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

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Thu, 09/19/2019 - 13:21

Take-Home Points

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

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

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

Case Report

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

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

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

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

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

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

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

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

Discussion

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Take-Home Points

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

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

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

Case Report

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

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

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

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

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

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

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

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

Discussion

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

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

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

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

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

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

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

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

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

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

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

Take-Home Points

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

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

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

Case Report

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

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

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

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

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

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

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

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

Discussion

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Trans-Scaphoid Transcapitate Perilunate Fracture-Dislocation

Take-Home Points

  • TSTC-PLFD is a rare hyperextension wrist injury characterized by fracture of both the scaphoid and the capitate and rotation of the proximal bone fragment of the capitate.
  • TSTC-PLFD is associated by a complex ligamentous injury of the wrist.
  • Impaction of the wrist in extension seems to be the most important predictor of this injury.
  • Optimal treatment for TSTC-PLFD is open reduction, anatomical alignment, and ligamentous and osseous stabilization.
  • The most important complications of scaphoid and capitate fractures and PLFD are osteonecrosis and nonunion.

Trans-scaphoid transcapitate (TSTC) perilunate fracture-dislocation (PLFD) is a rare hyperextension wrist injury characterized by fracture of both the scaphoid and the capitate and rotation of the proximal bone fragment of the capitate.1 Isolated capitate fractures with or without rotation of its proximal fragment have been well described.2,3 Obviously, this specific type of injury represents just the osseous part of a more complex ligamentous wrist injury.2,3

TSTC-PLFD was first described by Nicholson4 in 1940. In 1956, Fenton5 coined the term scaphocapitate syndrome, which became widely known. With PLFD, accurate diagnosis may be delayed. Usually, only the scaphoid fracture is identified by radiologic examination, and thus the severity of the injury is underestimated and appropriate treatment delayed.3,6,7 The English literature includes only case reports and small series on this rare perilunate injury.6-9 In this article, we report the case of an adult with TSTC-PLFD. We describe the radiographic and intraoperative findings, review the current surgical principles for reduction and stabilization of this injury, and assess the clinical and radiologic outcomes. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 32-year-old man sustained an isolated injury of his right (dominant) hand after falling from a height of 6 feet and landing on his outstretched right arm with the wrist in extension.

Figure 1.
Physical examination at admission revealed swelling over the dorsum of the wrist and pain on palpation. Radiographs showed a fracture of the waist of the scaphoid (Figure 1). In addition, the capitate was fractured with the proximal fragment rotated 180° (Figure 1, Figure 2). A small avulsion fracture on the dorsal surface of the wrist was obvious as well (Figure 2).
Figure 2.
A perilunate injury was diagnosed and surgical treatment recommended.

With the patient under general anesthesia and a humerus tourniquet applied, an external fixator was placed for spanning of the wrist joint. The dorsal aspect of the wrist joint was approached through a midline longitudinal 5-cm incision, centered over the Lister tubercle. For adequate exposure of the dorsal wrist, a flap of the dorsal capsule was raised with the apex at the triquetrum and a radial broad base, as previously described.9 An avulsion fracture at the insertion of the dorsal capsule to the triquetrum was observed. The dorsal surface of the hamate and lunate showed a small area of bone contusion with hemorrhagic infiltration. The scapholunate and lunotriquetral ligaments were intact. The proximal fragment of the capitate was identified deep into the space between the lunate and distal capitate fragment; the articular surface of the bone fragment was rotated 180° distally (Figure 3).

Figure 3.
Distraction was applied through the external fixator, and the bone fragment was removed from the surgical site. The cartilaginous surface was scratched, but no chondral flap or defect was observed. Hematoma and debris were removed, and the bone fragment was restored to its anatomical position. Two 1.6-mm Kirschner wires (K-wires) were inserted in a distal-to-proximal direction to stabilize the capitate fracture without engaging the lunate. The scaphoid fracture was reduced and stabilized with an antegrade double-threaded compression screw. Then, both K-wires were advanced proximally, engaging the lunate, to try to enhance midcarpus anteroposterior stability (Figure 4).
Figure 4.
The scapholunate and lunotriquetral intervals were stable. Last, the wound was sutured in layers, and the external fixator was locked with the wrist in 0° of flexion-extension and 0° of radioulnar deviation.

Skin sutures were removed 2 weeks after surgery, K-wires 6 weeks after surgery, and the external fixator 8 weeks after surgery. At 8 weeks, radiographs showed healing of both fractures, scaphoid and capitate. The patient was allowed gradual passive and active-assisted range-of-motion exercises of the wrist at 8 weeks, and he returned to work 3 months after surgery. At 12-month follow-up, all fractures were completely healed, and the wrist was stable and pain-free.
Figure 5.
At 24-month follow-up, the patient was asymptomatic, had no ulnar translation of the right wrist joint, and showed full range of pronation-supination, a 10° lag of wrist flexion, and a 20° lag of extension in comparison with the left wrist. Mayo wrist score was excellent (95 points). Radiographs of the right wrist showed fracture healing and ligamentous stability of the carpal joints (Figure 5).

 

 

Discussion

The exact biomechanism of TSTC-PLFD is unclear. Impaction of the wrist in extension seems to be the most important predictor of this injury.5,7,9-11 According to Stein and Siegel,10 scaphoid fractures first allow hyperextension of the wrist; the lunate and the capitate rotate dorsally, and the dorsal surface of the capitate impacts the dorsal edge of the distal radius, causing a fracture of the neck of the capitate. If the wrist continues to rotate into further hyperextension, the unsupported, proximal part of the capitate rotates 90° around itself.9,10 When the carpus returns to neutral position, the bone fragment of the capitate rotates further, reaching a position of 180°, with its proximal articular surface facing distally. In this type of injury, the axis of rotation is transverse (radioulnar), in contrast to the perpendicular (anteroposterior) axis of rotation suggested by the initial report by Fenton.5 The scaphoid is fractured by impaction of the radial styloid process. Monahan and Galasko11 reported a case of capitate fracture with palmar displacement and 90° rotation of the proximal bone fragment; the fragmented surface was facing dorsally. A transverse axis of rotation, as in our patient’s case, could explain this type of displacement supporting the mechanism of injury proposed by Stein and Siegel.10 Vance and colleagues7 described various patterns of scaphocapitate fractures and concluded that no single mechanism of injury accounts for these types of injuries. Other authors have considered scaphocapitate syndrome as a specific type of TSTC-PLFD, one that reduces either spontaneously or with manipulation.1,3,12 Detailed evaluation of standard anteroposterior and lateral wrist radiographs can provide enough evidence for the diagnosis of this injury. Computed tomography may define further the type and extent of injury.7 In our patient’s case, wrist impaction caused the scaphoid and capitate fractures and the avulsion of the capsule attachment to the triquetrum. The distal fragment of the capitate subluxated dorsally in relation to the lunate. The lateral radiograph of the wrist showed its position in the lunate fossa. According to the classification of Herzberg and colleagues12 and Mayfield and colleagues,13 this represents a dorsal PLFD of the greater carpal bones arc.

Conservative treatment is not recommended for PLFD because closed reduction usually is not possible, and poor functional outcomes are common. Instead, optimal treatment is open reduction, anatomical alignment, and ligamentous and osseous stabilization.7,12,14,15 Dorsal, palmar, and combined approaches have been used in surgery for perilunate injuries. A dorsal approach through a radius-based capsular flap allows excellent exposure of the dorsal wrist and facilitates reduction of fractures.9 Capitate reduction should precede scaphoid reduction because scaphoid reduction cannot be easily maintained, especially when the fracture interface is comminuted.7 In addition, scaphoid reduction may be guided from the radial surface of the capitate. Moreover, when the scaphoid is fixated first, reduction of the rotated head of the capitate usually is difficult. In our patient’s case, traction applied through the external fixator facilitated reduction and K-wire fixation of the capitate fracture. After scaphoid fixation, the K-wires were advanced through the capitate to the lunate to stabilize the capitolunate joint. The wrist must be immobilized for 6 to 8 weeks after surgical repair of PLFD. A cast can be used, but, as with our patient, an external fixator facilitates fracture reduction and wrist stability during osteosynthesis. During immobilization, the wrist should be maintained in neutral position to avoid stretching the dorsal and palmar wrist capsule and ligaments.16The most important complications of scaphoid and capitate fractures and PLFD are osteonecrosis and nonunion.17-20 Similar to scaphoid fractures, capitate fractures proximal to the waist of the capitate are associated with increased risk of osteonecrosis. Therefore, anatomical reduction and stabilization favor revascularization of the proximal bone fragment. Moreover, any osteonecrosis that occurs in the proximal part of the capitate is not an indication for further surgery as long as wrist height is maintained. Nonunion is not common after open reduction and internal fixation of PLFD (eg, our patient’s fractures healed completely).17 Radiographically, nonunion is characterized by bone absorption and sclerosis of the ends of the bone. Treatment of capitate nonunion depends on symptom severity, bone fragment size, and radiographic evidence of arthritic changes.3,7,21-23 Treatment options include resection of sclerotic edges, bone grafting, and stabilization21 and removal of the proximal capitate fragment and limited arthrodesis,22 as arthritic changes likely are inevitable.22,23TSTC-PLFD is a rare wrist injury. Careful radiographic evaluation of the carpal bones and their relationships on both anteroposterior and lateral views is mandatory in making the correct diagnosis. Open reduction (preferably with use of an external fixator) and internal fixation are recommended for optimal healing and functional outcomes.

Am J Orthop. 2017;46(4):E230-E234. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Johnson RP. The acutely injured wrist and its residuals. Clin Orthop Relat Res. 1980;(149):33-44.

2. Volk AG, Schnall SB, Merkle P, Stevanovic M. Unusual capitate fracture: a case report. J Hand Surg Am. 1995;20(4):581-582.

3. Apergis E, Darmanis S, Kastanis G, Papanikolaou A. Does the term scaphocapitate syndrome need to be revised? A report of 6 cases. J Hand Surg Br. 2001;26(5):441-445.

4. Nicholson CB. Fracture dislocation of the os magnum. J Roy Navy Med Serv. 1940;26:289-291.

5. Fenton RL. The naviculo-capitate fracture syndrome. J Bone Joint Surg Am. 1956;38(3):681-684.

6. Strohm PC, Laier P, Müller CA, Gutorski S, Pfister U. Scaphocapitate fracture syndrome of both hands—first description of a bilateral occurrence of a rare carpal injury [in German]. Unfallchirurg. 2003;106(4):339-342.

7. Vance RM, Gelberman R, Evans EF. Scaphocapitate fractures. Patterns of dislocation, mechanisms of injury, and preliminary results of treatment. J Bone Joint Surg Am. 1980;62(2):271-276.

8. Apostolides JG, Lifchez SD, Christy MR. Complex and rare fracture patterns in perilunate dislocations. Hand. 2011;6(3):287-294.

9. Berger RA, Bishop AT, Bettinger PC. New dorsal capsulotomy for the surgical exposure of the wrist. Ann Plast Surg. 1995;35(1):54-59.

10. Stein F, Siegel MW. Naviculocapitate fracture syndrome. A case report: new thoughts on the mechanism of injury. J Bone Joint Surg Am. 1969;51(2):391-395.

11. Monahan PR, Galasko CS. The scapho-capitate fracture syndrome. A mechanism of injury. J Bone Joint Surg Br. 1972;54(1):122-124.

12. Herzberg G, Comtet JJ, Linscheid RL, Amadio PC, Cooney WP, Stalder J. Perilunate dislocations and fracture-dislocations: a multicenter study. J Hand Surg Am. 1993;18(5):768-779.

13. Mayfield JK, Johnson RP, Kilcoyne RK. Carpal dislocations: pathomechanics and progressive perilunar instability. J Hand Surg Am. 1980;5(3):226-241.

14. Moneim MS, Hofammann KE 3rd, Omer GE. Transscaphoid perilunate fracture-dislocation. Result of open reduction and pin fixation. Clin Orthop Relat Res. 1984;(190):227-235.

15. Andreasi A, Coppo M, Danda F. Trans-scapho-capitate perilunar dislocation of the carpus. Ital J Orthop Traumatol. 1986;12(4):461-466.

16. Song D, Goodman S, Gilula LA, Wollstein R. Ulnocarpal translation in perilunate dislocations. J Hand Surg Eur. 2009;34(3):388-390.

17. Rand JA, Linscheid RL, Dobyns JH. Capitate fractures: a long-term follow-up. Clin Orthop Relat Res. 1982;(165):209-216.

18. Panagis JS, Gelberman RH, Taleisnik J, Baumgaertner M. The arterial anatomy of the human carpus. Part II: the intraosseous vascularity. J Hand Surg Am. 1983;8(4):375-382.

19. Freedman DM, Botte MJ, Gelberman RH. Vascularity of the carpus. Clin Orthop Relat Res. 2001;(383):47-59.

20. Vander Grend R, Dell PC, Glowczewskie F, Leslie B, Ruby LK. Intraosseous blood supply of the capitate and its correlation with aseptic necrosis. J Hand Surg Am. 1984;9(5):677-683.

21. Rico AA, Holguin PH, Martin JG. Pseudarthrosis of the capitate. J Hand Surg Br. 1999;24(3):382-384.

22. Kumar A, Olney DB. Multiple carpometacarpal dislocations. J Accid Emerg Med. 1994;11(4):257-258.

23. Kohut GN. Extra-articular fractures of the distal radius in young adults. A technique of closed reposition and stabilisation by mono-segmental, radio-radial external fixator. Ann Chir Main Memb Super. 1995;14(1):14-19.

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Take-Home Points

  • TSTC-PLFD is a rare hyperextension wrist injury characterized by fracture of both the scaphoid and the capitate and rotation of the proximal bone fragment of the capitate.
  • TSTC-PLFD is associated by a complex ligamentous injury of the wrist.
  • Impaction of the wrist in extension seems to be the most important predictor of this injury.
  • Optimal treatment for TSTC-PLFD is open reduction, anatomical alignment, and ligamentous and osseous stabilization.
  • The most important complications of scaphoid and capitate fractures and PLFD are osteonecrosis and nonunion.

Trans-scaphoid transcapitate (TSTC) perilunate fracture-dislocation (PLFD) is a rare hyperextension wrist injury characterized by fracture of both the scaphoid and the capitate and rotation of the proximal bone fragment of the capitate.1 Isolated capitate fractures with or without rotation of its proximal fragment have been well described.2,3 Obviously, this specific type of injury represents just the osseous part of a more complex ligamentous wrist injury.2,3

TSTC-PLFD was first described by Nicholson4 in 1940. In 1956, Fenton5 coined the term scaphocapitate syndrome, which became widely known. With PLFD, accurate diagnosis may be delayed. Usually, only the scaphoid fracture is identified by radiologic examination, and thus the severity of the injury is underestimated and appropriate treatment delayed.3,6,7 The English literature includes only case reports and small series on this rare perilunate injury.6-9 In this article, we report the case of an adult with TSTC-PLFD. We describe the radiographic and intraoperative findings, review the current surgical principles for reduction and stabilization of this injury, and assess the clinical and radiologic outcomes. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 32-year-old man sustained an isolated injury of his right (dominant) hand after falling from a height of 6 feet and landing on his outstretched right arm with the wrist in extension.

Figure 1.
Physical examination at admission revealed swelling over the dorsum of the wrist and pain on palpation. Radiographs showed a fracture of the waist of the scaphoid (Figure 1). In addition, the capitate was fractured with the proximal fragment rotated 180° (Figure 1, Figure 2). A small avulsion fracture on the dorsal surface of the wrist was obvious as well (Figure 2).
Figure 2.
A perilunate injury was diagnosed and surgical treatment recommended.

With the patient under general anesthesia and a humerus tourniquet applied, an external fixator was placed for spanning of the wrist joint. The dorsal aspect of the wrist joint was approached through a midline longitudinal 5-cm incision, centered over the Lister tubercle. For adequate exposure of the dorsal wrist, a flap of the dorsal capsule was raised with the apex at the triquetrum and a radial broad base, as previously described.9 An avulsion fracture at the insertion of the dorsal capsule to the triquetrum was observed. The dorsal surface of the hamate and lunate showed a small area of bone contusion with hemorrhagic infiltration. The scapholunate and lunotriquetral ligaments were intact. The proximal fragment of the capitate was identified deep into the space between the lunate and distal capitate fragment; the articular surface of the bone fragment was rotated 180° distally (Figure 3).

Figure 3.
Distraction was applied through the external fixator, and the bone fragment was removed from the surgical site. The cartilaginous surface was scratched, but no chondral flap or defect was observed. Hematoma and debris were removed, and the bone fragment was restored to its anatomical position. Two 1.6-mm Kirschner wires (K-wires) were inserted in a distal-to-proximal direction to stabilize the capitate fracture without engaging the lunate. The scaphoid fracture was reduced and stabilized with an antegrade double-threaded compression screw. Then, both K-wires were advanced proximally, engaging the lunate, to try to enhance midcarpus anteroposterior stability (Figure 4).
Figure 4.
The scapholunate and lunotriquetral intervals were stable. Last, the wound was sutured in layers, and the external fixator was locked with the wrist in 0° of flexion-extension and 0° of radioulnar deviation.

Skin sutures were removed 2 weeks after surgery, K-wires 6 weeks after surgery, and the external fixator 8 weeks after surgery. At 8 weeks, radiographs showed healing of both fractures, scaphoid and capitate. The patient was allowed gradual passive and active-assisted range-of-motion exercises of the wrist at 8 weeks, and he returned to work 3 months after surgery. At 12-month follow-up, all fractures were completely healed, and the wrist was stable and pain-free.
Figure 5.
At 24-month follow-up, the patient was asymptomatic, had no ulnar translation of the right wrist joint, and showed full range of pronation-supination, a 10° lag of wrist flexion, and a 20° lag of extension in comparison with the left wrist. Mayo wrist score was excellent (95 points). Radiographs of the right wrist showed fracture healing and ligamentous stability of the carpal joints (Figure 5).

 

 

Discussion

The exact biomechanism of TSTC-PLFD is unclear. Impaction of the wrist in extension seems to be the most important predictor of this injury.5,7,9-11 According to Stein and Siegel,10 scaphoid fractures first allow hyperextension of the wrist; the lunate and the capitate rotate dorsally, and the dorsal surface of the capitate impacts the dorsal edge of the distal radius, causing a fracture of the neck of the capitate. If the wrist continues to rotate into further hyperextension, the unsupported, proximal part of the capitate rotates 90° around itself.9,10 When the carpus returns to neutral position, the bone fragment of the capitate rotates further, reaching a position of 180°, with its proximal articular surface facing distally. In this type of injury, the axis of rotation is transverse (radioulnar), in contrast to the perpendicular (anteroposterior) axis of rotation suggested by the initial report by Fenton.5 The scaphoid is fractured by impaction of the radial styloid process. Monahan and Galasko11 reported a case of capitate fracture with palmar displacement and 90° rotation of the proximal bone fragment; the fragmented surface was facing dorsally. A transverse axis of rotation, as in our patient’s case, could explain this type of displacement supporting the mechanism of injury proposed by Stein and Siegel.10 Vance and colleagues7 described various patterns of scaphocapitate fractures and concluded that no single mechanism of injury accounts for these types of injuries. Other authors have considered scaphocapitate syndrome as a specific type of TSTC-PLFD, one that reduces either spontaneously or with manipulation.1,3,12 Detailed evaluation of standard anteroposterior and lateral wrist radiographs can provide enough evidence for the diagnosis of this injury. Computed tomography may define further the type and extent of injury.7 In our patient’s case, wrist impaction caused the scaphoid and capitate fractures and the avulsion of the capsule attachment to the triquetrum. The distal fragment of the capitate subluxated dorsally in relation to the lunate. The lateral radiograph of the wrist showed its position in the lunate fossa. According to the classification of Herzberg and colleagues12 and Mayfield and colleagues,13 this represents a dorsal PLFD of the greater carpal bones arc.

Conservative treatment is not recommended for PLFD because closed reduction usually is not possible, and poor functional outcomes are common. Instead, optimal treatment is open reduction, anatomical alignment, and ligamentous and osseous stabilization.7,12,14,15 Dorsal, palmar, and combined approaches have been used in surgery for perilunate injuries. A dorsal approach through a radius-based capsular flap allows excellent exposure of the dorsal wrist and facilitates reduction of fractures.9 Capitate reduction should precede scaphoid reduction because scaphoid reduction cannot be easily maintained, especially when the fracture interface is comminuted.7 In addition, scaphoid reduction may be guided from the radial surface of the capitate. Moreover, when the scaphoid is fixated first, reduction of the rotated head of the capitate usually is difficult. In our patient’s case, traction applied through the external fixator facilitated reduction and K-wire fixation of the capitate fracture. After scaphoid fixation, the K-wires were advanced through the capitate to the lunate to stabilize the capitolunate joint. The wrist must be immobilized for 6 to 8 weeks after surgical repair of PLFD. A cast can be used, but, as with our patient, an external fixator facilitates fracture reduction and wrist stability during osteosynthesis. During immobilization, the wrist should be maintained in neutral position to avoid stretching the dorsal and palmar wrist capsule and ligaments.16The most important complications of scaphoid and capitate fractures and PLFD are osteonecrosis and nonunion.17-20 Similar to scaphoid fractures, capitate fractures proximal to the waist of the capitate are associated with increased risk of osteonecrosis. Therefore, anatomical reduction and stabilization favor revascularization of the proximal bone fragment. Moreover, any osteonecrosis that occurs in the proximal part of the capitate is not an indication for further surgery as long as wrist height is maintained. Nonunion is not common after open reduction and internal fixation of PLFD (eg, our patient’s fractures healed completely).17 Radiographically, nonunion is characterized by bone absorption and sclerosis of the ends of the bone. Treatment of capitate nonunion depends on symptom severity, bone fragment size, and radiographic evidence of arthritic changes.3,7,21-23 Treatment options include resection of sclerotic edges, bone grafting, and stabilization21 and removal of the proximal capitate fragment and limited arthrodesis,22 as arthritic changes likely are inevitable.22,23TSTC-PLFD is a rare wrist injury. Careful radiographic evaluation of the carpal bones and their relationships on both anteroposterior and lateral views is mandatory in making the correct diagnosis. Open reduction (preferably with use of an external fixator) and internal fixation are recommended for optimal healing and functional outcomes.

Am J Orthop. 2017;46(4):E230-E234. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • TSTC-PLFD is a rare hyperextension wrist injury characterized by fracture of both the scaphoid and the capitate and rotation of the proximal bone fragment of the capitate.
  • TSTC-PLFD is associated by a complex ligamentous injury of the wrist.
  • Impaction of the wrist in extension seems to be the most important predictor of this injury.
  • Optimal treatment for TSTC-PLFD is open reduction, anatomical alignment, and ligamentous and osseous stabilization.
  • The most important complications of scaphoid and capitate fractures and PLFD are osteonecrosis and nonunion.

Trans-scaphoid transcapitate (TSTC) perilunate fracture-dislocation (PLFD) is a rare hyperextension wrist injury characterized by fracture of both the scaphoid and the capitate and rotation of the proximal bone fragment of the capitate.1 Isolated capitate fractures with or without rotation of its proximal fragment have been well described.2,3 Obviously, this specific type of injury represents just the osseous part of a more complex ligamentous wrist injury.2,3

TSTC-PLFD was first described by Nicholson4 in 1940. In 1956, Fenton5 coined the term scaphocapitate syndrome, which became widely known. With PLFD, accurate diagnosis may be delayed. Usually, only the scaphoid fracture is identified by radiologic examination, and thus the severity of the injury is underestimated and appropriate treatment delayed.3,6,7 The English literature includes only case reports and small series on this rare perilunate injury.6-9 In this article, we report the case of an adult with TSTC-PLFD. We describe the radiographic and intraoperative findings, review the current surgical principles for reduction and stabilization of this injury, and assess the clinical and radiologic outcomes. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 32-year-old man sustained an isolated injury of his right (dominant) hand after falling from a height of 6 feet and landing on his outstretched right arm with the wrist in extension.

Figure 1.
Physical examination at admission revealed swelling over the dorsum of the wrist and pain on palpation. Radiographs showed a fracture of the waist of the scaphoid (Figure 1). In addition, the capitate was fractured with the proximal fragment rotated 180° (Figure 1, Figure 2). A small avulsion fracture on the dorsal surface of the wrist was obvious as well (Figure 2).
Figure 2.
A perilunate injury was diagnosed and surgical treatment recommended.

With the patient under general anesthesia and a humerus tourniquet applied, an external fixator was placed for spanning of the wrist joint. The dorsal aspect of the wrist joint was approached through a midline longitudinal 5-cm incision, centered over the Lister tubercle. For adequate exposure of the dorsal wrist, a flap of the dorsal capsule was raised with the apex at the triquetrum and a radial broad base, as previously described.9 An avulsion fracture at the insertion of the dorsal capsule to the triquetrum was observed. The dorsal surface of the hamate and lunate showed a small area of bone contusion with hemorrhagic infiltration. The scapholunate and lunotriquetral ligaments were intact. The proximal fragment of the capitate was identified deep into the space between the lunate and distal capitate fragment; the articular surface of the bone fragment was rotated 180° distally (Figure 3).

Figure 3.
Distraction was applied through the external fixator, and the bone fragment was removed from the surgical site. The cartilaginous surface was scratched, but no chondral flap or defect was observed. Hematoma and debris were removed, and the bone fragment was restored to its anatomical position. Two 1.6-mm Kirschner wires (K-wires) were inserted in a distal-to-proximal direction to stabilize the capitate fracture without engaging the lunate. The scaphoid fracture was reduced and stabilized with an antegrade double-threaded compression screw. Then, both K-wires were advanced proximally, engaging the lunate, to try to enhance midcarpus anteroposterior stability (Figure 4).
Figure 4.
The scapholunate and lunotriquetral intervals were stable. Last, the wound was sutured in layers, and the external fixator was locked with the wrist in 0° of flexion-extension and 0° of radioulnar deviation.

Skin sutures were removed 2 weeks after surgery, K-wires 6 weeks after surgery, and the external fixator 8 weeks after surgery. At 8 weeks, radiographs showed healing of both fractures, scaphoid and capitate. The patient was allowed gradual passive and active-assisted range-of-motion exercises of the wrist at 8 weeks, and he returned to work 3 months after surgery. At 12-month follow-up, all fractures were completely healed, and the wrist was stable and pain-free.
Figure 5.
At 24-month follow-up, the patient was asymptomatic, had no ulnar translation of the right wrist joint, and showed full range of pronation-supination, a 10° lag of wrist flexion, and a 20° lag of extension in comparison with the left wrist. Mayo wrist score was excellent (95 points). Radiographs of the right wrist showed fracture healing and ligamentous stability of the carpal joints (Figure 5).

 

 

Discussion

The exact biomechanism of TSTC-PLFD is unclear. Impaction of the wrist in extension seems to be the most important predictor of this injury.5,7,9-11 According to Stein and Siegel,10 scaphoid fractures first allow hyperextension of the wrist; the lunate and the capitate rotate dorsally, and the dorsal surface of the capitate impacts the dorsal edge of the distal radius, causing a fracture of the neck of the capitate. If the wrist continues to rotate into further hyperextension, the unsupported, proximal part of the capitate rotates 90° around itself.9,10 When the carpus returns to neutral position, the bone fragment of the capitate rotates further, reaching a position of 180°, with its proximal articular surface facing distally. In this type of injury, the axis of rotation is transverse (radioulnar), in contrast to the perpendicular (anteroposterior) axis of rotation suggested by the initial report by Fenton.5 The scaphoid is fractured by impaction of the radial styloid process. Monahan and Galasko11 reported a case of capitate fracture with palmar displacement and 90° rotation of the proximal bone fragment; the fragmented surface was facing dorsally. A transverse axis of rotation, as in our patient’s case, could explain this type of displacement supporting the mechanism of injury proposed by Stein and Siegel.10 Vance and colleagues7 described various patterns of scaphocapitate fractures and concluded that no single mechanism of injury accounts for these types of injuries. Other authors have considered scaphocapitate syndrome as a specific type of TSTC-PLFD, one that reduces either spontaneously or with manipulation.1,3,12 Detailed evaluation of standard anteroposterior and lateral wrist radiographs can provide enough evidence for the diagnosis of this injury. Computed tomography may define further the type and extent of injury.7 In our patient’s case, wrist impaction caused the scaphoid and capitate fractures and the avulsion of the capsule attachment to the triquetrum. The distal fragment of the capitate subluxated dorsally in relation to the lunate. The lateral radiograph of the wrist showed its position in the lunate fossa. According to the classification of Herzberg and colleagues12 and Mayfield and colleagues,13 this represents a dorsal PLFD of the greater carpal bones arc.

Conservative treatment is not recommended for PLFD because closed reduction usually is not possible, and poor functional outcomes are common. Instead, optimal treatment is open reduction, anatomical alignment, and ligamentous and osseous stabilization.7,12,14,15 Dorsal, palmar, and combined approaches have been used in surgery for perilunate injuries. A dorsal approach through a radius-based capsular flap allows excellent exposure of the dorsal wrist and facilitates reduction of fractures.9 Capitate reduction should precede scaphoid reduction because scaphoid reduction cannot be easily maintained, especially when the fracture interface is comminuted.7 In addition, scaphoid reduction may be guided from the radial surface of the capitate. Moreover, when the scaphoid is fixated first, reduction of the rotated head of the capitate usually is difficult. In our patient’s case, traction applied through the external fixator facilitated reduction and K-wire fixation of the capitate fracture. After scaphoid fixation, the K-wires were advanced through the capitate to the lunate to stabilize the capitolunate joint. The wrist must be immobilized for 6 to 8 weeks after surgical repair of PLFD. A cast can be used, but, as with our patient, an external fixator facilitates fracture reduction and wrist stability during osteosynthesis. During immobilization, the wrist should be maintained in neutral position to avoid stretching the dorsal and palmar wrist capsule and ligaments.16The most important complications of scaphoid and capitate fractures and PLFD are osteonecrosis and nonunion.17-20 Similar to scaphoid fractures, capitate fractures proximal to the waist of the capitate are associated with increased risk of osteonecrosis. Therefore, anatomical reduction and stabilization favor revascularization of the proximal bone fragment. Moreover, any osteonecrosis that occurs in the proximal part of the capitate is not an indication for further surgery as long as wrist height is maintained. Nonunion is not common after open reduction and internal fixation of PLFD (eg, our patient’s fractures healed completely).17 Radiographically, nonunion is characterized by bone absorption and sclerosis of the ends of the bone. Treatment of capitate nonunion depends on symptom severity, bone fragment size, and radiographic evidence of arthritic changes.3,7,21-23 Treatment options include resection of sclerotic edges, bone grafting, and stabilization21 and removal of the proximal capitate fragment and limited arthrodesis,22 as arthritic changes likely are inevitable.22,23TSTC-PLFD is a rare wrist injury. Careful radiographic evaluation of the carpal bones and their relationships on both anteroposterior and lateral views is mandatory in making the correct diagnosis. Open reduction (preferably with use of an external fixator) and internal fixation are recommended for optimal healing and functional outcomes.

Am J Orthop. 2017;46(4):E230-E234. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Johnson RP. The acutely injured wrist and its residuals. Clin Orthop Relat Res. 1980;(149):33-44.

2. Volk AG, Schnall SB, Merkle P, Stevanovic M. Unusual capitate fracture: a case report. J Hand Surg Am. 1995;20(4):581-582.

3. Apergis E, Darmanis S, Kastanis G, Papanikolaou A. Does the term scaphocapitate syndrome need to be revised? A report of 6 cases. J Hand Surg Br. 2001;26(5):441-445.

4. Nicholson CB. Fracture dislocation of the os magnum. J Roy Navy Med Serv. 1940;26:289-291.

5. Fenton RL. The naviculo-capitate fracture syndrome. J Bone Joint Surg Am. 1956;38(3):681-684.

6. Strohm PC, Laier P, Müller CA, Gutorski S, Pfister U. Scaphocapitate fracture syndrome of both hands—first description of a bilateral occurrence of a rare carpal injury [in German]. Unfallchirurg. 2003;106(4):339-342.

7. Vance RM, Gelberman R, Evans EF. Scaphocapitate fractures. Patterns of dislocation, mechanisms of injury, and preliminary results of treatment. J Bone Joint Surg Am. 1980;62(2):271-276.

8. Apostolides JG, Lifchez SD, Christy MR. Complex and rare fracture patterns in perilunate dislocations. Hand. 2011;6(3):287-294.

9. Berger RA, Bishop AT, Bettinger PC. New dorsal capsulotomy for the surgical exposure of the wrist. Ann Plast Surg. 1995;35(1):54-59.

10. Stein F, Siegel MW. Naviculocapitate fracture syndrome. A case report: new thoughts on the mechanism of injury. J Bone Joint Surg Am. 1969;51(2):391-395.

11. Monahan PR, Galasko CS. The scapho-capitate fracture syndrome. A mechanism of injury. J Bone Joint Surg Br. 1972;54(1):122-124.

12. Herzberg G, Comtet JJ, Linscheid RL, Amadio PC, Cooney WP, Stalder J. Perilunate dislocations and fracture-dislocations: a multicenter study. J Hand Surg Am. 1993;18(5):768-779.

13. Mayfield JK, Johnson RP, Kilcoyne RK. Carpal dislocations: pathomechanics and progressive perilunar instability. J Hand Surg Am. 1980;5(3):226-241.

14. Moneim MS, Hofammann KE 3rd, Omer GE. Transscaphoid perilunate fracture-dislocation. Result of open reduction and pin fixation. Clin Orthop Relat Res. 1984;(190):227-235.

15. Andreasi A, Coppo M, Danda F. Trans-scapho-capitate perilunar dislocation of the carpus. Ital J Orthop Traumatol. 1986;12(4):461-466.

16. Song D, Goodman S, Gilula LA, Wollstein R. Ulnocarpal translation in perilunate dislocations. J Hand Surg Eur. 2009;34(3):388-390.

17. Rand JA, Linscheid RL, Dobyns JH. Capitate fractures: a long-term follow-up. Clin Orthop Relat Res. 1982;(165):209-216.

18. Panagis JS, Gelberman RH, Taleisnik J, Baumgaertner M. The arterial anatomy of the human carpus. Part II: the intraosseous vascularity. J Hand Surg Am. 1983;8(4):375-382.

19. Freedman DM, Botte MJ, Gelberman RH. Vascularity of the carpus. Clin Orthop Relat Res. 2001;(383):47-59.

20. Vander Grend R, Dell PC, Glowczewskie F, Leslie B, Ruby LK. Intraosseous blood supply of the capitate and its correlation with aseptic necrosis. J Hand Surg Am. 1984;9(5):677-683.

21. Rico AA, Holguin PH, Martin JG. Pseudarthrosis of the capitate. J Hand Surg Br. 1999;24(3):382-384.

22. Kumar A, Olney DB. Multiple carpometacarpal dislocations. J Accid Emerg Med. 1994;11(4):257-258.

23. Kohut GN. Extra-articular fractures of the distal radius in young adults. A technique of closed reposition and stabilisation by mono-segmental, radio-radial external fixator. Ann Chir Main Memb Super. 1995;14(1):14-19.

References

1. Johnson RP. The acutely injured wrist and its residuals. Clin Orthop Relat Res. 1980;(149):33-44.

2. Volk AG, Schnall SB, Merkle P, Stevanovic M. Unusual capitate fracture: a case report. J Hand Surg Am. 1995;20(4):581-582.

3. Apergis E, Darmanis S, Kastanis G, Papanikolaou A. Does the term scaphocapitate syndrome need to be revised? A report of 6 cases. J Hand Surg Br. 2001;26(5):441-445.

4. Nicholson CB. Fracture dislocation of the os magnum. J Roy Navy Med Serv. 1940;26:289-291.

5. Fenton RL. The naviculo-capitate fracture syndrome. J Bone Joint Surg Am. 1956;38(3):681-684.

6. Strohm PC, Laier P, Müller CA, Gutorski S, Pfister U. Scaphocapitate fracture syndrome of both hands—first description of a bilateral occurrence of a rare carpal injury [in German]. Unfallchirurg. 2003;106(4):339-342.

7. Vance RM, Gelberman R, Evans EF. Scaphocapitate fractures. Patterns of dislocation, mechanisms of injury, and preliminary results of treatment. J Bone Joint Surg Am. 1980;62(2):271-276.

8. Apostolides JG, Lifchez SD, Christy MR. Complex and rare fracture patterns in perilunate dislocations. Hand. 2011;6(3):287-294.

9. Berger RA, Bishop AT, Bettinger PC. New dorsal capsulotomy for the surgical exposure of the wrist. Ann Plast Surg. 1995;35(1):54-59.

10. Stein F, Siegel MW. Naviculocapitate fracture syndrome. A case report: new thoughts on the mechanism of injury. J Bone Joint Surg Am. 1969;51(2):391-395.

11. Monahan PR, Galasko CS. The scapho-capitate fracture syndrome. A mechanism of injury. J Bone Joint Surg Br. 1972;54(1):122-124.

12. Herzberg G, Comtet JJ, Linscheid RL, Amadio PC, Cooney WP, Stalder J. Perilunate dislocations and fracture-dislocations: a multicenter study. J Hand Surg Am. 1993;18(5):768-779.

13. Mayfield JK, Johnson RP, Kilcoyne RK. Carpal dislocations: pathomechanics and progressive perilunar instability. J Hand Surg Am. 1980;5(3):226-241.

14. Moneim MS, Hofammann KE 3rd, Omer GE. Transscaphoid perilunate fracture-dislocation. Result of open reduction and pin fixation. Clin Orthop Relat Res. 1984;(190):227-235.

15. Andreasi A, Coppo M, Danda F. Trans-scapho-capitate perilunar dislocation of the carpus. Ital J Orthop Traumatol. 1986;12(4):461-466.

16. Song D, Goodman S, Gilula LA, Wollstein R. Ulnocarpal translation in perilunate dislocations. J Hand Surg Eur. 2009;34(3):388-390.

17. Rand JA, Linscheid RL, Dobyns JH. Capitate fractures: a long-term follow-up. Clin Orthop Relat Res. 1982;(165):209-216.

18. Panagis JS, Gelberman RH, Taleisnik J, Baumgaertner M. The arterial anatomy of the human carpus. Part II: the intraosseous vascularity. J Hand Surg Am. 1983;8(4):375-382.

19. Freedman DM, Botte MJ, Gelberman RH. Vascularity of the carpus. Clin Orthop Relat Res. 2001;(383):47-59.

20. Vander Grend R, Dell PC, Glowczewskie F, Leslie B, Ruby LK. Intraosseous blood supply of the capitate and its correlation with aseptic necrosis. J Hand Surg Am. 1984;9(5):677-683.

21. Rico AA, Holguin PH, Martin JG. Pseudarthrosis of the capitate. J Hand Surg Br. 1999;24(3):382-384.

22. Kumar A, Olney DB. Multiple carpometacarpal dislocations. J Accid Emerg Med. 1994;11(4):257-258.

23. Kohut GN. Extra-articular fractures of the distal radius in young adults. A technique of closed reposition and stabilisation by mono-segmental, radio-radial external fixator. Ann Chir Main Memb Super. 1995;14(1):14-19.

