Management and Prevention of Intraoperative Acetabular Fracture in Primary Total Hip Arthroplasty

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Take Home Points

  • IAF is an uncommon, but serious complication of primary THA.
  • Small (<50 mm) cups are at higher risk for causing IAF.
  • Prompt recognition is critical to prevent component migration and need for revision.
  • Posterior column integrity is cirtical to a successful outcome when IAF occurs.
  • Initial stable fixation, with or without intraoperative acetabular revision, is critical for successful outcome when IAF is identified.

Intraoperative acetabular fracture (IAF) is a rare complication of primary total hip arthroplasty (THA).1-3 IAFs commonly occur with impaction of the acetabular component. Studies have found that underreaming of the acetabulum and impaction of relatively large, elliptic, or monoblock components may increase the risk of IAFs.2-5 There is a paucity of literature on risk factors, treatment strategies, and outcomes of this potentially devastating complication.

In this article, we report on the incidence of IAF in primary THA at our high-volume institution and present strategies for managing and preventing this rare fracture.

Materials and Methods

Between 1997 and 2015, more than 20 fellowship-trained arthroplasty surgeons performed 21,519 primary THAs at our institution. After obtaining Institutional Review Board approval for this study, we retrospectively searched the hospital database and identified 16 patients (16 hips) who sustained an IAF in primary THA. Mean age of the cohort (13 women, 3 men) at time of surgery was 70 years (range, 42-89 years). Of the 16 patients, 13 had a preoperative diagnosis of osteoarthritis, 2 had posttraumatic arthritis, and 1 had rheumatoid arthritis. A posterolateral approach was used with 14 patients and a modified anterolateral approach with the other 2. Surgical technique and implant selection varied among surgeons. Thirteen THAs were performed with an all-press-fit technique and 3 with a hybrid technique (uncemented acetabular component, cemented femoral component). In 9 cases, the acetabular component underwent supplemental screw fixation. Whether to use acetabular component screws or cemented femoral components was decided intraoperatively by the surgeon.

The cohort’s acetabular components were either elliptic modular or hemispheric modular. The elliptic modular component used was the Peripheral Self-Locking (PSL) implant (Stryker Howmedica Osteonics), and the hemispheric modular components used were either the Trident implant (Stryker Howmedica Osteonics) or the ZTT-II implant (DePuy Synthes). Elliptic acetabular components have a peripheral flare, in contrast to true hemispheric acetabular components. Ten elliptic modular and 6 hemispheric modular components were implanted. In all cases, the difference between the final reamer used to prepare the acetabular bed and the true largest external diameter of the impacted shell was 2 mm or less.

The cohort’s 16 femoral components consisted of 8 Secur-Fit uncemented components (Stryker Howmedica Osteonics), 3 Accolade uncemented components (Stryker Howmedica Osteonics), 3 Omnifit EON cemented components (Stryker Howmedica Osteonics), and 2 S-ROM uncemented components (DePuy Synthes).

After surgery, all patients were followed up according to individual surgeon protocol for radiographic and physical examination.

Data on IAF incidence were obtained from a hospital database and were confirmed with electronic medical record (EMR) documentation. Also obtained were IAF causes and locations recorded in operative notes. For fractures identified after surgery, location was obtained from the immediate postoperative radiograph. Fracture management (eg, supplemental screw fixation, fracture reduction and fixation, bone grafting, acetabular component revision, protected weight-bearing) was determined from EMR documentation.

Results

Sixteen patients sustained an IAF in primary THA. All IAFs occurred in cases involving cementless acetabular components. The institution’s incidence of IAF with use of cementless components was 0.0007%.

Table.

Of the 5 IAFs (31%) identified during surgery, 4 were noted during impaction of the acetabular component, and 1 was noted during reaming. Eighty percent of these IAFs occurred directly posterior, and 60% were addressed at time of index procedure secondary to acetabular component instability. The other 11 fractures (69%) were identified on standard postoperative anteroposterior pelvis radiographs obtained in the postanesthesia care unit (PACU). Details of component characteristics, fracture location, immediate treatment, and weight-bearing precautions for all 16 patients are listed in the Table.

