles in pediatric orthopedics,5 shoulder surgery,7 and arthroscopy.8 In our analysis, we included the top 25 journals by impact factor in the field of sports medicine, as rated by the Journal Citation Reports database. Within the highest-impact journals, we sorted all articles by those most often cited, and read them all to identify which ones discuss conditions commonly encountered in the clinical practice of sports medicine. We focused on clinical articles only and therefore excluded related basic science and cadaveric biomechanical studies. The 100 most cited articles were then further evaluated by primary author, journal of publication, institution, country of origin, year of publication, topic, and total number of citations. One-way analysis of variance (ANOVA) and linear regression analyses were used to determine if publication date correlated with mean number of citations.
Results
Eighty authors wrote the top 100 articles in sports medicine, and each publication garnered several hundred citations, ranging from 229 to 1629 with a mean of 408 (Table 114-113). Most of these articles were written in the past 3 decades, with equal distribution from the 1980s, 1990s, and 2000s (Figure 1A). We ran a linear regression to determine if publication date correlated with higher number of citations by virtue of longer time available for citation. The analysis poorly modeled the variability (R2 = 0.05), revealing no correlation between number of citations and publication date. Further, 1-way ANOVA found no significant difference between the number of citations per decade, F(5, 93) = 1.60, P = .17 (Figure 1B). Despite this finding, the oldest cited article, written by Fairbank39 in 1948, ranked high (position 7). Of these top 100 publications, the most recent, written by Knutsen and colleagues69 in 2007, ranked in the second half at position 66.
Seven journals published the top 100 articles, with the American volume of the Journal of Bone and Joint Surgery publishing nearly half (44%) (Table 2). In second place, with 28 articles, was the American Journal of Sports Medicine, followed by the British volume of the Journal of Bone and Joint Surgery, with 10 articles.
Thirty different topics were investigated in this collection of articles, encompassing nearly every major research area of sports medicine. There was a heavy emphasis on anterior cruciate ligament (ACL) injury and reconstruction, knee rating systems, rotator cuff reconstruction, and chondrocyte transplantation (Table 3).
In several cases, an author contributed more than 1 classic article. In fact, 31 of the top 100 articles were by an individual who had coauthored 2 or more of the publications on this list. The researchers with the largest number of first-authored articles were Noyes88-92 (5 articles), Neer81-84 (4 articles), and Rowe,102-104 Daniel,35-37 Peterson,97-99 and Hewett52-54 (3 articles each) (Table 417,19,21-24,29-31,35-37,42,44,45,52-54,58,61-65,69,70,72,74,80-84,87-92,97-99,101-105,107,109,110,113). Articles from authors with multiple publications had a common topic.
Last, these articles originated from a number of different countries and institutions. Of the 15 source countries (Figure 2), the United States contributed the most (61 articles). Other countries had prominent representation: Sweden and Switzerland (8 each), United Kingdom (5), and Canada, France, and Norway (3 each). These articles originated from 69 universities, hospitals, and clinics; 21 institutions had 2 or more articles (Table 5). The 5 institutions with the highest number of articles were Hospital for Special Surgery, University of Bern, Columbia College of Physicians and Surgeons/Columbia-Presbyterian Medical Center, Cincinnati Sports Medicine and Orthopaedic Center, and Massachusetts General Hospital.
Discussion
Several trends can be ascertained from analyzing the top 100 clinical articles cited in sports medicine. The 5 most frequent topics discussed were ACL injury and reconstruction, knee rating systems for injury and function, rotator cuff reconstruction, chondrocyte transplantation, and femoroacetabular impingement (Table 3). Of those 5 topics, only ACL injury and reconstruction falls within the top 10 most common orthopedic surgical procedures performed in the United States reported by one analysis.114 The most common orthopedic surgical procedure, knee arthroscopy, ranks 10th of all topics covered by the top 100 articles, whereas the second most common procedure, shoulder arthroscopy, was not discussed by any of those 100 articles. Also notable is the high frequency of knee rating system studies, which correlates well with the fact that 4 of the most common orthopedic surgical procedures are knee procedures. The prevalence of rating system articles reflects the importance of and need for accurate methods in the diagnosis of injuries in sports medicine.
The most cited sports medicine article was written by Insall and colleagues62 in 1989, more than 2 decades ago. In this article, “Rationale of the Knee Society Clinical Rating System,” they reported on a rigorous system that rates knee function and ability to walk and climb stairs. The second most cited article, “A Clinical Method of Functional Assessment of the Shoulder,” was written in 1987 by Constant and Murley.32 This article discusses another rating system but offers a functional assessment of the shoulder that is highly reproducible and time-efficient. “Rating Systems in the Evaluation of Knee Ligament Injuries,” the third most cited article, was written in 1985 by Tegner and Lysholm.113 This article details the complexities and variable uses of different knee ligament injury rating systems. These top 3 articles were all published in Clinical Orthopaedics and Related Research. In addition, all 3 discussed rating systems, reinforcing the need for accurate scoring systems to standardize the diagnosis of injury across the field of orthopedics and qualify outcomes after injury.
A number of studies have introduced physical examination findings, clinical tests, and rating systems used in the clinical setting of sports medicine (and named after the contributing authors). For example, the Neer sign82 and the Hawkins-Kennedy test51 are used to determine shoulder impingement. In knee ligament injuries, the Tegner knee activity score113 complements other functional scores (eg, Lysholm knee score74). For grading joint cartilage breakdown, the Outerbridge classification system96 is commonly used. The Fairbank test39 is used to gauge knee instability. In evaluating fatty degeneration of rotator cuff muscles through computed tomography scans, the Goutallier classification47 is used. Other metrics, such as the Knee Injury and Osteoarthritis Outcome Score, introduced by Roos and colleagues,101 measure knee injury and osteoarthritis. In other scenarios, studies have improved on surgical techniques—for example, the Neer open modification84 of the Bankart procedure. Many of these rating systems and named clinical findings are so ingrained in the practice and vernacular of orthopedics that it is possible they are in fact undercited in the literature.
As in other bibliometric analyses, one concession made here was to credit the first author listed for making the primary contribution to an article. As a result of journal variability and inconsistency, we were precluded from analyzing senior authors. When analyzed for authorship at any position, 3 of the top authors (Table 4) showed contributions to additional articles in the top 100 list. Noyes was listed as last author on 2 other articles,52,54 raising his total to 7. Daniel was listed as second author on 1 additional article,105 and Beck was listed as third author on 1 other article,42 raising their totals to 4 and 3, respectively.
A criticism of bibliometric analysis is its use of number of citations as an accurate measure of academic contribution. However, other methods for measuring the productivity and impact of researchers (eg, the recently developed Hirsch Index) have their own drawbacks,115,116 including being able to compare authors only at the same point in their careers and self-citation. It is important to note that our analyses focused strictly on publications related to clinical sports medicine, with the exclusion of basic science and cadaveric biomechanical studies.
Through bibliometric citation analysis, we have identified the authors who have made lasting contributions to the field of sports medicine, and we have highlighted the publications that have been cited by hundreds to thousands of authors. This list identifies trends within the articles that have become “classic,” by nature of their deep permeation into subsequent sports medicine literature, and offers guidance for trainees interested in studying the most high-yield sports medicine literature. Given that 69 institutions in 15 countries conducted these studies, we have also shown that orthopedic research can be readily disseminated internationally. Last, our study provides a thorough overview of the sports medicine literature over the past century and provides a strong framework for future research in our field.
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108. Sher JS, Uribe JW, Posada A, Murphy BJ, Zlatkin MB. Abnormal findings on magnetic resonance images of asymptomatic shoulders [see comments]. J Bone Joint Surg Am. 1995;77(1):10-15.
109. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoro-acetabular impingement due to acetabular retroversion. Treatment with periacetabular osteotomy. J Bone Joint Surg Am. 2003;85(2):278-286.
110. Solomonow M, Baratta R, Zhou BH, et al. The synergistic action of the anterior cruciate ligament and thigh muscles in maintaining joint stability. Am J Sports Med. 1987;15(3):207-213.
111. Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, Gill TJ, Rodkey WG. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy. 2003;19(5):477-484.