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Multimodality Approach to a Stener Lesion: Radiographic, Ultrasound, Magnetic Resonance Imaging, and Surgical Correlation

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Multimodality Approach to a Stener Lesion: Radiographic, Ultrasound, Magnetic Resonance Imaging, and Surgical Correlation

Take-Home Points

  • Torn, displaced, and entrapped UCL is a Stener lesion.
  • Hyperabduction injury with pain and joint laxity on examination.
  • MRI and ultrasound are useful in evaluating UCL tears.
  • Ultrasound offers dynamic evaluation.
  • Must be treated appropriately to avoid pain, instability, and osteoarthritis.

In the literature, hyperabduction injuries to the thumb metacarpophalangeal (MCP) joint have been referred to interchangeably as gamekeeper’s thumb and skier’s thumb. Historically, though, gamekeeper’s thumb was initially described in hunters with chronic injury to the ulnar collateral ligament (UCL),1 and skier’s thumb typically has been described as an acute hyperabduction injury of the UCL.2-5 The proximal portion of a torn UCL may retract with further abduction and displace dorsally, becoming entrapped by the adductor pollicis aponeurosis insertion, known as a Stener lesion.6

The first MCP joint is stabilized by static and dynamic structures that contribute in varying degrees in flexion and extension of the joint. The static stabilizers include the proper and accessory radial and UCLs, the palmar plate, and the dorsal capsule. The UCL originates at the dorsal ulnar aspect of the first metacarpal head at the metacarpal tubercle about 5 mm proximal to the articular surface. The UCL courses distally in the palmar direction to insert volar and proximal to the medial tubercle of the proximal phalanx about 3 mm distal to the articular surface.7 In flexion, the proper collateral ligament is taut and is the primary static stabilizer. In extension, the accessory collateral ligament, which inserts on the palmar plate, is taut and is the primary static stabilizer.8-11

The dynamic stabilizers include the extrinsic muscles (flexor pollicis longus, extensor pollicis longus and brevis) and the intrinsic muscles (abductor pollicis brevis, adductor pollicis, flexor pollicis brevis) inserting on the thumb at the distal phalanx and proximal phalanx and at the base of the first metacarpal.8-10

Figure 1.
The adductor pollicis originates from the volar third metacarpal, capitate, and hamate and has a dual insertion on the thumb.12 There is a direct insertion onto the palmar proximal phalanx at the medial tubercle, distal and dorsal to the phalangeal insertion of the UCL.
Figure 2.
There is also a broad aponeurosis that inserts onto the extensor hood expansion, dorsal to the insertion of the UCL (Figures 1A-1C and 2A, 2B).7,8,13

We report the case of an acute hyperabduction injury of the thumb MCP joint with radiographic, ultrasound, and magnetic resonance imaging (MRI) findings consistent with a Stener lesion and subsequently confirmed with intraoperative photographs. The patient provided written informed consent for print and electronic publication of this case report.

Clinical Findings

A 33-year-old healthy man had persistent left hand pain and grip weakness after performing a handstand. He presented to the orthopedic hand clinic 20 days after injury, having failed nonoperative management (use of nonsteroidal anti-inflammatory drugs and soft thumb spica splint). Physical examination revealed soft-tissue swelling and focal tenderness to palpation at the ulnar aspect of the thumb MCP joint. Despite bilateral first MCP joint laxity on varus and valgus stress without identification of a firm endpoint, pain was elicited only on valgus stress of the left first MCP joint. Given the laxity and the left thumb soft-tissue swelling with pain, plain radiographs, ultrasound, and MRI were used to evaluate for severity of presumed left thumb UCL injury.

Imaging Findings

Plain radiographs showed normal bony anatomy without fracture, normal joint space, and mild soft-tissue swelling at the left thumb MCP level (Figures 3A, 3B).

Figure 3.
Ultrasound confirmed a complete tear of the UCL, which was flipped in a proximal direction and projected dorsally in relation to the direct insertion of the adductor tendon (Figure 2B). MRI showed focal disruption of the UCL at the level of the left thumb MCP joint with associated MCP joint effusion (Figures 4A-4F).
Figure 4.
Low T1 signal intensity over the adductor aponeurosis at the level of the metacarpal head corresponded with the torn and proximally retracted UCL. There was associated bone marrow edema at the radial and volar aspects of the thumb metacarpal head and low-grade strain of the abductor pollicis brevis. The thumb flexor and extensor tendons appeared normal. Although possibly secondary to patient positioning, mild volar subluxation of the proximal phalanx in relation to the metacarpal head was queried.

 

 

Surgical Findings

Given laxity with pain at the UCL on stress testing, MRI and ultrasound findings, and continued pain and instability of the thumb with pinching and grasping during activities of daily living, the patient and orthopedic hand surgeon proceeded with surgical intervention. Preoperative examination under anesthesia confirmed significant laxity on valgus stress without a palpable endpoint (Figures 5A, 5B).

Figure 5.
During surgery, retraction of the extensor hood revealed the completely torn and displaced UCL, entrapped dorsally and proximally to the adductor aponeurosis, characteristic of a Stener lesion. After the primary repair of the UCL, the extensor hood was seen partially retracted in a normal location superficial to the normal deep position of the repaired UCL (Figures 6A, 6B).

Discussion

Hyperabduction injuries to the thumb may rupture the UCL of the MCP joint of the thumb or cause a bony avulsion of the base of the proximal phalanx. Injury to the UCL, most often at its distal portion,4,14,15 may result in a sprain or full-thickness tear of the ligament.

Figure 6.
Subsequently, the ligament may remain in situ, or the proximal segment may retract proximal to the adductor aponeurosis with continued abduction of the thumb. On release of the abduction force, the proximal UCL segment is displaced dorsally and proximally by the inferior aspect of the adductor aponeurosis. The UCL becomes entrapped by the adductor aponeurosis and cannot reduce spontaneously.15 This displacement was initially described by Stener6 in 1962 and is referred to as a Stener lesion (Figures 1A-1C).

It is vital for the radiologist to identify a Stener lesion because a nondisplaced tear of the UCL is often treated nonsurgically, but UCL tears displaced more than 3 mm and Stener lesions usually must be operated on to avoid chronic instability, pain, and osteoarthritis.2-5,8,12-23 Sensitivity and specificity of MRI in evaluating UCL injuries are reported to be almost 100%, with resolution of 1 mm using current surface coils.23 There are various UCL injury patterns, including partial tears, displaced and nondisplaced complete tears, and even complex injuries, such as an incomplete tear with the torn portion retracted as a Stener lesion.22 MRI is needed to establish the extent of injury, as 90% of complete tears that are displaced at least 3 mm, and all tears with retraction proximal and superficial to the aponeurosis (true Stener lesions), failed immobilization and required surgical treatment.23Although they vary in the literature, mean sensitivity and specificity of ultrasound in detecting UCL tears in level I studies have been reported as 76% and 81%, respectively.24 When Melville and colleagues21 applied their ultrasound criteria—including absence of normal UCL fibers traversing the first MCP joint as well as heterogeneous masslike tissue at least partially proximal to the apex of the metacarpal lateral tubercle—they were able to distinguish displaced full-thickness tears from nondisplaced full-thickness tears with 100% accuracy. Hergan and colleagues25 found that the diagnostic accuracy of MRI was superior to that of ultrasound; while MRI accuracy was perfect, 12% of patients were incorrectly diagnosed with ultrasound, with false-positive or false-negative tendon-edge displacement. In our experience, ultrasound is uniquely useful in its ability to characterize the real-time dynamic interaction of the UCL with the adductor aponeurosis. It has been observed that passive flexion of the first interphalangeal joint moves the adductor aponeurosis in isolation, allowing differentiation from the subjacent UCL.21 Had a partial tear been in the differential diagnosis of our patient’s Stener lesion, such a maneuver under ultrasound visualization would have solved the dilemma. In addition, ultrasound allows for comparison with the contralateral ligament at the time of examination should a diagnostic dilemma arise.

As many have reported both bony avulsion of the base of the proximal phalanx and concomitant injury to the UCL, identification of a bony avulsion does not exclude a ligamentous injury and the possibility of a Stener lesion (Figure 7).16,19

Figure 7.
In one study, 14% of patients with injury to the UCL sustained a concomitant bony avulsion of the UCL insertion.23 However, presence of the avulsion fragment did not alter management, and only those fragments involving more than 20% of the articular surface were considered true fractures and treated as such.

Conclusion

A Stener lesion—retraction of a completely torn UCL becoming entrapped dorsally and proximally to the adductor insertion—can cause pain, instability, and ultimately osteoarthritis if not treated appropriately. The orthopedic surgeon should have a high index of suspicion for a Stener lesion in the appropriate clinical scenario and consider all imaging modalities for diagnosis. Likewise, it is of utmost importance for the radiologist to identify imaging findings of a Stener lesion, as physical examination alone may be limited in its ability to characterize injury severity. Both MRI and ultrasound are useful in evaluating UCL tears, and ultrasound provides the additional benefit of dynamic visualization and comparison with the contralateral side.

Am J Orthop. 2017;46(3):E195-E199. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Campbell CS. Gamekeeper’s thumb. J Bone Joint Surg Br. 1955;37(1):148-149.

2. Anderson D. Skier’s thumb. Aust Family Physician. 2010;39(8):575-577.

3. Heim D. The skier’s thumb. Acta Orthop Belg. 1999;65(4):440-446.

4. Lohman M, Vasenius J, Kivisaari A, Kivisaari L. MR imaging in chronic rupture of the ulnar collateral ligament of the thumb. Acta Radiol. 2001;42(1):10-14.

5. Kundu N, Asfaw S, Polster J, Lohman R. The Stener lesion. Eplasty. 2012;12:ic11.

6. Stener B. Displacement of the ruptured ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Bone Joint Surg Br. 1962;44:869-879.

7. Carlson MG, Warner KK, Meyers KN, Hearns KA, Kok PL. Anatomy of the thumb metacarpophalangeal ulnar and radial collateral ligaments. J Hand Surg Am. 2012;37(10):2021-2026.

8. Heyman P. Injuries to the ulnar collateral ligament of the thumb metacarpophalangeal joint. J Am Acad Orthop Surg. 1997;5(4):224-229.

9. Minami A, An KN, Cooney WP 3rd, Linscheid RL, Chao EY. Ligamentous structures of the metacarpophalangeal joint: a quantitative anatomic study. J Orthop Res. 1984;1(4):361-368.

10. Heyman P, Gelberman RH, Duncan K, Hipp JA. Injuries of the ulnar collateral ligament of the thumb metacarpophalangeal joint. Biomechanical and prospective clinical studies on the usefulness of valgus stress testing. Clin Orthop Relat Res. 1993;(292):165-171.

11. Patel S, Potty A, Taylor EJ, Sorene ED. Collateral ligament injuries of the metacarpophalangeal joint of the thumb: a treatment algorithm. Strategies Trauma Limb Reconstr. 2010;5(1):1-10.

12. O’Callaghan BI, Kohut G, Hoogewoud HM. Gamekeeper thumb: identification of the Stener lesion with US. Radiology. 1994;192(2):477-480.

13. Ebrahim FS, De Maeseneer M, Jager T, Marcelis S, Jamadar DA, Jacobson JA. US diagnosis of UCL tears of the thumb and Stener lesions: technique, pattern-based approach, and differential diagnosis. Radiographics. 2006;26(4):1007-1020.

14. Haramati N, Hiller N, Dowdle J, et al. MRI of the Stener lesion. Skeletal Radiol. 1995;24(7):515-518.

15. Shinohara T, Horii E, Majima M, et al. Sonographic diagnosis of acute injuries of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Clin Ultrasound. 2007;35(2):73-77.

16. Giele H, Martin J. The two-level ulnar collateral ligament injury of the metacarpophalangeal joint of the thumb. J Hand Surg Br. 2003;28(1):92-93.

17. Kaplan SJ. The Stener lesion revisited: a case report. J Hand Surg Am. 1998;23(5):833-836.

18. Thirkannad S, Wolff TW. The “two fleck sign” for an occult Stener lesion. J Hand Surg Eur Vol. 2008;33(2):208-211.

19. Badawi RA, Hussain S, Compson JP. Two in one: a variant of the Stener lesion. Injury. 2002;33(4):379-380.

20. McKeon KE, Gelberman RH, Calfee RP. Ulnar collateral ligament injuries of the thumb: phalangeal translation during valgus stress in human cadavera. J Bone Joint Surg Am. 2013;95(10):881-887.

21. Melville D, Jacobson JA, Haase S, Brandon C, Brigido MK, Fessell D. Ultrasound of displaced ulnar collateral ligament tears of the thumb: the Stener lesion revisited. Skeletal Radiol. 2013;42(5):667-673.

22. Romano WM, Garvin G, Bhayana D, Chaudhary O. The spectrum of ulnar collateral ligament injuries as viewed on magnetic resonance imaging of the metacarpophalangeal joint of the thumb. Can Assoc Radiol J. 2003;54(4):243-248.

23. Milner CS, Manon-Matos Y, Thirkannad SM. Gamekeeper’s thumb—a treatment-oriented magnetic resonance imaging classification. J Hand Surg Am. 2015;40(1):90-95.

24. Papandrea RF, Fowler T. Injury at the thumb UCL: is there a Stener lesion? J Hand Surg Am. 2008;33(10):1882-1884.

25. Hergan K, Mittler C, Oser W. Ulnar collateral ligament: differentiation of displaced and nondisplaced tears with US and MR imaging. Radiology. 1995;194(1):65-71.

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Take-Home Points

  • Torn, displaced, and entrapped UCL is a Stener lesion.
  • Hyperabduction injury with pain and joint laxity on examination.
  • MRI and ultrasound are useful in evaluating UCL tears.
  • Ultrasound offers dynamic evaluation.
  • Must be treated appropriately to avoid pain, instability, and osteoarthritis.

In the literature, hyperabduction injuries to the thumb metacarpophalangeal (MCP) joint have been referred to interchangeably as gamekeeper’s thumb and skier’s thumb. Historically, though, gamekeeper’s thumb was initially described in hunters with chronic injury to the ulnar collateral ligament (UCL),1 and skier’s thumb typically has been described as an acute hyperabduction injury of the UCL.2-5 The proximal portion of a torn UCL may retract with further abduction and displace dorsally, becoming entrapped by the adductor pollicis aponeurosis insertion, known as a Stener lesion.6

The first MCP joint is stabilized by static and dynamic structures that contribute in varying degrees in flexion and extension of the joint. The static stabilizers include the proper and accessory radial and UCLs, the palmar plate, and the dorsal capsule. The UCL originates at the dorsal ulnar aspect of the first metacarpal head at the metacarpal tubercle about 5 mm proximal to the articular surface. The UCL courses distally in the palmar direction to insert volar and proximal to the medial tubercle of the proximal phalanx about 3 mm distal to the articular surface.7 In flexion, the proper collateral ligament is taut and is the primary static stabilizer. In extension, the accessory collateral ligament, which inserts on the palmar plate, is taut and is the primary static stabilizer.8-11

The dynamic stabilizers include the extrinsic muscles (flexor pollicis longus, extensor pollicis longus and brevis) and the intrinsic muscles (abductor pollicis brevis, adductor pollicis, flexor pollicis brevis) inserting on the thumb at the distal phalanx and proximal phalanx and at the base of the first metacarpal.8-10

Figure 1.
The adductor pollicis originates from the volar third metacarpal, capitate, and hamate and has a dual insertion on the thumb.12 There is a direct insertion onto the palmar proximal phalanx at the medial tubercle, distal and dorsal to the phalangeal insertion of the UCL.
Figure 2.
There is also a broad aponeurosis that inserts onto the extensor hood expansion, dorsal to the insertion of the UCL (Figures 1A-1C and 2A, 2B).7,8,13

We report the case of an acute hyperabduction injury of the thumb MCP joint with radiographic, ultrasound, and magnetic resonance imaging (MRI) findings consistent with a Stener lesion and subsequently confirmed with intraoperative photographs. The patient provided written informed consent for print and electronic publication of this case report.

Clinical Findings

A 33-year-old healthy man had persistent left hand pain and grip weakness after performing a handstand. He presented to the orthopedic hand clinic 20 days after injury, having failed nonoperative management (use of nonsteroidal anti-inflammatory drugs and soft thumb spica splint). Physical examination revealed soft-tissue swelling and focal tenderness to palpation at the ulnar aspect of the thumb MCP joint. Despite bilateral first MCP joint laxity on varus and valgus stress without identification of a firm endpoint, pain was elicited only on valgus stress of the left first MCP joint. Given the laxity and the left thumb soft-tissue swelling with pain, plain radiographs, ultrasound, and MRI were used to evaluate for severity of presumed left thumb UCL injury.

Imaging Findings

Plain radiographs showed normal bony anatomy without fracture, normal joint space, and mild soft-tissue swelling at the left thumb MCP level (Figures 3A, 3B).

Figure 3.
Ultrasound confirmed a complete tear of the UCL, which was flipped in a proximal direction and projected dorsally in relation to the direct insertion of the adductor tendon (Figure 2B). MRI showed focal disruption of the UCL at the level of the left thumb MCP joint with associated MCP joint effusion (Figures 4A-4F).
Figure 4.
Low T1 signal intensity over the adductor aponeurosis at the level of the metacarpal head corresponded with the torn and proximally retracted UCL. There was associated bone marrow edema at the radial and volar aspects of the thumb metacarpal head and low-grade strain of the abductor pollicis brevis. The thumb flexor and extensor tendons appeared normal. Although possibly secondary to patient positioning, mild volar subluxation of the proximal phalanx in relation to the metacarpal head was queried.

 

 

Surgical Findings

Given laxity with pain at the UCL on stress testing, MRI and ultrasound findings, and continued pain and instability of the thumb with pinching and grasping during activities of daily living, the patient and orthopedic hand surgeon proceeded with surgical intervention. Preoperative examination under anesthesia confirmed significant laxity on valgus stress without a palpable endpoint (Figures 5A, 5B).

Figure 5.
During surgery, retraction of the extensor hood revealed the completely torn and displaced UCL, entrapped dorsally and proximally to the adductor aponeurosis, characteristic of a Stener lesion. After the primary repair of the UCL, the extensor hood was seen partially retracted in a normal location superficial to the normal deep position of the repaired UCL (Figures 6A, 6B).

Discussion

Hyperabduction injuries to the thumb may rupture the UCL of the MCP joint of the thumb or cause a bony avulsion of the base of the proximal phalanx. Injury to the UCL, most often at its distal portion,4,14,15 may result in a sprain or full-thickness tear of the ligament.

Figure 6.
Subsequently, the ligament may remain in situ, or the proximal segment may retract proximal to the adductor aponeurosis with continued abduction of the thumb. On release of the abduction force, the proximal UCL segment is displaced dorsally and proximally by the inferior aspect of the adductor aponeurosis. The UCL becomes entrapped by the adductor aponeurosis and cannot reduce spontaneously.15 This displacement was initially described by Stener6 in 1962 and is referred to as a Stener lesion (Figures 1A-1C).

It is vital for the radiologist to identify a Stener lesion because a nondisplaced tear of the UCL is often treated nonsurgically, but UCL tears displaced more than 3 mm and Stener lesions usually must be operated on to avoid chronic instability, pain, and osteoarthritis.2-5,8,12-23 Sensitivity and specificity of MRI in evaluating UCL injuries are reported to be almost 100%, with resolution of 1 mm using current surface coils.23 There are various UCL injury patterns, including partial tears, displaced and nondisplaced complete tears, and even complex injuries, such as an incomplete tear with the torn portion retracted as a Stener lesion.22 MRI is needed to establish the extent of injury, as 90% of complete tears that are displaced at least 3 mm, and all tears with retraction proximal and superficial to the aponeurosis (true Stener lesions), failed immobilization and required surgical treatment.23Although they vary in the literature, mean sensitivity and specificity of ultrasound in detecting UCL tears in level I studies have been reported as 76% and 81%, respectively.24 When Melville and colleagues21 applied their ultrasound criteria—including absence of normal UCL fibers traversing the first MCP joint as well as heterogeneous masslike tissue at least partially proximal to the apex of the metacarpal lateral tubercle—they were able to distinguish displaced full-thickness tears from nondisplaced full-thickness tears with 100% accuracy. Hergan and colleagues25 found that the diagnostic accuracy of MRI was superior to that of ultrasound; while MRI accuracy was perfect, 12% of patients were incorrectly diagnosed with ultrasound, with false-positive or false-negative tendon-edge displacement. In our experience, ultrasound is uniquely useful in its ability to characterize the real-time dynamic interaction of the UCL with the adductor aponeurosis. It has been observed that passive flexion of the first interphalangeal joint moves the adductor aponeurosis in isolation, allowing differentiation from the subjacent UCL.21 Had a partial tear been in the differential diagnosis of our patient’s Stener lesion, such a maneuver under ultrasound visualization would have solved the dilemma. In addition, ultrasound allows for comparison with the contralateral ligament at the time of examination should a diagnostic dilemma arise.

As many have reported both bony avulsion of the base of the proximal phalanx and concomitant injury to the UCL, identification of a bony avulsion does not exclude a ligamentous injury and the possibility of a Stener lesion (Figure 7).16,19

Figure 7.
In one study, 14% of patients with injury to the UCL sustained a concomitant bony avulsion of the UCL insertion.23 However, presence of the avulsion fragment did not alter management, and only those fragments involving more than 20% of the articular surface were considered true fractures and treated as such.

Conclusion

A Stener lesion—retraction of a completely torn UCL becoming entrapped dorsally and proximally to the adductor insertion—can cause pain, instability, and ultimately osteoarthritis if not treated appropriately. The orthopedic surgeon should have a high index of suspicion for a Stener lesion in the appropriate clinical scenario and consider all imaging modalities for diagnosis. Likewise, it is of utmost importance for the radiologist to identify imaging findings of a Stener lesion, as physical examination alone may be limited in its ability to characterize injury severity. Both MRI and ultrasound are useful in evaluating UCL tears, and ultrasound provides the additional benefit of dynamic visualization and comparison with the contralateral side.

Am J Orthop. 2017;46(3):E195-E199. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Torn, displaced, and entrapped UCL is a Stener lesion.
  • Hyperabduction injury with pain and joint laxity on examination.
  • MRI and ultrasound are useful in evaluating UCL tears.
  • Ultrasound offers dynamic evaluation.
  • Must be treated appropriately to avoid pain, instability, and osteoarthritis.

In the literature, hyperabduction injuries to the thumb metacarpophalangeal (MCP) joint have been referred to interchangeably as gamekeeper’s thumb and skier’s thumb. Historically, though, gamekeeper’s thumb was initially described in hunters with chronic injury to the ulnar collateral ligament (UCL),1 and skier’s thumb typically has been described as an acute hyperabduction injury of the UCL.2-5 The proximal portion of a torn UCL may retract with further abduction and displace dorsally, becoming entrapped by the adductor pollicis aponeurosis insertion, known as a Stener lesion.6

The first MCP joint is stabilized by static and dynamic structures that contribute in varying degrees in flexion and extension of the joint. The static stabilizers include the proper and accessory radial and UCLs, the palmar plate, and the dorsal capsule. The UCL originates at the dorsal ulnar aspect of the first metacarpal head at the metacarpal tubercle about 5 mm proximal to the articular surface. The UCL courses distally in the palmar direction to insert volar and proximal to the medial tubercle of the proximal phalanx about 3 mm distal to the articular surface.7 In flexion, the proper collateral ligament is taut and is the primary static stabilizer. In extension, the accessory collateral ligament, which inserts on the palmar plate, is taut and is the primary static stabilizer.8-11

The dynamic stabilizers include the extrinsic muscles (flexor pollicis longus, extensor pollicis longus and brevis) and the intrinsic muscles (abductor pollicis brevis, adductor pollicis, flexor pollicis brevis) inserting on the thumb at the distal phalanx and proximal phalanx and at the base of the first metacarpal.8-10

Figure 1.
The adductor pollicis originates from the volar third metacarpal, capitate, and hamate and has a dual insertion on the thumb.12 There is a direct insertion onto the palmar proximal phalanx at the medial tubercle, distal and dorsal to the phalangeal insertion of the UCL.
Figure 2.
There is also a broad aponeurosis that inserts onto the extensor hood expansion, dorsal to the insertion of the UCL (Figures 1A-1C and 2A, 2B).7,8,13

We report the case of an acute hyperabduction injury of the thumb MCP joint with radiographic, ultrasound, and magnetic resonance imaging (MRI) findings consistent with a Stener lesion and subsequently confirmed with intraoperative photographs. The patient provided written informed consent for print and electronic publication of this case report.

Clinical Findings

A 33-year-old healthy man had persistent left hand pain and grip weakness after performing a handstand. He presented to the orthopedic hand clinic 20 days after injury, having failed nonoperative management (use of nonsteroidal anti-inflammatory drugs and soft thumb spica splint). Physical examination revealed soft-tissue swelling and focal tenderness to palpation at the ulnar aspect of the thumb MCP joint. Despite bilateral first MCP joint laxity on varus and valgus stress without identification of a firm endpoint, pain was elicited only on valgus stress of the left first MCP joint. Given the laxity and the left thumb soft-tissue swelling with pain, plain radiographs, ultrasound, and MRI were used to evaluate for severity of presumed left thumb UCL injury.

Imaging Findings

Plain radiographs showed normal bony anatomy without fracture, normal joint space, and mild soft-tissue swelling at the left thumb MCP level (Figures 3A, 3B).

Figure 3.
Ultrasound confirmed a complete tear of the UCL, which was flipped in a proximal direction and projected dorsally in relation to the direct insertion of the adductor tendon (Figure 2B). MRI showed focal disruption of the UCL at the level of the left thumb MCP joint with associated MCP joint effusion (Figures 4A-4F).
Figure 4.
Low T1 signal intensity over the adductor aponeurosis at the level of the metacarpal head corresponded with the torn and proximally retracted UCL. There was associated bone marrow edema at the radial and volar aspects of the thumb metacarpal head and low-grade strain of the abductor pollicis brevis. The thumb flexor and extensor tendons appeared normal. Although possibly secondary to patient positioning, mild volar subluxation of the proximal phalanx in relation to the metacarpal head was queried.

 

 

Surgical Findings

Given laxity with pain at the UCL on stress testing, MRI and ultrasound findings, and continued pain and instability of the thumb with pinching and grasping during activities of daily living, the patient and orthopedic hand surgeon proceeded with surgical intervention. Preoperative examination under anesthesia confirmed significant laxity on valgus stress without a palpable endpoint (Figures 5A, 5B).

Figure 5.
During surgery, retraction of the extensor hood revealed the completely torn and displaced UCL, entrapped dorsally and proximally to the adductor aponeurosis, characteristic of a Stener lesion. After the primary repair of the UCL, the extensor hood was seen partially retracted in a normal location superficial to the normal deep position of the repaired UCL (Figures 6A, 6B).

Discussion

Hyperabduction injuries to the thumb may rupture the UCL of the MCP joint of the thumb or cause a bony avulsion of the base of the proximal phalanx. Injury to the UCL, most often at its distal portion,4,14,15 may result in a sprain or full-thickness tear of the ligament.

Figure 6.
Subsequently, the ligament may remain in situ, or the proximal segment may retract proximal to the adductor aponeurosis with continued abduction of the thumb. On release of the abduction force, the proximal UCL segment is displaced dorsally and proximally by the inferior aspect of the adductor aponeurosis. The UCL becomes entrapped by the adductor aponeurosis and cannot reduce spontaneously.15 This displacement was initially described by Stener6 in 1962 and is referred to as a Stener lesion (Figures 1A-1C).

It is vital for the radiologist to identify a Stener lesion because a nondisplaced tear of the UCL is often treated nonsurgically, but UCL tears displaced more than 3 mm and Stener lesions usually must be operated on to avoid chronic instability, pain, and osteoarthritis.2-5,8,12-23 Sensitivity and specificity of MRI in evaluating UCL injuries are reported to be almost 100%, with resolution of 1 mm using current surface coils.23 There are various UCL injury patterns, including partial tears, displaced and nondisplaced complete tears, and even complex injuries, such as an incomplete tear with the torn portion retracted as a Stener lesion.22 MRI is needed to establish the extent of injury, as 90% of complete tears that are displaced at least 3 mm, and all tears with retraction proximal and superficial to the aponeurosis (true Stener lesions), failed immobilization and required surgical treatment.23Although they vary in the literature, mean sensitivity and specificity of ultrasound in detecting UCL tears in level I studies have been reported as 76% and 81%, respectively.24 When Melville and colleagues21 applied their ultrasound criteria—including absence of normal UCL fibers traversing the first MCP joint as well as heterogeneous masslike tissue at least partially proximal to the apex of the metacarpal lateral tubercle—they were able to distinguish displaced full-thickness tears from nondisplaced full-thickness tears with 100% accuracy. Hergan and colleagues25 found that the diagnostic accuracy of MRI was superior to that of ultrasound; while MRI accuracy was perfect, 12% of patients were incorrectly diagnosed with ultrasound, with false-positive or false-negative tendon-edge displacement. In our experience, ultrasound is uniquely useful in its ability to characterize the real-time dynamic interaction of the UCL with the adductor aponeurosis. It has been observed that passive flexion of the first interphalangeal joint moves the adductor aponeurosis in isolation, allowing differentiation from the subjacent UCL.21 Had a partial tear been in the differential diagnosis of our patient’s Stener lesion, such a maneuver under ultrasound visualization would have solved the dilemma. In addition, ultrasound allows for comparison with the contralateral ligament at the time of examination should a diagnostic dilemma arise.

As many have reported both bony avulsion of the base of the proximal phalanx and concomitant injury to the UCL, identification of a bony avulsion does not exclude a ligamentous injury and the possibility of a Stener lesion (Figure 7).16,19

Figure 7.
In one study, 14% of patients with injury to the UCL sustained a concomitant bony avulsion of the UCL insertion.23 However, presence of the avulsion fragment did not alter management, and only those fragments involving more than 20% of the articular surface were considered true fractures and treated as such.

Conclusion

A Stener lesion—retraction of a completely torn UCL becoming entrapped dorsally and proximally to the adductor insertion—can cause pain, instability, and ultimately osteoarthritis if not treated appropriately. The orthopedic surgeon should have a high index of suspicion for a Stener lesion in the appropriate clinical scenario and consider all imaging modalities for diagnosis. Likewise, it is of utmost importance for the radiologist to identify imaging findings of a Stener lesion, as physical examination alone may be limited in its ability to characterize injury severity. Both MRI and ultrasound are useful in evaluating UCL tears, and ultrasound provides the additional benefit of dynamic visualization and comparison with the contralateral side.

Am J Orthop. 2017;46(3):E195-E199. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Campbell CS. Gamekeeper’s thumb. J Bone Joint Surg Br. 1955;37(1):148-149.

2. Anderson D. Skier’s thumb. Aust Family Physician. 2010;39(8):575-577.

3. Heim D. The skier’s thumb. Acta Orthop Belg. 1999;65(4):440-446.

4. Lohman M, Vasenius J, Kivisaari A, Kivisaari L. MR imaging in chronic rupture of the ulnar collateral ligament of the thumb. Acta Radiol. 2001;42(1):10-14.

5. Kundu N, Asfaw S, Polster J, Lohman R. The Stener lesion. Eplasty. 2012;12:ic11.

6. Stener B. Displacement of the ruptured ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Bone Joint Surg Br. 1962;44:869-879.

7. Carlson MG, Warner KK, Meyers KN, Hearns KA, Kok PL. Anatomy of the thumb metacarpophalangeal ulnar and radial collateral ligaments. J Hand Surg Am. 2012;37(10):2021-2026.

8. Heyman P. Injuries to the ulnar collateral ligament of the thumb metacarpophalangeal joint. J Am Acad Orthop Surg. 1997;5(4):224-229.

9. Minami A, An KN, Cooney WP 3rd, Linscheid RL, Chao EY. Ligamentous structures of the metacarpophalangeal joint: a quantitative anatomic study. J Orthop Res. 1984;1(4):361-368.

10. Heyman P, Gelberman RH, Duncan K, Hipp JA. Injuries of the ulnar collateral ligament of the thumb metacarpophalangeal joint. Biomechanical and prospective clinical studies on the usefulness of valgus stress testing. Clin Orthop Relat Res. 1993;(292):165-171.

11. Patel S, Potty A, Taylor EJ, Sorene ED. Collateral ligament injuries of the metacarpophalangeal joint of the thumb: a treatment algorithm. Strategies Trauma Limb Reconstr. 2010;5(1):1-10.

12. O’Callaghan BI, Kohut G, Hoogewoud HM. Gamekeeper thumb: identification of the Stener lesion with US. Radiology. 1994;192(2):477-480.

13. Ebrahim FS, De Maeseneer M, Jager T, Marcelis S, Jamadar DA, Jacobson JA. US diagnosis of UCL tears of the thumb and Stener lesions: technique, pattern-based approach, and differential diagnosis. Radiographics. 2006;26(4):1007-1020.

14. Haramati N, Hiller N, Dowdle J, et al. MRI of the Stener lesion. Skeletal Radiol. 1995;24(7):515-518.

15. Shinohara T, Horii E, Majima M, et al. Sonographic diagnosis of acute injuries of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Clin Ultrasound. 2007;35(2):73-77.

16. Giele H, Martin J. The two-level ulnar collateral ligament injury of the metacarpophalangeal joint of the thumb. J Hand Surg Br. 2003;28(1):92-93.

17. Kaplan SJ. The Stener lesion revisited: a case report. J Hand Surg Am. 1998;23(5):833-836.

18. Thirkannad S, Wolff TW. The “two fleck sign” for an occult Stener lesion. J Hand Surg Eur Vol. 2008;33(2):208-211.

19. Badawi RA, Hussain S, Compson JP. Two in one: a variant of the Stener lesion. Injury. 2002;33(4):379-380.

20. McKeon KE, Gelberman RH, Calfee RP. Ulnar collateral ligament injuries of the thumb: phalangeal translation during valgus stress in human cadavera. J Bone Joint Surg Am. 2013;95(10):881-887.

21. Melville D, Jacobson JA, Haase S, Brandon C, Brigido MK, Fessell D. Ultrasound of displaced ulnar collateral ligament tears of the thumb: the Stener lesion revisited. Skeletal Radiol. 2013;42(5):667-673.

22. Romano WM, Garvin G, Bhayana D, Chaudhary O. The spectrum of ulnar collateral ligament injuries as viewed on magnetic resonance imaging of the metacarpophalangeal joint of the thumb. Can Assoc Radiol J. 2003;54(4):243-248.

23. Milner CS, Manon-Matos Y, Thirkannad SM. Gamekeeper’s thumb—a treatment-oriented magnetic resonance imaging classification. J Hand Surg Am. 2015;40(1):90-95.

24. Papandrea RF, Fowler T. Injury at the thumb UCL: is there a Stener lesion? J Hand Surg Am. 2008;33(10):1882-1884.

25. Hergan K, Mittler C, Oser W. Ulnar collateral ligament: differentiation of displaced and nondisplaced tears with US and MR imaging. Radiology. 1995;194(1):65-71.

References

1. Campbell CS. Gamekeeper’s thumb. J Bone Joint Surg Br. 1955;37(1):148-149.

2. Anderson D. Skier’s thumb. Aust Family Physician. 2010;39(8):575-577.

3. Heim D. The skier’s thumb. Acta Orthop Belg. 1999;65(4):440-446.

4. Lohman M, Vasenius J, Kivisaari A, Kivisaari L. MR imaging in chronic rupture of the ulnar collateral ligament of the thumb. Acta Radiol. 2001;42(1):10-14.

5. Kundu N, Asfaw S, Polster J, Lohman R. The Stener lesion. Eplasty. 2012;12:ic11.

6. Stener B. Displacement of the ruptured ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Bone Joint Surg Br. 1962;44:869-879.

7. Carlson MG, Warner KK, Meyers KN, Hearns KA, Kok PL. Anatomy of the thumb metacarpophalangeal ulnar and radial collateral ligaments. J Hand Surg Am. 2012;37(10):2021-2026.

8. Heyman P. Injuries to the ulnar collateral ligament of the thumb metacarpophalangeal joint. J Am Acad Orthop Surg. 1997;5(4):224-229.

9. Minami A, An KN, Cooney WP 3rd, Linscheid RL, Chao EY. Ligamentous structures of the metacarpophalangeal joint: a quantitative anatomic study. J Orthop Res. 1984;1(4):361-368.

10. Heyman P, Gelberman RH, Duncan K, Hipp JA. Injuries of the ulnar collateral ligament of the thumb metacarpophalangeal joint. Biomechanical and prospective clinical studies on the usefulness of valgus stress testing. Clin Orthop Relat Res. 1993;(292):165-171.

11. Patel S, Potty A, Taylor EJ, Sorene ED. Collateral ligament injuries of the metacarpophalangeal joint of the thumb: a treatment algorithm. Strategies Trauma Limb Reconstr. 2010;5(1):1-10.

12. O’Callaghan BI, Kohut G, Hoogewoud HM. Gamekeeper thumb: identification of the Stener lesion with US. Radiology. 1994;192(2):477-480.

13. Ebrahim FS, De Maeseneer M, Jager T, Marcelis S, Jamadar DA, Jacobson JA. US diagnosis of UCL tears of the thumb and Stener lesions: technique, pattern-based approach, and differential diagnosis. Radiographics. 2006;26(4):1007-1020.

14. Haramati N, Hiller N, Dowdle J, et al. MRI of the Stener lesion. Skeletal Radiol. 1995;24(7):515-518.

15. Shinohara T, Horii E, Majima M, et al. Sonographic diagnosis of acute injuries of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Clin Ultrasound. 2007;35(2):73-77.

16. Giele H, Martin J. The two-level ulnar collateral ligament injury of the metacarpophalangeal joint of the thumb. J Hand Surg Br. 2003;28(1):92-93.

17. Kaplan SJ. The Stener lesion revisited: a case report. J Hand Surg Am. 1998;23(5):833-836.

18. Thirkannad S, Wolff TW. The “two fleck sign” for an occult Stener lesion. J Hand Surg Eur Vol. 2008;33(2):208-211.

19. Badawi RA, Hussain S, Compson JP. Two in one: a variant of the Stener lesion. Injury. 2002;33(4):379-380.

20. McKeon KE, Gelberman RH, Calfee RP. Ulnar collateral ligament injuries of the thumb: phalangeal translation during valgus stress in human cadavera. J Bone Joint Surg Am. 2013;95(10):881-887.

21. Melville D, Jacobson JA, Haase S, Brandon C, Brigido MK, Fessell D. Ultrasound of displaced ulnar collateral ligament tears of the thumb: the Stener lesion revisited. Skeletal Radiol. 2013;42(5):667-673.