Figure 1.
The radiographs of patients 4 and 9, who were initially treated with observation, are presented in Figures 1A-1C and 2A-2C.
Figure 2.

There were additional complications. One patient sustained an intraoperative proximal femur fracture, which was addressed at the index THA with application of a cerclage wire and reinsertion of the femoral component; no further surgical intervention was required, and the femur fracture healed uneventfully. Another patient had a postoperative ileus that required nasogastric tube decompression and monitoring in the intensive care unit; the ileus resolved spontaneously. A third patient, initially treated with bone grafting and cemented cup insertion, was diagnosed with a periprosthetic joint infection 3 weeks after the index THA and was treated with explantation of all components and girdlestone resection arthroplasty; 1 month after the resection arthroplasty, a persistently draining wound was treated with irrigation and débridement. There were no other medical complications, thromboembolic events, or dislocations.

One to 7 weeks after surgery, patients returned for initial follow-up, and radiographs were obtained for component stability assessment. Three patients presented with gross acetabular instability, and revisions were performed. Standard clinical follow-up continued for all patients per individual surgeon protocol. Mean follow-up was 4 years.

Discussion

IAF is an uncommon complication of THA. The rarity of IAFs makes it difficult to obtain a cohort large enough to study the problem. Given the increasing incidence of primary THAs and the almost ubiquitous use of press-fit acetabular components, surgeons who perform THAs undoubtedly will encounter IAFs in their own practice. In this article, we report our institution’s experience with periprosthetic IAFs and provide a framework for making decisions regarding these complications.

Anatomical locations of IAFs have been associated with variable outcomes. In a 2015 series, Laflamme and colleagues6 found posterior column stability a crucial factor in implant stability. Fractures with posterior column instability had a 67% failure rate, and patients with an intact posterior column reliably had osteointegration occur without further intervention.6 In our series, fractures that violated the posterior column had similar results. All these fractures required further operative intervention, either at the index procedure or in the early postoperative period. Loss of posterior column stability prevents secure fixation of the acetabular component, thereby preventing successful hip reconstruction. One posterior column fracture in our series was not recognized until after surgery, on a PACU radiograph, and 1 posterior column fracture was fully appreciated only after postoperative computed tomography (CT) was obtained during immediate hospitalization after the index procedure. In both cases, conservative management was unsuccessful. Revision arthroplasty (and in 1 case late posterior column fixation) was performed to achieve adequate reconstruction. There were no failures after posterior column fixation. In cases of posterior wall or column fracture, we recommend early aggressive treatment, preferably at the time of index arthroplasty, to prevent catastrophic failure.

Most commonly, periprosthetic IAFs go unnoticed until initial postoperative radiographs are examined.6 Eleven of the 16 IAFs in our series were first recognized on radiographs obtained in the PACU. Surgeons thus have difficult decisions to make. The literature has little discussion on managing early postoperative periprosthetic IAFs. Most recent studies, which consist of small series and case reports, have focused on late and often traumatic IAFs.7-9 These were initially classified by Peterson and Lewallen10 as type I, which are stable radiographically (no movement relative to previous radiographs) and do not produce pain with minor movement of the extremity, or type II, which are unstable radiographically (gross displacement of component) or produce pain with any hip motion. Type I fractures were more common and were often managed with protected weight-bearing and observation. The authors concluded that, in type I fractures, retaining the original acetabular component is difficult; however, when these fractures are treated appropriately, a functional prosthesis can be salvaged, and fracture union can be expected.

Less common are acetabular fractures detected during surgery, as in our study. In an outcome series, Haidukewych and colleagues3 reported on 21 periprosthetic acetabular fractures, all recognized during surgery and managed according to perceived stability of the component. All fractures healed uneventfully, and there were no other complications.