112. Tapper EM, Hoover NW. Late results after meniscectomy. J Bone Joint Surg Am. 1969;51(3):517-526.
113. Tegner Y, Lysholm J. Rating systems in the evaluation of knee ligament injuries. Clin Orthop Relat Res. 1985;(198):43-49.
114. Garrett WE Jr, Swiontkowski MF, Weinstein JN, et al. American Board of Orthopaedic Surgery Practice of the Orthopaedic Surgeon: Part-II, certification examination case mix. J Bone Joint Surg Am. 2006;88(3):660-667.
115. Bartneck C, Kokkelmans S. Detecting h-index manipulation through self-citation analysis. Scientometrics. 2011;87(1):85-98.
116. Bornmann L, Daniel HD. The state of h index research. Is the h index the ideal way to measure research performance? EMBO Rep. 2009;10(1):2-6.
1. Adams AB, Simonson D. Publication, citations, and impact factors of leading investigators in critical care medicine. Respir Care. 2004;49(3):276-281.
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48. Guskiewicz KM, Weaver NL, Padua DA, Garrett WE Jr. Epidemiology of concussion in collegiate and high school football players. Am J Sports Med. 2000;28(5):643-650.
49. Hangody L, Fules P. Autologous osteochondral mosaicplasty for the treatment of full-thickness defects of weight-bearing joints: ten years of experimental and clinical experience. J Bone Joint Surg Am. 2003;85(suppl 2):25-32.
50. 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.
51. Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Sports Med. 1980;8(3):151-157.
52. Hewett TE, Lindenfeld TN, Riccobene JV, Noyes FR. The effect of neuromuscular training on the incidence of knee injury in female athletes. A prospective study. Am J Sports Med. 1999;27(6):699-706.
53. Hewett TE, Myer GD, Ford KR, et al. Biomechanical measures of neuromuscular control and valgus loading of the knee predict anterior cruciate ligament injury risk in female athletes: a prospective study. Am J Sports Med. 2005;33(4):492-501.
54. Hewett TE, Stroupe AL, Nance TA, Noyes FR. Plyometric training in female athletes. Decreased impact forces and increased hamstring torques. Am J Sports Med. 1996;24(6):765-773.
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56. Horas U, Pelinkovic D, Herr G, Aigner T, Schnettler R. Autologous chondrocyte implantation and osteochondral cylinder transplantation in cartilage repair of the knee joint. A prospective, comparative trial. J Bone Joint Surg Am. 2003;85(2):185-192.
57. Hovelius L, Augustini BG, Fredin H, Johansson O, Norlin R, Thorling J. Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J Bone Joint Surg Am. 1996;78(11):1677-1684.
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65. Ito K, Minka MA 2nd, Leunig M, Werlen S, Ganz R. Femoroacetabular impingement and the cam-effect. A MRI-based quantitative anatomical study of the femoral head-neck offset. J Bone Joint Surg Br. 2001;83(2):171-176.
66. Johnson RJ, Kettelkamp DB, Clark W, Leaverton P. Factors affecting late results after meniscectomy. J Bone Joint Surg Am. 1974;56(3):719-729.
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68. Jones KG. Reconstruction of the anterior cruciate ligament: a technique using the central one-third of the patellar ligament. J Bone Joint Surg Am. 1963;45(5):925-932.
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109. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoro-acetabular impingement due to acetabular retroversion. Treatment with periacetabular osteotomy. J Bone Joint Surg Am. 2003;85(2):278-286.
110. Solomonow M, Baratta R, Zhou BH, et al. The synergistic action of the anterior cruciate ligament and thigh muscles in maintaining joint stability. Am J Sports Med. 1987;15(3):207-213.
111. Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, Gill TJ, Rodkey WG. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy. 2003;19(5):477-484.
112. Tapper EM, Hoover NW. Late results after meniscectomy. J Bone Joint Surg Am. 1969;51(3):517-526.
113. Tegner Y, Lysholm J. Rating systems in the evaluation of knee ligament injuries. Clin Orthop Relat Res. 1985;(198):43-49.
114. Garrett WE Jr, Swiontkowski MF, Weinstein JN, et al. American Board of Orthopaedic Surgery Practice of the Orthopaedic Surgeon: Part-II, certification examination case mix. J Bone Joint Surg Am. 2006;88(3):660-667.
115. Bartneck C, Kokkelmans S. Detecting h-index manipulation through self-citation analysis. Scientometrics. 2011;87(1):85-98.
116. Bornmann L, Daniel HD. The state of h index research. Is the h index the ideal way to measure research performance? EMBO Rep. 2009;10(1):2-6.
Using Plate Osteosynthesis to Treat Isolated Greater Tuberosity Fractures
Proximal humerus fractures are the second most common fracture in the upper extremity, accounting for 4% to 5% of all fractures.1-4 The majority of these injuries can be treated without an operation. For fractures that require surgery, there are multiple options, including closed reduction, percutaneous pinning, open reduction and internal fixation (ORIF), hemiarthroplasty, and reverse total shoulder arthroplasty.3-9
Isolated greater tuberosity fractures (AO [Arbeitsgemeinschaft für Osteosynthesefragen] 11.A1) make up a small subset of proximal humerus fractures. In general, patients who sustain an isolated greater tuberosity fracture are younger and more active than those who sustain other proximal humerus fractures.2,10 As a result, in the treatment of greater tuberosity fractures, there is increased emphasis on return to high activity and function. Nondisplaced or minimally displaced fractures typically are treated nonoperatively with good success.11,12 Patients with fractures displaced more than 5 mm, and highly active patients with fractures displaced more than 3 mm, usually are recommended for surgical treatment.2,11-14 The many options for treating these difficult fractures include suture fixation, percutaneous techniques, screw fixation, and, more recently, arthroscopic suture techniques.2,5,13,15,16 The goal of any of these operative interventions is to restore normal function and minimize pain around the injured shoulder. Although most of the operative techniques for greater tuberosity fractures have predictable results, none has been established as the gold standard for the treatment of displaced greater tuberosity fractures.2,5,13,15-18 Use of plate osteosynthesis for displaced proximal humerus fractures not isolated to the greater tuberosity is becoming more widespread in the orthopedic community.1,4,19,20 However, the orthopedic literature includes very few reports of using this technique for isolated displaced greater tuberosity fractures.18 This surgical approach potentially provides increased stability, improved maintenance of reduction, and earlier range of motion (ROM) in the postoperative period. These outcomes in turn may allow for improved pain control and earlier return to normal activities than is the case with other operative interventions for these difficult injuries.
We conducted a study to determine the radiographic and clinical outcomes of plate osteosynthesis for displaced greater tuberosity fractures. We hypothesized that excellent clinical and radiographic outcomes could be achieved using this surgical technique.
Patients and Methods
After obtaining institutional review board approval for this study, we retrospectively identified 11 consecutive patients with an isolated displaced greater tuberosity fracture (AO 11.A1) treated with plate osteosynthesis by Dr. Getz between December 2009 and May 2011 (Figures 1A, 1B). We collected data on age at time of surgery, sex, length of follow-up, worker’s compensation status, and complications. At a minimum of 21 months (mean, 27 months; SD, 8 months; range, 16-44 months), we assessed ROM and administered validated outcome scores, including the Single Assessment Numeric Evaluation (SANE)21,22 and the Penn Shoulder Score (PSS).23
Surgical Technique
The deltopectoral approach was used in all 11 patients. A standard incision was made over the deltopectoral interval starting at the coracoid and extending about 6 cm toward the deltoid insertion. After the internervous plane was entered between the deltoid and pectoralis major, the clavipectoral fascia was divided. The greater tuberosity fracture was identified with the leading edge of the fracture 1 cm posterior to the bicipital groove in all cases. Organized hematoma was removed from the fracture site to allow reduction. Three 1-mm braided polyester tapes were placed into the rotator cuff at the insertion onto the greater tuberosity fragment. The sutures thus captured the fragment and were used to obtain reduction and fixation. The fragment was provisionally pinned by placing a 2.0-mm Kirschner wire high on the fragment as to not block plate application. Fluoroscopic imaging was used to determine the appropriate position of the fracture reduction. A standard periarticular proximal humerus 3.5-mm locking compression plate (Zimmer) was used in all patients. The plate was contoured to achieve more compression in several cases in which plastic deformation or comminution was present. The sutures that were attached to the greater tuberosity were then brought through the plate. The plate was then slid down onto the humerus and pinned under fluoroscopic guidance. Three bicortical screws were used to affix the plate to the humeral shaft to compress the fracture into the fracture bed. Two to 4 locking screws were placed into the humeral head to improve the rotational stability of the construct. Last, the sutures through the plate were tied for added fixation.