22. Romano WM, Garvin G, Bhayana D, Chaudhary O. The spectrum of ulnar collateral ligament injuries as viewed on magnetic resonance imaging of the metacarpophalangeal joint of the thumb. Can Assoc Radiol J. 2003;54(4):243-248.

23. Milner CS, Manon-Matos Y, Thirkannad SM. Gamekeeper’s thumb—a treatment-oriented magnetic resonance imaging classification. J Hand Surg Am. 2015;40(1):90-95.

24. Papandrea RF, Fowler T. Injury at the thumb UCL: is there a Stener lesion? J Hand Surg Am. 2008;33(10):1882-1884.

25. Hergan K, Mittler C, Oser W. Ulnar collateral ligament: differentiation of displaced and nondisplaced tears with US and MR imaging. Radiology. 1995;194(1):65-71.

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5 Points on Pyogenic Flexor Tenosynovitis of the Hand

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5 Points on Pyogenic Flexor Tenosynovitis of the Hand

Pyogenic flexor tenosynovitis (PFT) is a common closed space infection of the flexor tendon sheaths of the hand and remains one of the most challenging problems encountered in orthopedic and hand surgery (Figure 1). PFT also is known as septic flexor tenosynovitis and suppurative flexor tenosynovitis.

Figure 1.

Kanavel1 initially described 4 cardinal signs that characterize infection of the flexor tendon sheath: symmetric fusiform swelling of the entire digit, exquisite tenderness to palpation along the course of the tendon sheath, semiflexed posture at rest, and pain with attempted passive extension of the digit. The prevalence of this infection ranges from 2.5% to 9.4%.2 Once the infection is established in a patient, it can cause significant morbidity and disability and produce an economic burden. It can also present a significant treatment dilemma for the treating surgeon, as there is no standardized protocol for managing this common but challenging hand infection. For treatment, many surgeons combine surgical decompression, sheath irrigation, and empiric intravenous (IV) antibiotic administration. However, despite prompt treatment, and regardless of the protocol used, complication rates as high as 38% have been reported.3 Moreover, even after infection eradication, a significant proportion of patients continue to have pain, swelling, stiffness, loss of composite flexion, weakness, and recurrence that potentially requires amputation.

1. What Causes Pyogenic Flexor Tenosynovitis?

PFT can result from hematogenous spread, but local inoculation by a laceration, a puncture, or a bite also is common4-7 (Figure 1). As a consequence of these mechanisms of injury, the most common source of PFT is skin flora. Staphylococcus aureus has been found in up to 75% of positive cultures in several studies.2,5,6,8,9 Methicillin-resistant S aureus (MRSA) has been found in up to 29% of cases, and the incidence continues to increase, particularly in urban areas.2,9-12 Other common bacteria are Staphylococcus epidermidis, β-hemolytic Streptococcus species, and Pseudomonas aeruginosa.5,6,10 Infection by more than 1 species of bacteria is also fairly prevalent. Of 62 patients in a study, 38% had infections with 1 organism, and 62% with 2 or more.6 Twenty-six percent of cultures grew mixed anaerobic and aerobic organisms.6 PFT is seldom caused by Eikenella corrodens from a human bite or Pasteurella multocida from an animal bite.10 Other rare causes of PFT are Listeria monocytogenes13 and Clostridium difficile from a gastrointestinal source.14Neisseria gonorrhea can cause acute tenosynovitis, usually in the setting of disseminated gonococcal infection.15,16 Also reported is mycobacterial tenosynovitis, most commonly caused by Mycobacterium kansasii and Mycobacterium marinum.17

2. Which Antibiotics Are Best Suited to Empirical Management of PFT?

Management of PFT, regardless of the pathogen, includes prompt administration of empiric IV antibiotics, usually followed by surgical drainage.7,18-20 While cultures are being tested, antibiotics should be selected—including antibiotics for empiric coverage against common gram-positive organisms, including Staphylococcus and Streptococcus species.12 The Centers for Disease Control and Prevention recommends empiric coverage for MRSA if the local prevalence exceeds 10% to 15%. Recommended empiric antibiotics are trimethoprim-sulfamethoxazole (TMP-SMX) and clindamycin (both oral) and clindamycin, vancomycin, and daptomycin (all IV).

In addition, institutional and local antibiotic resistance patterns of bacteria should guide treatment and antibiotic selection. First-generation cephalosporins have long been the cornerstone of treatment for infections caused by S aureus, but increasing methicillin resistance has reduced their role in the treatment, particularly the empiric treatment, of MRSA infections. Methicillin resistance first appeared as nosocomial S aureus infections in 1961, only 1 year after the introduction of the semisynthetic penicillin class that includes methicillin. Over the past 2 decades, MRSA has emerged in the community in otherwise young and healthy individuals with no healthcare-associated risk factors. Fortunately, several readily available antibiotics have maintained their efficacy in managing these “community-acquired” MRSA hand infections. TMP-SMX provides adequate coverage for MRSA and is a relatively inexpensive medication, and clindamycin is an equally effective and cost-effective alternative.

Presumptive antibiotics should also cover gram-negative rods and anaerobes, including Clostridium species, especially in immunocompromised patients.7,9 These patients may require additional antibiotics for presumptive coverage of other rarer bacterial causes, especially when unique mechanisms of injury (eg, aquatic injury, farm injury) are involved. Once culture results are ready, antibiotic regimens should be narrowed to cover the specific organisms identified.

 

 

3. What Are the Timing and Indications for Surgery?

Nonoperative treatment may be appropriate for PFT patients who present early, typically within 48 hours after penetrating trauma to the hand.21 In a 4-patient series, Neviaser and Gunther19 successfully treated PFT nonoperatively, with IV antibiotics, splinting, and elevation. During nonoperative treatment, the affected hand should be regularly examined. If this treatment is to be successful, clinical symptoms should improve within 48 hours; if they do not, surgical irrigation and débridement should be performed.

Regardless of timing and type of irrigation, surgical treatment remains the treatment of choice for the majority of PFT cases. Michon22 developed a 3-tier PFT classification system that is based on intraoperative findings (Table).

Table.
According to Michon22, stage 1 and stage 2 PFT can be treated with limited incision and with drainage and irrigation of the sheath, and stage 3 PFT should be treated with extensile open débridement.

4. What Are the Surgical Techniques for PFT Drainage?

Several surgical methods have been developed to decompress and irrigate the flexor sheaths of the hand. However, debates about optimal timing of surgical intervention, surgery type (open surgery or closed catheter irrigation only), and irrigation method continue.

Open Irrigation and Débridement

Open irrigation and débridement procedures were originally described for surgical management of PFT.1 Midaxial and palmar (Bruner zigzag) incisions can be used to expose and open the entire sheath for complete drainage and washout. Both incisions afford good access to the flexor sheath, but the midaxial approach may provide more coverage of the sheath after surgery. Open irrigation and débridement is the treatment of choice for the most advanced cases of PFT and for atypical or chronic tenosynovial infections.4,23,24 The Bruner zigzag incision affords ease of surgical dissection, extension, and more exposure of the flexor tendon sheath at the expense of possible difficulty in closure or flap necrosis in the setting of a swollen digit. Alternatively, the midaxial incision has the advantage of a large, more robust skin flap for more reliable closure.

Closed Tendon Sheath Irrigation

In 1943, Dickson-Wright25 first described catheter irrigation of tendon sheath infections. Later, Neviaser4 described this technique in detail. A proximal incision is made over the metacarpal neck. The tendon sheath is cut transversely at the proximal edge of the A1 pulley. An angiocatheter is inserted 1 cm to 2 cm antegrade into the flexor tendon sheath. Then, a distal midaxial incision is made dorsal to the neurovascular bundle at the level of the distal interphalangeal joint on the ulnar aspect of the finger or the radial aspect of the thumb. The distal edge of the flexor sheath is exposed and resected distal to the distal-most pulley. A Penrose drain can be threaded into the tendon sheath beneath the A4 pulley to keep the wound open and allow for fluid drainage. The sheath is flushed gently in the operating room. After surgery, intermittent bedside irrigation can be continued on the floor.

Neviaser4 reported excellent initial results with this technique; 18 of 20 patients regained complete active and passive range of motion (ROM) by 1 week after surgery. Similarly, Juliano and Eglseder,26 using a similar method, reported 100% excellent results for mild PFT and 88.4% excellent results for more severe infection.

Gutowski and colleagues23 reviewed 47 PFT cases to determine if there is a difference in outcomes between PFT treated with open irrigation and débridement and PFT treated with closed catheter irrigation. Between these groups, they found no significant differences in early postoperative outcomes, including resolution of infection, need for additional surgery, and hospital length of stay.

There are also many differing opinions regarding the best irrigation method. Some authors have asserted that normal saline is sufficient,4,5,23 and others that local antibiotics provide added benefit.27-29 Recently, Draeger and colleagues30 reported promising results with local injection of antibiotics into the tendon sheath and the addition of locally administered corticosteroids in the treatment of PFT in an animal model.

Continuous Closed Irrigation

A continuous closed irrigation system with inlet and outlet tubes has yielded successful results.8,31,32 This system consists of 2 fenestrated tubes placed within the infected space, with the tip of the smaller caliber inlet tube positioned just inside the larger outlet tube. Advantages of this system include the patient’s ability to participate in hand therapy with the system in place and avoidance of pain caused by the high pressures involved in intermittent closed irrigation. Duration of this system has ranged from 2 days to 3 weeks, and results have been good.5,8

Postoperative Irrigation

Use of postoperative irrigation on the floor or at home is controversial, as leaving an indwelling catheter in the tendon sheath can lead to complications. Catheters may increase digital stiffness by decreasing the patient’s ability to participate in therapy or may cause additional injury and irritation to the sheath itself if left in place too long. Lille and colleagues6 retrospectively compared the results of intraoperative closed tendon sheath irrigation alone with those of intraoperative and postoperative closed tendon sheath irrigation. There were no significant differences in mean hospital length of stay, follow-up complication rates, or postoperative ROM—which suggests that postoperative intermittent or continuous irrigation is not necessary.

 

 

Our Preferred Technique

We recommend a palmar approach that begins with outlining a Bruner zigzag incision along the entire finger. Then, only the distal-most and proximal-most incision lines are opened, thereby exposing the A5 and A1 pulleys, respectively (Figure 2).

Figure 2.
The A1 pulley is released longitudinally, exposing the flexor tendons. A blush of seropurulent fluid is typical. Similarly, the A5 pulley is released in limited fashion, and a small Penrose drain is inserted. A 16-gauge angiocatheter needle is inserted antegrade at the level of the A1 pulley. The sheet is then repeatedly irrigated with antibiotic-impregnated irrigation, until clean. The finger is passively flexed and extended throughout to maximize tendon irrigation. Any enveloping tenosynovitis of the flexor tendons is débrided away. If the exposure or the extent of irrigation is too limited to adequately clear the infection, the entire marked incision can be opened to connect the initial 2 incisions. However, care should be taken to avoid taking down all the pulleys, particularly A2 and A4. After surgery, the incisions are loosely closed; floor irrigation is not performed. Repeat operative irrigation can be performed 2 days later, if necessary. Immediately after the infection is under control, the patient should start supervised therapy. Oral antibiotics should ultimately be tailored to the intraoperative cultures, and should be continued for 2 to 6 weeks after surgery.

5. What Are the Long-Term Outcomes of PFT?

The principal complication associated with PFT is stiffness with loss of ROM, which can be caused by flexor tendon adhesions, joint capsular thickening, or destruction of the sheath and pulley system.24 In several studies, up to one-fourth of patients with PFT did not obtain full ROM, despite adequate treatment.4-6,27 Therefore, full active ROM exercises should be initiated immediately after surgery to counteract the development of stiffness.

The most severe complication of PFT is amputation of the affected digit (Figures 3A, 3B).

Figure 3.
Amputation incidence was 17% in one study2 and 29% in another,9 despite appropriate management. Dailiana and colleagues9 found that amputation was necessary more often in patients with diabetes and in patients with delayed presentation.

Pang and colleagues2 identified 5 factors associated with increased risk of amputation in patients with PFT: (1) age >43 years; (2) diabetes mellitus, peripheral vascular disease, or renal failure; (3) subcutaneous purulence; (4) signs of digital ischemia at presentation; and (5) growth of more than 1 bacteria species on culture of specimens obtained at time of surgery.

Pang and colleagues2 classified these patients into 3 groups with distinct clinical features and reported each group’s outcomes. The authors based their PFT classification system on increasingly severe clinical presentation, which potentially predicts amputation risk. Patients in stage 1 presented with Kanavel signs of tenosynovitis but no evidence of subcutaneous purulence or ischemia; patients in stage 2 had concurrent localized subcutaneous purulence but no ischemia; and patients in stage 3 had concurrent extensive subcutaneous purulence involving more than 1 phalangeal segment or spreading circumferentially as well as signs of ischemia. These PFT stages were found to correlate with worse patient outcomes. In patients with stage 1 infection, amputation was not required, and average functional return was 80% of total active ROM of the affected digit. In patients with stage 2 infection, the amputation rate was 8%, and return of total active ROM in the remaining digits was 72%. The outcomes for the patients with stage 3 infection were the worst. The amputation rate for patients with all 3 classification criteria (Kanavel signs, subcutaneous purulence, digital ischemia) was 59%, and return of total active ROM in the remaining digits was only 49%. Use of this clinical classification system makes it possible to guide treatment and predict outcome and return to function.

Conclusion

PFT is a common hand infection that can cause significant morbidity. Early treatment is crucial: this requires use of IV antibiotics, or surgical irrigation and débridement in more advanced cases. However, despite prompt and thorough treatment, severe infection can lead to long-term impaired function and even amputation of the affected digit. More research is needed to determine optimal timing and technique for surgical intervention and to elucidate the role of local antibiotics and corticosteroids in treating this infection and potentially preventing the morbid outcomes we currently see.

Am J Orthop. 2017;46(3):E207-E212. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Kanavel AB. The symptoms, signs, and diagnosis of tenosynovitis and major fascial-space abscesses. In: Kanavel AB, ed. Infections of the Hand. 6th ed. Philadelphia, PA: Lea & Febiger; 1933:364-395.

2. Pang HN, Teoh LC, Yam AK, Lee JY, Puhaindran ME, Tan AB. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2007;89(8):1742-1748.

3. Stern PJ, Staneck JL, McDonough JJ, Neale HW, Tyler G. Established hand infections: a controlled, prospective study. J Hand Surg Am. 1983;8(5 pt 1):553-559.

4. Neviaser RJ. Closed tendon sheath irrigation for pyogenic flexor tenosynovitis. J Hand Surg Am. 1978;3(5):462-466.

5. Harris PA, Nanchahal J. Closed continuous irrigation in the treatment of hand infections. J Hand Surg Br. 1999;24(3):328-333.

6. Lille S, Hayakawa T, Neumeister MW, Brown RE, Zook EG, Murray K. Continuous postoperative catheter irrigation is not necessary for the treatment of suppurative flexor tenosynovitis. J Hand Surg Br. 2000;25(3):304-307.

7. Boles SD, Schmidt CC. Pyogenic flexor tenosynovitis. Hand Clin. 1998;14(4):567-578.

8. Nemoto K, Yanagida M, Nemoto T. Closed continuous irrigation as a treatment for infection in the hand. J Hand Surg Br. 1993;18(6):783-789.

9. Dailiana ZH, Rigopoulos N, Varitimidis S, Hantes M, Bargiotas K, Malizos KN. Purulent flexor tenosynovitis: factors influencing the functional outcome. J Hand Surg Eur Vol. 2008;33(3):280-285.

10. Small LN, Ross JJ. Suppurative tenosynovitis and septic bursitis. Infect Dis Clin North Am. 2005;19(4):991-1005, xi.

11. Katsoulis E, Bissell I, Hargreaves DG. MRSA pyogenic flexor tenosynovitis leading to digital ischaemic necrosis and amputation. J Hand Surg Br. 2006;31(3):350-352.

12. Fowler JR Greenhill D, Schaffer AA, Thoder JJ, Ilyas AM. Evolving incidence of MRSA in urban hand infections. Orthopedics. 2013;36(6):796-800.

13. Aubert JP, Stein A, Raoult D, Magalon G. Flexor tenosynovitis in the hand: an unusual aetiology. J Hand Surg Br. 1995;20(4):509-510.

14. Wright TW, Linscheid RL, O’Duffy JD. Acute flexor tenosynovitis in association with Clostridium difficile infection: a case report. J Hand Surg Am. 1996;21(2):304-306.

15. Schaefer RA, Enzenauer RJ, Pruitt A, Corpe RS. Acute gonococcal flexor tenosynovitis in an adolescent male with pharyngitis: a case report and literature review. Clin Orthop Relat Res. 1992;(281):212-215.

16. Mamane W, Falcone MO, Doursounian L, Nourissat G. Isolated gonococcal tenosynovitis. Case report and review of literature [in French]. Chir Main. 2010;29(5):335-337.

17. Regnard PJ, Barry P, Isselin J. Mycobacterial tenosynovitis of the flexor tendons of the hand. A report of five cases. J Hand Surg Br. 1996;21(3):351-354.

18. Abrams RA, Botte MJ. Hand infections: treatment recommendations for specific types. J Am Acad Orthop Surg. 1996;4(4):219-230.

19. Neviaser RJ, Gunther SF. Tenosynovial infections in the hand: diagnosis and management. Instr Course Lect. 1980;29:108-128.

20. Szabo R, Palumbo C. Infections of the hand. In: Chapman M, ed. Chapman’s Orthopedic Surgery. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001:1989-2008.

21. Neviaser R. Acute infections. In: Green D, Hotchkiss R, Pederson W, eds. Green’s Operative Hand Surgery. 4th ed. New York, NY: Churchill Livingstone; 1999:1033-1047.

22. Michon J. Phlegmon of the tendon sheaths [in French]. Ann Chir. 1974;28(4):277-280.

23. Gutowski KA, Ochoa O, Adams WP Jr. Closed-catheter irrigation is as effective as open drainage for treatment of pyogenic flexor tenosynovitis. Ann Plast Surg. 2002;49(4):350-354.

24. Stern PJ. Selected acute infections. Instr Course Lect. 1990;39:539-546.

25. Dickson-Wright A. Tendon sheath infection. Proc R Soc Med. 1943-1944;37:504-505.

26. Juliano PJ, Eglseder WA. Limited open-tendon-sheath irrigation in the treatment of pyogenic flexor tenosynovitis. Orthop Rev. 1991;20(12):1065-1069.

27. Pollen AG. Acute infection of the tendon sheaths. Hand. 1974;6(1):21-25.

28. Besser MI. Digital flexor tendon irrigation. Hand. 1976;8(1):72.

29. Carter SJ, Burman SO, Mersheimer WL. Treatment of digital tenosynovitis by irrigation with peroxide and oxytetracycline: review of nine cases. Ann Surg. 1966;163(4):645-650.

30. Draeger RW, Singh B, Bynum DK, Dahners LE. Corticosteroids as an adjunct to antibiotics and surgical drainage for the treatment of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2010;92(16):2653-2662.

31. Delsignore JL, Ritland D, Becker DR, Watson HK. Continuous catheter irrigation for the treatment of suppurative flexor synovitis. Conn Med. 1986;50(8):503-506.

32. Gosain AK, Markisson RE. Catheter irrigation for treatment of pyogenic closed space infections of the hand. Br J Plast Surg. 1991;44(4):270-273.

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Pyogenic flexor tenosynovitis (PFT) is a common closed space infection of the flexor tendon sheaths of the hand and remains one of the most challenging problems encountered in orthopedic and hand surgery (Figure 1). PFT also is known as septic flexor tenosynovitis and suppurative flexor tenosynovitis.

Figure 1.

Kanavel1 initially described 4 cardinal signs that characterize infection of the flexor tendon sheath: symmetric fusiform swelling of the entire digit, exquisite tenderness to palpation along the course of the tendon sheath, semiflexed posture at rest, and pain with attempted passive extension of the digit. The prevalence of this infection ranges from 2.5% to 9.4%.2 Once the infection is established in a patient, it can cause significant morbidity and disability and produce an economic burden. It can also present a significant treatment dilemma for the treating surgeon, as there is no standardized protocol for managing this common but challenging hand infection. For treatment, many surgeons combine surgical decompression, sheath irrigation, and empiric intravenous (IV) antibiotic administration. However, despite prompt treatment, and regardless of the protocol used, complication rates as high as 38% have been reported.3 Moreover, even after infection eradication, a significant proportion of patients continue to have pain, swelling, stiffness, loss of composite flexion, weakness, and recurrence that potentially requires amputation.

1. What Causes Pyogenic Flexor Tenosynovitis?

PFT can result from hematogenous spread, but local inoculation by a laceration, a puncture, or a bite also is common4-7 (Figure 1). As a consequence of these mechanisms of injury, the most common source of PFT is skin flora. Staphylococcus aureus has been found in up to 75% of positive cultures in several studies.2,5,6,8,9 Methicillin-resistant S aureus (MRSA) has been found in up to 29% of cases, and the incidence continues to increase, particularly in urban areas.2,9-12 Other common bacteria are Staphylococcus epidermidis, β-hemolytic Streptococcus species, and Pseudomonas aeruginosa.5,6,10 Infection by more than 1 species of bacteria is also fairly prevalent. Of 62 patients in a study, 38% had infections with 1 organism, and 62% with 2 or more.6 Twenty-six percent of cultures grew mixed anaerobic and aerobic organisms.6 PFT is seldom caused by Eikenella corrodens from a human bite or Pasteurella multocida from an animal bite.10 Other rare causes of PFT are Listeria monocytogenes13 and Clostridium difficile from a gastrointestinal source.14Neisseria gonorrhea can cause acute tenosynovitis, usually in the setting of disseminated gonococcal infection.15,16 Also reported is mycobacterial tenosynovitis, most commonly caused by Mycobacterium kansasii and Mycobacterium marinum.17

2. Which Antibiotics Are Best Suited to Empirical Management of PFT?

Management of PFT, regardless of the pathogen, includes prompt administration of empiric IV antibiotics, usually followed by surgical drainage.7,18-20 While cultures are being tested, antibiotics should be selected—including antibiotics for empiric coverage against common gram-positive organisms, including Staphylococcus and Streptococcus species.12 The Centers for Disease Control and Prevention recommends empiric coverage for MRSA if the local prevalence exceeds 10% to 15%. Recommended empiric antibiotics are trimethoprim-sulfamethoxazole (TMP-SMX) and clindamycin (both oral) and clindamycin, vancomycin, and daptomycin (all IV).

In addition, institutional and local antibiotic resistance patterns of bacteria should guide treatment and antibiotic selection. First-generation cephalosporins have long been the cornerstone of treatment for infections caused by S aureus, but increasing methicillin resistance has reduced their role in the treatment, particularly the empiric treatment, of MRSA infections. Methicillin resistance first appeared as nosocomial S aureus infections in 1961, only 1 year after the introduction of the semisynthetic penicillin class that includes methicillin. Over the past 2 decades, MRSA has emerged in the community in otherwise young and healthy individuals with no healthcare-associated risk factors. Fortunately, several readily available antibiotics have maintained their efficacy in managing these “community-acquired” MRSA hand infections. TMP-SMX provides adequate coverage for MRSA and is a relatively inexpensive medication, and clindamycin is an equally effective and cost-effective alternative.

Presumptive antibiotics should also cover gram-negative rods and anaerobes, including Clostridium species, especially in immunocompromised patients.7,9 These patients may require additional antibiotics for presumptive coverage of other rarer bacterial causes, especially when unique mechanisms of injury (eg, aquatic injury, farm injury) are involved. Once culture results are ready, antibiotic regimens should be narrowed to cover the specific organisms identified.

 

 

3. What Are the Timing and Indications for Surgery?

Nonoperative treatment may be appropriate for PFT patients who present early, typically within 48 hours after penetrating trauma to the hand.21 In a 4-patient series, Neviaser and Gunther19 successfully treated PFT nonoperatively, with IV antibiotics, splinting, and elevation. During nonoperative treatment, the affected hand should be regularly examined. If this treatment is to be successful, clinical symptoms should improve within 48 hours; if they do not, surgical irrigation and débridement should be performed.

Regardless of timing and type of irrigation, surgical treatment remains the treatment of choice for the majority of PFT cases. Michon22 developed a 3-tier PFT classification system that is based on intraoperative findings (Table).

Table.
According to Michon22, stage 1 and stage 2 PFT can be treated with limited incision and with drainage and irrigation of the sheath, and stage 3 PFT should be treated with extensile open débridement.

4. What Are the Surgical Techniques for PFT Drainage?

Several surgical methods have been developed to decompress and irrigate the flexor sheaths of the hand. However, debates about optimal timing of surgical intervention, surgery type (open surgery or closed catheter irrigation only), and irrigation method continue.

Open Irrigation and Débridement

Open irrigation and débridement procedures were originally described for surgical management of PFT.1 Midaxial and palmar (Bruner zigzag) incisions can be used to expose and open the entire sheath for complete drainage and washout. Both incisions afford good access to the flexor sheath, but the midaxial approach may provide more coverage of the sheath after surgery. Open irrigation and débridement is the treatment of choice for the most advanced cases of PFT and for atypical or chronic tenosynovial infections.4,23,24 The Bruner zigzag incision affords ease of surgical dissection, extension, and more exposure of the flexor tendon sheath at the expense of possible difficulty in closure or flap necrosis in the setting of a swollen digit. Alternatively, the midaxial incision has the advantage of a large, more robust skin flap for more reliable closure.

Closed Tendon Sheath Irrigation

In 1943, Dickson-Wright25 first described catheter irrigation of tendon sheath infections. Later, Neviaser4 described this technique in detail. A proximal incision is made over the metacarpal neck. The tendon sheath is cut transversely at the proximal edge of the A1 pulley. An angiocatheter is inserted 1 cm to 2 cm antegrade into the flexor tendon sheath. Then, a distal midaxial incision is made dorsal to the neurovascular bundle at the level of the distal interphalangeal joint on the ulnar aspect of the finger or the radial aspect of the thumb. The distal edge of the flexor sheath is exposed and resected distal to the distal-most pulley. A Penrose drain can be threaded into the tendon sheath beneath the A4 pulley to keep the wound open and allow for fluid drainage. The sheath is flushed gently in the operating room. After surgery, intermittent bedside irrigation can be continued on the floor.

Neviaser4 reported excellent initial results with this technique; 18 of 20 patients regained complete active and passive range of motion (ROM) by 1 week after surgery. Similarly, Juliano and Eglseder,26 using a similar method, reported 100% excellent results for mild PFT and 88.4% excellent results for more severe infection.

Gutowski and colleagues23 reviewed 47 PFT cases to determine if there is a difference in outcomes between PFT treated with open irrigation and débridement and PFT treated with closed catheter irrigation. Between these groups, they found no significant differences in early postoperative outcomes, including resolution of infection, need for additional surgery, and hospital length of stay.

There are also many differing opinions regarding the best irrigation method. Some authors have asserted that normal saline is sufficient,4,5,23 and others that local antibiotics provide added benefit.27-29 Recently, Draeger and colleagues30 reported promising results with local injection of antibiotics into the tendon sheath and the addition of locally administered corticosteroids in the treatment of PFT in an animal model.

Continuous Closed Irrigation

A continuous closed irrigation system with inlet and outlet tubes has yielded successful results.8,31,32 This system consists of 2 fenestrated tubes placed within the infected space, with the tip of the smaller caliber inlet tube positioned just inside the larger outlet tube. Advantages of this system include the patient’s ability to participate in hand therapy with the system in place and avoidance of pain caused by the high pressures involved in intermittent closed irrigation. Duration of this system has ranged from 2 days to 3 weeks, and results have been good.5,8

Postoperative Irrigation

Use of postoperative irrigation on the floor or at home is controversial, as leaving an indwelling catheter in the tendon sheath can lead to complications. Catheters may increase digital stiffness by decreasing the patient’s ability to participate in therapy or may cause additional injury and irritation to the sheath itself if left in place too long. Lille and colleagues6 retrospectively compared the results of intraoperative closed tendon sheath irrigation alone with those of intraoperative and postoperative closed tendon sheath irrigation. There were no significant differences in mean hospital length of stay, follow-up complication rates, or postoperative ROM—which suggests that postoperative intermittent or continuous irrigation is not necessary.

 

 

Our Preferred Technique

We recommend a palmar approach that begins with outlining a Bruner zigzag incision along the entire finger. Then, only the distal-most and proximal-most incision lines are opened, thereby exposing the A5 and A1 pulleys, respectively (Figure 2).

Figure 2.
The A1 pulley is released longitudinally, exposing the flexor tendons. A blush of seropurulent fluid is typical. Similarly, the A5 pulley is released in limited fashion, and a small Penrose drain is inserted. A 16-gauge angiocatheter needle is inserted antegrade at the level of the A1 pulley. The sheet is then repeatedly irrigated with antibiotic-impregnated irrigation, until clean. The finger is passively flexed and extended throughout to maximize tendon irrigation. Any enveloping tenosynovitis of the flexor tendons is débrided away. If the exposure or the extent of irrigation is too limited to adequately clear the infection, the entire marked incision can be opened to connect the initial 2 incisions. However, care should be taken to avoid taking down all the pulleys, particularly A2 and A4. After surgery, the incisions are loosely closed; floor irrigation is not performed. Repeat operative irrigation can be performed 2 days later, if necessary. Immediately after the infection is under control, the patient should start supervised therapy. Oral antibiotics should ultimately be tailored to the intraoperative cultures, and should be continued for 2 to 6 weeks after surgery.

5. What Are the Long-Term Outcomes of PFT?

The principal complication associated with PFT is stiffness with loss of ROM, which can be caused by flexor tendon adhesions, joint capsular thickening, or destruction of the sheath and pulley system.24 In several studies, up to one-fourth of patients with PFT did not obtain full ROM, despite adequate treatment.4-6,27 Therefore, full active ROM exercises should be initiated immediately after surgery to counteract the development of stiffness.

The most severe complication of PFT is amputation of the affected digit (Figures 3A, 3B).

Figure 3.
Amputation incidence was 17% in one study2 and 29% in another,9 despite appropriate management. Dailiana and colleagues9 found that amputation was necessary more often in patients with diabetes and in patients with delayed presentation.

Pang and colleagues2 identified 5 factors associated with increased risk of amputation in patients with PFT: (1) age >43 years; (2) diabetes mellitus, peripheral vascular disease, or renal failure; (3) subcutaneous purulence; (4) signs of digital ischemia at presentation; and (5) growth of more than 1 bacteria species on culture of specimens obtained at time of surgery.

Pang and colleagues2 classified these patients into 3 groups with distinct clinical features and reported each group’s outcomes. The authors based their PFT classification system on increasingly severe clinical presentation, which potentially predicts amputation risk. Patients in stage 1 presented with Kanavel signs of tenosynovitis but no evidence of subcutaneous purulence or ischemia; patients in stage 2 had concurrent localized subcutaneous purulence but no ischemia; and patients in stage 3 had concurrent extensive subcutaneous purulence involving more than 1 phalangeal segment or spreading circumferentially as well as signs of ischemia. These PFT stages were found to correlate with worse patient outcomes. In patients with stage 1 infection, amputation was not required, and average functional return was 80% of total active ROM of the affected digit. In patients with stage 2 infection, the amputation rate was 8%, and return of total active ROM in the remaining digits was 72%. The outcomes for the patients with stage 3 infection were the worst. The amputation rate for patients with all 3 classification criteria (Kanavel signs, subcutaneous purulence, digital ischemia) was 59%, and return of total active ROM in the remaining digits was only 49%. Use of this clinical classification system makes it possible to guide treatment and predict outcome and return to function.

Conclusion

PFT is a common hand infection that can cause significant morbidity. Early treatment is crucial: this requires use of IV antibiotics, or surgical irrigation and débridement in more advanced cases. However, despite prompt and thorough treatment, severe infection can lead to long-term impaired function and even amputation of the affected digit. More research is needed to determine optimal timing and technique for surgical intervention and to elucidate the role of local antibiotics and corticosteroids in treating this infection and potentially preventing the morbid outcomes we currently see.

Am J Orthop. 2017;46(3):E207-E212. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Pyogenic flexor tenosynovitis (PFT) is a common closed space infection of the flexor tendon sheaths of the hand and remains one of the most challenging problems encountered in orthopedic and hand surgery (Figure 1). PFT also is known as septic flexor tenosynovitis and suppurative flexor tenosynovitis.

Figure 1.

Kanavel1 initially described 4 cardinal signs that characterize infection of the flexor tendon sheath: symmetric fusiform swelling of the entire digit, exquisite tenderness to palpation along the course of the tendon sheath, semiflexed posture at rest, and pain with attempted passive extension of the digit. The prevalence of this infection ranges from 2.5% to 9.4%.2 Once the infection is established in a patient, it can cause significant morbidity and disability and produce an economic burden. It can also present a significant treatment dilemma for the treating surgeon, as there is no standardized protocol for managing this common but challenging hand infection. For treatment, many surgeons combine surgical decompression, sheath irrigation, and empiric intravenous (IV) antibiotic administration. However, despite prompt treatment, and regardless of the protocol used, complication rates as high as 38% have been reported.3 Moreover, even after infection eradication, a significant proportion of patients continue to have pain, swelling, stiffness, loss of composite flexion, weakness, and recurrence that potentially requires amputation.

1. What Causes Pyogenic Flexor Tenosynovitis?

PFT can result from hematogenous spread, but local inoculation by a laceration, a puncture, or a bite also is common4-7 (Figure 1). As a consequence of these mechanisms of injury, the most common source of PFT is skin flora. Staphylococcus aureus has been found in up to 75% of positive cultures in several studies.2,5,6,8,9 Methicillin-resistant S aureus (MRSA) has been found in up to 29% of cases, and the incidence continues to increase, particularly in urban areas.2,9-12 Other common bacteria are Staphylococcus epidermidis, β-hemolytic Streptococcus species, and Pseudomonas aeruginosa.5,6,10 Infection by more than 1 species of bacteria is also fairly prevalent. Of 62 patients in a study, 38% had infections with 1 organism, and 62% with 2 or more.6 Twenty-six percent of cultures grew mixed anaerobic and aerobic organisms.6 PFT is seldom caused by Eikenella corrodens from a human bite or Pasteurella multocida from an animal bite.10 Other rare causes of PFT are Listeria monocytogenes13 and Clostridium difficile from a gastrointestinal source.14Neisseria gonorrhea can cause acute tenosynovitis, usually in the setting of disseminated gonococcal infection.15,16 Also reported is mycobacterial tenosynovitis, most commonly caused by Mycobacterium kansasii and Mycobacterium marinum.17

2. Which Antibiotics Are Best Suited to Empirical Management of PFT?

Management of PFT, regardless of the pathogen, includes prompt administration of empiric IV antibiotics, usually followed by surgical drainage.7,18-20 While cultures are being tested, antibiotics should be selected—including antibiotics for empiric coverage against common gram-positive organisms, including Staphylococcus and Streptococcus species.12 The Centers for Disease Control and Prevention recommends empiric coverage for MRSA if the local prevalence exceeds 10% to 15%. Recommended empiric antibiotics are trimethoprim-sulfamethoxazole (TMP-SMX) and clindamycin (both oral) and clindamycin, vancomycin, and daptomycin (all IV).

In addition, institutional and local antibiotic resistance patterns of bacteria should guide treatment and antibiotic selection. First-generation cephalosporins have long been the cornerstone of treatment for infections caused by S aureus, but increasing methicillin resistance has reduced their role in the treatment, particularly the empiric treatment, of MRSA infections. Methicillin resistance first appeared as nosocomial S aureus infections in 1961, only 1 year after the introduction of the semisynthetic penicillin class that includes methicillin. Over the past 2 decades, MRSA has emerged in the community in otherwise young and healthy individuals with no healthcare-associated risk factors. Fortunately, several readily available antibiotics have maintained their efficacy in managing these “community-acquired” MRSA hand infections. TMP-SMX provides adequate coverage for MRSA and is a relatively inexpensive medication, and clindamycin is an equally effective and cost-effective alternative.

Presumptive antibiotics should also cover gram-negative rods and anaerobes, including Clostridium species, especially in immunocompromised patients.7,9 These patients may require additional antibiotics for presumptive coverage of other rarer bacterial causes, especially when unique mechanisms of injury (eg, aquatic injury, farm injury) are involved. Once culture results are ready, antibiotic regimens should be narrowed to cover the specific organisms identified.

 

 

3. What Are the Timing and Indications for Surgery?

Nonoperative treatment may be appropriate for PFT patients who present early, typically within 48 hours after penetrating trauma to the hand.21 In a 4-patient series, Neviaser and Gunther19 successfully treated PFT nonoperatively, with IV antibiotics, splinting, and elevation. During nonoperative treatment, the affected hand should be regularly examined. If this treatment is to be successful, clinical symptoms should improve within 48 hours; if they do not, surgical irrigation and débridement should be performed.

Regardless of timing and type of irrigation, surgical treatment remains the treatment of choice for the majority of PFT cases. Michon22 developed a 3-tier PFT classification system that is based on intraoperative findings (Table).

Table.
According to Michon22, stage 1 and stage 2 PFT can be treated with limited incision and with drainage and irrigation of the sheath, and stage 3 PFT should be treated with extensile open débridement.

4. What Are the Surgical Techniques for PFT Drainage?

Several surgical methods have been developed to decompress and irrigate the flexor sheaths of the hand. However, debates about optimal timing of surgical intervention, surgery type (open surgery or closed catheter irrigation only), and irrigation method continue.

Open Irrigation and Débridement

Open irrigation and débridement procedures were originally described for surgical management of PFT.1 Midaxial and palmar (Bruner zigzag) incisions can be used to expose and open the entire sheath for complete drainage and washout. Both incisions afford good access to the flexor sheath, but the midaxial approach may provide more coverage of the sheath after surgery. Open irrigation and débridement is the treatment of choice for the most advanced cases of PFT and for atypical or chronic tenosynovial infections.4,23,24 The Bruner zigzag incision affords ease of surgical dissection, extension, and more exposure of the flexor tendon sheath at the expense of possible difficulty in closure or flap necrosis in the setting of a swollen digit. Alternatively, the midaxial incision has the advantage of a large, more robust skin flap for more reliable closure.

Closed Tendon Sheath Irrigation

In 1943, Dickson-Wright25 first described catheter irrigation of tendon sheath infections. Later, Neviaser4 described this technique in detail. A proximal incision is made over the metacarpal neck. The tendon sheath is cut transversely at the proximal edge of the A1 pulley. An angiocatheter is inserted 1 cm to 2 cm antegrade into the flexor tendon sheath. Then, a distal midaxial incision is made dorsal to the neurovascular bundle at the level of the distal interphalangeal joint on the ulnar aspect of the finger or the radial aspect of the thumb. The distal edge of the flexor sheath is exposed and resected distal to the distal-most pulley. A Penrose drain can be threaded into the tendon sheath beneath the A4 pulley to keep the wound open and allow for fluid drainage. The sheath is flushed gently in the operating room. After surgery, intermittent bedside irrigation can be continued on the floor.