These studies provide a framework for addressing IAFs noticed in the early postoperative period. The diagnostic dilemma presented by these fractures was first discussed by Laflamme and colleagues.6 Nine of the 32 fractures in their series were classified as so-called type III fractures, recognized only after the early postoperative period. Additional radiographs (eg, Judet views) or CT scans were crucial in determining acetabular component stability, given the known poor outcomes associated with posterior column fracture. In our series, only 1 patient had CT performed after intraoperative recognition of fracture, and the extent of the fracture was not readily apparent on the patient’s postoperative radiograph. Given the successful recognition and treatment of these fractures in the early postoperative period in our series,

it is difficult to recommend advanced imaging for all periprosthetic IAFs. Perhaps this success is attributable to our almost universal use of screws for acetabular component fixation. Of the 11 patients with fractures recognized during the postoperative period, 8 had supplemental screw fixation at time of index surgery. If there is a question of fixation during component insertion, we recommend scrutinizing the acetabular rim for fracture and placing supplemental screw fixation. Screws placed for acetabular component fixation provide initial stability and may prevent early component failure in the setting of unrecognized medial or anterior fracture. In addition, when component stability is in question after impaction, we recommend using finger palpation to evaluate the sciatic notch for cortical step-off from an otherwise unrecognized fracture. Protected weight-bearing in the postoperative period may be left to the discretion of the surgeon, and the decision should be based on intraoperative stability of the acetabular component.

In our series, there was a disproportionate representation of fractures associated with elliptic acetabular components. All 5 of the fractures recognized during surgery and 5 of the 11 recognized after surgery occurred with elliptic components. The association between elliptic cup design and periprosthetic IAF was identified earlier, by Haidukewych and colleagues.3 Their series showed a statistically significant increase in fracture incidence with impaction of an elliptic cup into a bed prepared with a hemispheric reamer. In the present series, 75% of our acetabular components were impacted into a bed underreamed by 1 mm to 2 mm. It is typical of many surgeons at our institution to underream by 1 mm to 2 mm regardless of the type of component being implanted, though they show a growing trend to overream by only 1 mm with the PSL component, which has been both safe and reliable in preventing catastrophic posterior column fractures, especially with impaction of small (<50 mm) acetabular components. We have not observed early loosening or other evidence of failure with this technique. Cup impaction generates significant hoop stresses that can easily fracture sclerotic or otherwise poor-quality bone, and the dense bone around the acetabular rim experiences increased stress with impaction of elliptic components.2,11-15 Surgeons must understand the design traits of their components and be cognizant of the true difference between the diameter of the final reamer used and the real diameter of the acetabular component. We recommend having a difference of ≤1 mm to mitigate the risk of IAF occurring with cup insertion. With use of elliptic components, slight overreaming of the acetabular bed should be considered. More study is needed to better define these outcomes.

Study Limitations

Our study had several limitations, including the inherent biases of its retrospective design, small cohort size, and inclusion of multiple surgeons. Small cohort size is unavoidable given the low incidence of these injuries, and our study encompassed the experience of a high-volume hip arthroplasty service. There is the possibility that a subset of fractures may have persistently gone unrecognized, either during or after surgery, and the actual incidence of these complications may be higher. These outcomes represent our institutional experience addressing the complexities of these injuries. The lack of standardization in the management of these fractures in our series reflects the diagnostic dilemma they present, as well as the need for more study focused on their management and outcomes.

Conclusion

IAF, an uncommon complication of primary THA, most commonly occurs during component impaction. Acetabular component and surgical technique may influence the fracture rate. Intraoperative or prompt postoperative recognition of these fractures is crucial, as their location is associated with stability and outcome. Careful examination of postoperative radiographs, judicious use of advanced imaging, and close follow-up are needed to prevent early catastrophic failure. We argue against simply observing these unstable fractures and recommend early treatment with rigid fixation and, when necessary, acetabular component revision.

References

1. Sharkey PF, Hozack WJ, Callaghan JJ, et al. Acetabular fractures associated with cementless acetabular cup insertion: a report of 13 cases. J Arthroplasty.1999;14(4):426-431.

2. Kim YS, Callaghan JJ, Ahn PB, Brown TD. Fracture of the acetabulum during insertion of an oversized hemispherical component. J Bone Joint Surg Am. 1995;77(1):111-117.

3. Haidukewych GJ, Jacofsky DJ, Hanssen AD, Lewallen DG. Intraoperative fractures of the acetabulum during primary total hip arthroplasty. J Bone Joint Surg Am. 2006;88(9):1952-1956.

4. Curtis MJ, Jinnah RH, Wilson VD, Hungerford DS. The initial stability of uncemented acetabular components. J Bone Joint Surg Br. 1992;74(3):372-376.