Rehabilitation
In the immediate postoperative period, all patients were placed in a standard shoulder sling. The sling was worn for 6 weeks. At 2 weeks, patients started formal, standardized physical therapy, including passive ROM for elevation and external rotation. At 6 weeks, they began internal rotation stretching and active-assisted motion. Cuff strengthening began gently, as motion and pain allowed, after 8 weeks. Formal physical therapy continued until full or maximal improvement in motion and strength had been achieved.
Radiographic Measurements
Union/malunion was assessed by 2 orthopedic surgeons during their fellowship year in shoulder and elbow surgery. These surgeons were blinded to patients’ clinical outcomes. Each surgeon reviewed each patient’s radiographs twice to determine whether the reduction was anatomical. Anatomical reduction was achieved if the greater-tuberosity-to-head height was between 4 and 10 mm. Malunion was defined as loss of more than 3 mm of anatomical fracture reduction (from the original reduction) on any radiologic view at most recent follow-up. Loss of reduction was considered minimal if the fracture fragment was displaced less than 3 mm.
Statistical Analysis
A descriptive analysis of patient variables and outcomes was used for this small cohort of patients. Statistical significance was set at α = 0.05.
Results
Eleven patients (7 women, 4 men) underwent plate osteosynthesis for an isolated greater tuberosity fracture (Figure 2). Mean age at surgery was 60 years (range, 37-71 years). All patients were right-hand–dominant; 7 of the 11 sustained the injury on the dominant side. For all 11 patients, final postoperative ROM and complications were recorded. No patient required additional surgery. Before injury, all patients felt their shoulder was 100% normal. Nine of the 11 patients were available for assessment of functional outcome and ROM at a mean (SD) of 27 (8) months (range, 16-44 months). At final follow-up, mean (SD) forward elevation was 147° (28°; range, 100°-180°), and mean (SD) external rotation was 25° (15°; range, 10°-60°). Mean (SD) SANE score was 72 (17; range, 50-90), and mean (SD) PSS was 79 (16; range 43-90). On a 1-to-10 scale, patients’ mean (SD) overall satisfaction was 8.6 (1.9; range, 4-10). Of the 9 patients who worked before injury, 8 returned to preoperative duty. Six patients reported stiffness (consistent with ROM). All patients said they would have the surgery again (Table).
All patients experienced radiographic union. Three of the 11 had minimal (<3 mm) loss of reduction. Mean (SD) time to union was 10.7 (4.2) weeks (range, 6.1-21.6 weeks). There were no wound complications and no need for any hardware removal.
Discussion
Isolated greater tuberosity fractures are less common than other types of proximal humerus fractures but often require surgical intervention for less displacement when compared with those fractures.2,14 Multiple techniques (eg, suture fixation, percutaneous pinning, arthroscopic techniques) have been used, but none has established itself as the gold standard for treatment of these difficult injuries.2,5,9,11,13-16 The results of the present study show that plate osteosynthesis can reliably be used to achieve anatomical reduction and good functional outcomes in isolated greater tuberosity fractures. Even with the added stability of the plate and suture construct, a small number of fractures still displaced. In addition, despite having achieved anatomical union, many patients in this study experienced stiffness and functional loss, which speaks to the challenges associated with management of these fractures.
Self-reported outcomes were less favorable for patients in our study (despite achieving mean forward elevation of 147°) than for patients who underwent greater tuberosity repair in other studies.2,5,10 In a study of 12 patients who underwent ORIF of a 2-part displaced fracture of the greater tuberosity of the proximal part of the humerus, Flatow and colleagues5 found half the patients had an excellent outcome, and the other half had a good outcome with active elevation averaging 170°. In another study, conducted over 11 years, 165 patients with a proximal humeral fracture were treated with transosseous suture fixation. Union occurred in all patients except the 2 patients with 3-part fractures, and 155 patients had excellent or very good fracture reduction.10 Therefore, final ROM for these patients may not be a good indicator of actual final function, and previous reports likely underestimated the functional loss experienced by these patients.
The incidence of isolated greater tuberosity fractures likely will increase as the population ages and becomes more active.2,14,16 Patients with isolated greater tuberosity fractures are more likely to be male, to be younger, and to have fewer medical problems than patients with other types of proximal humerus fractures.14 In addition, patient expectations regarding life after displaced greater tuberosity fractures are unique compared with expectations of patients who have other proximal humerus fractures; displaced greater tuberosity fractures usually occur in more active patients, who may expect to return to work and may place higher demands on themselves after treatment,2,14,16,24 possibly leading to lower subjective clinical outcomes.
Various operative treatment techniques for isolated greater tuberosity fractures have been described. Flatow and colleagues5 reported excellent return of forward elevation after ORIF with heavy suture, and half the patients reported excellent outcomes. Other techniques have had mixed results. Bhatia and colleagues11 reported on long-term outcomes of internal fixation using a double row of suture anchors in isolated, displaced greater tuberosity fractures in 21 patients. Outcomes were rated excellent in 8 patients, good in 10, satisfactory in 2, and unsatisfactory in 1. Braunstein and colleagues12 examined the biomechanical strength of various fixation constructs and found that tension band wiring or cancellous screws were superior to suture fixation. More recently, Ji and colleagues13 described encouraging outcomes of arthroscopic fixation of isolated displaced proximal humerus fractures in 16 patients. Mean postoperative American Shoulder and Elbow Surgeons (ASES) score was 88, and mean improvement in University of California, Los Angeles (UCLA) score was 31 points. In addition, mean forward elevation was 148.7° at most recent follow-up.
Our technique supplements the literature on greater tuberosity fracture fixation by using a plate as the point for suture fixation rather than suture anchors or screw fixation. As has been shown with 3- and 4-part fractures, plate osteosynthesis provides proximal suture fixation points and locking screws (often in poor-quality bone) that can prevent suture cut-out and isolated screw failure. In addition, compared with other techniques for greater tuberosity fixation, meta-diaphyseal cortical plate fixation bypasses the often poor bone quality of the greater tuberosity, preventing these modes of failure.18 Schoffl and colleagues18 reported on 10 patients who received a Bamberg plate; all 10 had excellent postoperative outcomes with no complications or secondary loss of reduction. Outcomes in the present study mirror those in the literature for operative fixation of displaced greater tuberosity fractures. Despite the near anatomical reduction in the majority of patients (mean forward elevation, 147°), functional results in this patient population remain guarded, with many patients reporting only good clinical outcomes.
This study had a few limitations. First is the inherent limitation of a retrospective study. Second, the small sample size limited the subgroup analysis. However, given the rarity of the injury and the single-surgeon series, we would have to have added considerable time to the study to increase its power. Third, there was no control group. This is a difficult situation with displaced fractures, as clinical outcomes are poorer with nonoperative management than with operative intervention.2,16,17 Compared with historical operative controls in the literature, our patients compare favorably over medium-term follow-up.2,5,15,16
Conclusion
Plate osteosynthesis is a novel technique in the treatment of displaced greater tuberosity fractures. It results in excellent fracture reduction, a 100% union rate, minimal fracture migration, and good return of ROM. However, self-reported functional assessment of the shoulder was about three-fourths of what is expected of normal or preinjury function.
1. Gardner MJ, Boraiah S, Helfet DL, Lorich DG. Indirect medial reduction and strut support of proximal humerus fractures using an endosteal implant.
J Orthop Trauma. 2008;22(3):195-200.
2. Green A, Izzi J Jr. Isolated fractures of the greater tuberosity of the proximal humerus. J Shoulder Elbow Surg. 2003;12(6):641-649.
3. Neer CS 2nd. Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am. 1970;52(6):1077-1089.
4. Ricchetti ET, DeMola PM, Roman D, Abboud JA. The use of precontoured humeral locking plates in the management of displaced proximal humerus fracture. J Am Acad Orthop Surg. 2009;17(9):582-590.