Neviaser4 reported excellent initial results with this technique; 18 of 20 patients regained complete active and passive range of motion (ROM) by 1 week after surgery. Similarly, Juliano and Eglseder,26 using a similar method, reported 100% excellent results for mild PFT and 88.4% excellent results for more severe infection.

Gutowski and colleagues23 reviewed 47 PFT cases to determine if there is a difference in outcomes between PFT treated with open irrigation and débridement and PFT treated with closed catheter irrigation. Between these groups, they found no significant differences in early postoperative outcomes, including resolution of infection, need for additional surgery, and hospital length of stay.

There are also many differing opinions regarding the best irrigation method. Some authors have asserted that normal saline is sufficient,4,5,23 and others that local antibiotics provide added benefit.27-29 Recently, Draeger and colleagues30 reported promising results with local injection of antibiotics into the tendon sheath and the addition of locally administered corticosteroids in the treatment of PFT in an animal model.

Continuous Closed Irrigation

A continuous closed irrigation system with inlet and outlet tubes has yielded successful results.8,31,32 This system consists of 2 fenestrated tubes placed within the infected space, with the tip of the smaller caliber inlet tube positioned just inside the larger outlet tube. Advantages of this system include the patient’s ability to participate in hand therapy with the system in place and avoidance of pain caused by the high pressures involved in intermittent closed irrigation. Duration of this system has ranged from 2 days to 3 weeks, and results have been good.5,8

Postoperative Irrigation

Use of postoperative irrigation on the floor or at home is controversial, as leaving an indwelling catheter in the tendon sheath can lead to complications. Catheters may increase digital stiffness by decreasing the patient’s ability to participate in therapy or may cause additional injury and irritation to the sheath itself if left in place too long. Lille and colleagues6 retrospectively compared the results of intraoperative closed tendon sheath irrigation alone with those of intraoperative and postoperative closed tendon sheath irrigation. There were no significant differences in mean hospital length of stay, follow-up complication rates, or postoperative ROM—which suggests that postoperative intermittent or continuous irrigation is not necessary.

 

 

Our Preferred Technique

We recommend a palmar approach that begins with outlining a Bruner zigzag incision along the entire finger. Then, only the distal-most and proximal-most incision lines are opened, thereby exposing the A5 and A1 pulleys, respectively (Figure 2).

Figure 2.
The A1 pulley is released longitudinally, exposing the flexor tendons. A blush of seropurulent fluid is typical. Similarly, the A5 pulley is released in limited fashion, and a small Penrose drain is inserted. A 16-gauge angiocatheter needle is inserted antegrade at the level of the A1 pulley. The sheet is then repeatedly irrigated with antibiotic-impregnated irrigation, until clean. The finger is passively flexed and extended throughout to maximize tendon irrigation. Any enveloping tenosynovitis of the flexor tendons is débrided away. If the exposure or the extent of irrigation is too limited to adequately clear the infection, the entire marked incision can be opened to connect the initial 2 incisions. However, care should be taken to avoid taking down all the pulleys, particularly A2 and A4. After surgery, the incisions are loosely closed; floor irrigation is not performed. Repeat operative irrigation can be performed 2 days later, if necessary. Immediately after the infection is under control, the patient should start supervised therapy. Oral antibiotics should ultimately be tailored to the intraoperative cultures, and should be continued for 2 to 6 weeks after surgery.

5. What Are the Long-Term Outcomes of PFT?

The principal complication associated with PFT is stiffness with loss of ROM, which can be caused by flexor tendon adhesions, joint capsular thickening, or destruction of the sheath and pulley system.24 In several studies, up to one-fourth of patients with PFT did not obtain full ROM, despite adequate treatment.4-6,27 Therefore, full active ROM exercises should be initiated immediately after surgery to counteract the development of stiffness.

The most severe complication of PFT is amputation of the affected digit (Figures 3A, 3B).

Figure 3.
Amputation incidence was 17% in one study2 and 29% in another,9 despite appropriate management. Dailiana and colleagues9 found that amputation was necessary more often in patients with diabetes and in patients with delayed presentation.

Pang and colleagues2 identified 5 factors associated with increased risk of amputation in patients with PFT: (1) age >43 years; (2) diabetes mellitus, peripheral vascular disease, or renal failure; (3) subcutaneous purulence; (4) signs of digital ischemia at presentation; and (5) growth of more than 1 bacteria species on culture of specimens obtained at time of surgery.

Pang and colleagues2 classified these patients into 3 groups with distinct clinical features and reported each group’s outcomes. The authors based their PFT classification system on increasingly severe clinical presentation, which potentially predicts amputation risk. Patients in stage 1 presented with Kanavel signs of tenosynovitis but no evidence of subcutaneous purulence or ischemia; patients in stage 2 had concurrent localized subcutaneous purulence but no ischemia; and patients in stage 3 had concurrent extensive subcutaneous purulence involving more than 1 phalangeal segment or spreading circumferentially as well as signs of ischemia. These PFT stages were found to correlate with worse patient outcomes. In patients with stage 1 infection, amputation was not required, and average functional return was 80% of total active ROM of the affected digit. In patients with stage 2 infection, the amputation rate was 8%, and return of total active ROM in the remaining digits was 72%. The outcomes for the patients with stage 3 infection were the worst. The amputation rate for patients with all 3 classification criteria (Kanavel signs, subcutaneous purulence, digital ischemia) was 59%, and return of total active ROM in the remaining digits was only 49%. Use of this clinical classification system makes it possible to guide treatment and predict outcome and return to function.

Conclusion

PFT is a common hand infection that can cause significant morbidity. Early treatment is crucial: this requires use of IV antibiotics, or surgical irrigation and débridement in more advanced cases. However, despite prompt and thorough treatment, severe infection can lead to long-term impaired function and even amputation of the affected digit. More research is needed to determine optimal timing and technique for surgical intervention and to elucidate the role of local antibiotics and corticosteroids in treating this infection and potentially preventing the morbid outcomes we currently see.

Am J Orthop. 2017;46(3):E207-E212. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Kanavel AB. The symptoms, signs, and diagnosis of tenosynovitis and major fascial-space abscesses. In: Kanavel AB, ed. Infections of the Hand. 6th ed. Philadelphia, PA: Lea & Febiger; 1933:364-395.

2. Pang HN, Teoh LC, Yam AK, Lee JY, Puhaindran ME, Tan AB. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2007;89(8):1742-1748.

3. Stern PJ, Staneck JL, McDonough JJ, Neale HW, Tyler G. Established hand infections: a controlled, prospective study. J Hand Surg Am. 1983;8(5 pt 1):553-559.

4. Neviaser RJ. Closed tendon sheath irrigation for pyogenic flexor tenosynovitis. J Hand Surg Am. 1978;3(5):462-466.

5. Harris PA, Nanchahal J. Closed continuous irrigation in the treatment of hand infections. J Hand Surg Br. 1999;24(3):328-333.

6. Lille S, Hayakawa T, Neumeister MW, Brown RE, Zook EG, Murray K. Continuous postoperative catheter irrigation is not necessary for the treatment of suppurative flexor tenosynovitis. J Hand Surg Br. 2000;25(3):304-307.

7. Boles SD, Schmidt CC. Pyogenic flexor tenosynovitis. Hand Clin. 1998;14(4):567-578.

8. Nemoto K, Yanagida M, Nemoto T. Closed continuous irrigation as a treatment for infection in the hand. J Hand Surg Br. 1993;18(6):783-789.

9. Dailiana ZH, Rigopoulos N, Varitimidis S, Hantes M, Bargiotas K, Malizos KN. Purulent flexor tenosynovitis: factors influencing the functional outcome. J Hand Surg Eur Vol. 2008;33(3):280-285.

10. Small LN, Ross JJ. Suppurative tenosynovitis and septic bursitis. Infect Dis Clin North Am. 2005;19(4):991-1005, xi.

11. Katsoulis E, Bissell I, Hargreaves DG. MRSA pyogenic flexor tenosynovitis leading to digital ischaemic necrosis and amputation. J Hand Surg Br. 2006;31(3):350-352.

12. Fowler JR Greenhill D, Schaffer AA, Thoder JJ, Ilyas AM. Evolving incidence of MRSA in urban hand infections. Orthopedics. 2013;36(6):796-800.

13. Aubert JP, Stein A, Raoult D, Magalon G. Flexor tenosynovitis in the hand: an unusual aetiology. J Hand Surg Br. 1995;20(4):509-510.

14. Wright TW, Linscheid RL, O’Duffy JD. Acute flexor tenosynovitis in association with Clostridium difficile infection: a case report. J Hand Surg Am. 1996;21(2):304-306.

15. Schaefer RA, Enzenauer RJ, Pruitt A, Corpe RS. Acute gonococcal flexor tenosynovitis in an adolescent male with pharyngitis: a case report and literature review. Clin Orthop Relat Res. 1992;(281):212-215.

16. Mamane W, Falcone MO, Doursounian L, Nourissat G. Isolated gonococcal tenosynovitis. Case report and review of literature [in French]. Chir Main. 2010;29(5):335-337.

17. Regnard PJ, Barry P, Isselin J. Mycobacterial tenosynovitis of the flexor tendons of the hand. A report of five cases. J Hand Surg Br. 1996;21(3):351-354.

18. Abrams RA, Botte MJ. Hand infections: treatment recommendations for specific types. J Am Acad Orthop Surg. 1996;4(4):219-230.

19. Neviaser RJ, Gunther SF. Tenosynovial infections in the hand: diagnosis and management. Instr Course Lect. 1980;29:108-128.

20. Szabo R, Palumbo C. Infections of the hand. In: Chapman M, ed. Chapman’s Orthopedic Surgery. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001:1989-2008.

21. Neviaser R. Acute infections. In: Green D, Hotchkiss R, Pederson W, eds. Green’s Operative Hand Surgery. 4th ed. New York, NY: Churchill Livingstone; 1999:1033-1047.

22. Michon J. Phlegmon of the tendon sheaths [in French]. Ann Chir. 1974;28(4):277-280.

23. Gutowski KA, Ochoa O, Adams WP Jr. Closed-catheter irrigation is as effective as open drainage for treatment of pyogenic flexor tenosynovitis. Ann Plast Surg. 2002;49(4):350-354.

24. Stern PJ. Selected acute infections. Instr Course Lect. 1990;39:539-546.

25. Dickson-Wright A. Tendon sheath infection. Proc R Soc Med. 1943-1944;37:504-505.

26. Juliano PJ, Eglseder WA. Limited open-tendon-sheath irrigation in the treatment of pyogenic flexor tenosynovitis. Orthop Rev. 1991;20(12):1065-1069.

27. Pollen AG. Acute infection of the tendon sheaths. Hand. 1974;6(1):21-25.

28. Besser MI. Digital flexor tendon irrigation. Hand. 1976;8(1):72.

29. Carter SJ, Burman SO, Mersheimer WL. Treatment of digital tenosynovitis by irrigation with peroxide and oxytetracycline: review of nine cases. Ann Surg. 1966;163(4):645-650.

30. Draeger RW, Singh B, Bynum DK, Dahners LE. Corticosteroids as an adjunct to antibiotics and surgical drainage for the treatment of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2010;92(16):2653-2662.

31. Delsignore JL, Ritland D, Becker DR, Watson HK. Continuous catheter irrigation for the treatment of suppurative flexor synovitis. Conn Med. 1986;50(8):503-506.

32. Gosain AK, Markisson RE. Catheter irrigation for treatment of pyogenic closed space infections of the hand. Br J Plast Surg. 1991;44(4):270-273.

References

1. Kanavel AB. The symptoms, signs, and diagnosis of tenosynovitis and major fascial-space abscesses. In: Kanavel AB, ed. Infections of the Hand. 6th ed. Philadelphia, PA: Lea & Febiger; 1933:364-395.

2. Pang HN, Teoh LC, Yam AK, Lee JY, Puhaindran ME, Tan AB. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2007;89(8):1742-1748.

3. Stern PJ, Staneck JL, McDonough JJ, Neale HW, Tyler G. Established hand infections: a controlled, prospective study. J Hand Surg Am. 1983;8(5 pt 1):553-559.

4. Neviaser RJ. Closed tendon sheath irrigation for pyogenic flexor tenosynovitis. J Hand Surg Am. 1978;3(5):462-466.

5. Harris PA, Nanchahal J. Closed continuous irrigation in the treatment of hand infections. J Hand Surg Br. 1999;24(3):328-333.

6. Lille S, Hayakawa T, Neumeister MW, Brown RE, Zook EG, Murray K. Continuous postoperative catheter irrigation is not necessary for the treatment of suppurative flexor tenosynovitis. J Hand Surg Br. 2000;25(3):304-307.

7. Boles SD, Schmidt CC. Pyogenic flexor tenosynovitis. Hand Clin. 1998;14(4):567-578.

8. Nemoto K, Yanagida M, Nemoto T. Closed continuous irrigation as a treatment for infection in the hand. J Hand Surg Br. 1993;18(6):783-789.

9. Dailiana ZH, Rigopoulos N, Varitimidis S, Hantes M, Bargiotas K, Malizos KN. Purulent flexor tenosynovitis: factors influencing the functional outcome. J Hand Surg Eur Vol. 2008;33(3):280-285.

10. Small LN, Ross JJ. Suppurative tenosynovitis and septic bursitis. Infect Dis Clin North Am. 2005;19(4):991-1005, xi.

11. Katsoulis E, Bissell I, Hargreaves DG. MRSA pyogenic flexor tenosynovitis leading to digital ischaemic necrosis and amputation. J Hand Surg Br. 2006;31(3):350-352.

12. Fowler JR Greenhill D, Schaffer AA, Thoder JJ, Ilyas AM. Evolving incidence of MRSA in urban hand infections. Orthopedics. 2013;36(6):796-800.

13. Aubert JP, Stein A, Raoult D, Magalon G. Flexor tenosynovitis in the hand: an unusual aetiology. J Hand Surg Br. 1995;20(4):509-510.

14. Wright TW, Linscheid RL, O’Duffy JD. Acute flexor tenosynovitis in association with Clostridium difficile infection: a case report. J Hand Surg Am. 1996;21(2):304-306.

15. Schaefer RA, Enzenauer RJ, Pruitt A, Corpe RS. Acute gonococcal flexor tenosynovitis in an adolescent male with pharyngitis: a case report and literature review. Clin Orthop Relat Res. 1992;(281):212-215.

16. Mamane W, Falcone MO, Doursounian L, Nourissat G. Isolated gonococcal tenosynovitis. Case report and review of literature [in French]. Chir Main. 2010;29(5):335-337.

17. Regnard PJ, Barry P, Isselin J. Mycobacterial tenosynovitis of the flexor tendons of the hand. A report of five cases. J Hand Surg Br. 1996;21(3):351-354.

18. Abrams RA, Botte MJ. Hand infections: treatment recommendations for specific types. J Am Acad Orthop Surg. 1996;4(4):219-230.

19. Neviaser RJ, Gunther SF. Tenosynovial infections in the hand: diagnosis and management. Instr Course Lect. 1980;29:108-128.

20. Szabo R, Palumbo C. Infections of the hand. In: Chapman M, ed. Chapman’s Orthopedic Surgery. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001:1989-2008.

21. Neviaser R. Acute infections. In: Green D, Hotchkiss R, Pederson W, eds. Green’s Operative Hand Surgery. 4th ed. New York, NY: Churchill Livingstone; 1999:1033-1047.

22. Michon J. Phlegmon of the tendon sheaths [in French]. Ann Chir. 1974;28(4):277-280.

23. Gutowski KA, Ochoa O, Adams WP Jr. Closed-catheter irrigation is as effective as open drainage for treatment of pyogenic flexor tenosynovitis. Ann Plast Surg. 2002;49(4):350-354.

24. Stern PJ. Selected acute infections. Instr Course Lect. 1990;39:539-546.

25. Dickson-Wright A. Tendon sheath infection. Proc R Soc Med. 1943-1944;37:504-505.

26. Juliano PJ, Eglseder WA. Limited open-tendon-sheath irrigation in the treatment of pyogenic flexor tenosynovitis. Orthop Rev. 1991;20(12):1065-1069.

27. Pollen AG. Acute infection of the tendon sheaths. Hand. 1974;6(1):21-25.

28. Besser MI. Digital flexor tendon irrigation. Hand. 1976;8(1):72.

29. Carter SJ, Burman SO, Mersheimer WL. Treatment of digital tenosynovitis by irrigation with peroxide and oxytetracycline: review of nine cases. Ann Surg. 1966;163(4):645-650.

30. Draeger RW, Singh B, Bynum DK, Dahners LE. Corticosteroids as an adjunct to antibiotics and surgical drainage for the treatment of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2010;92(16):2653-2662.

31. Delsignore JL, Ritland D, Becker DR, Watson HK. Continuous catheter irrigation for the treatment of suppurative flexor synovitis. Conn Med. 1986;50(8):503-506.

32. Gosain AK, Markisson RE. Catheter irrigation for treatment of pyogenic closed space infections of the hand. Br J Plast Surg. 1991;44(4):270-273.

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How Should the Treatment Costs of Distal Radius Fractures Be Measured?

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Take-Home Points

  • Physician fees, operating room costs, therapy costs, and missed work account for most (92%) of the costs in distal radius fractures.
  • Indirect costs (especially missed work) contribute a significant amount to the total cost of injury.
  • Patients continue to accrue costs up to 3-6 months post-injury.
  • Implant costs make up only 6% of the total costs of operatively treated distal radius fractures.

Distal radius fractures (DRFs) account for 20% of all fractures seen in the emergency department, and are the most common fractures in all patients under age 75 years.1,2 Apart from causing pain and disability, DRFs have a large associated economic burden.3-6 In addition, over the past decade, the fixation technology used for DRF treatment has expanded rapidly and revolutionized operative management. With this expansion has come a growing body of high-level evidence guiding treatment decisions regarding patient outcomes.7-11 As operative treatment of these injuries has evolved, researchers have begun to critically evaluate both health outcomes and the cost-effectiveness of treatment choices.12,13

Determining the cost-effectiveness of any medical intervention requires an accurate and standardized method for measuring the total cost of a course of treatment. Although several studies have attempted to evaluate the treatment costs of DRFs,14-18 none has rigorously examined exactly what needs to be measured, and for how long, to accurately describe the overall cost. Many studies have examined only direct costs (treatment-related costs incurred in the hospital or clinic itself) and neglected indirect costs (eg, missed work, time in treatment, additional care requirements). As patient-reported disability from these injuries can be high,19-22 it is likely that the additional indirect costs, often borne by the patient, are correspondingly high. This relationship has been suggested by indirect data from large retrospective epidemiologic studies3-6 but has never been evaluated with primary data obtained in a prospective study.

Given these questions, we conducted an in-depth study of the treatment costs of these injuries to identify which factors should be captured, and for how long, to accurately describe the overall cost without missing any of the major cost-drivers. We hypothesized that indirect costs (particularly missed work) would be significant and variable cost-drivers in the overall economic impact of these injuries, and that direct prospective measurement of these costs would be the most reliable method for accurately assessing them. In short, this was a prospective, observational study of all the direct and indirect costs associated with treating DRFs. Its 2 main goals were to determine how much of the overall cost was attributable to indirect costs, and which cost factors should be measured, and for how long, to capture the true economic cost of these injuries.

Patients and Methods

Study Design

This prospective, observational study was approved by our hospital’s Institutional Review Board, and patients gave informed consent to participate. Patients with an isolated DRF that was treated either operatively or nonoperatively and followed at our hospital were eligible for the study. Treatment decisions for each patient were made by the treating surgeon and were based on injury characteristics. Patients with multiple concomitant injuries (polytrauma) were excluded. The AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) classification system was used to grade all fractures.23

Patients were seen 2 weeks, 1 month, 3 months, 6 months, and 1 year after injury. Each time, clinical data (strength, range of motion, patient-rated outcome forms) and economic data were collected. A patient’s economic data were considered complete if the patient had full follow-up in our clinic up to 1 year after injury or, if applicable, the patient returned to work and had all recurring direct and indirect costs resolved. Costs were measured and calculated from the broadest possible perspective (overall societal costs) rather than from payer-specific perspectives (eg, institution costs, insurance costs).

Treatment and Rehabilitation Protocol

Each patient who underwent nonoperative treatment was placed in a molded sugar-tong splint with hand motion encouraged and followed in clinic. At 4 to 6 weeks, the splint was removed, and the patient was placed in a removable cock-up wrist splint for another 2 to 4 weeks. Throughout this period, the patient worked on elbow and finger motion with an occupational therapist (OT). On discontinuation of the wrist splint, the patient returned to the OT for gentle wrist motion and continuation of elbow and finger motion.

For each patient who underwent operative treatment, implant and approach were based on fracture pattern. Implants used included isolated Kirschner wires (K-wires), volar locked plates, dorsal plates, radial column plates, and ulnar plates. After fixation, the patient was placed in a well-padded volar splint and encouraged to start immediate finger motion. Ten to 14 days after surgery, the splint was removed, and the patient was referred to an OT for gentle wrist, finger, and elbow motion. Therapy was continued until wrist, finger, and elbow motion was full.

 

 

Direct Costs

Direct costs were obtained from hospital billing and collections records. Cost items measured included physician fees, imaging fees, inpatient bed fees (when applicable), operating room (OR) facility fees, implant costs, and OT costs. Whenever possible, the final amount collected (vs charged) was used for the cost, as this was thought to be the most reliable indicator of the real cost of an item. Total cost was obtained from ultimate collection/reimbursement for all physician, imaging, and OT fees.

In a few cases, ultimate amount collected was not in our system and instead was calculated by normalizing the charges based on internal departmental cost-to-charge ratios. Cost-to-charge ratios were used for OR/emergency department facility fees, inpatient bed fees, and implant costs.

Indirect Costs

Indirect costs were calculated from questionnaires completed by patients at initial enrollment and at each follow-up visit. The initial enrollment form captured basic demographic information, employment status and work type, and annual income. The follow-up form included questions about current work status, physical/occupational therapy frequency, and extra recurring expenses related to transportation, household chores, and personal care, among other items. Total recurring expenses from transportation, chores, and personal care were calculated by multiplying the weekly expenses listed at a given visit by the time since the previous visit.

Costs for missed work were estimated as a function of preinjury wages multiplied by decreased level of productivity and period of work missed. For a patient who indicated part-time work status, decreased level of productivity was calculated by dividing the patient’s weekly hours by 40 (assumes 40-hour week is full-time), which yielded a percentage of full-time capacity. The patient was also asked to indicate any change in work status, which allowed for an accurate accounting of how long the patient was away from work and how much the patient’s capacity was decreased, ultimately providing an estimate of total amount of work missed. Multiplying that period by annual preinjury wages gave the value used for total cost of missed work.

Results

Of the 82 patients enrolled in the study, 36 were treated operatively and 46 nonoperatively. Table 1 lists additional demographic information about the study population.

Table 1.
Complete financial data, defined as 1-year follow-up data, or data collected until recurring indirect costs were negligible, were ultimately available for 75 patients; the other 7 patients were lost to follow-up while they were still incurring indirect costs.

Table 2 provides a full breakdown of costs. OT costs were similar between groups but proportionally made up 27% of the costs for the nonoperative group and 4.9% for the operative group.

Table 2.
Of note, implant costs comprised about 6.3% of total costs in the operative group. Of the 36 patients in that group, 2 were treated with K-wires only (average cost, $356), 26 with a single volar locked plate (average cost, $871), and 8 with a volar plate plus supplemental fixation, such as a radial column plate, a dorsal plate, or an ulnar plate (average cost, $1479).

Indirect costs accounted for 28% of the total cost for the operative group and 36% for the nonoperative group. Missed work was the major contributor to overall indirect cost, accounting for 93% of all indirect costs. Additional transportation, household chores, and personal care costs accounted for 4.7%, 1.7%, and 0.8% of total indirect costs, respectively.

Of the nonoperatively treated patients who had been working before being injured, 25% missed at least some work. Except for 1 patient, all were back working full-time within 3 months after injury. Of the operatively treated patients who had been working before injury, 48% missed at least some work, and 24% were still missing at least some work between 3 and 6 months after injury. All patients in both groups were back working within 1 year after injury.

Indirect costs largely paralleled work status, with 50% of patients still incurring some costs up to 6 months after injury (Figure).
Figure.
For the nonoperative group, 92% of all indirect costs were incurred within the first 3 months; for the operative group, 74%. For all patients, more than 96% of all indirect costs were incurred within 6 months after injury.

Discussion

The drive to use evidence-based treatments in medicine has led to increased scrutiny of the benefits of novel treatments and technologies. However, in addition to carefully measuring clinical benefits, we must monitor costs. Implementation of new treatments based on small clinical advantages, without consideration of economic impact, will not be sustainable over the long term.

This study was not intended to report the “true” cost of treating these injuries, or to make direct comparisons between operative and nonoperative groups (regional and institutional costs and practices vary so much that no single-site study can report a meaningful number for cost). Furthermore, the observational (nonrandomized) nature of this study makes direct comparison of operative and nonoperative groups too confounded to draw conclusions. Simply, this study was conducted to help determine what needs to be measured, with the ultimate goal being to obtain a relatively reliable estimate of the total cost to society of a given injury and its treatment.

In this study, physician fees and facility fees were major direct expenses—not surprising given the value of physician time and OR time. In addition, OT was a fairly large direct-cost driver, particularly for nonoperative patients, for whom other costs were relatively low. This finding supports what has been reported in studies of the frequency and duration of therapy as potential targets for cost containment.24 Surprisingly, OT costs were lower for operatively (vs nonoperatively) treated patients. This finding may be attributable to earlier wrist motion in operatively treated patients (10-14 days) relative to nonoperatively treated patients (6-8 weeks), as earlier wrist motion may reduce stiffness and total need for therapy. Alternatively, the finding may be attributable to sampling error caused by difficulty in obtaining accurate OT costs, as some patients received therapy at multiple private offices, with records unavailable.

Although significant attention is often focused on implant costs, these actually comprised a relatively small portion (6%) of the total treatment costs for these injuries. However, implant costs vary significantly between institutions.

Indirect costs were a major factor, accounting for about one-third of total cost. Missed work was the single largest cost item in this study, comprising 93% of the indirect cost and 27% of the total cost. These findings suggest that the cost of missed work is crucial and should be measured in any study that compares the cost-effectiveness of different treatment modalities.

In orthopedic trauma, earlier return to work is often cited as a potential benefit of surgical intervention. However, without defining the exact economic impact of missed work, it is difficult to decide if earlier return to work justifies the added cost of surgery. The situation is further muddled by conflicting priorities, as the entities that bear the cost of missed work (patient, disability insurance) are often different from the entity that bears the cost of surgery (medical insurance). In the light of this complex decision-making with multiple and sometimes conflicting stakeholders, accurate understanding of the economic impact of missed work is paramount. Our data showed return to work took slightly longer for operatively (vs nonoperatively) treated patients, though we think this is more likely a result of higher injury severity than treatment choice.

Patients in both groups were still not back working up to 6 months after injury, indicating that return of function after these injuries is not as rapid as we might hope or expect, and may play a role in setting expectations during initial discussions with patients.

The major strength of this study is that it was the first of its kind to prospectively measure these costs at a single institution in order to make direct comparisons of different cost factors. Whenever possible, rather than relying on cost-to-charge ratio estimates, we analyzed costs obtained directly from collections reports, which improved the validity of the results generated. Missed work was captured by directly asking patients about work capacity, not by retrospectively reviewing disability applications, which for a variety of reasons often inaccurately reflects true work productivity. In addition, our final follow-up rate was relatively high (91%), which helped minimize bias. Although this study focused on DRFs, the hope is that these data can serve as a template for the kinds of factors that need to be measured to accurately describe the cost of many different upper extremity injuries. This idea, however, needs to be formally tested.

This study had several limitations. First, some costs (OR time, facility fees) still had to be estimated with cost-to-charge ratios—a less precise method. Second, measuring the societal cost of missed work is controversial. We calculated this cost by using standard economic techniques, valuing the decreased productivity period according to baseline salary, though the true “loss” to society is less clear. Third, our data represent the costs at one hospital in one city and might be very different at other institutions with different cost structures. Fourth, this study was observational (vs randomized) and subject to the usual bias of such studies, so conclusions between treatment choices and cost or clinical outcomes could not be drawn (which was not our intent in this study). Although these issues limited our ability to calculate the exact “cost” of these injuries, the relative impact of the different cost factors could be measured (which was our intent).

DRFs are common injuries that can have significant associated expenses, many of which were not captured in previous cost analyses. In the present study, we found that measuring physician, OR, therapy, and missed work costs for at least 6 months after injury was generally sufficient for accurate capture of major costs. We hope these data can help in planning studies of the treatment costs of upper extremity injuries. Only through accurate and conscientious data gathering can we evaluate the clinical and economic effects of novel technologies and ensure delivery of high-quality care while containing costs and improving efficiency.

Am J Orthop. 2017;46(1):E54-E59. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Simic PM, Weiland AJ. Fractures of the distal aspect of the radius: changes in treatment over the past two decades. Instr Course Lect. 2003;52:185-195.

2. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26(5):908-915.

3. Trybus M, Guzik P. The economic impact of hand injury [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2003;68(4):269-273.

4. Dias JJ, Garcia-Elias M. Hand injury costs. Injury. 2006;37(11):1071-1077.

5. Wüthrich P. Epidemiology and socioeconomic significance of hand injuries [in German]. Z Unfallchir Versicherungsmed Berufskr. 1986;79(1):5-14.

6. de Putter CE, Selles RW, Polinder S, Panneman MJ, Hovius SE, van Beeck EF. Economic impact of hand and wrist injuries: health-care costs and productivity costs in a population-based study. J Bone Joint Surg Am. 2012;94(9):e56.

7. Wong TC, Chiu Y, Tsang WL, Leung WY, Yam SK, Yeung SH. Casting versus percutaneous pinning for extra-articular fractures of the distal radius in an elderly Chinese population: a prospective randomised controlled trial. J Hand Surg Eur Vol. 2010;35(3):202-208.

8. Krukhaug Y, Ugland S, Lie SA, Hove LM. External fixation of fractures of the distal radius: a randomized comparison of the Hoffman Compact II non-bridging fixator and the Dynawrist fixator in 75 patients followed for 1 year. Acta Orthop. 2009;80(1):104-108.

9. Xu GG, Chan SP, Puhaindran ME, Chew WY. Prospective randomised study of intra-articular fractures of the distal radius: comparison between external fixation and plate fixation. Ann Acad Med Singapore. 2009;38(7):600-606.

10. Egol K, Walsh M, Tejwani N, McLaurin T, Wynn C, Paksima N. Bridging external fixation and supplementary Kirschner-wire fixation versus volar locked plating for unstable fractures of the distal radius: a randomised, prospective trial. J Bone Joint Surg Br. 2008;90(9):1214-1221.

11. Wei DH, Raizman NM, Bottino CJ, Jobin CM, Strauch RJ, Rosenwasser MP. Unstable distal radial fractures treated with external fixation, a radial column plate, or a volar plate. A prospective randomized trial. J Bone Joint Surg Am. 2009;91(7):1568-1577.

12. Shauver MJ, Clapham PJ, Chung KC. An economic analysis of outcomes and complications of treating distal radius fractures in the elderly. J Hand Surg Am. 2011;36(12):1912-1918.e1-e3.

13. Espinosa Gutiérrez A, Moreno Velázquez A. Cost–benefit of various treatments for patients with distal radius fracture [in Spanish]. Acta Ortop Mex. 2010;24(2):61-65.

14. Shyamalan G, Theokli C, Pearse Y, Tennent D. Volar locking plates versus Kirschner wires for distal radial fractures—a cost analysis study. Injury. 2009;40(12):1279-1281.

15. Kakarlapudi TK, Santini A, Shahane SA, Douglas D. The cost of treatment of distal radial fractures. Injury. 2000;31(4):229-232.

16. Do TT, Strub WM, Foad SL, Mehlman CT, Crawford AH. Reduction versus remodeling in pediatric distal forearm fractures: a preliminary cost analysis. J Pediatr Orthop B. 2003;12(2):109-115.

17. Miller BS, Taylor B, Widmann RF, Bae DS, Snyder BD, Waters PM. Cast immobilization versus percutaneous pin fixation of displaced distal radius fractures in children: a prospective, randomized study. J Pediatr Orthop. 2005;25(4):490-494.

18. Shauver MJ, Yin H, Banerjee M, Chung KC. Current and future national costs to Medicare for the treatment of distal radius fracture in the elderly. J Hand Surg Am. 2011;36(8):1282-1287.

19. Handoll HH, Madhok R, Howe TE. Rehabilitation for distal radial fractures in adults. Cochrane Database Syst Rev. 2006;(3):CD003324.

20. Handoll HH, Huntley JS, Madhok R. External fixation versus conservative treatment for distal radial fractures in adults. Cochrane Database Syst Rev. 2007;(3):CD006194.

21. Handoll HH, Vaghela MV, Madhok R. Percutaneous pinning for treating distal radial fractures in adults. Cochrane Database Syst Rev. 2007;(3):CD006080.

22. Handoll HH, Huntley JS, Madhok R. Different methods of external fixation for treating distal radial fractures in adults. Cochrane Database Syst Rev. 2008;(1):CD006522.

23. Marsh JL, Slongo TF, Agel J, et al. Fracture and dislocation classification compendium—2007: Orthopaedic Trauma Association classification, database and outcomes committee. J Orthop Trauma. 2007;21(10 suppl):S1-S133.

24. Souer JS, Buijze G, Ring D. A prospective randomized controlled trial comparing occupational therapy with independent exercises after volar plate fixation of a fracture of the distal part of the radius. J Bone Joint Surg Am. 2011;93(19):1761-1766.

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Authors’ Disclosure Statement: This study was funded through a generous resident grant from the Orthopaedic Trauma Association. Dr. Rosenwasser reports that he is a consultant for Stryker and Zimmer Biomet and receives royalties from Zimmer Biomet. The other authors report no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: This study was funded through a generous resident grant from the Orthopaedic Trauma Association. Dr. Rosenwasser reports that he is a consultant for Stryker and Zimmer Biomet and receives royalties from Zimmer Biomet. The other authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors’ Disclosure Statement: This study was funded through a generous resident grant from the Orthopaedic Trauma Association. Dr. Rosenwasser reports that he is a consultant for Stryker and Zimmer Biomet and receives royalties from Zimmer Biomet. The other authors report no actual or potential conflict of interest in relation to this article.

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Take-Home Points

  • Physician fees, operating room costs, therapy costs, and missed work account for most (92%) of the costs in distal radius fractures.
  • Indirect costs (especially missed work) contribute a significant amount to the total cost of injury.
  • Patients continue to accrue costs up to 3-6 months post-injury.
  • Implant costs make up only 6% of the total costs of operatively treated distal radius fractures.

Distal radius fractures (DRFs) account for 20% of all fractures seen in the emergency department, and are the most common fractures in all patients under age 75 years.1,2 Apart from causing pain and disability, DRFs have a large associated economic burden.3-6 In addition, over the past decade, the fixation technology used for DRF treatment has expanded rapidly and revolutionized operative management. With this expansion has come a growing body of high-level evidence guiding treatment decisions regarding patient outcomes.7-11 As operative treatment of these injuries has evolved, researchers have begun to critically evaluate both health outcomes and the cost-effectiveness of treatment choices.12,13

Determining the cost-effectiveness of any medical intervention requires an accurate and standardized method for measuring the total cost of a course of treatment. Although several studies have attempted to evaluate the treatment costs of DRFs,14-18 none has rigorously examined exactly what needs to be measured, and for how long, to accurately describe the overall cost. Many studies have examined only direct costs (treatment-related costs incurred in the hospital or clinic itself) and neglected indirect costs (eg, missed work, time in treatment, additional care requirements). As patient-reported disability from these injuries can be high,19-22 it is likely that the additional indirect costs, often borne by the patient, are correspondingly high. This relationship has been suggested by indirect data from large retrospective epidemiologic studies3-6 but has never been evaluated with primary data obtained in a prospective study.

Given these questions, we conducted an in-depth study of the treatment costs of these injuries to identify which factors should be captured, and for how long, to accurately describe the overall cost without missing any of the major cost-drivers. We hypothesized that indirect costs (particularly missed work) would be significant and variable cost-drivers in the overall economic impact of these injuries, and that direct prospective measurement of these costs would be the most reliable method for accurately assessing them. In short, this was a prospective, observational study of all the direct and indirect costs associated with treating DRFs. Its 2 main goals were to determine how much of the overall cost was attributable to indirect costs, and which cost factors should be measured, and for how long, to capture the true economic cost of these injuries.

Patients and Methods

Study Design

This prospective, observational study was approved by our hospital’s Institutional Review Board, and patients gave informed consent to participate. Patients with an isolated DRF that was treated either operatively or nonoperatively and followed at our hospital were eligible for the study. Treatment decisions for each patient were made by the treating surgeon and were based on injury characteristics. Patients with multiple concomitant injuries (polytrauma) were excluded. The AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) classification system was used to grade all fractures.23

Patients were seen 2 weeks, 1 month, 3 months, 6 months, and 1 year after injury. Each time, clinical data (strength, range of motion, patient-rated outcome forms) and economic data were collected. A patient’s economic data were considered complete if the patient had full follow-up in our clinic up to 1 year after injury or, if applicable, the patient returned to work and had all recurring direct and indirect costs resolved. Costs were measured and calculated from the broadest possible perspective (overall societal costs) rather than from payer-specific perspectives (eg, institution costs, insurance costs).

Treatment and Rehabilitation Protocol

Each patient who underwent nonoperative treatment was placed in a molded sugar-tong splint with hand motion encouraged and followed in clinic. At 4 to 6 weeks, the splint was removed, and the patient was placed in a removable cock-up wrist splint for another 2 to 4 weeks. Throughout this period, the patient worked on elbow and finger motion with an occupational therapist (OT). On discontinuation of the wrist splint, the patient returned to the OT for gentle wrist motion and continuation of elbow and finger motion.

For each patient who underwent operative treatment, implant and approach were based on fracture pattern. Implants used included isolated Kirschner wires (K-wires), volar locked plates, dorsal plates, radial column plates, and ulnar plates. After fixation, the patient was placed in a well-padded volar splint and encouraged to start immediate finger motion. Ten to 14 days after surgery, the splint was removed, and the patient was referred to an OT for gentle wrist, finger, and elbow motion. Therapy was continued until wrist, finger, and elbow motion was full.

 

 

Direct Costs

Direct costs were obtained from hospital billing and collections records. Cost items measured included physician fees, imaging fees, inpatient bed fees (when applicable), operating room (OR) facility fees, implant costs, and OT costs. Whenever possible, the final amount collected (vs charged) was used for the cost, as this was thought to be the most reliable indicator of the real cost of an item. Total cost was obtained from ultimate collection/reimbursement for all physician, imaging, and OT fees.

In a few cases, ultimate amount collected was not in our system and instead was calculated by normalizing the charges based on internal departmental cost-to-charge ratios. Cost-to-charge ratios were used for OR/emergency department facility fees, inpatient bed fees, and implant costs.