5. Flatow EL, Cuomo F, Maday MG, Miller SR, McIlveen SJ, Bigliani LU. Open reduction and internal fixation of two-part displaced fractures of the greater tuberosity of the proximal part of the humerus. J Bone Joint Surg Am. 1991;73(8):1213-1218.
6. Lenarz C, Shishani Y, McCrum C, Nowinski RJ, Edwards TB, Gobezie R. Is reverse shoulder arthroplasty appropriate for the treatment of fractures in the older patient? Early observations. Clin Orthop Relat Res. 2011;469(12):3324-3331.
7. Park MC, Murthi AM, Roth NS, Blaine TA, Levine WN, Bigliani LU. Two-part and three-part fractures of the proximal humerus treated with suture fixation. J Orthop Trauma. 2003;17(5):319-325.
8. Young SW, Segal BS, Turner PC, Poon PC. Comparison of functional outcomes of reverse shoulder arthroplasty versus hemiarthroplasty in the primary treatment of acute proximal humerus fracture. ANZ J Surg. 2010;80(11):789-793.
9. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. J Bone Joint Surg Am. 2007;89(8):1700-1709.
10. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. Surgical technique. J Bone Joint Surg Am. 2009;91(suppl 2, pt 1):8-21.
11. Bhatia DN, van Rooyen KS, du Toit DF, de Beer JF. Surgical treatment of comminuted, displaced fractures of the greater tuberosity of the proximal humerus: a new technique of double-row suture-anchor fixation and long-term results. Injury. 2006;37(10):946-952.
12. Braunstein V, Wiedemann E, Plitz W, Muensterer OJ, Mutschler W, Hinterwimmer S. Operative treatment of greater tuberosity fractures of the humerus—a biomechanical analysis. Clin Biomech. 2007;22(6):652-657.
13. Ji JH, Shafi M, Song IS, Kim YY, McFarland EG, Moon CY. Arthroscopic fixation technique for comminuted, displaced greater tuberosity fracture. Arthroscopy. 2010;26(5):600-609.
14. Kim E, Shin HK, Kim CH. Characteristics of an isolated greater tuberosity fracture of the humerus. J Orthop Sci. 2005;10(5):441-444.
15. Lee SU, Jeong C, Park IJ. Arthroscopic fixation of displaced greater tuberosity fracture of the proximal humerus. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):378-380.
16. Mattyasovszky SG, Burkhart KJ, Ahlers C, et al. Isolated fractures of the greater tuberosity of the proximal humerus. Acta Orthop. 2011;82(6):714-720.
17. Platzer P, Thalhammer G, Oberleitner G, et al. Displaced fractures of the greater tuberosity: a comparison of operative and nonoperative treatment. J Trauma. 2008;65(4):843-848.
18. Schoffl V, Popp D, Strecker W. A simple and effective implant for displaced fractures of the greater tuberosity: the “Bamberg” plate. Arch Orthop Trauma Surg. 2011;131(4):509-512.
19. Gardner MJ, Boraiah S, Helfet DL, Lorich DG. The anterolateral acromial approach for fractures of the proximal humerus. J Orthop Trauma. 2008;22(2):132-137.
20. Ricchetti ET, Warrender WJ, Abboud JA. Use of locking plates in the treatment of proximal humerus fractures. J Shoulder Elbow Surg. 2010;19(2 suppl):66-75.
21. 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.
22. Williams GN, Taylor DC, Gangel TJ, Uhorchak JM, Arciero RA. Comparison of the Single Assessment Numeric Evaluation method and the Lysholm score. Clin Orthop Relat Res. 2000;(373):184-192.
23. Leggin BG, Michener LA, Shaffer MA, Brenneman SK, Iannotti JP, Williams GR Jr. The Penn Shoulder Score: reliability and validity. J Orthop Sports Phys Ther. 2006;36(3):138-151.
24. Gruson KI, Ruchelsman DE, Tejwani NC. Isolated tuberosity fractures of the proximal humeral: current concepts. Injury. 2008;39(3):284-298.
Proximal humerus fractures are the second most common fracture in the upper extremity, accounting for 4% to 5% of all fractures.1-4 The majority of these injuries can be treated without an operation. For fractures that require surgery, there are multiple options, including closed reduction, percutaneous pinning, open reduction and internal fixation (ORIF), hemiarthroplasty, and reverse total shoulder arthroplasty.3-9
Isolated greater tuberosity fractures (AO [Arbeitsgemeinschaft für Osteosynthesefragen] 11.A1) make up a small subset of proximal humerus fractures. In general, patients who sustain an isolated greater tuberosity fracture are younger and more active than those who sustain other proximal humerus fractures.2,10 As a result, in the treatment of greater tuberosity fractures, there is increased emphasis on return to high activity and function. Nondisplaced or minimally displaced fractures typically are treated nonoperatively with good success.11,12 Patients with fractures displaced more than 5 mm, and highly active patients with fractures displaced more than 3 mm, usually are recommended for surgical treatment.2,11-14 The many options for treating these difficult fractures include suture fixation, percutaneous techniques, screw fixation, and, more recently, arthroscopic suture techniques.2,5,13,15,16 The goal of any of these operative interventions is to restore normal function and minimize pain around the injured shoulder. Although most of the operative techniques for greater tuberosity fractures have predictable results, none has been established as the gold standard for the treatment of displaced greater tuberosity fractures.2,5,13,15-18 Use of plate osteosynthesis for displaced proximal humerus fractures not isolated to the greater tuberosity is becoming more widespread in the orthopedic community.1,4,19,20 However, the orthopedic literature includes very few reports of using this technique for isolated displaced greater tuberosity fractures.18 This surgical approach potentially provides increased stability, improved maintenance of reduction, and earlier range of motion (ROM) in the postoperative period. These outcomes in turn may allow for improved pain control and earlier return to normal activities than is the case with other operative interventions for these difficult injuries.
We conducted a study to determine the radiographic and clinical outcomes of plate osteosynthesis for displaced greater tuberosity fractures. We hypothesized that excellent clinical and radiographic outcomes could be achieved using this surgical technique.
Patients and Methods
After obtaining institutional review board approval for this study, we retrospectively identified 11 consecutive patients with an isolated displaced greater tuberosity fracture (AO 11.A1) treated with plate osteosynthesis by Dr. Getz between December 2009 and May 2011 (Figures 1A, 1B). We collected data on age at time of surgery, sex, length of follow-up, worker’s compensation status, and complications. At a minimum of 21 months (mean, 27 months; SD, 8 months; range, 16-44 months), we assessed ROM and administered validated outcome scores, including the Single Assessment Numeric Evaluation (SANE)21,22 and the Penn Shoulder Score (PSS).23
Surgical Technique
The deltopectoral approach was used in all 11 patients. A standard incision was made over the deltopectoral interval starting at the coracoid and extending about 6 cm toward the deltoid insertion. After the internervous plane was entered between the deltoid and pectoralis major, the clavipectoral fascia was divided. The greater tuberosity fracture was identified with the leading edge of the fracture 1 cm posterior to the bicipital groove in all cases. Organized hematoma was removed from the fracture site to allow reduction. Three 1-mm braided polyester tapes were placed into the rotator cuff at the insertion onto the greater tuberosity fragment. The sutures thus captured the fragment and were used to obtain reduction and fixation. The fragment was provisionally pinned by placing a 2.0-mm Kirschner wire high on the fragment as to not block plate application. Fluoroscopic imaging was used to determine the appropriate position of the fracture reduction. A standard periarticular proximal humerus 3.5-mm locking compression plate (Zimmer) was used in all patients. The plate was contoured to achieve more compression in several cases in which plastic deformation or comminution was present. The sutures that were attached to the greater tuberosity were then brought through the plate. The plate was then slid down onto the humerus and pinned under fluoroscopic guidance. Three bicortical screws were used to affix the plate to the humeral shaft to compress the fracture into the fracture bed. Two to 4 locking screws were placed into the humeral head to improve the rotational stability of the construct. Last, the sutures through the plate were tied for added fixation.
Rehabilitation
In the immediate postoperative period, all patients were placed in a standard shoulder sling. The sling was worn for 6 weeks. At 2 weeks, patients started formal, standardized physical therapy, including passive ROM for elevation and external rotation. At 6 weeks, they began internal rotation stretching and active-assisted motion. Cuff strengthening began gently, as motion and pain allowed, after 8 weeks. Formal physical therapy continued until full or maximal improvement in motion and strength had been achieved.
Radiographic Measurements
Union/malunion was assessed by 2 orthopedic surgeons during their fellowship year in shoulder and elbow surgery. These surgeons were blinded to patients’ clinical outcomes. Each surgeon reviewed each patient’s radiographs twice to determine whether the reduction was anatomical. Anatomical reduction was achieved if the greater-tuberosity-to-head height was between 4 and 10 mm. Malunion was defined as loss of more than 3 mm of anatomical fracture reduction (from the original reduction) on any radiologic view at most recent follow-up. Loss of reduction was considered minimal if the fracture fragment was displaced less than 3 mm.
Statistical Analysis
A descriptive analysis of patient variables and outcomes was used for this small cohort of patients. Statistical significance was set at α = 0.05.
Results
Eleven patients (7 women, 4 men) underwent plate osteosynthesis for an isolated greater tuberosity fracture (Figure 2). Mean age at surgery was 60 years (range, 37-71 years). All patients were right-hand–dominant; 7 of the 11 sustained the injury on the dominant side. For all 11 patients, final postoperative ROM and complications were recorded. No patient required additional surgery. Before injury, all patients felt their shoulder was 100% normal. Nine of the 11 patients were available for assessment of functional outcome and ROM at a mean (SD) of 27 (8) months (range, 16-44 months). At final follow-up, mean (SD) forward elevation was 147° (28°; range, 100°-180°), and mean (SD) external rotation was 25° (15°; range, 10°-60°). Mean (SD) SANE score was 72 (17; range, 50-90), and mean (SD) PSS was 79 (16; range 43-90). On a 1-to-10 scale, patients’ mean (SD) overall satisfaction was 8.6 (1.9; range, 4-10). Of the 9 patients who worked before injury, 8 returned to preoperative duty. Six patients reported stiffness (consistent with ROM). All patients said they would have the surgery again (Table).
All patients experienced radiographic union. Three of the 11 had minimal (<3 mm) loss of reduction. Mean (SD) time to union was 10.7 (4.2) weeks (range, 6.1-21.6 weeks). There were no wound complications and no need for any hardware removal.
Discussion
Isolated greater tuberosity fractures are less common than other types of proximal humerus fractures but often require surgical intervention for less displacement when compared with those fractures.2,14 Multiple techniques (eg, suture fixation, percutaneous pinning, arthroscopic techniques) have been used, but none has established itself as the gold standard for treatment of these difficult injuries.2,5,9,11,13-16 The results of the present study show that plate osteosynthesis can reliably be used to achieve anatomical reduction and good functional outcomes in isolated greater tuberosity fractures. Even with the added stability of the plate and suture construct, a small number of fractures still displaced. In addition, despite having achieved anatomical union, many patients in this study experienced stiffness and functional loss, which speaks to the challenges associated with management of these fractures.
Self-reported outcomes were less favorable for patients in our study (despite achieving mean forward elevation of 147°) than for patients who underwent greater tuberosity repair in other studies.2,5,10 In a study of 12 patients who underwent ORIF of a 2-part displaced fracture of the greater tuberosity of the proximal part of the humerus, Flatow and colleagues5 found half the patients had an excellent outcome, and the other half had a good outcome with active elevation averaging 170°. In another study, conducted over 11 years, 165 patients with a proximal humeral fracture were treated with transosseous suture fixation. Union occurred in all patients except the 2 patients with 3-part fractures, and 155 patients had excellent or very good fracture reduction.10 Therefore, final ROM for these patients may not be a good indicator of actual final function, and previous reports likely underestimated the functional loss experienced by these patients.
The incidence of isolated greater tuberosity fractures likely will increase as the population ages and becomes more active.2,14,16 Patients with isolated greater tuberosity fractures are more likely to be male, to be younger, and to have fewer medical problems than patients with other types of proximal humerus fractures.14 In addition, patient expectations regarding life after displaced greater tuberosity fractures are unique compared with expectations of patients who have other proximal humerus fractures; displaced greater tuberosity fractures usually occur in more active patients, who may expect to return to work and may place higher demands on themselves after treatment,2,14,16,24 possibly leading to lower subjective clinical outcomes.
Various operative treatment techniques for isolated greater tuberosity fractures have been described. Flatow and colleagues5 reported excellent return of forward elevation after ORIF with heavy suture, and half the patients reported excellent outcomes. Other techniques have had mixed results. Bhatia and colleagues11 reported on long-term outcomes of internal fixation using a double row of suture anchors in isolated, displaced greater tuberosity fractures in 21 patients. Outcomes were rated excellent in 8 patients, good in 10, satisfactory in 2, and unsatisfactory in 1. Braunstein and colleagues12 examined the biomechanical strength of various fixation constructs and found that tension band wiring or cancellous screws were superior to suture fixation. More recently, Ji and colleagues13 described encouraging outcomes of arthroscopic fixation of isolated displaced proximal humerus fractures in 16 patients. Mean postoperative American Shoulder and Elbow Surgeons (ASES) score was 88, and mean improvement in University of California, Los Angeles (UCLA) score was 31 points. In addition, mean forward elevation was 148.7° at most recent follow-up.
Our technique supplements the literature on greater tuberosity fracture fixation by using a plate as the point for suture fixation rather than suture anchors or screw fixation. As has been shown with 3- and 4-part fractures, plate osteosynthesis provides proximal suture fixation points and locking screws (often in poor-quality bone) that can prevent suture cut-out and isolated screw failure. In addition, compared with other techniques for greater tuberosity fixation, meta-diaphyseal cortical plate fixation bypasses the often poor bone quality of the greater tuberosity, preventing these modes of failure.18 Schoffl and colleagues18 reported on 10 patients who received a Bamberg plate; all 10 had excellent postoperative outcomes with no complications or secondary loss of reduction. Outcomes in the present study mirror those in the literature for operative fixation of displaced greater tuberosity fractures. Despite the near anatomical reduction in the majority of patients (mean forward elevation, 147°), functional results in this patient population remain guarded, with many patients reporting only good clinical outcomes.
This study had a few limitations. First is the inherent limitation of a retrospective study. Second, the small sample size limited the subgroup analysis. However, given the rarity of the injury and the single-surgeon series, we would have to have added considerable time to the study to increase its power. Third, there was no control group. This is a difficult situation with displaced fractures, as clinical outcomes are poorer with nonoperative management than with operative intervention.2,16,17 Compared with historical operative controls in the literature, our patients compare favorably over medium-term follow-up.2,5,15,16
Conclusion
Plate osteosynthesis is a novel technique in the treatment of displaced greater tuberosity fractures. It results in excellent fracture reduction, a 100% union rate, minimal fracture migration, and good return of ROM. However, self-reported functional assessment of the shoulder was about three-fourths of what is expected of normal or preinjury function.
Proximal humerus fractures are the second most common fracture in the upper extremity, accounting for 4% to 5% of all fractures.1-4 The majority of these injuries can be treated without an operation. For fractures that require surgery, there are multiple options, including closed reduction, percutaneous pinning, open reduction and internal fixation (ORIF), hemiarthroplasty, and reverse total shoulder arthroplasty.3-9
Isolated greater tuberosity fractures (AO [Arbeitsgemeinschaft für Osteosynthesefragen] 11.A1) make up a small subset of proximal humerus fractures. In general, patients who sustain an isolated greater tuberosity fracture are younger and more active than those who sustain other proximal humerus fractures.2,10 As a result, in the treatment of greater tuberosity fractures, there is increased emphasis on return to high activity and function. Nondisplaced or minimally displaced fractures typically are treated nonoperatively with good success.11,12 Patients with fractures displaced more than 5 mm, and highly active patients with fractures displaced more than 3 mm, usually are recommended for surgical treatment.2,11-14 The many options for treating these difficult fractures include suture fixation, percutaneous techniques, screw fixation, and, more recently, arthroscopic suture techniques.2,5,13,15,16 The goal of any of these operative interventions is to restore normal function and minimize pain around the injured shoulder. Although most of the operative techniques for greater tuberosity fractures have predictable results, none has been established as the gold standard for the treatment of displaced greater tuberosity fractures.2,5,13,15-18 Use of plate osteosynthesis for displaced proximal humerus fractures not isolated to the greater tuberosity is becoming more widespread in the orthopedic community.1,4,19,20 However, the orthopedic literature includes very few reports of using this technique for isolated displaced greater tuberosity fractures.18 This surgical approach potentially provides increased stability, improved maintenance of reduction, and earlier range of motion (ROM) in the postoperative period. These outcomes in turn may allow for improved pain control and earlier return to normal activities than is the case with other operative interventions for these difficult injuries.