Indirect Costs

Indirect costs were calculated from questionnaires completed by patients at initial enrollment and at each follow-up visit. The initial enrollment form captured basic demographic information, employment status and work type, and annual income. The follow-up form included questions about current work status, physical/occupational therapy frequency, and extra recurring expenses related to transportation, household chores, and personal care, among other items. Total recurring expenses from transportation, chores, and personal care were calculated by multiplying the weekly expenses listed at a given visit by the time since the previous visit.

Costs for missed work were estimated as a function of preinjury wages multiplied by decreased level of productivity and period of work missed. For a patient who indicated part-time work status, decreased level of productivity was calculated by dividing the patient’s weekly hours by 40 (assumes 40-hour week is full-time), which yielded a percentage of full-time capacity. The patient was also asked to indicate any change in work status, which allowed for an accurate accounting of how long the patient was away from work and how much the patient’s capacity was decreased, ultimately providing an estimate of total amount of work missed. Multiplying that period by annual preinjury wages gave the value used for total cost of missed work.

Results

Of the 82 patients enrolled in the study, 36 were treated operatively and 46 nonoperatively. Table 1 lists additional demographic information about the study population.

Table 1.
Complete financial data, defined as 1-year follow-up data, or data collected until recurring indirect costs were negligible, were ultimately available for 75 patients; the other 7 patients were lost to follow-up while they were still incurring indirect costs.

Table 2 provides a full breakdown of costs. OT costs were similar between groups but proportionally made up 27% of the costs for the nonoperative group and 4.9% for the operative group.

Table 2.
Of note, implant costs comprised about 6.3% of total costs in the operative group. Of the 36 patients in that group, 2 were treated with K-wires only (average cost, $356), 26 with a single volar locked plate (average cost, $871), and 8 with a volar plate plus supplemental fixation, such as a radial column plate, a dorsal plate, or an ulnar plate (average cost, $1479).

Indirect costs accounted for 28% of the total cost for the operative group and 36% for the nonoperative group. Missed work was the major contributor to overall indirect cost, accounting for 93% of all indirect costs. Additional transportation, household chores, and personal care costs accounted for 4.7%, 1.7%, and 0.8% of total indirect costs, respectively.

Of the nonoperatively treated patients who had been working before being injured, 25% missed at least some work. Except for 1 patient, all were back working full-time within 3 months after injury. Of the operatively treated patients who had been working before injury, 48% missed at least some work, and 24% were still missing at least some work between 3 and 6 months after injury. All patients in both groups were back working within 1 year after injury.

Indirect costs largely paralleled work status, with 50% of patients still incurring some costs up to 6 months after injury (Figure).
Figure.
For the nonoperative group, 92% of all indirect costs were incurred within the first 3 months; for the operative group, 74%. For all patients, more than 96% of all indirect costs were incurred within 6 months after injury.

Discussion

The drive to use evidence-based treatments in medicine has led to increased scrutiny of the benefits of novel treatments and technologies. However, in addition to carefully measuring clinical benefits, we must monitor costs. Implementation of new treatments based on small clinical advantages, without consideration of economic impact, will not be sustainable over the long term.

This study was not intended to report the “true” cost of treating these injuries, or to make direct comparisons between operative and nonoperative groups (regional and institutional costs and practices vary so much that no single-site study can report a meaningful number for cost). Furthermore, the observational (nonrandomized) nature of this study makes direct comparison of operative and nonoperative groups too confounded to draw conclusions. Simply, this study was conducted to help determine what needs to be measured, with the ultimate goal being to obtain a relatively reliable estimate of the total cost to society of a given injury and its treatment.

In this study, physician fees and facility fees were major direct expenses—not surprising given the value of physician time and OR time. In addition, OT was a fairly large direct-cost driver, particularly for nonoperative patients, for whom other costs were relatively low. This finding supports what has been reported in studies of the frequency and duration of therapy as potential targets for cost containment.24 Surprisingly, OT costs were lower for operatively (vs nonoperatively) treated patients. This finding may be attributable to earlier wrist motion in operatively treated patients (10-14 days) relative to nonoperatively treated patients (6-8 weeks), as earlier wrist motion may reduce stiffness and total need for therapy. Alternatively, the finding may be attributable to sampling error caused by difficulty in obtaining accurate OT costs, as some patients received therapy at multiple private offices, with records unavailable.

Although significant attention is often focused on implant costs, these actually comprised a relatively small portion (6%) of the total treatment costs for these injuries. However, implant costs vary significantly between institutions.

Indirect costs were a major factor, accounting for about one-third of total cost. Missed work was the single largest cost item in this study, comprising 93% of the indirect cost and 27% of the total cost. These findings suggest that the cost of missed work is crucial and should be measured in any study that compares the cost-effectiveness of different treatment modalities.

In orthopedic trauma, earlier return to work is often cited as a potential benefit of surgical intervention. However, without defining the exact economic impact of missed work, it is difficult to decide if earlier return to work justifies the added cost of surgery. The situation is further muddled by conflicting priorities, as the entities that bear the cost of missed work (patient, disability insurance) are often different from the entity that bears the cost of surgery (medical insurance). In the light of this complex decision-making with multiple and sometimes conflicting stakeholders, accurate understanding of the economic impact of missed work is paramount. Our data showed return to work took slightly longer for operatively (vs nonoperatively) treated patients, though we think this is more likely a result of higher injury severity than treatment choice.

Patients in both groups were still not back working up to 6 months after injury, indicating that return of function after these injuries is not as rapid as we might hope or expect, and may play a role in setting expectations during initial discussions with patients.

The major strength of this study is that it was the first of its kind to prospectively measure these costs at a single institution in order to make direct comparisons of different cost factors. Whenever possible, rather than relying on cost-to-charge ratio estimates, we analyzed costs obtained directly from collections reports, which improved the validity of the results generated. Missed work was captured by directly asking patients about work capacity, not by retrospectively reviewing disability applications, which for a variety of reasons often inaccurately reflects true work productivity. In addition, our final follow-up rate was relatively high (91%), which helped minimize bias. Although this study focused on DRFs, the hope is that these data can serve as a template for the kinds of factors that need to be measured to accurately describe the cost of many different upper extremity injuries. This idea, however, needs to be formally tested.

This study had several limitations. First, some costs (OR time, facility fees) still had to be estimated with cost-to-charge ratios—a less precise method. Second, measuring the societal cost of missed work is controversial. We calculated this cost by using standard economic techniques, valuing the decreased productivity period according to baseline salary, though the true “loss” to society is less clear. Third, our data represent the costs at one hospital in one city and might be very different at other institutions with different cost structures. Fourth, this study was observational (vs randomized) and subject to the usual bias of such studies, so conclusions between treatment choices and cost or clinical outcomes could not be drawn (which was not our intent in this study). Although these issues limited our ability to calculate the exact “cost” of these injuries, the relative impact of the different cost factors could be measured (which was our intent).

DRFs are common injuries that can have significant associated expenses, many of which were not captured in previous cost analyses. In the present study, we found that measuring physician, OR, therapy, and missed work costs for at least 6 months after injury was generally sufficient for accurate capture of major costs. We hope these data can help in planning studies of the treatment costs of upper extremity injuries. Only through accurate and conscientious data gathering can we evaluate the clinical and economic effects of novel technologies and ensure delivery of high-quality care while containing costs and improving efficiency.

Am J Orthop. 2017;46(1):E54-E59. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Physician fees, operating room costs, therapy costs, and missed work account for most (92%) of the costs in distal radius fractures.
  • Indirect costs (especially missed work) contribute a significant amount to the total cost of injury.
  • Patients continue to accrue costs up to 3-6 months post-injury.
  • Implant costs make up only 6% of the total costs of operatively treated distal radius fractures.

Distal radius fractures (DRFs) account for 20% of all fractures seen in the emergency department, and are the most common fractures in all patients under age 75 years.1,2 Apart from causing pain and disability, DRFs have a large associated economic burden.3-6 In addition, over the past decade, the fixation technology used for DRF treatment has expanded rapidly and revolutionized operative management. With this expansion has come a growing body of high-level evidence guiding treatment decisions regarding patient outcomes.7-11 As operative treatment of these injuries has evolved, researchers have begun to critically evaluate both health outcomes and the cost-effectiveness of treatment choices.12,13

Determining the cost-effectiveness of any medical intervention requires an accurate and standardized method for measuring the total cost of a course of treatment. Although several studies have attempted to evaluate the treatment costs of DRFs,14-18 none has rigorously examined exactly what needs to be measured, and for how long, to accurately describe the overall cost. Many studies have examined only direct costs (treatment-related costs incurred in the hospital or clinic itself) and neglected indirect costs (eg, missed work, time in treatment, additional care requirements). As patient-reported disability from these injuries can be high,19-22 it is likely that the additional indirect costs, often borne by the patient, are correspondingly high. This relationship has been suggested by indirect data from large retrospective epidemiologic studies3-6 but has never been evaluated with primary data obtained in a prospective study.

Given these questions, we conducted an in-depth study of the treatment costs of these injuries to identify which factors should be captured, and for how long, to accurately describe the overall cost without missing any of the major cost-drivers. We hypothesized that indirect costs (particularly missed work) would be significant and variable cost-drivers in the overall economic impact of these injuries, and that direct prospective measurement of these costs would be the most reliable method for accurately assessing them. In short, this was a prospective, observational study of all the direct and indirect costs associated with treating DRFs. Its 2 main goals were to determine how much of the overall cost was attributable to indirect costs, and which cost factors should be measured, and for how long, to capture the true economic cost of these injuries.

Patients and Methods

Study Design

This prospective, observational study was approved by our hospital’s Institutional Review Board, and patients gave informed consent to participate. Patients with an isolated DRF that was treated either operatively or nonoperatively and followed at our hospital were eligible for the study. Treatment decisions for each patient were made by the treating surgeon and were based on injury characteristics. Patients with multiple concomitant injuries (polytrauma) were excluded. The AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) classification system was used to grade all fractures.23

Patients were seen 2 weeks, 1 month, 3 months, 6 months, and 1 year after injury. Each time, clinical data (strength, range of motion, patient-rated outcome forms) and economic data were collected. A patient’s economic data were considered complete if the patient had full follow-up in our clinic up to 1 year after injury or, if applicable, the patient returned to work and had all recurring direct and indirect costs resolved. Costs were measured and calculated from the broadest possible perspective (overall societal costs) rather than from payer-specific perspectives (eg, institution costs, insurance costs).

Treatment and Rehabilitation Protocol

Each patient who underwent nonoperative treatment was placed in a molded sugar-tong splint with hand motion encouraged and followed in clinic. At 4 to 6 weeks, the splint was removed, and the patient was placed in a removable cock-up wrist splint for another 2 to 4 weeks. Throughout this period, the patient worked on elbow and finger motion with an occupational therapist (OT). On discontinuation of the wrist splint, the patient returned to the OT for gentle wrist motion and continuation of elbow and finger motion.

For each patient who underwent operative treatment, implant and approach were based on fracture pattern. Implants used included isolated Kirschner wires (K-wires), volar locked plates, dorsal plates, radial column plates, and ulnar plates. After fixation, the patient was placed in a well-padded volar splint and encouraged to start immediate finger motion. Ten to 14 days after surgery, the splint was removed, and the patient was referred to an OT for gentle wrist, finger, and elbow motion. Therapy was continued until wrist, finger, and elbow motion was full.

 

 

Direct Costs

Direct costs were obtained from hospital billing and collections records. Cost items measured included physician fees, imaging fees, inpatient bed fees (when applicable), operating room (OR) facility fees, implant costs, and OT costs. Whenever possible, the final amount collected (vs charged) was used for the cost, as this was thought to be the most reliable indicator of the real cost of an item. Total cost was obtained from ultimate collection/reimbursement for all physician, imaging, and OT fees.

In a few cases, ultimate amount collected was not in our system and instead was calculated by normalizing the charges based on internal departmental cost-to-charge ratios. Cost-to-charge ratios were used for OR/emergency department facility fees, inpatient bed fees, and implant costs.

Indirect Costs

Indirect costs were calculated from questionnaires completed by patients at initial enrollment and at each follow-up visit. The initial enrollment form captured basic demographic information, employment status and work type, and annual income. The follow-up form included questions about current work status, physical/occupational therapy frequency, and extra recurring expenses related to transportation, household chores, and personal care, among other items. Total recurring expenses from transportation, chores, and personal care were calculated by multiplying the weekly expenses listed at a given visit by the time since the previous visit.

Costs for missed work were estimated as a function of preinjury wages multiplied by decreased level of productivity and period of work missed. For a patient who indicated part-time work status, decreased level of productivity was calculated by dividing the patient’s weekly hours by 40 (assumes 40-hour week is full-time), which yielded a percentage of full-time capacity. The patient was also asked to indicate any change in work status, which allowed for an accurate accounting of how long the patient was away from work and how much the patient’s capacity was decreased, ultimately providing an estimate of total amount of work missed. Multiplying that period by annual preinjury wages gave the value used for total cost of missed work.

Results

Of the 82 patients enrolled in the study, 36 were treated operatively and 46 nonoperatively. Table 1 lists additional demographic information about the study population.

Table 1.
Complete financial data, defined as 1-year follow-up data, or data collected until recurring indirect costs were negligible, were ultimately available for 75 patients; the other 7 patients were lost to follow-up while they were still incurring indirect costs.

Table 2 provides a full breakdown of costs. OT costs were similar between groups but proportionally made up 27% of the costs for the nonoperative group and 4.9% for the operative group.

Table 2.
Of note, implant costs comprised about 6.3% of total costs in the operative group. Of the 36 patients in that group, 2 were treated with K-wires only (average cost, $356), 26 with a single volar locked plate (average cost, $871), and 8 with a volar plate plus supplemental fixation, such as a radial column plate, a dorsal plate, or an ulnar plate (average cost, $1479).

Indirect costs accounted for 28% of the total cost for the operative group and 36% for the nonoperative group. Missed work was the major contributor to overall indirect cost, accounting for 93% of all indirect costs. Additional transportation, household chores, and personal care costs accounted for 4.7%, 1.7%, and 0.8% of total indirect costs, respectively.

Of the nonoperatively treated patients who had been working before being injured, 25% missed at least some work. Except for 1 patient, all were back working full-time within 3 months after injury. Of the operatively treated patients who had been working before injury, 48% missed at least some work, and 24% were still missing at least some work between 3 and 6 months after injury. All patients in both groups were back working within 1 year after injury.

Indirect costs largely paralleled work status, with 50% of patients still incurring some costs up to 6 months after injury (Figure).
Figure.
For the nonoperative group, 92% of all indirect costs were incurred within the first 3 months; for the operative group, 74%. For all patients, more than 96% of all indirect costs were incurred within 6 months after injury.

Discussion

The drive to use evidence-based treatments in medicine has led to increased scrutiny of the benefits of novel treatments and technologies. However, in addition to carefully measuring clinical benefits, we must monitor costs. Implementation of new treatments based on small clinical advantages, without consideration of economic impact, will not be sustainable over the long term.

This study was not intended to report the “true” cost of treating these injuries, or to make direct comparisons between operative and nonoperative groups (regional and institutional costs and practices vary so much that no single-site study can report a meaningful number for cost). Furthermore, the observational (nonrandomized) nature of this study makes direct comparison of operative and nonoperative groups too confounded to draw conclusions. Simply, this study was conducted to help determine what needs to be measured, with the ultimate goal being to obtain a relatively reliable estimate of the total cost to society of a given injury and its treatment.

In this study, physician fees and facility fees were major direct expenses—not surprising given the value of physician time and OR time. In addition, OT was a fairly large direct-cost driver, particularly for nonoperative patients, for whom other costs were relatively low. This finding supports what has been reported in studies of the frequency and duration of therapy as potential targets for cost containment.24 Surprisingly, OT costs were lower for operatively (vs nonoperatively) treated patients. This finding may be attributable to earlier wrist motion in operatively treated patients (10-14 days) relative to nonoperatively treated patients (6-8 weeks), as earlier wrist motion may reduce stiffness and total need for therapy. Alternatively, the finding may be attributable to sampling error caused by difficulty in obtaining accurate OT costs, as some patients received therapy at multiple private offices, with records unavailable.

Although significant attention is often focused on implant costs, these actually comprised a relatively small portion (6%) of the total treatment costs for these injuries. However, implant costs vary significantly between institutions.

Indirect costs were a major factor, accounting for about one-third of total cost. Missed work was the single largest cost item in this study, comprising 93% of the indirect cost and 27% of the total cost. These findings suggest that the cost of missed work is crucial and should be measured in any study that compares the cost-effectiveness of different treatment modalities.

In orthopedic trauma, earlier return to work is often cited as a potential benefit of surgical intervention. However, without defining the exact economic impact of missed work, it is difficult to decide if earlier return to work justifies the added cost of surgery. The situation is further muddled by conflicting priorities, as the entities that bear the cost of missed work (patient, disability insurance) are often different from the entity that bears the cost of surgery (medical insurance). In the light of this complex decision-making with multiple and sometimes conflicting stakeholders, accurate understanding of the economic impact of missed work is paramount. Our data showed return to work took slightly longer for operatively (vs nonoperatively) treated patients, though we think this is more likely a result of higher injury severity than treatment choice.

Patients in both groups were still not back working up to 6 months after injury, indicating that return of function after these injuries is not as rapid as we might hope or expect, and may play a role in setting expectations during initial discussions with patients.

The major strength of this study is that it was the first of its kind to prospectively measure these costs at a single institution in order to make direct comparisons of different cost factors. Whenever possible, rather than relying on cost-to-charge ratio estimates, we analyzed costs obtained directly from collections reports, which improved the validity of the results generated. Missed work was captured by directly asking patients about work capacity, not by retrospectively reviewing disability applications, which for a variety of reasons often inaccurately reflects true work productivity. In addition, our final follow-up rate was relatively high (91%), which helped minimize bias. Although this study focused on DRFs, the hope is that these data can serve as a template for the kinds of factors that need to be measured to accurately describe the cost of many different upper extremity injuries. This idea, however, needs to be formally tested.

This study had several limitations. First, some costs (OR time, facility fees) still had to be estimated with cost-to-charge ratios—a less precise method. Second, measuring the societal cost of missed work is controversial. We calculated this cost by using standard economic techniques, valuing the decreased productivity period according to baseline salary, though the true “loss” to society is less clear. Third, our data represent the costs at one hospital in one city and might be very different at other institutions with different cost structures. Fourth, this study was observational (vs randomized) and subject to the usual bias of such studies, so conclusions between treatment choices and cost or clinical outcomes could not be drawn (which was not our intent in this study). Although these issues limited our ability to calculate the exact “cost” of these injuries, the relative impact of the different cost factors could be measured (which was our intent).

DRFs are common injuries that can have significant associated expenses, many of which were not captured in previous cost analyses. In the present study, we found that measuring physician, OR, therapy, and missed work costs for at least 6 months after injury was generally sufficient for accurate capture of major costs. We hope these data can help in planning studies of the treatment costs of upper extremity injuries. Only through accurate and conscientious data gathering can we evaluate the clinical and economic effects of novel technologies and ensure delivery of high-quality care while containing costs and improving efficiency.

Am J Orthop. 2017;46(1):E54-E59. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Simic PM, Weiland AJ. Fractures of the distal aspect of the radius: changes in treatment over the past two decades. Instr Course Lect. 2003;52:185-195.

2. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26(5):908-915.

3. Trybus M, Guzik P. The economic impact of hand injury [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2003;68(4):269-273.

4. Dias JJ, Garcia-Elias M. Hand injury costs. Injury. 2006;37(11):1071-1077.

5. Wüthrich P. Epidemiology and socioeconomic significance of hand injuries [in German]. Z Unfallchir Versicherungsmed Berufskr. 1986;79(1):5-14.

6. de Putter CE, Selles RW, Polinder S, Panneman MJ, Hovius SE, van Beeck EF. Economic impact of hand and wrist injuries: health-care costs and productivity costs in a population-based study. J Bone Joint Surg Am. 2012;94(9):e56.

7. Wong TC, Chiu Y, Tsang WL, Leung WY, Yam SK, Yeung SH. Casting versus percutaneous pinning for extra-articular fractures of the distal radius in an elderly Chinese population: a prospective randomised controlled trial. J Hand Surg Eur Vol. 2010;35(3):202-208.

8. Krukhaug Y, Ugland S, Lie SA, Hove LM. External fixation of fractures of the distal radius: a randomized comparison of the Hoffman Compact II non-bridging fixator and the Dynawrist fixator in 75 patients followed for 1 year. Acta Orthop. 2009;80(1):104-108.

9. Xu GG, Chan SP, Puhaindran ME, Chew WY. Prospective randomised study of intra-articular fractures of the distal radius: comparison between external fixation and plate fixation. Ann Acad Med Singapore. 2009;38(7):600-606.

10. Egol K, Walsh M, Tejwani N, McLaurin T, Wynn C, Paksima N. Bridging external fixation and supplementary Kirschner-wire fixation versus volar locked plating for unstable fractures of the distal radius: a randomised, prospective trial. J Bone Joint Surg Br. 2008;90(9):1214-1221.

11. Wei DH, Raizman NM, Bottino CJ, Jobin CM, Strauch RJ, Rosenwasser MP. Unstable distal radial fractures treated with external fixation, a radial column plate, or a volar plate. A prospective randomized trial. J Bone Joint Surg Am. 2009;91(7):1568-1577.

12. Shauver MJ, Clapham PJ, Chung KC. An economic analysis of outcomes and complications of treating distal radius fractures in the elderly. J Hand Surg Am. 2011;36(12):1912-1918.e1-e3.

13. Espinosa Gutiérrez A, Moreno Velázquez A. Cost–benefit of various treatments for patients with distal radius fracture [in Spanish]. Acta Ortop Mex. 2010;24(2):61-65.

14. Shyamalan G, Theokli C, Pearse Y, Tennent D. Volar locking plates versus Kirschner wires for distal radial fractures—a cost analysis study. Injury. 2009;40(12):1279-1281.

15. Kakarlapudi TK, Santini A, Shahane SA, Douglas D. The cost of treatment of distal radial fractures. Injury. 2000;31(4):229-232.

16. Do TT, Strub WM, Foad SL, Mehlman CT, Crawford AH. Reduction versus remodeling in pediatric distal forearm fractures: a preliminary cost analysis. J Pediatr Orthop B. 2003;12(2):109-115.

17. Miller BS, Taylor B, Widmann RF, Bae DS, Snyder BD, Waters PM. Cast immobilization versus percutaneous pin fixation of displaced distal radius fractures in children: a prospective, randomized study. J Pediatr Orthop. 2005;25(4):490-494.

18. Shauver MJ, Yin H, Banerjee M, Chung KC. Current and future national costs to Medicare for the treatment of distal radius fracture in the elderly. J Hand Surg Am. 2011;36(8):1282-1287.

19. Handoll HH, Madhok R, Howe TE. Rehabilitation for distal radial fractures in adults. Cochrane Database Syst Rev. 2006;(3):CD003324.

20. Handoll HH, Huntley JS, Madhok R. External fixation versus conservative treatment for distal radial fractures in adults. Cochrane Database Syst Rev. 2007;(3):CD006194.

21. Handoll HH, Vaghela MV, Madhok R. Percutaneous pinning for treating distal radial fractures in adults. Cochrane Database Syst Rev. 2007;(3):CD006080.

22. Handoll HH, Huntley JS, Madhok R. Different methods of external fixation for treating distal radial fractures in adults. Cochrane Database Syst Rev. 2008;(1):CD006522.

23. Marsh JL, Slongo TF, Agel J, et al. Fracture and dislocation classification compendium—2007: Orthopaedic Trauma Association classification, database and outcomes committee. J Orthop Trauma. 2007;21(10 suppl):S1-S133.

24. Souer JS, Buijze G, Ring D. A prospective randomized controlled trial comparing occupational therapy with independent exercises after volar plate fixation of a fracture of the distal part of the radius. J Bone Joint Surg Am. 2011;93(19):1761-1766.

References

1. Simic PM, Weiland AJ. Fractures of the distal aspect of the radius: changes in treatment over the past two decades. Instr Course Lect. 2003;52:185-195.

2. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26(5):908-915.

3. Trybus M, Guzik P. The economic impact of hand injury [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2003;68(4):269-273.

4. Dias JJ, Garcia-Elias M. Hand injury costs. Injury. 2006;37(11):1071-1077.

5. Wüthrich P. Epidemiology and socioeconomic significance of hand injuries [in German]. Z Unfallchir Versicherungsmed Berufskr. 1986;79(1):5-14.

6. de Putter CE, Selles RW, Polinder S, Panneman MJ, Hovius SE, van Beeck EF. Economic impact of hand and wrist injuries: health-care costs and productivity costs in a population-based study. J Bone Joint Surg Am. 2012;94(9):e56.

7. Wong TC, Chiu Y, Tsang WL, Leung WY, Yam SK, Yeung SH. Casting versus percutaneous pinning for extra-articular fractures of the distal radius in an elderly Chinese population: a prospective randomised controlled trial. J Hand Surg Eur Vol. 2010;35(3):202-208.

8. Krukhaug Y, Ugland S, Lie SA, Hove LM. External fixation of fractures of the distal radius: a randomized comparison of the Hoffman Compact II non-bridging fixator and the Dynawrist fixator in 75 patients followed for 1 year. Acta Orthop. 2009;80(1):104-108.

9. Xu GG, Chan SP, Puhaindran ME, Chew WY. Prospective randomised study of intra-articular fractures of the distal radius: comparison between external fixation and plate fixation. Ann Acad Med Singapore. 2009;38(7):600-606.

10. Egol K, Walsh M, Tejwani N, McLaurin T, Wynn C, Paksima N. Bridging external fixation and supplementary Kirschner-wire fixation versus volar locked plating for unstable fractures of the distal radius: a randomised, prospective trial. J Bone Joint Surg Br. 2008;90(9):1214-1221.

11. Wei DH, Raizman NM, Bottino CJ, Jobin CM, Strauch RJ, Rosenwasser MP. Unstable distal radial fractures treated with external fixation, a radial column plate, or a volar plate. A prospective randomized trial. J Bone Joint Surg Am. 2009;91(7):1568-1577.

12. Shauver MJ, Clapham PJ, Chung KC. An economic analysis of outcomes and complications of treating distal radius fractures in the elderly. J Hand Surg Am. 2011;36(12):1912-1918.e1-e3.

13. Espinosa Gutiérrez A, Moreno Velázquez A. Cost–benefit of various treatments for patients with distal radius fracture [in Spanish]. Acta Ortop Mex. 2010;24(2):61-65.

14. Shyamalan G, Theokli C, Pearse Y, Tennent D. Volar locking plates versus Kirschner wires for distal radial fractures—a cost analysis study. Injury. 2009;40(12):1279-1281.

15. Kakarlapudi TK, Santini A, Shahane SA, Douglas D. The cost of treatment of distal radial fractures. Injury. 2000;31(4):229-232.

16. Do TT, Strub WM, Foad SL, Mehlman CT, Crawford AH. Reduction versus remodeling in pediatric distal forearm fractures: a preliminary cost analysis. J Pediatr Orthop B. 2003;12(2):109-115.

17. Miller BS, Taylor B, Widmann RF, Bae DS, Snyder BD, Waters PM. Cast immobilization versus percutaneous pin fixation of displaced distal radius fractures in children: a prospective, randomized study. J Pediatr Orthop. 2005;25(4):490-494.

18. Shauver MJ, Yin H, Banerjee M, Chung KC. Current and future national costs to Medicare for the treatment of distal radius fracture in the elderly. J Hand Surg Am. 2011;36(8):1282-1287.

19. Handoll HH, Madhok R, Howe TE. Rehabilitation for distal radial fractures in adults. Cochrane Database Syst Rev. 2006;(3):CD003324.

20. Handoll HH, Huntley JS, Madhok R. External fixation versus conservative treatment for distal radial fractures in adults. Cochrane Database Syst Rev. 2007;(3):CD006194.

21. Handoll HH, Vaghela MV, Madhok R. Percutaneous pinning for treating distal radial fractures in adults. Cochrane Database Syst Rev. 2007;(3):CD006080.

22. Handoll HH, Huntley JS, Madhok R. Different methods of external fixation for treating distal radial fractures in adults. Cochrane Database Syst Rev. 2008;(1):CD006522.

23. Marsh JL, Slongo TF, Agel J, et al. Fracture and dislocation classification compendium—2007: Orthopaedic Trauma Association classification, database and outcomes committee. J Orthop Trauma. 2007;21(10 suppl):S1-S133.

24. Souer JS, Buijze G, Ring D. A prospective randomized controlled trial comparing occupational therapy with independent exercises after volar plate fixation of a fracture of the distal part of the radius. J Bone Joint Surg Am. 2011;93(19):1761-1766.

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Prospective Evaluation of Opioid Consumption After Distal Radius Fracture Repair Surgery

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Take-Home Points

  • Prescription opioid abuse and overdose-related deaths are on the rise in the United States.
  • Following Open Reduction Internal Fixation (ORIF) of a distal radius fracture (DRF), patients consumed an average of 14.6 opioid pills. We recommend prescribing no more than 15-20 opioid pills after DRF ORIF.
  • There was no difference in opioid consumption between patients who underwent general anesthesia vs regional anesthesia.
  • There was a significant trend towards less opioid consumption with increasing age.
  • There was a trend towards increased opioid consumption in patients with worsening fracture type as well as in self-pay/Medicaid patients.

Over the past 2 decades, prescription opioid abuse in the United States has risen steadily.1,2 Although use of opioid analgesics in the US far exceeds use in other countries, US patients do not report less pain or more satisfaction with pain relief.3-5 Between 1999 and 2002, oxycodone prescriptions increased by 50%, fentanyl prescriptions by 150%, and morphine prescriptions by 60%.6 Furthermore, the Centers for Disease Control and Prevention (CDC) reported in 2012 that, for every 100 people in the United States, US physicians wrote a mean of 82.5 opioid prescriptions and 37.6 benzodiazepine prescriptions; in total, US clinicians wrote 259 million opioid prescriptions in 2012, enough for every adult to have a bottle.7 The increase in prescription opioid abuse, not surprisingly, has paralleled a 124% increase in opioid overdose-related deaths.8 Cicero and colleagues2,9 recently found that, over the past 50 years, heroin use has dramatically shifted from being a problem mainly of urban centers and minorities toward one of older, suburban Caucasians with a previous history of prescription pain killer abuse. Deaths from prescription opioid overdoses now exceed deaths from heroin and cocaine overdoses combined.10 According to the CDC, emergency department visits related to nonmedical use of prescription opioid medications jumped 111% between 2004 and 2008.11

Opioid analgesics are often prescribed for the management of musculoskeletal pain and injuries.12-16 Orthopedic surgeons, who prescribe more opioids than physicians in any other surgical field, represent the third largest group of opioid prescribers, trailing only primary care physicians and internists, who far outnumber them.17 A study focused on opioid consumption after upper extremity surgery found that upper extremity surgeons tended to overprescribe opioids for postoperative analgesia.18 Many patients saved their remaining medication for later use and were never instructed on proper disposal. There is a developing consensus that opioid medication is not as safe and effective as once thought, and that a high-dose prescription or prolonged opioid therapy do not improve outcomes.19 In addition, patients may experience numerous opioid-associated adverse effects, including nausea, vomiting, constipation, lightheadedness, dizziness, blurred vision, headache, dry mouth, sweating, and itching.

In October 2012, patient satisfaction scores on the Hospital Consumer Assessment of Healthcare Providers and Systems started affecting Medicare reimbursements.20 By 2017, up to 6% of Medicare reimbursement will be at risk, given the poor outcomes caused by uncontrolled pain.21-24 The US healthcare culture has made it more important than ever for physicians to adequately manage postoperative pain while limiting opioid availability and the risk for abuse.

Distal radius fracture (DRF) open reduction and internal fixation (ORIF) is commonly performed by orthopedic surgeons and hand surgeons. Pain management and opioid consumption after DRF repair may be influenced by several variables. We conducted a study to investigate the impact of several clinical variables on postoperative opioid use; to test the hypothesis that post-DRF-ORIF opioid consumption would increase with worsening fracture classification and certain patient demographics; and to seek postoperative opioid consumption insights that would facilitate optimization of future opioid prescribing.

Materials and Methods

Institutional Review Board approval was obtained before initiation of the study. All outpatients who underwent DRF-ORIF (performed by 9 hand surgery fellowship-trained orthopedic surgeons) were consecutively enrolled over a 6-month period in 2014. All procedures were performed with a standard volar plating technique through a flexor carpi radialis approach. The postoperative rehabilitation protocol was standardized for all patients. Data collected on each patient included age, sex, payer type, fracture type, opioid prescribed, amount prescribed, amount consumed, reasons for stopping, adverse events, and any postoperative adjunctive pain medications. The data were taken from questionnaires completed by patients at their first visit within 2 weeks after surgery. Anesthesia type (general or regional) was noted as well. All fractures were classified by Dr. O’Neil using the AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) classification of long-bone fractures based on preoperative radiographs.

 

 

Amount of opioid analgesic consumed was converted into morphine equivalents to adjust for the different opioids prescribed after surgery: oxycodone/acetaminophen or oxycodone equivalent, hydrocodone/acetaminophen or hydrocodone equivalent, and acetaminophen/codeine.

Patients were excluded from the study if their procedure was performed on an inpatient basis, if they sustained other injuries or fractures from their trauma, or if an adjunctive procedure (including carpal tunnel release) was performed during the DRF repair.

We used the Spearman rank correlation coefficient and a count data model to examine the relationship between opioid use and age. The Kruskal-Wallis test was used to examine the relationships between opioid use and payer type, anesthesia type, and fracture type.

Results

Of the 109 patients eligible for the study, 11 were excluded for incomplete postoperative questionnaires, leaving 98 patients (79 females, 19 males) for analysis. Mean age was 58 years (range, 13-92 years). Of the 98 patients, 45 received general anesthesia, and 53 received regional anesthesia with a single-shot peripheral nerve block before surgery and sedation perioperatively (Table).

Table.
A single-shot supraclavicular nerve block (30 mL of 0.5% ropivacaine plus 5 mg of dexamethasone) was administered by a board-certified anesthesiologist. Mean opioid consumption (morphine equivalents) was 58.5 mg (range, 0-280 mg), roughly equivalent to 14.6 tabs of oxycodone/acetaminophen 5/325 mg. Sixty-seven patients (68.4%) consumed <75 mg of morphine equivalents, or <20 tabs of oxycodone/acetaminophen 5/325 mg. Mean duration of use was 4.8 days (range, 0-16 days) after surgery.
Figure 1.
There were no significant differences (P = .74) in opioid consumption between patients who received general anesthesia and patients who received regional anesthesia (Figure 1).

Of the 98 study patients, 61 reported using over-the-counter adjunctive pain medications during the postoperative period, and 37 reported no use. Mean opioid consumption was 64.7 mg of morphine equivalents for the adjunctive medication users and 48.3 mg for the nonusers (P = .1947).

Demographic analysis revealed an inverse relationship between age and opioid use (Figure 2). The Spearman ρ between age and opioid consumption was –0.2958, which suggests decreased opioid use by older patients (P = .003).

Figure 2.
A count data model with negative binomial distribution suggested opioid consumption decreased by 1.72% per year of age (95% confidence interval, 0.35%-3.06%).
Figure 3.
Similarly, a relationship was found between opioid consumption and payer type (Figure 3), with consumption highest for self-pay and Medicaid patients (P = .063). However, this finding should be interpreted carefully, as it was underpowered—there were only 3 patients in the self-pay/Medicaid group.

All fractures were graded with the AO/OTA long-bone fracture classification system. Mean opioid consumption for the 3 fracture-type groups was 57.7 mg (class A), 60.3 mg (class B), and 62.0 mg (class C) (Figure 4).
Figure 4.
Although the data demonstrate a trend toward increasing opioid consumption in patients who underwent fixation of complete intra-articular DRFs, as opposed to partial articular and extra-articular fractures, the difference was not significant (P = .99).

Discussion

The US healthcare culture has elevated physicians’ responsibility in adequately and aggressively managing their patients’ pain experience. Moreover, reimbursement may be affected by patient satisfaction scores, which are partly predicated on pain control.20-24 However, as rates of opioid use and abuse rise, it is important that physicians prescribe such medications judiciously. This is particularly germane to orthopedic surgeons, who prescribe more opioid analgesics than surgeons in any other field.17 Rodgers and colleagues18 found upper extremity surgeons, in particular, tended to overprescribe postoperative opioid analgesics. In the present study, we sought to identify the crucial risk factors that influence post-DRF-ORIF pain management and opioid consumption.

Mean postoperative opioid consumption (morphine equivalents) was 58.5 mg, roughly equivalent to 14.6 tabs of oxycodone/acetaminophen 5/325 mg, an opioid analgesic commonly used during the acute postoperative period. In addition, almost 70% of our patients required <75 mg of morphine equivalents, or <20 tabs of oxycodone/acetaminophen 5/325 mg. For upper extremity surgeons, these numbers may be better guides in determining the most appropriate amount of opioid to prescribe after DRF repair.

As for predicting levels of postoperative opioid medication, there was a significant trend toward less consumption with increasing age. Given this finding, surgeons prescribing for elderly patients should expect less opioid use. Regarding payer type, there was a trend toward more opioid use by self-pay/Medicaid patients; however, there were only 3 patients in this group. The situation in the study by Rodgers and colleagues18 is similar: Their finding that Medicaid patients consumed more pain pills after surgery was underpowered (only 5 patients in the group).

In the orthopedic community, support for use of regional anesthesia has been widespread for several reasons, including the belief that it reduces postoperative pain and therefore should reduce postoperative opioid consumption.25 However, we found no significant difference in postoperative opioid consumption between patients who received general anesthesia (with and without local anesthesia) and patients who received regional anesthesia (nerve block). Mean opioid consumption was 57.93 mg in the general anesthesia group and 58.98 mg in the regional anesthesia group. However, this finding could have been confounded by the variability in success and operator dependence inherent in regional anesthesia. In addition, the anatomical location for the peripheral nerve block and anesthetic could have affected the efficacy of the block and played a role in postoperative opioid consumption.

In this study, we tested the hypothesis that there would be more postoperative opioid consumption with worsening fracture type. Although our results did not reach statistical significance, there was a trend toward increased opioid consumption in patients with a complete intra-articular fracture (AO/OTA class C) vs patients with a partial articular fracture (class B) or an extra-articular fracture (class A). In addition, patients with a partial articular fracture tended to use more postoperative opioids than patients with an extra-articular fracture. In short, postoperative opioid consumption tended to be higher with increasing articular involvement of the fracture.