We conducted a study to determine the radiographic and clinical outcomes of plate osteosynthesis for displaced greater tuberosity fractures. We hypothesized that excellent clinical and radiographic outcomes could be achieved using this surgical technique.
Patients and Methods
After obtaining institutional review board approval for this study, we retrospectively identified 11 consecutive patients with an isolated displaced greater tuberosity fracture (AO 11.A1) treated with plate osteosynthesis by Dr. Getz between December 2009 and May 2011 (Figures 1A, 1B). We collected data on age at time of surgery, sex, length of follow-up, worker’s compensation status, and complications. At a minimum of 21 months (mean, 27 months; SD, 8 months; range, 16-44 months), we assessed ROM and administered validated outcome scores, including the Single Assessment Numeric Evaluation (SANE)21,22 and the Penn Shoulder Score (PSS).23
Surgical Technique
The deltopectoral approach was used in all 11 patients. A standard incision was made over the deltopectoral interval starting at the coracoid and extending about 6 cm toward the deltoid insertion. After the internervous plane was entered between the deltoid and pectoralis major, the clavipectoral fascia was divided. The greater tuberosity fracture was identified with the leading edge of the fracture 1 cm posterior to the bicipital groove in all cases. Organized hematoma was removed from the fracture site to allow reduction. Three 1-mm braided polyester tapes were placed into the rotator cuff at the insertion onto the greater tuberosity fragment. The sutures thus captured the fragment and were used to obtain reduction and fixation. The fragment was provisionally pinned by placing a 2.0-mm Kirschner wire high on the fragment as to not block plate application. Fluoroscopic imaging was used to determine the appropriate position of the fracture reduction. A standard periarticular proximal humerus 3.5-mm locking compression plate (Zimmer) was used in all patients. The plate was contoured to achieve more compression in several cases in which plastic deformation or comminution was present. The sutures that were attached to the greater tuberosity were then brought through the plate. The plate was then slid down onto the humerus and pinned under fluoroscopic guidance. Three bicortical screws were used to affix the plate to the humeral shaft to compress the fracture into the fracture bed. Two to 4 locking screws were placed into the humeral head to improve the rotational stability of the construct. Last, the sutures through the plate were tied for added fixation.
Rehabilitation
In the immediate postoperative period, all patients were placed in a standard shoulder sling. The sling was worn for 6 weeks. At 2 weeks, patients started formal, standardized physical therapy, including passive ROM for elevation and external rotation. At 6 weeks, they began internal rotation stretching and active-assisted motion. Cuff strengthening began gently, as motion and pain allowed, after 8 weeks. Formal physical therapy continued until full or maximal improvement in motion and strength had been achieved.
Radiographic Measurements
Union/malunion was assessed by 2 orthopedic surgeons during their fellowship year in shoulder and elbow surgery. These surgeons were blinded to patients’ clinical outcomes. Each surgeon reviewed each patient’s radiographs twice to determine whether the reduction was anatomical. Anatomical reduction was achieved if the greater-tuberosity-to-head height was between 4 and 10 mm. Malunion was defined as loss of more than 3 mm of anatomical fracture reduction (from the original reduction) on any radiologic view at most recent follow-up. Loss of reduction was considered minimal if the fracture fragment was displaced less than 3 mm.
Statistical Analysis
A descriptive analysis of patient variables and outcomes was used for this small cohort of patients. Statistical significance was set at α = 0.05.
Results
Eleven patients (7 women, 4 men) underwent plate osteosynthesis for an isolated greater tuberosity fracture (Figure 2). Mean age at surgery was 60 years (range, 37-71 years). All patients were right-hand–dominant; 7 of the 11 sustained the injury on the dominant side. For all 11 patients, final postoperative ROM and complications were recorded. No patient required additional surgery. Before injury, all patients felt their shoulder was 100% normal. Nine of the 11 patients were available for assessment of functional outcome and ROM at a mean (SD) of 27 (8) months (range, 16-44 months). At final follow-up, mean (SD) forward elevation was 147° (28°; range, 100°-180°), and mean (SD) external rotation was 25° (15°; range, 10°-60°). Mean (SD) SANE score was 72 (17; range, 50-90), and mean (SD) PSS was 79 (16; range 43-90). On a 1-to-10 scale, patients’ mean (SD) overall satisfaction was 8.6 (1.9; range, 4-10). Of the 9 patients who worked before injury, 8 returned to preoperative duty. Six patients reported stiffness (consistent with ROM). All patients said they would have the surgery again (Table).
All patients experienced radiographic union. Three of the 11 had minimal (<3 mm) loss of reduction. Mean (SD) time to union was 10.7 (4.2) weeks (range, 6.1-21.6 weeks). There were no wound complications and no need for any hardware removal.
Discussion
Isolated greater tuberosity fractures are less common than other types of proximal humerus fractures but often require surgical intervention for less displacement when compared with those fractures.2,14 Multiple techniques (eg, suture fixation, percutaneous pinning, arthroscopic techniques) have been used, but none has established itself as the gold standard for treatment of these difficult injuries.2,5,9,11,13-16 The results of the present study show that plate osteosynthesis can reliably be used to achieve anatomical reduction and good functional outcomes in isolated greater tuberosity fractures. Even with the added stability of the plate and suture construct, a small number of fractures still displaced. In addition, despite having achieved anatomical union, many patients in this study experienced stiffness and functional loss, which speaks to the challenges associated with management of these fractures.
Self-reported outcomes were less favorable for patients in our study (despite achieving mean forward elevation of 147°) than for patients who underwent greater tuberosity repair in other studies.2,5,10 In a study of 12 patients who underwent ORIF of a 2-part displaced fracture of the greater tuberosity of the proximal part of the humerus, Flatow and colleagues5 found half the patients had an excellent outcome, and the other half had a good outcome with active elevation averaging 170°. In another study, conducted over 11 years, 165 patients with a proximal humeral fracture were treated with transosseous suture fixation. Union occurred in all patients except the 2 patients with 3-part fractures, and 155 patients had excellent or very good fracture reduction.10 Therefore, final ROM for these patients may not be a good indicator of actual final function, and previous reports likely underestimated the functional loss experienced by these patients.
The incidence of isolated greater tuberosity fractures likely will increase as the population ages and becomes more active.2,14,16 Patients with isolated greater tuberosity fractures are more likely to be male, to be younger, and to have fewer medical problems than patients with other types of proximal humerus fractures.14 In addition, patient expectations regarding life after displaced greater tuberosity fractures are unique compared with expectations of patients who have other proximal humerus fractures; displaced greater tuberosity fractures usually occur in more active patients, who may expect to return to work and may place higher demands on themselves after treatment,2,14,16,24 possibly leading to lower subjective clinical outcomes.
Various operative treatment techniques for isolated greater tuberosity fractures have been described. Flatow and colleagues5 reported excellent return of forward elevation after ORIF with heavy suture, and half the patients reported excellent outcomes. Other techniques have had mixed results. Bhatia and colleagues11 reported on long-term outcomes of internal fixation using a double row of suture anchors in isolated, displaced greater tuberosity fractures in 21 patients. Outcomes were rated excellent in 8 patients, good in 10, satisfactory in 2, and unsatisfactory in 1. Braunstein and colleagues12 examined the biomechanical strength of various fixation constructs and found that tension band wiring or cancellous screws were superior to suture fixation. More recently, Ji and colleagues13 described encouraging outcomes of arthroscopic fixation of isolated displaced proximal humerus fractures in 16 patients. Mean postoperative American Shoulder and Elbow Surgeons (ASES) score was 88, and mean improvement in University of California, Los Angeles (UCLA) score was 31 points. In addition, mean forward elevation was 148.7° at most recent follow-up.