This study was limited in that it relied on patient self-reporting. Given the social stigma attached to opioid use, patients may have underreported their postoperative opioid consumption, been affected by recall bias, or both. The study also did not control for preoperative opioid use or history of opioid or substance abuse. Chronic preoperative opioid consumption may have affected postoperative opioid use. Other patient-related factors, such as body mass index (BMI) and hepatorenal dysfunction, can create tremendous variability in opioid metabolism across a population. Such factors were not controlled for in this study and therefore may have affected its results. That could help explain why older patients, who are more likely to have lower BMI and less efficient organ function for opioid metabolism, had lower postoperative opioid consumption. In addition, although we excluded patients with concomitant injuries and procedures, we did not screen patients for concomitant complex regional pain syndrome, fibromyalgia, or other medical conditions that might have had a significant impact on postoperative pain management needs. Last, some findings, such as the relationship between opioid use and payer type, were underpowered: Although self-pay/Medicaid patients had higher postoperative opioid consumption, they were few in number. The same was true of the Medicaid patients in the study by Rodgers and colleagues.18Our results demonstrated that post-DRF-ORIF opioid consumption decreased with age and was independent of type of perioperative anesthesia. There was a trend toward more opioid consumption with both self- and Medicaid payment and worsening fracture classification. It has become more important than ever for orthopedic surgeons to adequately manage postoperative pain while limiting opioid availability and the risk for abuse. Surgeons must remain aware of the variables in their patients’ postoperative pain experience in order to better optimize prescribing patterns and provide a safe and effective postoperative pain regimen.

Am J Orthop. 2017;46(1):E35-E40. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

References

1. Kuehn BM. Opioid prescriptions soar: increase in legitimate use as well as abuse. JAMA. 2007;297(3):249-251.

2. Cicero TJ, Ellis MS, Surratt HL, Kurtz SP. The changing face of heroin use in the United States: a retrospective analysis of the past 50 years. JAMA Psychiatry. 2014;71(7):821-826.

3. Helmerhorst GT, Lindenhovius AL, Vrahas M, Ring D, Kloen P. Satisfaction with pain relief after operative treatment of an ankle fracture. Injury. 2012;43(11):1958-1961.

4. Lindenhovius AL, Helmerhorst GT, Schnellen AC, Vrahas M, Ring D, Kloen P. Differences in prescription of narcotic pain medication after operative treatment of hip and ankle fractures in the United States and the Netherlands. J Trauma. 2009;67(1):160-164.

5. Seya MJ, Gelders SF, Achara OU, Milani B, Scholten WK. A first comparison between the consumption of and the need for opioid analgesics at country, regional, and global levels. J Pain Palliat Care Pharmacother. 2011;25(1):6-18.

6. Bohnert AS, Valenstein M, Bair MJ, et al. Association between opioid prescribing patterns and opioid overdose-related deaths. JAMA. 2011;305(13):1315-1321.

7. Kuehn BM. CDC: major disparities in opioid prescribing among states: some states crack down on excess prescribing. JAMA. 2014;312(7):684-686.

8. Paulozzi LJ, Budnitz DS, Xi Y. Increasing deaths from opioid analgesics in the United States. Pharmacoepidemiol Drug Saf. 2006;15(9):618-627.

9. Cicero TJ, Kuehn BM. Driven by prescription drug abuse, heroin use increases among suburban and rural whites. JAMA. 2014;312(2):118-119.

10. Painkillers fuel growth in drug addiction. Harvard Ment Health Lett. Harvard Medical School website. http://www.health.harvard.edu/newsletter_article/painkillers-fuel-growth-in-drug-addiction. Published January 2011. Accessed March 18, 2015.

11. Cai R, Crane E, Poneleit K, Paulozzi L. Emergency department visits involving nonmedical use of selected prescription drugs in the United States, 2004-2008. J Pain Palliat Care Pharmacother. 2010;24(3):293-297.

12. Armaghani SJ, Lee DS, Bible JE, et al. Preoperative narcotic use and its relation to depression and anxiety in patients undergoing spine surgery. Spine. 2013;38(25):2196-2200.

13. Caudill-Slosberg MA, Schwartz LM, Woloshin S. Office visits and analgesic prescriptions for musculoskeletal pain in US: 1980 vs. 2000. Pain. 2004;109(3):514-519.

14. Deyo RA, Mirza SK, Turner JA, Martin BI. Overtreating chronic back pain: time to back off? J Am Board Fam Med. 2009;22(1):62-68.

15. Lee D, Armaghani S, Archer KR, et al. Preoperative opioid use as a predictor of adverse postoperative self-reported outcomes in patients undergoing spine surgery. J Bone Joint Surg Am. 2014;96(11):e89.

16. Webster BS, Verma SK, Gatchel RJ. Relationship between early opioid prescribing for acute occupational low back pain and disability duration, medical costs, subsequent surgery and late opioid use. Spine. 2007;32(19):2127-2132.

17. Volkow ND, McLellan TA, Cotto JH, Karithanom M, Weiss SR. Characteristics of opioid prescriptions in 2009. JAMA. 2011;305(13):1299-1301.

18. Rodgers J, Cunningham K, Fitzgerald K, Finnerty E. Opioid consumption following outpatient upper extremity surgery. J Hand Surg Am. 2012;37(4):645-650.

19. Chen L, Vo T, Seefeld L, et al. Lack of correlation between opioid dose adjustment and pain score change in a group of chronic pain patients. J Pain. 2013;14(4):384-392.

20. Bush H. Doubling down on the patient experience. Hosp Health Netw. 2011;85(12):22-25, 1.

21. Centers for Medicare & Medicaid Services, US Department of Health and Human Services. Medicare program; hospital inpatient prospective payment systems for acute care hospitals and the long-term care hospital prospective payment system and fiscal year 2013 rates; hospitals’ resident caps for graduate medical education payment purposes; quality reporting requirements for specific providers and for ambulatory surgical centers. Final rule. Fed Regist. 2012;77(170):53257-53750.

22. Centers for Medicare & Medicaid Services, US Department of Health and Human Services. Hospital Value-Based Purchasing. http://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/downloads/Hospital_VBPurchasing_Fact_Sheet_ICN907664.pdf. Published September 2015. Accessed October 2015.

23. Manchikanti L, Singh V, Caraway DL, Benyamin RM, Falco FJ, Hirsch JA. Proposed physician payment schedule for 2013: guarded prognosis for interventional pain management. Pain Physician. 2012;15(5):E615-E627.

24. Bot AG, Bekkers S, Arnstein PM, Smith RM, Ring D. Opioid use after fracture surgery correlates with pain intensity and satisfaction with pain relief. Clin Orthop Relat Res. 2014;472(8):2542-2549.

25. Oldman M, McCartney CJ, Leung A, et al. A survey of orthopedic surgeons’ attitudes and knowledge regarding regional anesthesia. Anesth Analg. 2004;98(5):1486-1490.

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Take-Home Points

  • Prescription opioid abuse and overdose-related deaths are on the rise in the United States.
  • Following Open Reduction Internal Fixation (ORIF) of a distal radius fracture (DRF), patients consumed an average of 14.6 opioid pills. We recommend prescribing no more than 15-20 opioid pills after DRF ORIF.
  • There was no difference in opioid consumption between patients who underwent general anesthesia vs regional anesthesia.
  • There was a significant trend towards less opioid consumption with increasing age.
  • There was a trend towards increased opioid consumption in patients with worsening fracture type as well as in self-pay/Medicaid patients.

Over the past 2 decades, prescription opioid abuse in the United States has risen steadily.1,2 Although use of opioid analgesics in the US far exceeds use in other countries, US patients do not report less pain or more satisfaction with pain relief.3-5 Between 1999 and 2002, oxycodone prescriptions increased by 50%, fentanyl prescriptions by 150%, and morphine prescriptions by 60%.6 Furthermore, the Centers for Disease Control and Prevention (CDC) reported in 2012 that, for every 100 people in the United States, US physicians wrote a mean of 82.5 opioid prescriptions and 37.6 benzodiazepine prescriptions; in total, US clinicians wrote 259 million opioid prescriptions in 2012, enough for every adult to have a bottle.7 The increase in prescription opioid abuse, not surprisingly, has paralleled a 124% increase in opioid overdose-related deaths.8 Cicero and colleagues2,9 recently found that, over the past 50 years, heroin use has dramatically shifted from being a problem mainly of urban centers and minorities toward one of older, suburban Caucasians with a previous history of prescription pain killer abuse. Deaths from prescription opioid overdoses now exceed deaths from heroin and cocaine overdoses combined.10 According to the CDC, emergency department visits related to nonmedical use of prescription opioid medications jumped 111% between 2004 and 2008.11

Opioid analgesics are often prescribed for the management of musculoskeletal pain and injuries.12-16 Orthopedic surgeons, who prescribe more opioids than physicians in any other surgical field, represent the third largest group of opioid prescribers, trailing only primary care physicians and internists, who far outnumber them.17 A study focused on opioid consumption after upper extremity surgery found that upper extremity surgeons tended to overprescribe opioids for postoperative analgesia.18 Many patients saved their remaining medication for later use and were never instructed on proper disposal. There is a developing consensus that opioid medication is not as safe and effective as once thought, and that a high-dose prescription or prolonged opioid therapy do not improve outcomes.19 In addition, patients may experience numerous opioid-associated adverse effects, including nausea, vomiting, constipation, lightheadedness, dizziness, blurred vision, headache, dry mouth, sweating, and itching.

In October 2012, patient satisfaction scores on the Hospital Consumer Assessment of Healthcare Providers and Systems started affecting Medicare reimbursements.20 By 2017, up to 6% of Medicare reimbursement will be at risk, given the poor outcomes caused by uncontrolled pain.21-24 The US healthcare culture has made it more important than ever for physicians to adequately manage postoperative pain while limiting opioid availability and the risk for abuse.

Distal radius fracture (DRF) open reduction and internal fixation (ORIF) is commonly performed by orthopedic surgeons and hand surgeons. Pain management and opioid consumption after DRF repair may be influenced by several variables. We conducted a study to investigate the impact of several clinical variables on postoperative opioid use; to test the hypothesis that post-DRF-ORIF opioid consumption would increase with worsening fracture classification and certain patient demographics; and to seek postoperative opioid consumption insights that would facilitate optimization of future opioid prescribing.

Materials and Methods

Institutional Review Board approval was obtained before initiation of the study. All outpatients who underwent DRF-ORIF (performed by 9 hand surgery fellowship-trained orthopedic surgeons) were consecutively enrolled over a 6-month period in 2014. All procedures were performed with a standard volar plating technique through a flexor carpi radialis approach. The postoperative rehabilitation protocol was standardized for all patients. Data collected on each patient included age, sex, payer type, fracture type, opioid prescribed, amount prescribed, amount consumed, reasons for stopping, adverse events, and any postoperative adjunctive pain medications. The data were taken from questionnaires completed by patients at their first visit within 2 weeks after surgery. Anesthesia type (general or regional) was noted as well. All fractures were classified by Dr. O’Neil using the AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) classification of long-bone fractures based on preoperative radiographs.

 

 

Amount of opioid analgesic consumed was converted into morphine equivalents to adjust for the different opioids prescribed after surgery: oxycodone/acetaminophen or oxycodone equivalent, hydrocodone/acetaminophen or hydrocodone equivalent, and acetaminophen/codeine.

Patients were excluded from the study if their procedure was performed on an inpatient basis, if they sustained other injuries or fractures from their trauma, or if an adjunctive procedure (including carpal tunnel release) was performed during the DRF repair.

We used the Spearman rank correlation coefficient and a count data model to examine the relationship between opioid use and age. The Kruskal-Wallis test was used to examine the relationships between opioid use and payer type, anesthesia type, and fracture type.

Results

Of the 109 patients eligible for the study, 11 were excluded for incomplete postoperative questionnaires, leaving 98 patients (79 females, 19 males) for analysis. Mean age was 58 years (range, 13-92 years). Of the 98 patients, 45 received general anesthesia, and 53 received regional anesthesia with a single-shot peripheral nerve block before surgery and sedation perioperatively (Table).

Table.
A single-shot supraclavicular nerve block (30 mL of 0.5% ropivacaine plus 5 mg of dexamethasone) was administered by a board-certified anesthesiologist. Mean opioid consumption (morphine equivalents) was 58.5 mg (range, 0-280 mg), roughly equivalent to 14.6 tabs of oxycodone/acetaminophen 5/325 mg. Sixty-seven patients (68.4%) consumed <75 mg of morphine equivalents, or <20 tabs of oxycodone/acetaminophen 5/325 mg. Mean duration of use was 4.8 days (range, 0-16 days) after surgery.
Figure 1.
There were no significant differences (P = .74) in opioid consumption between patients who received general anesthesia and patients who received regional anesthesia (Figure 1).

Of the 98 study patients, 61 reported using over-the-counter adjunctive pain medications during the postoperative period, and 37 reported no use. Mean opioid consumption was 64.7 mg of morphine equivalents for the adjunctive medication users and 48.3 mg for the nonusers (P = .1947).

Demographic analysis revealed an inverse relationship between age and opioid use (Figure 2). The Spearman ρ between age and opioid consumption was –0.2958, which suggests decreased opioid use by older patients (P = .003).

Figure 2.
A count data model with negative binomial distribution suggested opioid consumption decreased by 1.72% per year of age (95% confidence interval, 0.35%-3.06%).
Figure 3.
Similarly, a relationship was found between opioid consumption and payer type (Figure 3), with consumption highest for self-pay and Medicaid patients (P = .063). However, this finding should be interpreted carefully, as it was underpowered—there were only 3 patients in the self-pay/Medicaid group.

All fractures were graded with the AO/OTA long-bone fracture classification system. Mean opioid consumption for the 3 fracture-type groups was 57.7 mg (class A), 60.3 mg (class B), and 62.0 mg (class C) (Figure 4).
Figure 4.
Although the data demonstrate a trend toward increasing opioid consumption in patients who underwent fixation of complete intra-articular DRFs, as opposed to partial articular and extra-articular fractures, the difference was not significant (P = .99).

Discussion

The US healthcare culture has elevated physicians’ responsibility in adequately and aggressively managing their patients’ pain experience. Moreover, reimbursement may be affected by patient satisfaction scores, which are partly predicated on pain control.20-24 However, as rates of opioid use and abuse rise, it is important that physicians prescribe such medications judiciously. This is particularly germane to orthopedic surgeons, who prescribe more opioid analgesics than surgeons in any other field.17 Rodgers and colleagues18 found upper extremity surgeons, in particular, tended to overprescribe postoperative opioid analgesics. In the present study, we sought to identify the crucial risk factors that influence post-DRF-ORIF pain management and opioid consumption.

Mean postoperative opioid consumption (morphine equivalents) was 58.5 mg, roughly equivalent to 14.6 tabs of oxycodone/acetaminophen 5/325 mg, an opioid analgesic commonly used during the acute postoperative period. In addition, almost 70% of our patients required <75 mg of morphine equivalents, or <20 tabs of oxycodone/acetaminophen 5/325 mg. For upper extremity surgeons, these numbers may be better guides in determining the most appropriate amount of opioid to prescribe after DRF repair.

As for predicting levels of postoperative opioid medication, there was a significant trend toward less consumption with increasing age. Given this finding, surgeons prescribing for elderly patients should expect less opioid use. Regarding payer type, there was a trend toward more opioid use by self-pay/Medicaid patients; however, there were only 3 patients in this group. The situation in the study by Rodgers and colleagues18 is similar: Their finding that Medicaid patients consumed more pain pills after surgery was underpowered (only 5 patients in the group).

In the orthopedic community, support for use of regional anesthesia has been widespread for several reasons, including the belief that it reduces postoperative pain and therefore should reduce postoperative opioid consumption.25 However, we found no significant difference in postoperative opioid consumption between patients who received general anesthesia (with and without local anesthesia) and patients who received regional anesthesia (nerve block). Mean opioid consumption was 57.93 mg in the general anesthesia group and 58.98 mg in the regional anesthesia group. However, this finding could have been confounded by the variability in success and operator dependence inherent in regional anesthesia. In addition, the anatomical location for the peripheral nerve block and anesthetic could have affected the efficacy of the block and played a role in postoperative opioid consumption.

In this study, we tested the hypothesis that there would be more postoperative opioid consumption with worsening fracture type. Although our results did not reach statistical significance, there was a trend toward increased opioid consumption in patients with a complete intra-articular fracture (AO/OTA class C) vs patients with a partial articular fracture (class B) or an extra-articular fracture (class A). In addition, patients with a partial articular fracture tended to use more postoperative opioids than patients with an extra-articular fracture. In short, postoperative opioid consumption tended to be higher with increasing articular involvement of the fracture.

This study was limited in that it relied on patient self-reporting. Given the social stigma attached to opioid use, patients may have underreported their postoperative opioid consumption, been affected by recall bias, or both. The study also did not control for preoperative opioid use or history of opioid or substance abuse. Chronic preoperative opioid consumption may have affected postoperative opioid use. Other patient-related factors, such as body mass index (BMI) and hepatorenal dysfunction, can create tremendous variability in opioid metabolism across a population. Such factors were not controlled for in this study and therefore may have affected its results. That could help explain why older patients, who are more likely to have lower BMI and less efficient organ function for opioid metabolism, had lower postoperative opioid consumption. In addition, although we excluded patients with concomitant injuries and procedures, we did not screen patients for concomitant complex regional pain syndrome, fibromyalgia, or other medical conditions that might have had a significant impact on postoperative pain management needs. Last, some findings, such as the relationship between opioid use and payer type, were underpowered: Although self-pay/Medicaid patients had higher postoperative opioid consumption, they were few in number. The same was true of the Medicaid patients in the study by Rodgers and colleagues.18Our results demonstrated that post-DRF-ORIF opioid consumption decreased with age and was independent of type of perioperative anesthesia. There was a trend toward more opioid consumption with both self- and Medicaid payment and worsening fracture classification. It has become more important than ever for orthopedic surgeons to adequately manage postoperative pain while limiting opioid availability and the risk for abuse. Surgeons must remain aware of the variables in their patients’ postoperative pain experience in order to better optimize prescribing patterns and provide a safe and effective postoperative pain regimen.

Am J Orthop. 2017;46(1):E35-E40. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

Take-Home Points

  • Prescription opioid abuse and overdose-related deaths are on the rise in the United States.
  • Following Open Reduction Internal Fixation (ORIF) of a distal radius fracture (DRF), patients consumed an average of 14.6 opioid pills. We recommend prescribing no more than 15-20 opioid pills after DRF ORIF.
  • There was no difference in opioid consumption between patients who underwent general anesthesia vs regional anesthesia.
  • There was a significant trend towards less opioid consumption with increasing age.
  • There was a trend towards increased opioid consumption in patients with worsening fracture type as well as in self-pay/Medicaid patients.

Over the past 2 decades, prescription opioid abuse in the United States has risen steadily.1,2 Although use of opioid analgesics in the US far exceeds use in other countries, US patients do not report less pain or more satisfaction with pain relief.3-5 Between 1999 and 2002, oxycodone prescriptions increased by 50%, fentanyl prescriptions by 150%, and morphine prescriptions by 60%.6 Furthermore, the Centers for Disease Control and Prevention (CDC) reported in 2012 that, for every 100 people in the United States, US physicians wrote a mean of 82.5 opioid prescriptions and 37.6 benzodiazepine prescriptions; in total, US clinicians wrote 259 million opioid prescriptions in 2012, enough for every adult to have a bottle.7 The increase in prescription opioid abuse, not surprisingly, has paralleled a 124% increase in opioid overdose-related deaths.8 Cicero and colleagues2,9 recently found that, over the past 50 years, heroin use has dramatically shifted from being a problem mainly of urban centers and minorities toward one of older, suburban Caucasians with a previous history of prescription pain killer abuse. Deaths from prescription opioid overdoses now exceed deaths from heroin and cocaine overdoses combined.10 According to the CDC, emergency department visits related to nonmedical use of prescription opioid medications jumped 111% between 2004 and 2008.11

Opioid analgesics are often prescribed for the management of musculoskeletal pain and injuries.12-16 Orthopedic surgeons, who prescribe more opioids than physicians in any other surgical field, represent the third largest group of opioid prescribers, trailing only primary care physicians and internists, who far outnumber them.17 A study focused on opioid consumption after upper extremity surgery found that upper extremity surgeons tended to overprescribe opioids for postoperative analgesia.18 Many patients saved their remaining medication for later use and were never instructed on proper disposal. There is a developing consensus that opioid medication is not as safe and effective as once thought, and that a high-dose prescription or prolonged opioid therapy do not improve outcomes.19 In addition, patients may experience numerous opioid-associated adverse effects, including nausea, vomiting, constipation, lightheadedness, dizziness, blurred vision, headache, dry mouth, sweating, and itching.

In October 2012, patient satisfaction scores on the Hospital Consumer Assessment of Healthcare Providers and Systems started affecting Medicare reimbursements.20 By 2017, up to 6% of Medicare reimbursement will be at risk, given the poor outcomes caused by uncontrolled pain.21-24 The US healthcare culture has made it more important than ever for physicians to adequately manage postoperative pain while limiting opioid availability and the risk for abuse.

Distal radius fracture (DRF) open reduction and internal fixation (ORIF) is commonly performed by orthopedic surgeons and hand surgeons. Pain management and opioid consumption after DRF repair may be influenced by several variables. We conducted a study to investigate the impact of several clinical variables on postoperative opioid use; to test the hypothesis that post-DRF-ORIF opioid consumption would increase with worsening fracture classification and certain patient demographics; and to seek postoperative opioid consumption insights that would facilitate optimization of future opioid prescribing.

Materials and Methods

Institutional Review Board approval was obtained before initiation of the study. All outpatients who underwent DRF-ORIF (performed by 9 hand surgery fellowship-trained orthopedic surgeons) were consecutively enrolled over a 6-month period in 2014. All procedures were performed with a standard volar plating technique through a flexor carpi radialis approach. The postoperative rehabilitation protocol was standardized for all patients. Data collected on each patient included age, sex, payer type, fracture type, opioid prescribed, amount prescribed, amount consumed, reasons for stopping, adverse events, and any postoperative adjunctive pain medications. The data were taken from questionnaires completed by patients at their first visit within 2 weeks after surgery. Anesthesia type (general or regional) was noted as well. All fractures were classified by Dr. O’Neil using the AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) classification of long-bone fractures based on preoperative radiographs.

 

 

Amount of opioid analgesic consumed was converted into morphine equivalents to adjust for the different opioids prescribed after surgery: oxycodone/acetaminophen or oxycodone equivalent, hydrocodone/acetaminophen or hydrocodone equivalent, and acetaminophen/codeine.

Patients were excluded from the study if their procedure was performed on an inpatient basis, if they sustained other injuries or fractures from their trauma, or if an adjunctive procedure (including carpal tunnel release) was performed during the DRF repair.

We used the Spearman rank correlation coefficient and a count data model to examine the relationship between opioid use and age. The Kruskal-Wallis test was used to examine the relationships between opioid use and payer type, anesthesia type, and fracture type.

Results

Of the 109 patients eligible for the study, 11 were excluded for incomplete postoperative questionnaires, leaving 98 patients (79 females, 19 males) for analysis. Mean age was 58 years (range, 13-92 years). Of the 98 patients, 45 received general anesthesia, and 53 received regional anesthesia with a single-shot peripheral nerve block before surgery and sedation perioperatively (Table).

Table.
A single-shot supraclavicular nerve block (30 mL of 0.5% ropivacaine plus 5 mg of dexamethasone) was administered by a board-certified anesthesiologist. Mean opioid consumption (morphine equivalents) was 58.5 mg (range, 0-280 mg), roughly equivalent to 14.6 tabs of oxycodone/acetaminophen 5/325 mg. Sixty-seven patients (68.4%) consumed <75 mg of morphine equivalents, or <20 tabs of oxycodone/acetaminophen 5/325 mg. Mean duration of use was 4.8 days (range, 0-16 days) after surgery.
Figure 1.
There were no significant differences (P = .74) in opioid consumption between patients who received general anesthesia and patients who received regional anesthesia (Figure 1).

Of the 98 study patients, 61 reported using over-the-counter adjunctive pain medications during the postoperative period, and 37 reported no use. Mean opioid consumption was 64.7 mg of morphine equivalents for the adjunctive medication users and 48.3 mg for the nonusers (P = .1947).

Demographic analysis revealed an inverse relationship between age and opioid use (Figure 2). The Spearman ρ between age and opioid consumption was –0.2958, which suggests decreased opioid use by older patients (P = .003).

Figure 2.
A count data model with negative binomial distribution suggested opioid consumption decreased by 1.72% per year of age (95% confidence interval, 0.35%-3.06%).
Figure 3.
Similarly, a relationship was found between opioid consumption and payer type (Figure 3), with consumption highest for self-pay and Medicaid patients (P = .063). However, this finding should be interpreted carefully, as it was underpowered—there were only 3 patients in the self-pay/Medicaid group.

All fractures were graded with the AO/OTA long-bone fracture classification system. Mean opioid consumption for the 3 fracture-type groups was 57.7 mg (class A), 60.3 mg (class B), and 62.0 mg (class C) (Figure 4).
Figure 4.
Although the data demonstrate a trend toward increasing opioid consumption in patients who underwent fixation of complete intra-articular DRFs, as opposed to partial articular and extra-articular fractures, the difference was not significant (P = .99).

Discussion

The US healthcare culture has elevated physicians’ responsibility in adequately and aggressively managing their patients’ pain experience. Moreover, reimbursement may be affected by patient satisfaction scores, which are partly predicated on pain control.20-24 However, as rates of opioid use and abuse rise, it is important that physicians prescribe such medications judiciously. This is particularly germane to orthopedic surgeons, who prescribe more opioid analgesics than surgeons in any other field.17 Rodgers and colleagues18 found upper extremity surgeons, in particular, tended to overprescribe postoperative opioid analgesics. In the present study, we sought to identify the crucial risk factors that influence post-DRF-ORIF pain management and opioid consumption.

Mean postoperative opioid consumption (morphine equivalents) was 58.5 mg, roughly equivalent to 14.6 tabs of oxycodone/acetaminophen 5/325 mg, an opioid analgesic commonly used during the acute postoperative period. In addition, almost 70% of our patients required <75 mg of morphine equivalents, or <20 tabs of oxycodone/acetaminophen 5/325 mg. For upper extremity surgeons, these numbers may be better guides in determining the most appropriate amount of opioid to prescribe after DRF repair.

As for predicting levels of postoperative opioid medication, there was a significant trend toward less consumption with increasing age. Given this finding, surgeons prescribing for elderly patients should expect less opioid use. Regarding payer type, there was a trend toward more opioid use by self-pay/Medicaid patients; however, there were only 3 patients in this group. The situation in the study by Rodgers and colleagues18 is similar: Their finding that Medicaid patients consumed more pain pills after surgery was underpowered (only 5 patients in the group).

In the orthopedic community, support for use of regional anesthesia has been widespread for several reasons, including the belief that it reduces postoperative pain and therefore should reduce postoperative opioid consumption.25 However, we found no significant difference in postoperative opioid consumption between patients who received general anesthesia (with and without local anesthesia) and patients who received regional anesthesia (nerve block). Mean opioid consumption was 57.93 mg in the general anesthesia group and 58.98 mg in the regional anesthesia group. However, this finding could have been confounded by the variability in success and operator dependence inherent in regional anesthesia. In addition, the anatomical location for the peripheral nerve block and anesthetic could have affected the efficacy of the block and played a role in postoperative opioid consumption.

In this study, we tested the hypothesis that there would be more postoperative opioid consumption with worsening fracture type. Although our results did not reach statistical significance, there was a trend toward increased opioid consumption in patients with a complete intra-articular fracture (AO/OTA class C) vs patients with a partial articular fracture (class B) or an extra-articular fracture (class A). In addition, patients with a partial articular fracture tended to use more postoperative opioids than patients with an extra-articular fracture. In short, postoperative opioid consumption tended to be higher with increasing articular involvement of the fracture.

This study was limited in that it relied on patient self-reporting. Given the social stigma attached to opioid use, patients may have underreported their postoperative opioid consumption, been affected by recall bias, or both. The study also did not control for preoperative opioid use or history of opioid or substance abuse. Chronic preoperative opioid consumption may have affected postoperative opioid use. Other patient-related factors, such as body mass index (BMI) and hepatorenal dysfunction, can create tremendous variability in opioid metabolism across a population. Such factors were not controlled for in this study and therefore may have affected its results. That could help explain why older patients, who are more likely to have lower BMI and less efficient organ function for opioid metabolism, had lower postoperative opioid consumption. In addition, although we excluded patients with concomitant injuries and procedures, we did not screen patients for concomitant complex regional pain syndrome, fibromyalgia, or other medical conditions that might have had a significant impact on postoperative pain management needs. Last, some findings, such as the relationship between opioid use and payer type, were underpowered: Although self-pay/Medicaid patients had higher postoperative opioid consumption, they were few in number. The same was true of the Medicaid patients in the study by Rodgers and colleagues.18Our results demonstrated that post-DRF-ORIF opioid consumption decreased with age and was independent of type of perioperative anesthesia. There was a trend toward more opioid consumption with both self- and Medicaid payment and worsening fracture classification. It has become more important than ever for orthopedic surgeons to adequately manage postoperative pain while limiting opioid availability and the risk for abuse. Surgeons must remain aware of the variables in their patients’ postoperative pain experience in order to better optimize prescribing patterns and provide a safe and effective postoperative pain regimen.

Am J Orthop. 2017;46(1):E35-E40. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

References

1. Kuehn BM. Opioid prescriptions soar: increase in legitimate use as well as abuse. JAMA. 2007;297(3):249-251.

2. Cicero TJ, Ellis MS, Surratt HL, Kurtz SP. The changing face of heroin use in the United States: a retrospective analysis of the past 50 years. JAMA Psychiatry. 2014;71(7):821-826.

3. Helmerhorst GT, Lindenhovius AL, Vrahas M, Ring D, Kloen P. Satisfaction with pain relief after operative treatment of an ankle fracture. Injury. 2012;43(11):1958-1961.

4. Lindenhovius AL, Helmerhorst GT, Schnellen AC, Vrahas M, Ring D, Kloen P. Differences in prescription of narcotic pain medication after operative treatment of hip and ankle fractures in the United States and the Netherlands. J Trauma. 2009;67(1):160-164.

5. Seya MJ, Gelders SF, Achara OU, Milani B, Scholten WK. A first comparison between the consumption of and the need for opioid analgesics at country, regional, and global levels. J Pain Palliat Care Pharmacother. 2011;25(1):6-18.

6. Bohnert AS, Valenstein M, Bair MJ, et al. Association between opioid prescribing patterns and opioid overdose-related deaths. JAMA. 2011;305(13):1315-1321.

7. Kuehn BM. CDC: major disparities in opioid prescribing among states: some states crack down on excess prescribing. JAMA. 2014;312(7):684-686.

8. Paulozzi LJ, Budnitz DS, Xi Y. Increasing deaths from opioid analgesics in the United States. Pharmacoepidemiol Drug Saf. 2006;15(9):618-627.

9. Cicero TJ, Kuehn BM. Driven by prescription drug abuse, heroin use increases among suburban and rural whites. JAMA. 2014;312(2):118-119.

10. Painkillers fuel growth in drug addiction. Harvard Ment Health Lett. Harvard Medical School website. http://www.health.harvard.edu/newsletter_article/painkillers-fuel-growth-in-drug-addiction. Published January 2011. Accessed March 18, 2015.

11. Cai R, Crane E, Poneleit K, Paulozzi L. Emergency department visits involving nonmedical use of selected prescription drugs in the United States, 2004-2008. J Pain Palliat Care Pharmacother. 2010;24(3):293-297.

12. Armaghani SJ, Lee DS, Bible JE, et al. Preoperative narcotic use and its relation to depression and anxiety in patients undergoing spine surgery. Spine. 2013;38(25):2196-2200.

13. Caudill-Slosberg MA, Schwartz LM, Woloshin S. Office visits and analgesic prescriptions for musculoskeletal pain in US: 1980 vs. 2000. Pain. 2004;109(3):514-519.

14. Deyo RA, Mirza SK, Turner JA, Martin BI. Overtreating chronic back pain: time to back off? J Am Board Fam Med. 2009;22(1):62-68.

15. Lee D, Armaghani S, Archer KR, et al. Preoperative opioid use as a predictor of adverse postoperative self-reported outcomes in patients undergoing spine surgery. J Bone Joint Surg Am. 2014;96(11):e89.

16. Webster BS, Verma SK, Gatchel RJ. Relationship between early opioid prescribing for acute occupational low back pain and disability duration, medical costs, subsequent surgery and late opioid use. Spine. 2007;32(19):2127-2132.

17. Volkow ND, McLellan TA, Cotto JH, Karithanom M, Weiss SR. Characteristics of opioid prescriptions in 2009. JAMA. 2011;305(13):1299-1301.

18. Rodgers J, Cunningham K, Fitzgerald K, Finnerty E. Opioid consumption following outpatient upper extremity surgery. J Hand Surg Am. 2012;37(4):645-650.

19. Chen L, Vo T, Seefeld L, et al. Lack of correlation between opioid dose adjustment and pain score change in a group of chronic pain patients. J Pain. 2013;14(4):384-392.

20. Bush H. Doubling down on the patient experience. Hosp Health Netw. 2011;85(12):22-25, 1.

21. Centers for Medicare & Medicaid Services, US Department of Health and Human Services. Medicare program; hospital inpatient prospective payment systems for acute care hospitals and the long-term care hospital prospective payment system and fiscal year 2013 rates; hospitals’ resident caps for graduate medical education payment purposes; quality reporting requirements for specific providers and for ambulatory surgical centers. Final rule. Fed Regist. 2012;77(170):53257-53750.

22. Centers for Medicare & Medicaid Services, US Department of Health and Human Services. Hospital Value-Based Purchasing. http://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/downloads/Hospital_VBPurchasing_Fact_Sheet_ICN907664.pdf. Published September 2015. Accessed October 2015.

23. Manchikanti L, Singh V, Caraway DL, Benyamin RM, Falco FJ, Hirsch JA. Proposed physician payment schedule for 2013: guarded prognosis for interventional pain management. Pain Physician. 2012;15(5):E615-E627.

24. Bot AG, Bekkers S, Arnstein PM, Smith RM, Ring D. Opioid use after fracture surgery correlates with pain intensity and satisfaction with pain relief. Clin Orthop Relat Res. 2014;472(8):2542-2549.

25. Oldman M, McCartney CJ, Leung A, et al. A survey of orthopedic surgeons’ attitudes and knowledge regarding regional anesthesia. Anesth Analg. 2004;98(5):1486-1490.

References

1. Kuehn BM. Opioid prescriptions soar: increase in legitimate use as well as abuse. JAMA. 2007;297(3):249-251.

2. Cicero TJ, Ellis MS, Surratt HL, Kurtz SP. The changing face of heroin use in the United States: a retrospective analysis of the past 50 years. JAMA Psychiatry. 2014;71(7):821-826.

3. Helmerhorst GT, Lindenhovius AL, Vrahas M, Ring D, Kloen P. Satisfaction with pain relief after operative treatment of an ankle fracture. Injury. 2012;43(11):1958-1961.

4. Lindenhovius AL, Helmerhorst GT, Schnellen AC, Vrahas M, Ring D, Kloen P. Differences in prescription of narcotic pain medication after operative treatment of hip and ankle fractures in the United States and the Netherlands. J Trauma. 2009;67(1):160-164.

5. Seya MJ, Gelders SF, Achara OU, Milani B, Scholten WK. A first comparison between the consumption of and the need for opioid analgesics at country, regional, and global levels. J Pain Palliat Care Pharmacother. 2011;25(1):6-18.

6. Bohnert AS, Valenstein M, Bair MJ, et al. Association between opioid prescribing patterns and opioid overdose-related deaths. JAMA. 2011;305(13):1315-1321.

7. Kuehn BM. CDC: major disparities in opioid prescribing among states: some states crack down on excess prescribing. JAMA. 2014;312(7):684-686.

8. Paulozzi LJ, Budnitz DS, Xi Y. Increasing deaths from opioid analgesics in the United States. Pharmacoepidemiol Drug Saf. 2006;15(9):618-627.

9. Cicero TJ, Kuehn BM. Driven by prescription drug abuse, heroin use increases among suburban and rural whites. JAMA. 2014;312(2):118-119.

10. Painkillers fuel growth in drug addiction. Harvard Ment Health Lett. Harvard Medical School website. http://www.health.harvard.edu/newsletter_article/painkillers-fuel-growth-in-drug-addiction. Published January 2011. Accessed March 18, 2015.

11. Cai R, Crane E, Poneleit K, Paulozzi L. Emergency department visits involving nonmedical use of selected prescription drugs in the United States, 2004-2008. J Pain Palliat Care Pharmacother. 2010;24(3):293-297.

12. Armaghani SJ, Lee DS, Bible JE, et al. Preoperative narcotic use and its relation to depression and anxiety in patients undergoing spine surgery. Spine. 2013;38(25):2196-2200.

13. Caudill-Slosberg MA, Schwartz LM, Woloshin S. Office visits and analgesic prescriptions for musculoskeletal pain in US: 1980 vs. 2000. Pain. 2004;109(3):514-519.

14. Deyo RA, Mirza SK, Turner JA, Martin BI. Overtreating chronic back pain: time to back off? J Am Board Fam Med. 2009;22(1):62-68.

15. Lee D, Armaghani S, Archer KR, et al. Preoperative opioid use as a predictor of adverse postoperative self-reported outcomes in patients undergoing spine surgery. J Bone Joint Surg Am. 2014;96(11):e89.

16. Webster BS, Verma SK, Gatchel RJ. Relationship between early opioid prescribing for acute occupational low back pain and disability duration, medical costs, subsequent surgery and late opioid use. Spine. 2007;32(19):2127-2132.

17. Volkow ND, McLellan TA, Cotto JH, Karithanom M, Weiss SR. Characteristics of opioid prescriptions in 2009. JAMA. 2011;305(13):1299-1301.

18. Rodgers J, Cunningham K, Fitzgerald K, Finnerty E. Opioid consumption following outpatient upper extremity surgery. J Hand Surg Am. 2012;37(4):645-650.

19. Chen L, Vo T, Seefeld L, et al. Lack of correlation between opioid dose adjustment and pain score change in a group of chronic pain patients. J Pain. 2013;14(4):384-392.

20. Bush H. Doubling down on the patient experience. Hosp Health Netw. 2011;85(12):22-25, 1.

21. Centers for Medicare & Medicaid Services, US Department of Health and Human Services. Medicare program; hospital inpatient prospective payment systems for acute care hospitals and the long-term care hospital prospective payment system and fiscal year 2013 rates; hospitals’ resident caps for graduate medical education payment purposes; quality reporting requirements for specific providers and for ambulatory surgical centers. Final rule. Fed Regist. 2012;77(170):53257-53750.

22. Centers for Medicare & Medicaid Services, US Department of Health and Human Services. Hospital Value-Based Purchasing. http://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/downloads/Hospital_VBPurchasing_Fact_Sheet_ICN907664.pdf. Published September 2015. Accessed October 2015.

23. Manchikanti L, Singh V, Caraway DL, Benyamin RM, Falco FJ, Hirsch JA. Proposed physician payment schedule for 2013: guarded prognosis for interventional pain management. Pain Physician. 2012;15(5):E615-E627.