Our technique supplements the literature on greater tuberosity fracture fixation by using a plate as the point for suture fixation rather than suture anchors or screw fixation. As has been shown with 3- and 4-part fractures, plate osteosynthesis provides proximal suture fixation points and locking screws (often in poor-quality bone) that can prevent suture cut-out and isolated screw failure. In addition, compared with other techniques for greater tuberosity fixation, meta-diaphyseal cortical plate fixation bypasses the often poor bone quality of the greater tuberosity, preventing these modes of failure.18 Schoffl and colleagues18 reported on 10 patients who received a Bamberg plate; all 10 had excellent postoperative outcomes with no complications or secondary loss of reduction. Outcomes in the present study mirror those in the literature for operative fixation of displaced greater tuberosity fractures. Despite the near anatomical reduction in the majority of patients (mean forward elevation, 147°), functional results in this patient population remain guarded, with many patients reporting only good clinical outcomes.
This study had a few limitations. First is the inherent limitation of a retrospective study. Second, the small sample size limited the subgroup analysis. However, given the rarity of the injury and the single-surgeon series, we would have to have added considerable time to the study to increase its power. Third, there was no control group. This is a difficult situation with displaced fractures, as clinical outcomes are poorer with nonoperative management than with operative intervention.2,16,17 Compared with historical operative controls in the literature, our patients compare favorably over medium-term follow-up.2,5,15,16
Conclusion
Plate osteosynthesis is a novel technique in the treatment of displaced greater tuberosity fractures. It results in excellent fracture reduction, a 100% union rate, minimal fracture migration, and good return of ROM. However, self-reported functional assessment of the shoulder was about three-fourths of what is expected of normal or preinjury function.
1. Gardner MJ, Boraiah S, Helfet DL, Lorich DG. Indirect medial reduction and strut support of proximal humerus fractures using an endosteal implant.
J Orthop Trauma. 2008;22(3):195-200.
2. Green A, Izzi J Jr. Isolated fractures of the greater tuberosity of the proximal humerus. J Shoulder Elbow Surg. 2003;12(6):641-649.
3. Neer CS 2nd. Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am. 1970;52(6):1077-1089.
4. Ricchetti ET, DeMola PM, Roman D, Abboud JA. The use of precontoured humeral locking plates in the management of displaced proximal humerus fracture. J Am Acad Orthop Surg. 2009;17(9):582-590.
5. Flatow EL, Cuomo F, Maday MG, Miller SR, McIlveen SJ, Bigliani LU. Open reduction and internal fixation of two-part displaced fractures of the greater tuberosity of the proximal part of the humerus. J Bone Joint Surg Am. 1991;73(8):1213-1218.
6. Lenarz C, Shishani Y, McCrum C, Nowinski RJ, Edwards TB, Gobezie R. Is reverse shoulder arthroplasty appropriate for the treatment of fractures in the older patient? Early observations. Clin Orthop Relat Res. 2011;469(12):3324-3331.
7. Park MC, Murthi AM, Roth NS, Blaine TA, Levine WN, Bigliani LU. Two-part and three-part fractures of the proximal humerus treated with suture fixation. J Orthop Trauma. 2003;17(5):319-325.
8. Young SW, Segal BS, Turner PC, Poon PC. Comparison of functional outcomes of reverse shoulder arthroplasty versus hemiarthroplasty in the primary treatment of acute proximal humerus fracture. ANZ J Surg. 2010;80(11):789-793.
9. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. J Bone Joint Surg Am. 2007;89(8):1700-1709.
10. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. Surgical technique. J Bone Joint Surg Am. 2009;91(suppl 2, pt 1):8-21.
11. Bhatia DN, van Rooyen KS, du Toit DF, de Beer JF. Surgical treatment of comminuted, displaced fractures of the greater tuberosity of the proximal humerus: a new technique of double-row suture-anchor fixation and long-term results. Injury. 2006;37(10):946-952.
12. Braunstein V, Wiedemann E, Plitz W, Muensterer OJ, Mutschler W, Hinterwimmer S. Operative treatment of greater tuberosity fractures of the humerus—a biomechanical analysis. Clin Biomech. 2007;22(6):652-657.
13. Ji JH, Shafi M, Song IS, Kim YY, McFarland EG, Moon CY. Arthroscopic fixation technique for comminuted, displaced greater tuberosity fracture. Arthroscopy. 2010;26(5):600-609.
14. Kim E, Shin HK, Kim CH. Characteristics of an isolated greater tuberosity fracture of the humerus. J Orthop Sci. 2005;10(5):441-444.
15. Lee SU, Jeong C, Park IJ. Arthroscopic fixation of displaced greater tuberosity fracture of the proximal humerus. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):378-380.
16. Mattyasovszky SG, Burkhart KJ, Ahlers C, et al. Isolated fractures of the greater tuberosity of the proximal humerus. Acta Orthop. 2011;82(6):714-720.
17. Platzer P, Thalhammer G, Oberleitner G, et al. Displaced fractures of the greater tuberosity: a comparison of operative and nonoperative treatment. J Trauma. 2008;65(4):843-848.
18. Schoffl V, Popp D, Strecker W. A simple and effective implant for displaced fractures of the greater tuberosity: the “Bamberg” plate. Arch Orthop Trauma Surg. 2011;131(4):509-512.
19. Gardner MJ, Boraiah S, Helfet DL, Lorich DG. The anterolateral acromial approach for fractures of the proximal humerus. J Orthop Trauma. 2008;22(2):132-137.
20. Ricchetti ET, Warrender WJ, Abboud JA. Use of locking plates in the treatment of proximal humerus fractures. J Shoulder Elbow Surg. 2010;19(2 suppl):66-75.
21. 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.
22. Williams GN, Taylor DC, Gangel TJ, Uhorchak JM, Arciero RA. Comparison of the Single Assessment Numeric Evaluation method and the Lysholm score. Clin Orthop Relat Res. 2000;(373):184-192.
23. Leggin BG, Michener LA, Shaffer MA, Brenneman SK, Iannotti JP, Williams GR Jr. The Penn Shoulder Score: reliability and validity. J Orthop Sports Phys Ther. 2006;36(3):138-151.
24. Gruson KI, Ruchelsman DE, Tejwani NC. Isolated tuberosity fractures of the proximal humeral: current concepts. Injury. 2008;39(3):284-298.
1. Gardner MJ, Boraiah S, Helfet DL, Lorich DG. Indirect medial reduction and strut support of proximal humerus fractures using an endosteal implant.
J Orthop Trauma. 2008;22(3):195-200.
2. Green A, Izzi J Jr. Isolated fractures of the greater tuberosity of the proximal humerus. J Shoulder Elbow Surg. 2003;12(6):641-649.
3. Neer CS 2nd. Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am. 1970;52(6):1077-1089.
4. Ricchetti ET, DeMola PM, Roman D, Abboud JA. The use of precontoured humeral locking plates in the management of displaced proximal humerus fracture. J Am Acad Orthop Surg. 2009;17(9):582-590.
5. Flatow EL, Cuomo F, Maday MG, Miller SR, McIlveen SJ, Bigliani LU. Open reduction and internal fixation of two-part displaced fractures of the greater tuberosity of the proximal part of the humerus. J Bone Joint Surg Am. 1991;73(8):1213-1218.
6. Lenarz C, Shishani Y, McCrum C, Nowinski RJ, Edwards TB, Gobezie R. Is reverse shoulder arthroplasty appropriate for the treatment of fractures in the older patient? Early observations. Clin Orthop Relat Res. 2011;469(12):3324-3331.
7. Park MC, Murthi AM, Roth NS, Blaine TA, Levine WN, Bigliani LU. Two-part and three-part fractures of the proximal humerus treated with suture fixation. J Orthop Trauma. 2003;17(5):319-325.
8. Young SW, Segal BS, Turner PC, Poon PC. Comparison of functional outcomes of reverse shoulder arthroplasty versus hemiarthroplasty in the primary treatment of acute proximal humerus fracture. ANZ J Surg. 2010;80(11):789-793.
9. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. J Bone Joint Surg Am. 2007;89(8):1700-1709.
10. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. Surgical technique. J Bone Joint Surg Am. 2009;91(suppl 2, pt 1):8-21.
11. Bhatia DN, van Rooyen KS, du Toit DF, de Beer JF. Surgical treatment of comminuted, displaced fractures of the greater tuberosity of the proximal humerus: a new technique of double-row suture-anchor fixation and long-term results. Injury. 2006;37(10):946-952.