24. Bot AG, Bekkers S, Arnstein PM, Smith RM, Ring D. Opioid use after fracture surgery correlates with pain intensity and satisfaction with pain relief. Clin Orthop Relat Res. 2014;472(8):2542-2549.

25. Oldman M, McCartney CJ, Leung A, et al. A survey of orthopedic surgeons’ attitudes and knowledge regarding regional anesthesia. Anesth Analg. 2004;98(5):1486-1490.

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The Effect of Ligament Injuries on Outcomes of Operatively Treated Distal Radius Fractures

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The Effect of Ligament Injuries on Outcomes of Operatively Treated Distal Radius Fractures

Take-Home Points

  • Patients sustaining DRFs commonly have associated ligament injuries and chondral damage as well.
  • Many of these associated injuries do not seem to affect outcomes up to 1 year after surgery.
  • Plain radiographs have a 74% sensitivity and 73% specificity for detecting intra-articular fractures.
  • ”Minor” injuries identified incidentally by arthroscopy during fixation of DRFs may not require dedicated treatment.
  • The optimal treatment for high-grade ligament or chondral injuries in patients with DRFs remains incompletely understood.

Distal radius fracture (DRF) is one of the most common upper extremity injuries, with up to 20% to 50% requiring surgical fixation.1 With increasing use of wrist arthroscopy to assist in managing these fractures,2-6 it has become easier to accurately assess concomitant wrist ligament injuries. Reported injury rates are 18% to 86% for the scapholunate interosseous ligament (SLIL),7,8 5% to 29% for the lunotriquetral ligament (LTL),8,9 and 17% to 60% for the triangular fibrocartilage complex (TFCC).10,11 Reported chondral injury rates range from 18% to 60%.7,9,12 Despite the common occurrence of these injuries, it is unclear how they affect outcomes and how aggressively they should be treated when detected during fracture surgery.

As the use of arthroscopy in DRF management becomes more common, surgeons often must decide how to treat ligamentous/chondral injuries incidentally discovered during surgery. To date, only 1 study prospectively evaluated how these injuries affect DRF outcomes,8 though it did not use a validated, patient-based outcome measure.

We conducted a study to address a common clinical scenario: When arthroscopy is used to assist with intra-articular reduction during DRF fixation, how should the surgeon respond to incidentally identified ligament and chondral injuries? Specifically, we wanted to address 3 questions: What is the overall incidence of SLIL, TFCC, and chondral surface injuries in patients undergoing operative fracture fixation? On initial injury films, do any radiographic parameters predict specific soft-tissue injuries or ultimate functional outcomes? Do wrist ligament and chondral injuries affect patient-rated outcomes (disability, pain) and objective measures (range of motion [ROM], grip strength, pinch strength) up to 1 year after fracture surgery?

Materials and Methods

Patient Selection/Population

This observational, prognostic study was approved by our Institutional Review Board. Inclusion criteria were age over 18 years, isolated acute operatively treated DRF (surgery within 14 days of injury), and informed consent. All patients were treated by the same surgeon. Exclusion criteria were open DRF, dorsal shear pattern, fractures requiring dorsal arthrotomy for reduction because of significant intra-articular damage, prior ipsilateral DRF, and prior SLIL or TFCC injury.

Surgery was indicated according to general radiographic parameters as measured on postreduction films: radial height, <8 mm; radial inclination, <15°; positive ulnar variance, >3 mm, or 3 mm more than contralateral side; dorsal tilt, >10°; and volar tilt, >15°. With these parameters within acceptable limits, surgery was also indicated when fractures were deemed unstable and likely to displace because of dorsal tilt >20°, dorsal comminution, intra-articular step-off of ≥2 mm on the posterior-anterior (PA) film, associated ulnar fracture, and age >60 years.13Over a 2-year period, 42 patients (12 male, 30 female) met the inclusion criteria and were enrolled in the study. The dominant arm was affected in 17 patients (40%). Mean (SD) age at time of injury was 56.6 (16.4) years (median, 54 years; range, 20-85 years).

Operative Technique

During surgery, damage to the SLIL, the TFCC, and chondral surfaces (scaphoid, lunate, scaphoid fossa, lunate fossa) and to the intra-articular extension of the DRF was assessed and recorded. Wrist arthroscopy was performed with the 3, 4 portal as the primary portal. When significant damage to the TFCC warranted débridement, the 6R (radial) portal was used as an accessory portal. As a midcarpal portal was not used for SLIL assessment, we used a novel classification system: 0 = no injury, normal-appearing ligament without hemorrhage and smooth transition from scaphoid to lunate surface except for slight concave indentation at the ligament; 1 = attenuation, no visible tear with convex shape of ligament with or without hemorrhage; 2 = partial tear with or without step-off at junction between scaphoid and lunate, but 2.7-mm arthroscope cannot “drive through” to midcarpal joint; and 3 = complete tear with positive “drive-through” sign. TFCC injuries were classified according to the system described by Palmer14: Avulsions were central (1A), ulnar (1B), distal (1C), or radial (1D). The trampoline test was performed through a 6R portal by using a probe to evaluate ligament tension/laxity. In some cases, a 6R portal was deemed unnecessary, and a modified trampoline test was performed—tension/laxity/displacement was evaluated by manually palpating at the fovea and observing TFCC motion with the arthroscope. When appropriate, the TFCC was débrided with a shaver through the 6R portal. In cases of significant instability at the SLIL interval, two 0.062-inch K-wires were placed percutaneously through the scaphoid and lunate, and one was placed from the scaphoid to the capitate.

 

 

All DRFs underwent internal fixation with a locked volar plate. When necessary, K-wires and/or a locked radial column plate was used for additional fixation. External fixation was not used. The postoperative protocol began with a dorsal wrist splint placed on the patient in the operating room and worn for 10 to 14 days. At the first postoperative visit, the patient received a removable splint that was to be worn at all times except during showers, therapy, and home exercises. Occupational therapy, initiated the week of the first postoperative visit, consisted of active and passive ROM exercises. At 6 weeks, the splint was removed and strengthening initiated.

Outcome Measures

Our primary outcome measure was the Disabilities of the Arm, Shoulder, and Hand (DASH) questionnaire at 1 year.15 Secondary outcome measures were visual analog scale (VAS) pain rating, ROM, and radiographic measurements. Patients returned for evaluation 2, 6, 12, 24, and 52 weeks after surgery. At each follow-up visit, the DASH questionnaire and the pain VAS were administered, and ROM and strength were measured. Patient-reported pain was recorded on a standard VAS and measured on a scale from 0 (no pain) to 10 (worst possible pain). Wrist flexion and extension and radioulnar deviation were assessed with a goniometer. Forearm supination and pronation were assessed with the elbow flexed 90° at the patient’s side. Grip strength was measured with a calibrated Jamar dynamometer (Sammons Preston Rolyan), and lateral pinch strength was measured with a hydraulic pinch gauge (Sammons Preston Rolyan). The average of 3 trials for both hands was recorded for all strength measurements.

Radiographs were obtained on presentation. When appropriate, the fracture was manually reduced with a hematoma block, and postreduction radiographs were obtained. Then, radiographs were obtained at each postoperative visit until union. Radial height, radial inclination, tilt, and ulnar variance were measured on preoperative and postoperative radiographs according to standard methods.16 Radiographs were used to classify the fracture patterns according to the AO/ASIF (Arbeitsgemeinschaft für Osteosynthesefragen/Association for the Study of Internal Fixation) classification. Union was determined by radiographic healing, absence of tenderness to palpation, absence of pain with motion, and continued functional improvement.

Data Analysis

To evaluate for relationships between patient injury parameters and outcome measures, we used a 1-way analysis of variance seeking statistically significant differences between groups. Patients were divided into 4 groups: no ligament injuries; isolated SLIL injuries; isolated TFCC injuries; and both SLIL and TFCC injuries. These injury classification categories were then evaluated independently against our chosen outcome measures, which included DASH and VAS pain scores, ROM, and grip/pinch strength.

To determine the optimal sample size, we performed a power analysis to estimate the number of patients required to detect a clinically significant difference in DASH scores at 1 year among the 4 groups. According to the literature, standard deviations of DASH scores in healthy volunteers range from 10 to 15,17 consistent with values found in other recent trials of patients with DRFs.18 The recent literature on DASH construct validity has established a DASH score difference of 19 as representing a disability change being “much better or much worse.”19 As such, power analysis for a 1-way analysis of variance among 4 categories, detecting a DASH score difference of 19 with a standard deviation ranging from 10 to 15, would require 28 to 60 patients to detect a difference with an α of 0.05 and a power of 0.8.

In addition, radiographic parameters at time of injury were compared with injury characteristics to assess for significant relationships. Multivariate linear regression analysis was performed to evaluate radial height, radial inclination, and volar tilt as possible predictors of SLIL injury, TFCC injury, and chondral surface damage. A statistically significant result was defined as a correlation with P < .05.

Results

Of the 42 patients included in the study, 11 (26%) had no ligament injuries, 10 (24%) had isolated SLIL injuries, 12 (29%) had isolated TFCC injuries, and 9 (21%) had injuries to both the SLIL and the TFCC. In addition, in 12 patients (29%), the articular cartilage had visible damage (Table 1).

Table 1.
According to the AO/ASIF classification, 18 patients had type A fractures, 8 had type B, and 16 had type C. Twenty patients had an intra-articular component seen on preoperative radiographs and confirmed arthroscopically, and another 7 were thought to have an extra-articular fracture pattern but were found to have an intra-articular component arthroscopically.

In all patients, bony union occurred. After union, 1 patient underwent hardware removal for hardware-related pain. The same patient had a dorsal ulnar cutaneous nerve neurolysis at the ulnar styloid fixation site. Another patient developed a partial extensor pollicis longus tear from a prominent dorsal screw tip.

All patients returned for their 2- and 6-week follow-ups. At 1 year, 30 patients (71%) returned for follow-up, 11 could not be contacted, and 1 was removed because of an olecranon fracture from a subsequent fall.

Regarding the primary outcome measure, mean DASH score at 1-year follow-up was 30.8 for the group without injuries, 10.8 for the group with SLIL injuries, 14.7 for the group with TFCC injuries, and 21.9 for the group with SLIL and TFCC injuries (Table 2).

Table 2.
There were no statistical differences between the groups at any point. The secondary outcome measures (VAS pain, wrist ROM, grip/pinch strength) also showed no statistically significant relationship at any point. Controlling for AO/ASIF fracture type did not affect significance, and there was no subdivision or subanalysis of injury characteristic or classification that correlated with DASH scores, VAS pain, or physical examination results at any point.

Radiographic parameters were restored to acceptable limits in all patients (Table 3).
Table 3.
A linear regression analysis comparing these injury radiographic parameters with the incidence of SLIL, TFCC, or chondral injuries showed that none of these measurements were a significant predictor of soft-tissue injury.

 

 

Discussion

Use of wrist arthroscopy in DRF management has allowed assessment of the incidence of intra-articular injuries, including ligament and chondral surface injuries. Although the literature on the incidence of these injuries has been expanding, their clinical significance remains unclear.

Authors have postulated that some patients do not do well after DRF repair because of undetected ligament injuries. With the current trend of internal fixation, locked plating, and early motion—contrasting with older trends of prolonged immobilization in a cast or external fixation—concerns have been raised that early mobilization results in inadequate treatment of ligament injuries. However, data from the present study suggest no significant morbidity from early mobilization despite the presence of ligament injuries in more than half of all operatively treated DRFs. It is possible morbidity was not appreciated, as most patients with DRFs end up with some stiffness, which masks the effects of ligament injuries during healing.

We found no correlation between injury radiographic parameters, observed soft-tissue injuries, or final subjective outcomes. Interestingly, in this study, there was some discordance between the appearance of intra-articular fractures on radiographs and the direct arthroscopic observation of intra-articular fracture extension. With the present data and with arthroscopic visualization as the gold standard, radiographs had 74% sensitivity and 73% specificity for detecting intra-articular fractures (the corresponding positive predictive value was 83%, and the negative predictive value was 61%). As we typically rely on radiographs as the primary tool in assessing the articular component of a fracture, these results should be taken into account when basing management decisions exclusively on static injury films.

Observational studies of arthroscopy in DRFs have revealed a wide range of injury rates: For SLILs, the average injury rate was 44%; for LTLs, 13%; for TFCCs, 43%; and for chondral surfaces, 32% (Table 4).

Table 4.
We found comparable rates in the present study, indicating the injuries in our patient population are comparable with those in similar studies.

This study had several limitations, including loss to follow-up at the primary endpoint (we were unable to contact 29% of patients). In addition, because of resource limitations, we were able to enroll only a limited number of patients, and as a result were able to power the study to detect only major effects on DASH scores. Therefore, although our 32 patients with long-term follow-up are within the range dictated by the power analysis, this study was not powered to capture more subtle differences in disability. Furthermore, because we used 1 year as the longest follow-up point, the long-term sequelae (eg, arthritis) of these injuries may not have been captured. Last, despite the high incidence of soft-tissue injuries overall, the number of patients with severe ligament injuries was relatively low, which makes it difficult to make definitive statements about their contribution to outcomes. A likely explanation is that patients with high-energy injuries and significant intra-articular displacement requiring open arthrotomies were excluded.

At 1-year follow-up, with use of DASH as the gold standard for disability, we found no major difference in subjective or objective outcome measures between patients with and without ligament injuries. Radiographs did not predict soft-tissue injury or ultimate outcome. Rates of ligament injuries in our operatively treated DRFs were similar to those in the literature. Overall, these findings suggest that “minor” injuries incidentally discovered with arthroscopy during DRF surgery may not have a significant effect on outcomes, with the caveat that the significance of very severe injuries (eg, Geissler grade 4 injuries with frank scapholunate diastasis) remains incompletely understood. The decision by the treating surgeon to perform arthroscopy and/or to repair soft-tissue injuries should be made on a case-by-case basis.

Am J Orthop. 2017;46(1):E41-E46. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Róbertsson GO, Jónsson GT, Sigurjónsson K. Epidemiology of distal radius fractures in Iceland in 1985. Acta Orthop Scand. 1990;61(5):457-459.

2. Geissler WB. Arthroscopically assisted reduction of intra-articular fractures of the distal radius. Hand Clin. 1995;11(1):19-29.

3. Trybus M, Guzik P. The economic impact of hand injury [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2003;68(4):269-273.

4. Wolfe SW, Easterling KJ, Yoo HH. Arthroscopic-assisted reduction of distal radius fractures. Arthroscopy. 1995;11(6):706-714.

5. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26(5):908-915.

6. Doi K, Hattori Y, Otsuka K, Abe Y, Yamamoto H. Intra-articular fractures of the distal aspect of the radius: arthroscopically assisted reduction compared with open reduction and internal fixation. J Bone Joint Surg Am. 1999;81(8):1093-1110.

7. Shih JT, Lee HM, Hou YT, Tan CM. Arthroscopically-assisted reduction of intra-articular fractures and soft tissue management of distal radius. Hand Surg. 2001;6(2):127-135.

8. Forward DP, Lindau TR, Melsom DS. Intercarpal ligament injuries associated with fractures of the distal part of the radius. J Bone Joint Surg Am. 2007;89(11):2334-2340.

9. Espinosa-Gutiérrez A, Rivas-Montero JA, Elias-Escobedo A, Alisedo-Ochoa PG. Wrist arthroscopy for fractures of the distal end of the radius [in Spanish]. Acta Ortop Mex. 2009;23(6):358-365.

10. Hardy P, Gomes N, Chebil M, Bauer T. Wrist arthroscopy and intra-articular fractures of the distal radius in young adults. Knee Surg Sports Traumatol Arthrosc. 2006;14(11):1225-1230.

11. Varitimidis SE, Basdekis GK, Dailiana ZH, Hantes ME, Bargiotas K, Malizos K. Treatment of intra-articular fractures of the distal radius: fluoroscopic or arthroscopic reduction? J Bone Joint Surg Br. 2008;90(6):778-785.

12. Kordasiewicz B, Pomianowski S, Rylski W, Antolak L, Marczak D. Intraarticular distal radius fractures—arthroscopic assessment of injuries [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2006;71(2):113-116.

13. Lafontaine M, Hardy D, Delince P. Stability assessment of distal radius fractures. Injury. 1989;20(4):208-210.

14. Palmer AK. Triangular fibrocartilage complex lesions: a classification. J Hand Surg Am. 1989;14(4):594-606.

15. Hudak PL, Amadio PC, Bombardier C. Development of an upper extremity outcome measure: the DASH (Disabilities of the Arm, Shoulder and Hand) [corrected]. The Upper Extremity Collaborative Group (UECG) [published correction appears in Am J Ind Med. 1996;30(3):372]. Am J Ind Med. 1996;29(6):602-608.

16. Fernandez DL, Jupiter JB. Fractures of the Distal Radius: A Practical Approach to Management. New York, NY: Springer; 1996.

17. Jester A, Harth A, Wind G, Germann G, Sauerbier M. Does the Disability of Shoulder, Arm and Hand questionnaire (DASH) replace grip strength and range of motion in outcome-evaluation? [in German]. Handchir Mikrochir Plast Chir. 2005;37(2):126-130.

18. Wei DH, Raizman NM, Bottino CJ, Jobin CM, Strauch RJ, Rosenwasser MP. Unstable distal radial fractures treated with external fixation, a radial column plate, or a volar plate. A prospective randomized trial. J Bone Joint Surg Am. 2009;91(7):1568-1577.

19. Gummesson C, Atroshi I, Ekdahl C. The Disabilities of the Arm, Shoulder and Hand (DASH) outcome questionnaire: longitudinal construct validity and measuring self-rated health change after surgery. BMC Musculoskelet Disord. 2003;4:11.

20. Richards RS, Bennett JD, Roth JH, Milne K Jr. Arthroscopic diagnosis of intra-articular soft tissue injuries associated with distal radial fractures. J Hand Surg Am. 1997;22(5):772-776.

21. Peicha G, Seibert F, Fellinger M, Grechenig W. Midterm results of arthroscopic treatment of scapholunate ligament lesions associated with intra-articular distal radius fractures. Knee Surg Sports Traumatol Arthrosc. 1999;7(5):327-333.

22. Schädel-Höpfner M, Böhringer G, Junge A, Celik I, Gotzen L. [Arthroscopic diagnosis of concomitant scapholunate ligament injuries in fractures of the distal radius]. Handchir Mikrochir Plast Chir. 2001;33(4):229-233.

23. Ruch DS, Yang CC, Smith BP. Results of acute arthroscopically repaired triangular fibrocartilage complex injuries associated with intra-articular distal radius fractures. Arthroscopy. 2003;19(5):511-516.

24. Hattori Y, Doi K, Estrella EP, Chen G. Arthroscopically assisted reduction with volar plating or external fixation for displaced intra-articular fractures of the distal radius in the elderly patients. Hand Surg. 2007;12(1):1-12.

25. Hohendorff B, Eck M, Mühldorfer M, Fodor S, Schmitt R, Prommersberger KJ. [Palmar wrist arthroscopy for evaluation of concomitant carpal lesions in operative treatment of distal intraarticular radius fractures]. Handchir Mikrochir Plast Chir. 2009;41(5):295-299.

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Take-Home Points

  • Patients sustaining DRFs commonly have associated ligament injuries and chondral damage as well.
  • Many of these associated injuries do not seem to affect outcomes up to 1 year after surgery.
  • Plain radiographs have a 74% sensitivity and 73% specificity for detecting intra-articular fractures.
  • ”Minor” injuries identified incidentally by arthroscopy during fixation of DRFs may not require dedicated treatment.
  • The optimal treatment for high-grade ligament or chondral injuries in patients with DRFs remains incompletely understood.

Distal radius fracture (DRF) is one of the most common upper extremity injuries, with up to 20% to 50% requiring surgical fixation.1 With increasing use of wrist arthroscopy to assist in managing these fractures,2-6 it has become easier to accurately assess concomitant wrist ligament injuries. Reported injury rates are 18% to 86% for the scapholunate interosseous ligament (SLIL),7,8 5% to 29% for the lunotriquetral ligament (LTL),8,9 and 17% to 60% for the triangular fibrocartilage complex (TFCC).10,11 Reported chondral injury rates range from 18% to 60%.7,9,12 Despite the common occurrence of these injuries, it is unclear how they affect outcomes and how aggressively they should be treated when detected during fracture surgery.

As the use of arthroscopy in DRF management becomes more common, surgeons often must decide how to treat ligamentous/chondral injuries incidentally discovered during surgery. To date, only 1 study prospectively evaluated how these injuries affect DRF outcomes,8 though it did not use a validated, patient-based outcome measure.

We conducted a study to address a common clinical scenario: When arthroscopy is used to assist with intra-articular reduction during DRF fixation, how should the surgeon respond to incidentally identified ligament and chondral injuries? Specifically, we wanted to address 3 questions: What is the overall incidence of SLIL, TFCC, and chondral surface injuries in patients undergoing operative fracture fixation? On initial injury films, do any radiographic parameters predict specific soft-tissue injuries or ultimate functional outcomes? Do wrist ligament and chondral injuries affect patient-rated outcomes (disability, pain) and objective measures (range of motion [ROM], grip strength, pinch strength) up to 1 year after fracture surgery?

Materials and Methods

Patient Selection/Population

This observational, prognostic study was approved by our Institutional Review Board. Inclusion criteria were age over 18 years, isolated acute operatively treated DRF (surgery within 14 days of injury), and informed consent. All patients were treated by the same surgeon. Exclusion criteria were open DRF, dorsal shear pattern, fractures requiring dorsal arthrotomy for reduction because of significant intra-articular damage, prior ipsilateral DRF, and prior SLIL or TFCC injury.

Surgery was indicated according to general radiographic parameters as measured on postreduction films: radial height, <8 mm; radial inclination, <15°; positive ulnar variance, >3 mm, or 3 mm more than contralateral side; dorsal tilt, >10°; and volar tilt, >15°. With these parameters within acceptable limits, surgery was also indicated when fractures were deemed unstable and likely to displace because of dorsal tilt >20°, dorsal comminution, intra-articular step-off of ≥2 mm on the posterior-anterior (PA) film, associated ulnar fracture, and age >60 years.13Over a 2-year period, 42 patients (12 male, 30 female) met the inclusion criteria and were enrolled in the study. The dominant arm was affected in 17 patients (40%). Mean (SD) age at time of injury was 56.6 (16.4) years (median, 54 years; range, 20-85 years).

Operative Technique

During surgery, damage to the SLIL, the TFCC, and chondral surfaces (scaphoid, lunate, scaphoid fossa, lunate fossa) and to the intra-articular extension of the DRF was assessed and recorded. Wrist arthroscopy was performed with the 3, 4 portal as the primary portal. When significant damage to the TFCC warranted débridement, the 6R (radial) portal was used as an accessory portal. As a midcarpal portal was not used for SLIL assessment, we used a novel classification system: 0 = no injury, normal-appearing ligament without hemorrhage and smooth transition from scaphoid to lunate surface except for slight concave indentation at the ligament; 1 = attenuation, no visible tear with convex shape of ligament with or without hemorrhage; 2 = partial tear with or without step-off at junction between scaphoid and lunate, but 2.7-mm arthroscope cannot “drive through” to midcarpal joint; and 3 = complete tear with positive “drive-through” sign. TFCC injuries were classified according to the system described by Palmer14: Avulsions were central (1A), ulnar (1B), distal (1C), or radial (1D). The trampoline test was performed through a 6R portal by using a probe to evaluate ligament tension/laxity. In some cases, a 6R portal was deemed unnecessary, and a modified trampoline test was performed—tension/laxity/displacement was evaluated by manually palpating at the fovea and observing TFCC motion with the arthroscope. When appropriate, the TFCC was débrided with a shaver through the 6R portal. In cases of significant instability at the SLIL interval, two 0.062-inch K-wires were placed percutaneously through the scaphoid and lunate, and one was placed from the scaphoid to the capitate.

 

 

All DRFs underwent internal fixation with a locked volar plate. When necessary, K-wires and/or a locked radial column plate was used for additional fixation. External fixation was not used. The postoperative protocol began with a dorsal wrist splint placed on the patient in the operating room and worn for 10 to 14 days. At the first postoperative visit, the patient received a removable splint that was to be worn at all times except during showers, therapy, and home exercises. Occupational therapy, initiated the week of the first postoperative visit, consisted of active and passive ROM exercises. At 6 weeks, the splint was removed and strengthening initiated.

Outcome Measures

Our primary outcome measure was the Disabilities of the Arm, Shoulder, and Hand (DASH) questionnaire at 1 year.15 Secondary outcome measures were visual analog scale (VAS) pain rating, ROM, and radiographic measurements. Patients returned for evaluation 2, 6, 12, 24, and 52 weeks after surgery. At each follow-up visit, the DASH questionnaire and the pain VAS were administered, and ROM and strength were measured. Patient-reported pain was recorded on a standard VAS and measured on a scale from 0 (no pain) to 10 (worst possible pain). Wrist flexion and extension and radioulnar deviation were assessed with a goniometer. Forearm supination and pronation were assessed with the elbow flexed 90° at the patient’s side. Grip strength was measured with a calibrated Jamar dynamometer (Sammons Preston Rolyan), and lateral pinch strength was measured with a hydraulic pinch gauge (Sammons Preston Rolyan). The average of 3 trials for both hands was recorded for all strength measurements.

Radiographs were obtained on presentation. When appropriate, the fracture was manually reduced with a hematoma block, and postreduction radiographs were obtained. Then, radiographs were obtained at each postoperative visit until union. Radial height, radial inclination, tilt, and ulnar variance were measured on preoperative and postoperative radiographs according to standard methods.16 Radiographs were used to classify the fracture patterns according to the AO/ASIF (Arbeitsgemeinschaft für Osteosynthesefragen/Association for the Study of Internal Fixation) classification. Union was determined by radiographic healing, absence of tenderness to palpation, absence of pain with motion, and continued functional improvement.

Data Analysis

To evaluate for relationships between patient injury parameters and outcome measures, we used a 1-way analysis of variance seeking statistically significant differences between groups. Patients were divided into 4 groups: no ligament injuries; isolated SLIL injuries; isolated TFCC injuries; and both SLIL and TFCC injuries. These injury classification categories were then evaluated independently against our chosen outcome measures, which included DASH and VAS pain scores, ROM, and grip/pinch strength.

To determine the optimal sample size, we performed a power analysis to estimate the number of patients required to detect a clinically significant difference in DASH scores at 1 year among the 4 groups. According to the literature, standard deviations of DASH scores in healthy volunteers range from 10 to 15,17 consistent with values found in other recent trials of patients with DRFs.18 The recent literature on DASH construct validity has established a DASH score difference of 19 as representing a disability change being “much better or much worse.”19 As such, power analysis for a 1-way analysis of variance among 4 categories, detecting a DASH score difference of 19 with a standard deviation ranging from 10 to 15, would require 28 to 60 patients to detect a difference with an α of 0.05 and a power of 0.8.

In addition, radiographic parameters at time of injury were compared with injury characteristics to assess for significant relationships. Multivariate linear regression analysis was performed to evaluate radial height, radial inclination, and volar tilt as possible predictors of SLIL injury, TFCC injury, and chondral surface damage. A statistically significant result was defined as a correlation with P < .05.

Results

Of the 42 patients included in the study, 11 (26%) had no ligament injuries, 10 (24%) had isolated SLIL injuries, 12 (29%) had isolated TFCC injuries, and 9 (21%) had injuries to both the SLIL and the TFCC. In addition, in 12 patients (29%), the articular cartilage had visible damage (Table 1).

Table 1.
According to the AO/ASIF classification, 18 patients had type A fractures, 8 had type B, and 16 had type C. Twenty patients had an intra-articular component seen on preoperative radiographs and confirmed arthroscopically, and another 7 were thought to have an extra-articular fracture pattern but were found to have an intra-articular component arthroscopically.

In all patients, bony union occurred. After union, 1 patient underwent hardware removal for hardware-related pain. The same patient had a dorsal ulnar cutaneous nerve neurolysis at the ulnar styloid fixation site. Another patient developed a partial extensor pollicis longus tear from a prominent dorsal screw tip.

All patients returned for their 2- and 6-week follow-ups. At 1 year, 30 patients (71%) returned for follow-up, 11 could not be contacted, and 1 was removed because of an olecranon fracture from a subsequent fall.

Regarding the primary outcome measure, mean DASH score at 1-year follow-up was 30.8 for the group without injuries, 10.8 for the group with SLIL injuries, 14.7 for the group with TFCC injuries, and 21.9 for the group with SLIL and TFCC injuries (Table 2).

Table 2.
There were no statistical differences between the groups at any point. The secondary outcome measures (VAS pain, wrist ROM, grip/pinch strength) also showed no statistically significant relationship at any point. Controlling for AO/ASIF fracture type did not affect significance, and there was no subdivision or subanalysis of injury characteristic or classification that correlated with DASH scores, VAS pain, or physical examination results at any point.

Radiographic parameters were restored to acceptable limits in all patients (Table 3).
Table 3.
A linear regression analysis comparing these injury radiographic parameters with the incidence of SLIL, TFCC, or chondral injuries showed that none of these measurements were a significant predictor of soft-tissue injury.

 

 

Discussion

Use of wrist arthroscopy in DRF management has allowed assessment of the incidence of intra-articular injuries, including ligament and chondral surface injuries. Although the literature on the incidence of these injuries has been expanding, their clinical significance remains unclear.

Authors have postulated that some patients do not do well after DRF repair because of undetected ligament injuries. With the current trend of internal fixation, locked plating, and early motion—contrasting with older trends of prolonged immobilization in a cast or external fixation—concerns have been raised that early mobilization results in inadequate treatment of ligament injuries. However, data from the present study suggest no significant morbidity from early mobilization despite the presence of ligament injuries in more than half of all operatively treated DRFs. It is possible morbidity was not appreciated, as most patients with DRFs end up with some stiffness, which masks the effects of ligament injuries during healing.

We found no correlation between injury radiographic parameters, observed soft-tissue injuries, or final subjective outcomes. Interestingly, in this study, there was some discordance between the appearance of intra-articular fractures on radiographs and the direct arthroscopic observation of intra-articular fracture extension. With the present data and with arthroscopic visualization as the gold standard, radiographs had 74% sensitivity and 73% specificity for detecting intra-articular fractures (the corresponding positive predictive value was 83%, and the negative predictive value was 61%). As we typically rely on radiographs as the primary tool in assessing the articular component of a fracture, these results should be taken into account when basing management decisions exclusively on static injury films.

Observational studies of arthroscopy in DRFs have revealed a wide range of injury rates: For SLILs, the average injury rate was 44%; for LTLs, 13%; for TFCCs, 43%; and for chondral surfaces, 32% (Table 4).

Table 4.
We found comparable rates in the present study, indicating the injuries in our patient population are comparable with those in similar studies.

This study had several limitations, including loss to follow-up at the primary endpoint (we were unable to contact 29% of patients). In addition, because of resource limitations, we were able to enroll only a limited number of patients, and as a result were able to power the study to detect only major effects on DASH scores. Therefore, although our 32 patients with long-term follow-up are within the range dictated by the power analysis, this study was not powered to capture more subtle differences in disability. Furthermore, because we used 1 year as the longest follow-up point, the long-term sequelae (eg, arthritis) of these injuries may not have been captured. Last, despite the high incidence of soft-tissue injuries overall, the number of patients with severe ligament injuries was relatively low, which makes it difficult to make definitive statements about their contribution to outcomes. A likely explanation is that patients with high-energy injuries and significant intra-articular displacement requiring open arthrotomies were excluded.

At 1-year follow-up, with use of DASH as the gold standard for disability, we found no major difference in subjective or objective outcome measures between patients with and without ligament injuries. Radiographs did not predict soft-tissue injury or ultimate outcome. Rates of ligament injuries in our operatively treated DRFs were similar to those in the literature. Overall, these findings suggest that “minor” injuries incidentally discovered with arthroscopy during DRF surgery may not have a significant effect on outcomes, with the caveat that the significance of very severe injuries (eg, Geissler grade 4 injuries with frank scapholunate diastasis) remains incompletely understood. The decision by the treating surgeon to perform arthroscopy and/or to repair soft-tissue injuries should be made on a case-by-case basis.

Am J Orthop. 2017;46(1):E41-E46. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Patients sustaining DRFs commonly have associated ligament injuries and chondral damage as well.
  • Many of these associated injuries do not seem to affect outcomes up to 1 year after surgery.
  • Plain radiographs have a 74% sensitivity and 73% specificity for detecting intra-articular fractures.
  • ”Minor” injuries identified incidentally by arthroscopy during fixation of DRFs may not require dedicated treatment.
  • The optimal treatment for high-grade ligament or chondral injuries in patients with DRFs remains incompletely understood.

Distal radius fracture (DRF) is one of the most common upper extremity injuries, with up to 20% to 50% requiring surgical fixation.1 With increasing use of wrist arthroscopy to assist in managing these fractures,2-6 it has become easier to accurately assess concomitant wrist ligament injuries. Reported injury rates are 18% to 86% for the scapholunate interosseous ligament (SLIL),7,8 5% to 29% for the lunotriquetral ligament (LTL),8,9 and 17% to 60% for the triangular fibrocartilage complex (TFCC).10,11 Reported chondral injury rates range from 18% to 60%.7,9,12 Despite the common occurrence of these injuries, it is unclear how they affect outcomes and how aggressively they should be treated when detected during fracture surgery.

As the use of arthroscopy in DRF management becomes more common, surgeons often must decide how to treat ligamentous/chondral injuries incidentally discovered during surgery. To date, only 1 study prospectively evaluated how these injuries affect DRF outcomes,8 though it did not use a validated, patient-based outcome measure.

We conducted a study to address a common clinical scenario: When arthroscopy is used to assist with intra-articular reduction during DRF fixation, how should the surgeon respond to incidentally identified ligament and chondral injuries? Specifically, we wanted to address 3 questions: What is the overall incidence of SLIL, TFCC, and chondral surface injuries in patients undergoing operative fracture fixation? On initial injury films, do any radiographic parameters predict specific soft-tissue injuries or ultimate functional outcomes? Do wrist ligament and chondral injuries affect patient-rated outcomes (disability, pain) and objective measures (range of motion [ROM], grip strength, pinch strength) up to 1 year after fracture surgery?

Materials and Methods

Patient Selection/Population

This observational, prognostic study was approved by our Institutional Review Board. Inclusion criteria were age over 18 years, isolated acute operatively treated DRF (surgery within 14 days of injury), and informed consent. All patients were treated by the same surgeon. Exclusion criteria were open DRF, dorsal shear pattern, fractures requiring dorsal arthrotomy for reduction because of significant intra-articular damage, prior ipsilateral DRF, and prior SLIL or TFCC injury.

Surgery was indicated according to general radiographic parameters as measured on postreduction films: radial height, <8 mm; radial inclination, <15°; positive ulnar variance, >3 mm, or 3 mm more than contralateral side; dorsal tilt, >10°; and volar tilt, >15°. With these parameters within acceptable limits, surgery was also indicated when fractures were deemed unstable and likely to displace because of dorsal tilt >20°, dorsal comminution, intra-articular step-off of ≥2 mm on the posterior-anterior (PA) film, associated ulnar fracture, and age >60 years.13Over a 2-year period, 42 patients (12 male, 30 female) met the inclusion criteria and were enrolled in the study. The dominant arm was affected in 17 patients (40%). Mean (SD) age at time of injury was 56.6 (16.4) years (median, 54 years; range, 20-85 years).

Operative Technique

During surgery, damage to the SLIL, the TFCC, and chondral surfaces (scaphoid, lunate, scaphoid fossa, lunate fossa) and to the intra-articular extension of the DRF was assessed and recorded. Wrist arthroscopy was performed with the 3, 4 portal as the primary portal. When significant damage to the TFCC warranted débridement, the 6R (radial) portal was used as an accessory portal. As a midcarpal portal was not used for SLIL assessment, we used a novel classification system: 0 = no injury, normal-appearing ligament without hemorrhage and smooth transition from scaphoid to lunate surface except for slight concave indentation at the ligament; 1 = attenuation, no visible tear with convex shape of ligament with or without hemorrhage; 2 = partial tear with or without step-off at junction between scaphoid and lunate, but 2.7-mm arthroscope cannot “drive through” to midcarpal joint; and 3 = complete tear with positive “drive-through” sign. TFCC injuries were classified according to the system described by Palmer14: Avulsions were central (1A), ulnar (1B), distal (1C), or radial (1D). The trampoline test was performed through a 6R portal by using a probe to evaluate ligament tension/laxity. In some cases, a 6R portal was deemed unnecessary, and a modified trampoline test was performed—tension/laxity/displacement was evaluated by manually palpating at the fovea and observing TFCC motion with the arthroscope. When appropriate, the TFCC was débrided with a shaver through the 6R portal. In cases of significant instability at the SLIL interval, two 0.062-inch K-wires were placed percutaneously through the scaphoid and lunate, and one was placed from the scaphoid to the capitate.

 

 

All DRFs underwent internal fixation with a locked volar plate. When necessary, K-wires and/or a locked radial column plate was used for additional fixation. External fixation was not used. The postoperative protocol began with a dorsal wrist splint placed on the patient in the operating room and worn for 10 to 14 days. At the first postoperative visit, the patient received a removable splint that was to be worn at all times except during showers, therapy, and home exercises. Occupational therapy, initiated the week of the first postoperative visit, consisted of active and passive ROM exercises. At 6 weeks, the splint was removed and strengthening initiated.

Outcome Measures

Our primary outcome measure was the Disabilities of the Arm, Shoulder, and Hand (DASH) questionnaire at 1 year.15 Secondary outcome measures were visual analog scale (VAS) pain rating, ROM, and radiographic measurements. Patients returned for evaluation 2, 6, 12, 24, and 52 weeks after surgery. At each follow-up visit, the DASH questionnaire and the pain VAS were administered, and ROM and strength were measured. Patient-reported pain was recorded on a standard VAS and measured on a scale from 0 (no pain) to 10 (worst possible pain). Wrist flexion and extension and radioulnar deviation were assessed with a goniometer. Forearm supination and pronation were assessed with the elbow flexed 90° at the patient’s side. Grip strength was measured with a calibrated Jamar dynamometer (Sammons Preston Rolyan), and lateral pinch strength was measured with a hydraulic pinch gauge (Sammons Preston Rolyan). The average of 3 trials for both hands was recorded for all strength measurements.

Radiographs were obtained on presentation. When appropriate, the fracture was manually reduced with a hematoma block, and postreduction radiographs were obtained. Then, radiographs were obtained at each postoperative visit until union. Radial height, radial inclination, tilt, and ulnar variance were measured on preoperative and postoperative radiographs according to standard methods.16 Radiographs were used to classify the fracture patterns according to the AO/ASIF (Arbeitsgemeinschaft für Osteosynthesefragen/Association for the Study of Internal Fixation) classification. Union was determined by radiographic healing, absence of tenderness to palpation, absence of pain with motion, and continued functional improvement.

Data Analysis

To evaluate for relationships between patient injury parameters and outcome measures, we used a 1-way analysis of variance seeking statistically significant differences between groups. Patients were divided into 4 groups: no ligament injuries; isolated SLIL injuries; isolated TFCC injuries; and both SLIL and TFCC injuries. These injury classification categories were then evaluated independently against our chosen outcome measures, which included DASH and VAS pain scores, ROM, and grip/pinch strength.

To determine the optimal sample size, we performed a power analysis to estimate the number of patients required to detect a clinically significant difference in DASH scores at 1 year among the 4 groups. According to the literature, standard deviations of DASH scores in healthy volunteers range from 10 to 15,17 consistent with values found in other recent trials of patients with DRFs.18 The recent literature on DASH construct validity has established a DASH score difference of 19 as representing a disability change being “much better or much worse.”19 As such, power analysis for a 1-way analysis of variance among 4 categories, detecting a DASH score difference of 19 with a standard deviation ranging from 10 to 15, would require 28 to 60 patients to detect a difference with an α of 0.05 and a power of 0.8.

In addition, radiographic parameters at time of injury were compared with injury characteristics to assess for significant relationships. Multivariate linear regression analysis was performed to evaluate radial height, radial inclination, and volar tilt as possible predictors of SLIL injury, TFCC injury, and chondral surface damage. A statistically significant result was defined as a correlation with P < .05.

Results

Of the 42 patients included in the study, 11 (26%) had no ligament injuries, 10 (24%) had isolated SLIL injuries, 12 (29%) had isolated TFCC injuries, and 9 (21%) had injuries to both the SLIL and the TFCC. In addition, in 12 patients (29%), the articular cartilage had visible damage (Table 1).

Table 1.
According to the AO/ASIF classification, 18 patients had type A fractures, 8 had type B, and 16 had type C. Twenty patients had an intra-articular component seen on preoperative radiographs and confirmed arthroscopically, and another 7 were thought to have an extra-articular fracture pattern but were found to have an intra-articular component arthroscopically.

In all patients, bony union occurred. After union, 1 patient underwent hardware removal for hardware-related pain. The same patient had a dorsal ulnar cutaneous nerve neurolysis at the ulnar styloid fixation site. Another patient developed a partial extensor pollicis longus tear from a prominent dorsal screw tip.

All patients returned for their 2- and 6-week follow-ups. At 1 year, 30 patients (71%) returned for follow-up, 11 could not be contacted, and 1 was removed because of an olecranon fracture from a subsequent fall.

Regarding the primary outcome measure, mean DASH score at 1-year follow-up was 30.8 for the group without injuries, 10.8 for the group with SLIL injuries, 14.7 for the group with TFCC injuries, and 21.9 for the group with SLIL and TFCC injuries (Table 2).

Table 2.
There were no statistical differences between the groups at any point. The secondary outcome measures (VAS pain, wrist ROM, grip/pinch strength) also showed no statistically significant relationship at any point. Controlling for AO/ASIF fracture type did not affect significance, and there was no subdivision or subanalysis of injury characteristic or classification that correlated with DASH scores, VAS pain, or physical examination results at any point.

Radiographic parameters were restored to acceptable limits in all patients (Table 3).
Table 3.
A linear regression analysis comparing these injury radiographic parameters with the incidence of SLIL, TFCC, or chondral injuries showed that none of these measurements were a significant predictor of soft-tissue injury.

 

 

Discussion

Use of wrist arthroscopy in DRF management has allowed assessment of the incidence of intra-articular injuries, including ligament and chondral surface injuries. Although the literature on the incidence of these injuries has been expanding, their clinical significance remains unclear.

Authors have postulated that some patients do not do well after DRF repair because of undetected ligament injuries. With the current trend of internal fixation, locked plating, and early motion—contrasting with older trends of prolonged immobilization in a cast or external fixation—concerns have been raised that early mobilization results in inadequate treatment of ligament injuries. However, data from the present study suggest no significant morbidity from early mobilization despite the presence of ligament injuries in more than half of all operatively treated DRFs. It is possible morbidity was not appreciated, as most patients with DRFs end up with some stiffness, which masks the effects of ligament injuries during healing.

We found no correlation between injury radiographic parameters, observed soft-tissue injuries, or final subjective outcomes. Interestingly, in this study, there was some discordance between the appearance of intra-articular fractures on radiographs and the direct arthroscopic observation of intra-articular fracture extension. With the present data and with arthroscopic visualization as the gold standard, radiographs had 74% sensitivity and 73% specificity for detecting intra-articular fractures (the corresponding positive predictive value was 83%, and the negative predictive value was 61%). As we typically rely on radiographs as the primary tool in assessing the articular component of a fracture, these results should be taken into account when basing management decisions exclusively on static injury films.

Observational studies of arthroscopy in DRFs have revealed a wide range of injury rates: For SLILs, the average injury rate was 44%; for LTLs, 13%; for TFCCs, 43%; and for chondral surfaces, 32% (Table 4).

Table 4.
We found comparable rates in the present study, indicating the injuries in our patient population are comparable with those in similar studies.

This study had several limitations, including loss to follow-up at the primary endpoint (we were unable to contact 29% of patients). In addition, because of resource limitations, we were able to enroll only a limited number of patients, and as a result were able to power the study to detect only major effects on DASH scores. Therefore, although our 32 patients with long-term follow-up are within the range dictated by the power analysis, this study was not powered to capture more subtle differences in disability. Furthermore, because we used 1 year as the longest follow-up point, the long-term sequelae (eg, arthritis) of these injuries may not have been captured. Last, despite the high incidence of soft-tissue injuries overall, the number of patients with severe ligament injuries was relatively low, which makes it difficult to make definitive statements about their contribution to outcomes. A likely explanation is that patients with high-energy injuries and significant intra-articular displacement requiring open arthrotomies were excluded.

At 1-year follow-up, with use of DASH as the gold standard for disability, we found no major difference in subjective or objective outcome measures between patients with and without ligament injuries. Radiographs did not predict soft-tissue injury or ultimate outcome. Rates of ligament injuries in our operatively treated DRFs were similar to those in the literature. Overall, these findings suggest that “minor” injuries incidentally discovered with arthroscopy during DRF surgery may not have a significant effect on outcomes, with the caveat that the significance of very severe injuries (eg, Geissler grade 4 injuries with frank scapholunate diastasis) remains incompletely understood. The decision by the treating surgeon to perform arthroscopy and/or to repair soft-tissue injuries should be made on a case-by-case basis.

Am J Orthop. 2017;46(1):E41-E46. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Róbertsson GO, Jónsson GT, Sigurjónsson K. Epidemiology of distal radius fractures in Iceland in 1985. Acta Orthop Scand. 1990;61(5):457-459.

2. Geissler WB. Arthroscopically assisted reduction of intra-articular fractures of the distal radius. Hand Clin. 1995;11(1):19-29.

3. Trybus M, Guzik P. The economic impact of hand injury [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2003;68(4):269-273.

4. Wolfe SW, Easterling KJ, Yoo HH. Arthroscopic-assisted reduction of distal radius fractures. Arthroscopy. 1995;11(6):706-714.

5. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26(5):908-915.

6. Doi K, Hattori Y, Otsuka K, Abe Y, Yamamoto H. Intra-articular fractures of the distal aspect of the radius: arthroscopically assisted reduction compared with open reduction and internal fixation. J Bone Joint Surg Am. 1999;81(8):1093-1110.

7. Shih JT, Lee HM, Hou YT, Tan CM. Arthroscopically-assisted reduction of intra-articular fractures and soft tissue management of distal radius. Hand Surg. 2001;6(2):127-135.

8. Forward DP, Lindau TR, Melsom DS. Intercarpal ligament injuries associated with fractures of the distal part of the radius. J Bone Joint Surg Am. 2007;89(11):2334-2340.

9. Espinosa-Gutiérrez A, Rivas-Montero JA, Elias-Escobedo A, Alisedo-Ochoa PG. Wrist arthroscopy for fractures of the distal end of the radius [in Spanish]. Acta Ortop Mex. 2009;23(6):358-365.

10. Hardy P, Gomes N, Chebil M, Bauer T. Wrist arthroscopy and intra-articular fractures of the distal radius in young adults. Knee Surg Sports Traumatol Arthrosc. 2006;14(11):1225-1230.

11. Varitimidis SE, Basdekis GK, Dailiana ZH, Hantes ME, Bargiotas K, Malizos K. Treatment of intra-articular fractures of the distal radius: fluoroscopic or arthroscopic reduction? J Bone Joint Surg Br. 2008;90(6):778-785.

12. Kordasiewicz B, Pomianowski S, Rylski W, Antolak L, Marczak D. Intraarticular distal radius fractures—arthroscopic assessment of injuries [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2006;71(2):113-116.

13. Lafontaine M, Hardy D, Delince P. Stability assessment of distal radius fractures. Injury. 1989;20(4):208-210.

14. Palmer AK. Triangular fibrocartilage complex lesions: a classification. J Hand Surg Am. 1989;14(4):594-606.

15. Hudak PL, Amadio PC, Bombardier C. Development of an upper extremity outcome measure: the DASH (Disabilities of the Arm, Shoulder and Hand) [corrected]. The Upper Extremity Collaborative Group (UECG) [published correction appears in Am J Ind Med. 1996;30(3):372]. Am J Ind Med. 1996;29(6):602-608.

16. Fernandez DL, Jupiter JB. Fractures of the Distal Radius: A Practical Approach to Management. New York, NY: Springer; 1996.

17. Jester A, Harth A, Wind G, Germann G, Sauerbier M. Does the Disability of Shoulder, Arm and Hand questionnaire (DASH) replace grip strength and range of motion in outcome-evaluation? [in German]. Handchir Mikrochir Plast Chir. 2005;37(2):126-130.

18. Wei DH, Raizman NM, Bottino CJ, Jobin CM, Strauch RJ, Rosenwasser MP. Unstable distal radial fractures treated with external fixation, a radial column plate, or a volar plate. A prospective randomized trial. J Bone Joint Surg Am. 2009;91(7):1568-1577.

19. Gummesson C, Atroshi I, Ekdahl C. The Disabilities of the Arm, Shoulder and Hand (DASH) outcome questionnaire: longitudinal construct validity and measuring self-rated health change after surgery. BMC Musculoskelet Disord. 2003;4:11.

20. Richards RS, Bennett JD, Roth JH, Milne K Jr. Arthroscopic diagnosis of intra-articular soft tissue injuries associated with distal radial fractures. J Hand Surg Am. 1997;22(5):772-776.

21. Peicha G, Seibert F, Fellinger M, Grechenig W. Midterm results of arthroscopic treatment of scapholunate ligament lesions associated with intra-articular distal radius fractures. Knee Surg Sports Traumatol Arthrosc. 1999;7(5):327-333.

22. Schädel-Höpfner M, Böhringer G, Junge A, Celik I, Gotzen L. [Arthroscopic diagnosis of concomitant scapholunate ligament injuries in fractures of the distal radius]. Handchir Mikrochir Plast Chir. 2001;33(4):229-233.

23. Ruch DS, Yang CC, Smith BP. Results of acute arthroscopically repaired triangular fibrocartilage complex injuries associated with intra-articular distal radius fractures. Arthroscopy. 2003;19(5):511-516.

24. Hattori Y, Doi K, Estrella EP, Chen G. Arthroscopically assisted reduction with volar plating or external fixation for displaced intra-articular fractures of the distal radius in the elderly patients. Hand Surg. 2007;12(1):1-12.

25. Hohendorff B, Eck M, Mühldorfer M, Fodor S, Schmitt R, Prommersberger KJ. [Palmar wrist arthroscopy for evaluation of concomitant carpal lesions in operative treatment of distal intraarticular radius fractures]. Handchir Mikrochir Plast Chir. 2009;41(5):295-299.

References

1. Róbertsson GO, Jónsson GT, Sigurjónsson K. Epidemiology of distal radius fractures in Iceland in 1985. Acta Orthop Scand. 1990;61(5):457-459.

2. Geissler WB. Arthroscopically assisted reduction of intra-articular fractures of the distal radius. Hand Clin. 1995;11(1):19-29.

3. Trybus M, Guzik P. The economic impact of hand injury [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2003;68(4):269-273.

4. Wolfe SW, Easterling KJ, Yoo HH. Arthroscopic-assisted reduction of distal radius fractures. Arthroscopy. 1995;11(6):706-714.

5. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26(5):908-915.

6. Doi K, Hattori Y, Otsuka K, Abe Y, Yamamoto H. Intra-articular fractures of the distal aspect of the radius: arthroscopically assisted reduction compared with open reduction and internal fixation. J Bone Joint Surg Am. 1999;81(8):1093-1110.

7. Shih JT, Lee HM, Hou YT, Tan CM. Arthroscopically-assisted reduction of intra-articular fractures and soft tissue management of distal radius. Hand Surg. 2001;6(2):127-135.

8. Forward DP, Lindau TR, Melsom DS. Intercarpal ligament injuries associated with fractures of the distal part of the radius. J Bone Joint Surg Am. 2007;89(11):2334-2340.

9. Espinosa-Gutiérrez A, Rivas-Montero JA, Elias-Escobedo A, Alisedo-Ochoa PG. Wrist arthroscopy for fractures of the distal end of the radius [in Spanish]. Acta Ortop Mex. 2009;23(6):358-365.

10. Hardy P, Gomes N, Chebil M, Bauer T. Wrist arthroscopy and intra-articular fractures of the distal radius in young adults. Knee Surg Sports Traumatol Arthrosc. 2006;14(11):1225-1230.

11. Varitimidis SE, Basdekis GK, Dailiana ZH, Hantes ME, Bargiotas K, Malizos K. Treatment of intra-articular fractures of the distal radius: fluoroscopic or arthroscopic reduction? J Bone Joint Surg Br. 2008;90(6):778-785.

12. Kordasiewicz B, Pomianowski S, Rylski W, Antolak L, Marczak D. Intraarticular distal radius fractures—arthroscopic assessment of injuries [in Polish]. Chir Narzadow Ruchu Ortop Pol. 2006;71(2):113-116.

13. Lafontaine M, Hardy D, Delince P. Stability assessment of distal radius fractures. Injury. 1989;20(4):208-210.

14. Palmer AK. Triangular fibrocartilage complex lesions: a classification. J Hand Surg Am. 1989;14(4):594-606.

15. Hudak PL, Amadio PC, Bombardier C. Development of an upper extremity outcome measure: the DASH (Disabilities of the Arm, Shoulder and Hand) [corrected]. The Upper Extremity Collaborative Group (UECG) [published correction appears in Am J Ind Med. 1996;30(3):372]. Am J Ind Med. 1996;29(6):602-608.

16. Fernandez DL, Jupiter JB. Fractures of the Distal Radius: A Practical Approach to Management. New York, NY: Springer; 1996.

17. Jester A, Harth A, Wind G, Germann G, Sauerbier M. Does the Disability of Shoulder, Arm and Hand questionnaire (DASH) replace grip strength and range of motion in outcome-evaluation? [in German]. Handchir Mikrochir Plast Chir. 2005;37(2):126-130.

18. Wei DH, Raizman NM, Bottino CJ, Jobin CM, Strauch RJ, Rosenwasser MP. Unstable distal radial fractures treated with external fixation, a radial column plate, or a volar plate. A prospective randomized trial. J Bone Joint Surg Am. 2009;91(7):1568-1577.

19. Gummesson C, Atroshi I, Ekdahl C. The Disabilities of the Arm, Shoulder and Hand (DASH) outcome questionnaire: longitudinal construct validity and measuring self-rated health change after surgery. BMC Musculoskelet Disord. 2003;4:11.

20. Richards RS, Bennett JD, Roth JH, Milne K Jr. Arthroscopic diagnosis of intra-articular soft tissue injuries associated with distal radial fractures. J Hand Surg Am. 1997;22(5):772-776.

21. Peicha G, Seibert F, Fellinger M, Grechenig W. Midterm results of arthroscopic treatment of scapholunate ligament lesions associated with intra-articular distal radius fractures. Knee Surg Sports Traumatol Arthrosc. 1999;7(5):327-333.

22. Schädel-Höpfner M, Böhringer G, Junge A, Celik I, Gotzen L. [Arthroscopic diagnosis of concomitant scapholunate ligament injuries in fractures of the distal radius]. Handchir Mikrochir Plast Chir. 2001;33(4):229-233.

23. Ruch DS, Yang CC, Smith BP. Results of acute arthroscopically repaired triangular fibrocartilage complex injuries associated with intra-articular distal radius fractures. Arthroscopy. 2003;19(5):511-516.

24. Hattori Y, Doi K, Estrella EP, Chen G. Arthroscopically assisted reduction with volar plating or external fixation for displaced intra-articular fractures of the distal radius in the elderly patients. Hand Surg. 2007;12(1):1-12.

25. Hohendorff B, Eck M, Mühldorfer M, Fodor S, Schmitt R, Prommersberger KJ. [Palmar wrist arthroscopy for evaluation of concomitant carpal lesions in operative treatment of distal intraarticular radius fractures]. Handchir Mikrochir Plast Chir. 2009;41(5):295-299.

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Silicone joint arthroplasty for RA shows sustained improvements at 7 years

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Rheumatoid arthritis patients who underwent silicone metacarpophalangeal joint replacement maintained significant improvement in ulnar drift and extensor lag after 7 years of follow-up in the prospective, multicenter Silicone Arthroplasty in Rheumatoid Arthritis (SARA) study.

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Rhumatoid arthritis hands with ulnar drift
Investigators led by Kevin C. Chung, MD, and his colleagues from the University of Michigan, Ann Arbor, conducted what they claim is the largest prospective cohort study yet of RA joint replacement surgery by following 170 patients with RA, 73 of whom had elected to undergo SMPA with a Swanson implant and 97 who chose nonsurgical management. Patients were selected because they had severe deformity at the MCP joints, based on their combined ulnar deviation and an extensor lag greater than or equal to 50 degrees on average for each finger.

The practice of replacing deformed MCP joints with a hinged silicone implant has been around for almost half a century, the investigators noted, but despite widespread use, there is a lack of high-quality surgical outcomes data for the procedure. The authors suggested that the scarcity of data may create a barrier for surgical referrals from rheumatologists and could account for the declining rate of surgical intervention for RA joint deformities.

The significant improvement in ulnar drift that occurred in patients who underwent SMPA versus no surgery remained even after adjustment for baseline severity, age, sex, and use of biologics. The adjustment was especially important because the nonsurgical group had better function at baseline, with significantly stronger grip and pinch strength, better Michigan Hand Questionnaire (MHQ) scores, and significantly better ulnar drift, extensor lag, and arc of motion than in the surgical group (Arthritis Care Res. 2016 Oct 1. doi: 10.1002/acr.23105).

The nonsurgical group largely maintained its baseline functional state during the 7-year follow-up period except for a decline in pinch strength.

“When the SMPA cohort was compared with the non-SMPA cohort, the covariate-adjusted difference showed significant benefits associated with SMPA hand outcome as measured by the MHQ function, aesthetics, and satisfaction scores, with no measures showing significantly better outcomes for the non-SMPA group,” the researchers wrote. “Although the average treatment effect estimate (ATT estimate) showed a decline over time for the average benefit from SMPA in those treated, the function score benefit as shown by the ATT estimate remained significant at year 5.”

Patients in the nonsurgical group were also given the option to crossover and receive surgery after 1 year, which two did. Eleven patients in the surgical group also decided to undergo surgery on their other hand.

Researchers saw one mild and three moderate implant-related adverse events during the study, including one patient who experienced ulnar deviation and needed a new joint replacement, one who dislocated the implant of the little finger a few weeks after insertion, and one who experienced sepsis in the joints 6 years after insertion and needed replacements for two implants. The fracture incidence of about 10% fits into the mid-range of previously reported fracture rates with this implant.

The study experienced significant losses to follow-up, particularly in the surgical group in which 7-year data were only available for 43% of participants in this group. The authors suggested this could have been because the surgical patients achieved their goals and were less inclined to the follow-up visits.

The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. No conflicts of interest were declared.

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Rheumatoid arthritis patients who underwent silicone metacarpophalangeal joint replacement maintained significant improvement in ulnar drift and extensor lag after 7 years of follow-up in the prospective, multicenter Silicone Arthroplasty in Rheumatoid Arthritis (SARA) study.

iStock
Rhumatoid arthritis hands with ulnar drift
Investigators led by Kevin C. Chung, MD, and his colleagues from the University of Michigan, Ann Arbor, conducted what they claim is the largest prospective cohort study yet of RA joint replacement surgery by following 170 patients with RA, 73 of whom had elected to undergo SMPA with a Swanson implant and 97 who chose nonsurgical management. Patients were selected because they had severe deformity at the MCP joints, based on their combined ulnar deviation and an extensor lag greater than or equal to 50 degrees on average for each finger.

The practice of replacing deformed MCP joints with a hinged silicone implant has been around for almost half a century, the investigators noted, but despite widespread use, there is a lack of high-quality surgical outcomes data for the procedure. The authors suggested that the scarcity of data may create a barrier for surgical referrals from rheumatologists and could account for the declining rate of surgical intervention for RA joint deformities.

The significant improvement in ulnar drift that occurred in patients who underwent SMPA versus no surgery remained even after adjustment for baseline severity, age, sex, and use of biologics. The adjustment was especially important because the nonsurgical group had better function at baseline, with significantly stronger grip and pinch strength, better Michigan Hand Questionnaire (MHQ) scores, and significantly better ulnar drift, extensor lag, and arc of motion than in the surgical group (Arthritis Care Res. 2016 Oct 1. doi: 10.1002/acr.23105).

The nonsurgical group largely maintained its baseline functional state during the 7-year follow-up period except for a decline in pinch strength.

“When the SMPA cohort was compared with the non-SMPA cohort, the covariate-adjusted difference showed significant benefits associated with SMPA hand outcome as measured by the MHQ function, aesthetics, and satisfaction scores, with no measures showing significantly better outcomes for the non-SMPA group,” the researchers wrote. “Although the average treatment effect estimate (ATT estimate) showed a decline over time for the average benefit from SMPA in those treated, the function score benefit as shown by the ATT estimate remained significant at year 5.”

Patients in the nonsurgical group were also given the option to crossover and receive surgery after 1 year, which two did. Eleven patients in the surgical group also decided to undergo surgery on their other hand.

Researchers saw one mild and three moderate implant-related adverse events during the study, including one patient who experienced ulnar deviation and needed a new joint replacement, one who dislocated the implant of the little finger a few weeks after insertion, and one who experienced sepsis in the joints 6 years after insertion and needed replacements for two implants. The fracture incidence of about 10% fits into the mid-range of previously reported fracture rates with this implant.

The study experienced significant losses to follow-up, particularly in the surgical group in which 7-year data were only available for 43% of participants in this group. The authors suggested this could have been because the surgical patients achieved their goals and were less inclined to the follow-up visits.

The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. No conflicts of interest were declared.

 

Rheumatoid arthritis patients who underwent silicone metacarpophalangeal joint replacement maintained significant improvement in ulnar drift and extensor lag after 7 years of follow-up in the prospective, multicenter Silicone Arthroplasty in Rheumatoid Arthritis (SARA) study.

iStock
Rhumatoid arthritis hands with ulnar drift
Investigators led by Kevin C. Chung, MD, and his colleagues from the University of Michigan, Ann Arbor, conducted what they claim is the largest prospective cohort study yet of RA joint replacement surgery by following 170 patients with RA, 73 of whom had elected to undergo SMPA with a Swanson implant and 97 who chose nonsurgical management. Patients were selected because they had severe deformity at the MCP joints, based on their combined ulnar deviation and an extensor lag greater than or equal to 50 degrees on average for each finger.

The practice of replacing deformed MCP joints with a hinged silicone implant has been around for almost half a century, the investigators noted, but despite widespread use, there is a lack of high-quality surgical outcomes data for the procedure. The authors suggested that the scarcity of data may create a barrier for surgical referrals from rheumatologists and could account for the declining rate of surgical intervention for RA joint deformities.

The significant improvement in ulnar drift that occurred in patients who underwent SMPA versus no surgery remained even after adjustment for baseline severity, age, sex, and use of biologics. The adjustment was especially important because the nonsurgical group had better function at baseline, with significantly stronger grip and pinch strength, better Michigan Hand Questionnaire (MHQ) scores, and significantly better ulnar drift, extensor lag, and arc of motion than in the surgical group (Arthritis Care Res. 2016 Oct 1. doi: 10.1002/acr.23105).

The nonsurgical group largely maintained its baseline functional state during the 7-year follow-up period except for a decline in pinch strength.

“When the SMPA cohort was compared with the non-SMPA cohort, the covariate-adjusted difference showed significant benefits associated with SMPA hand outcome as measured by the MHQ function, aesthetics, and satisfaction scores, with no measures showing significantly better outcomes for the non-SMPA group,” the researchers wrote. “Although the average treatment effect estimate (ATT estimate) showed a decline over time for the average benefit from SMPA in those treated, the function score benefit as shown by the ATT estimate remained significant at year 5.”

Patients in the nonsurgical group were also given the option to crossover and receive surgery after 1 year, which two did. Eleven patients in the surgical group also decided to undergo surgery on their other hand.

Researchers saw one mild and three moderate implant-related adverse events during the study, including one patient who experienced ulnar deviation and needed a new joint replacement, one who dislocated the implant of the little finger a few weeks after insertion, and one who experienced sepsis in the joints 6 years after insertion and needed replacements for two implants. The fracture incidence of about 10% fits into the mid-range of previously reported fracture rates with this implant.

The study experienced significant losses to follow-up, particularly in the surgical group in which 7-year data were only available for 43% of participants in this group. The authors suggested this could have been because the surgical patients achieved their goals and were less inclined to the follow-up visits.

The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. No conflicts of interest were declared.

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Key clinical point: Silicone MCP joint replacement in rheumatoid arthritis is associated with significant and sustained improvements in ulnar drift and extensor lag.

Major finding: Patients who elected to undergo silicone MCP joint replacement showed significant improvements in ulnar drift and extensor lag, as well as in function, aesthetics, and satisfaction scores at 7 years after the procedure.

Data source: Cohort study of 170 patients with rheumatoid arthritis–related severe deformity at the metacarpophalangeal joints.

Disclosures: The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. No conflicts of interest were declared.

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Pain starting in knee later arises in other joints

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Pain starting in knee later arises in other joints

People who develop knee pain associated with osteoarthritis often subsequently develop pain in other joints, according to a study of two observational, community-based cohorts that could not discern any pattern of new pain sites.

In the “first investigation of the association of knee pain with pain in multiple other sites,” David T. Felson, MD, of Boston University and his colleagues reported that the regions where pain developed after first appearing in the knee varied from person to person and occurred in both upper and lower extremities, which goes against the hypothesis that adjacent joints are most often affected by knee pain.

 

Dr. David T. Felson

The study involved patients from the MOST (Multicenter Osteoarthritis Study) trial, including 281 with knee pain at the index visit (168 unilaterally) and 852 without, as well as patients from OAI (the Osteoarthritis Initiative), including 412 with knee pain at the index visit (241 unilaterally), and 1,941 without. The investigators assessed the patients’ data for 14 total joints outside of the knees: 2 each of feet, ankles, hips, hands, wrists, elbows, and shoulders (Arthritis Rheumatol. 2016 Sep 2. doi: 10.1002/art.39848).

Patients with new-onset knee pain at the index visit reported a mean of 2.3 painful joints outside the knee, compared with a significantly lower number of 1.3 reported by those without knee pain. The mean number of nonknee joints with pain was higher among patients with bilateral knee pain, compared with unilateral knee pain. The percentage of patients who reported pain outside the knee rose with the number of painful knees: 80% for two, 64% for one, and 50% for none.

The patients who developed new unilateral knee pain at the index visit also experienced an increase in prevalent joint pain in multiple joints in upper- and lower-extremity sites. In particular, the investigators noted that ipsilateral prevalent hip joint pain, which they characterized as pain in the groin or front of the thigh, was more than twice as likely to occur among those with new unilateral knee pain at the index visit, but the odds for contralateral hip joint pain did not reach statistical significance. The comparisons were adjusted for age, sex, body mass index, depression at the index visit, study (MOST or OAI), and count of painful upper and lower limb joints at the index visit (excluding knees).

When examining only patients with new-onset joint pain outside of the knee, the odds of patients with new knee pain to later develop new-onset joint pain outside the knee were 30% higher than for those without knee pain. Patients with new knee pain had a mean 2.6 new painful joints out of 12.1 eligible joints, compared with 2.0 new painful joints in those without knee pain out of 12.7 eligible joints. (Joint regions with prevalent symptoms at the index visit were excluded as incident painful sites.) Patients with knee pain also had a consistently higher rate of new-onset pain in nonknee joints when compared with patients without knee pain in at least half of the follow-up visits over the course of the MOST and OAI studies. Sensitivity analyses indicated that the association between knee pain and subsequent pain in other joints was not driven by the inclusion of patients with widespread pain.

“There was no clear-cut predilection for pain in any specific lower-extremity joint region,” the investigators wrote.

The investigators noted that other researchers have suggested that patients with knee pain may be at higher risk for lower-extremity joint pain because of changes to their gait that gradually cause damage to other joints, but evidence in this study doesn’t “necessarily support the argument that in persons with knee pain, aberrant loading by altered movement patterns induces pain in only nearby joints. Our findings suggest that the sites affected are more than just hip and ankle and that there is no special predilection for pain in these locations.”

While the investigators cannot differentiate underlying mechanisms for their study’s finding of multiple co-occurring sites of joint pain in people with new-onset knee pain, they suggested that it “supports either a predilection for osteoarthritic changes at multiple joint sites and/or raises the possibility that nervous system–driven pain sensitization increases the risk not only of widespread pain but even of regional pain. Since symptomatic OA is unusual in some of these painful sites (e.g., elbow, shoulder, ankle), pain sensitization would seem a more likely explanation.”

Some of the study’s limitations described by the investigators included the uncertainty surrounding whether new-onset knee pain was truly new onset or whether it was a reoccurrence, and also the fact that most of the people in the two cohorts had multiple sites of joint pain at both the baseline and the index visit and there were too few people with no sites of pain outside the knee to carry out subanalyses in that group, which “speaks to the high prevalence of multiple joint pains in older adult cohorts.”

 

 

The research was supported by grants from the National Institutes of Health. The authors had no disclosures to report.

jevans@frontlinemedcom.com

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People who develop knee pain associated with osteoarthritis often subsequently develop pain in other joints, according to a study of two observational, community-based cohorts that could not discern any pattern of new pain sites.

In the “first investigation of the association of knee pain with pain in multiple other sites,” David T. Felson, MD, of Boston University and his colleagues reported that the regions where pain developed after first appearing in the knee varied from person to person and occurred in both upper and lower extremities, which goes against the hypothesis that adjacent joints are most often affected by knee pain.

 

Dr. David T. Felson

The study involved patients from the MOST (Multicenter Osteoarthritis Study) trial, including 281 with knee pain at the index visit (168 unilaterally) and 852 without, as well as patients from OAI (the Osteoarthritis Initiative), including 412 with knee pain at the index visit (241 unilaterally), and 1,941 without. The investigators assessed the patients’ data for 14 total joints outside of the knees: 2 each of feet, ankles, hips, hands, wrists, elbows, and shoulders (Arthritis Rheumatol. 2016 Sep 2. doi: 10.1002/art.39848).

Patients with new-onset knee pain at the index visit reported a mean of 2.3 painful joints outside the knee, compared with a significantly lower number of 1.3 reported by those without knee pain. The mean number of nonknee joints with pain was higher among patients with bilateral knee pain, compared with unilateral knee pain. The percentage of patients who reported pain outside the knee rose with the number of painful knees: 80% for two, 64% for one, and 50% for none.

The patients who developed new unilateral knee pain at the index visit also experienced an increase in prevalent joint pain in multiple joints in upper- and lower-extremity sites. In particular, the investigators noted that ipsilateral prevalent hip joint pain, which they characterized as pain in the groin or front of the thigh, was more than twice as likely to occur among those with new unilateral knee pain at the index visit, but the odds for contralateral hip joint pain did not reach statistical significance. The comparisons were adjusted for age, sex, body mass index, depression at the index visit, study (MOST or OAI), and count of painful upper and lower limb joints at the index visit (excluding knees).

When examining only patients with new-onset joint pain outside of the knee, the odds of patients with new knee pain to later develop new-onset joint pain outside the knee were 30% higher than for those without knee pain. Patients with new knee pain had a mean 2.6 new painful joints out of 12.1 eligible joints, compared with 2.0 new painful joints in those without knee pain out of 12.7 eligible joints. (Joint regions with prevalent symptoms at the index visit were excluded as incident painful sites.) Patients with knee pain also had a consistently higher rate of new-onset pain in nonknee joints when compared with patients without knee pain in at least half of the follow-up visits over the course of the MOST and OAI studies. Sensitivity analyses indicated that the association between knee pain and subsequent pain in other joints was not driven by the inclusion of patients with widespread pain.

“There was no clear-cut predilection for pain in any specific lower-extremity joint region,” the investigators wrote.

The investigators noted that other researchers have suggested that patients with knee pain may be at higher risk for lower-extremity joint pain because of changes to their gait that gradually cause damage to other joints, but evidence in this study doesn’t “necessarily support the argument that in persons with knee pain, aberrant loading by altered movement patterns induces pain in only nearby joints. Our findings suggest that the sites affected are more than just hip and ankle and that there is no special predilection for pain in these locations.”

While the investigators cannot differentiate underlying mechanisms for their study’s finding of multiple co-occurring sites of joint pain in people with new-onset knee pain, they suggested that it “supports either a predilection for osteoarthritic changes at multiple joint sites and/or raises the possibility that nervous system–driven pain sensitization increases the risk not only of widespread pain but even of regional pain. Since symptomatic OA is unusual in some of these painful sites (e.g., elbow, shoulder, ankle), pain sensitization would seem a more likely explanation.”

Some of the study’s limitations described by the investigators included the uncertainty surrounding whether new-onset knee pain was truly new onset or whether it was a reoccurrence, and also the fact that most of the people in the two cohorts had multiple sites of joint pain at both the baseline and the index visit and there were too few people with no sites of pain outside the knee to carry out subanalyses in that group, which “speaks to the high prevalence of multiple joint pains in older adult cohorts.”

 

 

The research was supported by grants from the National Institutes of Health. The authors had no disclosures to report.

jevans@frontlinemedcom.com

People who develop knee pain associated with osteoarthritis often subsequently develop pain in other joints, according to a study of two observational, community-based cohorts that could not discern any pattern of new pain sites.

In the “first investigation of the association of knee pain with pain in multiple other sites,” David T. Felson, MD, of Boston University and his colleagues reported that the regions where pain developed after first appearing in the knee varied from person to person and occurred in both upper and lower extremities, which goes against the hypothesis that adjacent joints are most often affected by knee pain.

 

Dr. David T. Felson

The study involved patients from the MOST (Multicenter Osteoarthritis Study) trial, including 281 with knee pain at the index visit (168 unilaterally) and 852 without, as well as patients from OAI (the Osteoarthritis Initiative), including 412 with knee pain at the index visit (241 unilaterally), and 1,941 without. The investigators assessed the patients’ data for 14 total joints outside of the knees: 2 each of feet, ankles, hips, hands, wrists, elbows, and shoulders (Arthritis Rheumatol. 2016 Sep 2. doi: 10.1002/art.39848).

Patients with new-onset knee pain at the index visit reported a mean of 2.3 painful joints outside the knee, compared with a significantly lower number of 1.3 reported by those without knee pain. The mean number of nonknee joints with pain was higher among patients with bilateral knee pain, compared with unilateral knee pain. The percentage of patients who reported pain outside the knee rose with the number of painful knees: 80% for two, 64% for one, and 50% for none.

The patients who developed new unilateral knee pain at the index visit also experienced an increase in prevalent joint pain in multiple joints in upper- and lower-extremity sites. In particular, the investigators noted that ipsilateral prevalent hip joint pain, which they characterized as pain in the groin or front of the thigh, was more than twice as likely to occur among those with new unilateral knee pain at the index visit, but the odds for contralateral hip joint pain did not reach statistical significance. The comparisons were adjusted for age, sex, body mass index, depression at the index visit, study (MOST or OAI), and count of painful upper and lower limb joints at the index visit (excluding knees).

When examining only patients with new-onset joint pain outside of the knee, the odds of patients with new knee pain to later develop new-onset joint pain outside the knee were 30% higher than for those without knee pain. Patients with new knee pain had a mean 2.6 new painful joints out of 12.1 eligible joints, compared with 2.0 new painful joints in those without knee pain out of 12.7 eligible joints. (Joint regions with prevalent symptoms at the index visit were excluded as incident painful sites.) Patients with knee pain also had a consistently higher rate of new-onset pain in nonknee joints when compared with patients without knee pain in at least half of the follow-up visits over the course of the MOST and OAI studies. Sensitivity analyses indicated that the association between knee pain and subsequent pain in other joints was not driven by the inclusion of patients with widespread pain.

“There was no clear-cut predilection for pain in any specific lower-extremity joint region,” the investigators wrote.

The investigators noted that other researchers have suggested that patients with knee pain may be at higher risk for lower-extremity joint pain because of changes to their gait that gradually cause damage to other joints, but evidence in this study doesn’t “necessarily support the argument that in persons with knee pain, aberrant loading by altered movement patterns induces pain in only nearby joints. Our findings suggest that the sites affected are more than just hip and ankle and that there is no special predilection for pain in these locations.”

While the investigators cannot differentiate underlying mechanisms for their study’s finding of multiple co-occurring sites of joint pain in people with new-onset knee pain, they suggested that it “supports either a predilection for osteoarthritic changes at multiple joint sites and/or raises the possibility that nervous system–driven pain sensitization increases the risk not only of widespread pain but even of regional pain. Since symptomatic OA is unusual in some of these painful sites (e.g., elbow, shoulder, ankle), pain sensitization would seem a more likely explanation.”

Some of the study’s limitations described by the investigators included the uncertainty surrounding whether new-onset knee pain was truly new onset or whether it was a reoccurrence, and also the fact that most of the people in the two cohorts had multiple sites of joint pain at both the baseline and the index visit and there were too few people with no sites of pain outside the knee to carry out subanalyses in that group, which “speaks to the high prevalence of multiple joint pains in older adult cohorts.”

 

 

The research was supported by grants from the National Institutes of Health. The authors had no disclosures to report.

jevans@frontlinemedcom.com

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Pain starting in knee later arises in other joints
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Pain starting in knee later arises in other joints
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Key clinical point:People with frequently painful knees often develop pain in joints outside the knee, and the sites vary from person to person.

Major finding: The odds of patients with new knee pain to later develop joint pain outside the knee were 30% higher than for those without knee pain.

Data source: A study of 693 persons with index visit knee pain and 2,793 without it from two community-based cohorts.

Disclosures: The research was supported by grants from the National Institutes of Health. The authors had no disclosures to report.

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