12. Braunstein V, Wiedemann E, Plitz W, Muensterer OJ, Mutschler W, Hinterwimmer S. Operative treatment of greater tuberosity fractures of the humerus—a biomechanical analysis. Clin Biomech. 2007;22(6):652-657.
13. Ji JH, Shafi M, Song IS, Kim YY, McFarland EG, Moon CY. Arthroscopic fixation technique for comminuted, displaced greater tuberosity fracture. Arthroscopy. 2010;26(5):600-609.
14. Kim E, Shin HK, Kim CH. Characteristics of an isolated greater tuberosity fracture of the humerus. J Orthop Sci. 2005;10(5):441-444.
15. Lee SU, Jeong C, Park IJ. Arthroscopic fixation of displaced greater tuberosity fracture of the proximal humerus. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):378-380.
16. Mattyasovszky SG, Burkhart KJ, Ahlers C, et al. Isolated fractures of the greater tuberosity of the proximal humerus. Acta Orthop. 2011;82(6):714-720.
17. Platzer P, Thalhammer G, Oberleitner G, et al. Displaced fractures of the greater tuberosity: a comparison of operative and nonoperative treatment. J Trauma. 2008;65(4):843-848.
18. Schoffl V, Popp D, Strecker W. A simple and effective implant for displaced fractures of the greater tuberosity: the “Bamberg” plate. Arch Orthop Trauma Surg. 2011;131(4):509-512.
19. Gardner MJ, Boraiah S, Helfet DL, Lorich DG. The anterolateral acromial approach for fractures of the proximal humerus. J Orthop Trauma. 2008;22(2):132-137.
20. Ricchetti ET, Warrender WJ, Abboud JA. Use of locking plates in the treatment of proximal humerus fractures. J Shoulder Elbow Surg. 2010;19(2 suppl):66-75.
21. 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.
22. Williams GN, Taylor DC, Gangel TJ, Uhorchak JM, Arciero RA. Comparison of the Single Assessment Numeric Evaluation method and the Lysholm score. Clin Orthop Relat Res. 2000;(373):184-192.
23. Leggin BG, Michener LA, Shaffer MA, Brenneman SK, Iannotti JP, Williams GR Jr. The Penn Shoulder Score: reliability and validity. J Orthop Sports Phys Ther. 2006;36(3):138-151.
24. Gruson KI, Ruchelsman DE, Tejwani NC. Isolated tuberosity fractures of the proximal humeral: current concepts. Injury. 2008;39(3):284-298.
CMS Proposes Major Initiative for Hip and Knee Replacements
In an attempt to reduce the rate and cost of complications following hip and knee replacements among Medicare beneficiaries, the Centers for Medicare & Medicaid Services (CMS) announced a new Comprehensive Care for Joint Replacement payment model. With this new measure, the CMS proposes to hold hospitals accountable for the quality of care they deliver to Medicare fee-for-service beneficiaries for hip and knee replacements from surgery through recovery.
“We are committed to changing our health care system to pay for quality over quantity, so that we spend our dollars more wisely and improve care for patients,” said Sylvia M. Burwell, Secretary of Health and Human Services.
Through the proposed 5-year payment model, health care providers in 75 geographic areas would continue to be paid under existing Medicare payment systems. However, the hospital where the hip or knee replacement is performed would be held liable for the quality and costs of care for the duration of care, from the time of the surgery through 90 days after discharge.
Depending on the hospital’s quality and cost performance during the episode, the hospital may receive an additional payment or be required to repay Medicare for a portion of the episode costs. As a result, hospitals would have an incentive to work with physicians, home health agencies, and nursing facilities to ensure that beneficiaries receive the coordinated care they need, with the goal of reducing avoidable hospitalizations and complications. Hospitals would receive tools, such as spending and utilization data and sharing of best practices, to improve the effectiveness of care coordination.
These bundled payments for joint replacement surgeries would build upon successful demonstration programs already underway in Medicare. This model is also consistent with the private sector, where major employers and leading providers and care systems are moving towards bundled payments for orthopedic services.
“Today, we are taking another important step to improve the quality of care for the hundreds of thousands of Americans who have hip and knee replacements through Medicare every year. By focusing on episodes of care, rather than a piecemeal system, hospitals and physicians have an incentive to work together to deliver more effective and efficient care. This model will incentivize providing patients with the right care the first time and finding better ways to help them recover successfully. It will reward providers and doctors for helping patients get and stay healthy, ” stated Ms. Burwell.
In an attempt to reduce the rate and cost of complications following hip and knee replacements among Medicare beneficiaries, the Centers for Medicare & Medicaid Services (CMS) announced a new Comprehensive Care for Joint Replacement payment model. With this new measure, the CMS proposes to hold hospitals accountable for the quality of care they deliver to Medicare fee-for-service beneficiaries for hip and knee replacements from surgery through recovery.
“We are committed to changing our health care system to pay for quality over quantity, so that we spend our dollars more wisely and improve care for patients,” said Sylvia M. Burwell, Secretary of Health and Human Services.
Through the proposed 5-year payment model, health care providers in 75 geographic areas would continue to be paid under existing Medicare payment systems. However, the hospital where the hip or knee replacement is performed would be held liable for the quality and costs of care for the duration of care, from the time of the surgery through 90 days after discharge.
Depending on the hospital’s quality and cost performance during the episode, the hospital may receive an additional payment or be required to repay Medicare for a portion of the episode costs. As a result, hospitals would have an incentive to work with physicians, home health agencies, and nursing facilities to ensure that beneficiaries receive the coordinated care they need, with the goal of reducing avoidable hospitalizations and complications. Hospitals would receive tools, such as spending and utilization data and sharing of best practices, to improve the effectiveness of care coordination.
These bundled payments for joint replacement surgeries would build upon successful demonstration programs already underway in Medicare. This model is also consistent with the private sector, where major employers and leading providers and care systems are moving towards bundled payments for orthopedic services.
“Today, we are taking another important step to improve the quality of care for the hundreds of thousands of Americans who have hip and knee replacements through Medicare every year. By focusing on episodes of care, rather than a piecemeal system, hospitals and physicians have an incentive to work together to deliver more effective and efficient care. This model will incentivize providing patients with the right care the first time and finding better ways to help them recover successfully. It will reward providers and doctors for helping patients get and stay healthy, ” stated Ms. Burwell.
In an attempt to reduce the rate and cost of complications following hip and knee replacements among Medicare beneficiaries, the Centers for Medicare & Medicaid Services (CMS) announced a new Comprehensive Care for Joint Replacement payment model. With this new measure, the CMS proposes to hold hospitals accountable for the quality of care they deliver to Medicare fee-for-service beneficiaries for hip and knee replacements from surgery through recovery.
“We are committed to changing our health care system to pay for quality over quantity, so that we spend our dollars more wisely and improve care for patients,” said Sylvia M. Burwell, Secretary of Health and Human Services.
Through the proposed 5-year payment model, health care providers in 75 geographic areas would continue to be paid under existing Medicare payment systems. However, the hospital where the hip or knee replacement is performed would be held liable for the quality and costs of care for the duration of care, from the time of the surgery through 90 days after discharge.
Depending on the hospital’s quality and cost performance during the episode, the hospital may receive an additional payment or be required to repay Medicare for a portion of the episode costs. As a result, hospitals would have an incentive to work with physicians, home health agencies, and nursing facilities to ensure that beneficiaries receive the coordinated care they need, with the goal of reducing avoidable hospitalizations and complications. Hospitals would receive tools, such as spending and utilization data and sharing of best practices, to improve the effectiveness of care coordination.
These bundled payments for joint replacement surgeries would build upon successful demonstration programs already underway in Medicare. This model is also consistent with the private sector, where major employers and leading providers and care systems are moving towards bundled payments for orthopedic services.
“Today, we are taking another important step to improve the quality of care for the hundreds of thousands of Americans who have hip and knee replacements through Medicare every year. By focusing on episodes of care, rather than a piecemeal system, hospitals and physicians have an incentive to work together to deliver more effective and efficient care. This model will incentivize providing patients with the right care the first time and finding better ways to help them recover successfully. It will reward providers and doctors for helping patients get and stay healthy, ” stated Ms. Burwell.