5. Lachiewicz PF, Suh PB, Gilbert JA. In vitro initial fixation of porous-coated acetabular total hip components. A biomechanical and comparative study. J Arthroplasty. 1989;4(3):201-205.

6. Laflamme GY, Belzile EL, Fernandes JC, Vendittoli PA, Hébert-Davies J. Periprosthetic fractures of the acetabulum during component insertion: posterior column stability
is crucial. J Arthroplasty. 2015;30(2):265-269.

7. Desai G, Reis MD. Early postoperative acetabular discontinuity after total hip arthroplasty. J Arthroplasty. 2011;26(8):1570.e17-e19.

8. Gelalis ID, Politis AN, Arnaoutoglou CM, Georgakopoulos N, Mitsiou D, Xenakis TA. Traumatic periprosthetic acetabular fracture treated by acute one-stage revision arthroplasty. A case report and review of the literature. Injury. 2010;41(4):421-424.

9. Gras F, Marintschev I, Klos K, Fujak A, Mückley T, Hofmann GO. Navigated percutaneous screw fixation of a periprosthetic acetabular fracture. J Arthroplasty. 2010;25(7):1169.e1-e4.

10. Peterson CA, Lewallen DG. Periprosthetic fracture of the acetabulum after total hip arthroplasty. J Bone Joint Surg Am. 1996;78(8):1206-1213.

11. Hansen TM, Koenman JB, Headley AK. 3-D FEM analysis of interface fixation of acetabular implants. Trans Orthop Res Soc. 1992;17:400.

12. Yerby SA, Taylor JK, Murzic WJ. Acetabular component interface: press-fit fixation. Trans Orthop Res Soc. 1992;17:384.

13. Callaghan JJ. The clinical results and basic science of total hip arthroplasty with porous-coated prostheses. J Bone Joint Surg Am. 1993;75(2):299-310.

14. Cheng SL, Binnington AG, Bragdon CR, Jasty M, Harris WH, Davey JR. The effect of sizing mismatch on bone ingrowth into uncemented porous coated acetabular components: an in vivo canine study. Trans Orthop Res Soc. 1990;15:442.

15. Morscher E, Bereiter H, Lampert C, Cementless press-fit cup: principles, experimental data, and three-year follow-up study. Clin Orthop Relat Res. 1989;(249):12-20.

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Take Home Points

  • IAF is an uncommon, but serious complication of primary THA.
  • Small (<50 mm) cups are at higher risk for causing IAF.
  • Prompt recognition is critical to prevent component migration and need for revision.
  • Posterior column integrity is cirtical to a successful outcome when IAF occurs.
  • Initial stable fixation, with or without intraoperative acetabular revision, is critical for successful outcome when IAF is identified.

Intraoperative acetabular fracture (IAF) is a rare complication of primary total hip arthroplasty (THA).1-3 IAFs commonly occur with impaction of the acetabular component. Studies have found that underreaming of the acetabulum and impaction of relatively large, elliptic, or monoblock components may increase the risk of IAFs.2-5 There is a paucity of literature on risk factors, treatment strategies, and outcomes of this potentially devastating complication.

In this article, we report on the incidence of IAF in primary THA at our high-volume institution and present strategies for managing and preventing this rare fracture.

Materials and Methods

Between 1997 and 2015, more than 20 fellowship-trained arthroplasty surgeons performed 21,519 primary THAs at our institution. After obtaining Institutional Review Board approval for this study, we retrospectively searched the hospital database and identified 16 patients (16 hips) who sustained an IAF in primary THA. Mean age of the cohort (13 women, 3 men) at time of surgery was 70 years (range, 42-89 years). Of the 16 patients, 13 had a preoperative diagnosis of osteoarthritis, 2 had posttraumatic arthritis, and 1 had rheumatoid arthritis. A posterolateral approach was used with 14 patients and a modified anterolateral approach with the other 2. Surgical technique and implant selection varied among surgeons. Thirteen THAs were performed with an all-press-fit technique and 3 with a hybrid technique (uncemented acetabular component, cemented femoral component). In 9 cases, the acetabular component underwent supplemental screw fixation. Whether to use acetabular component screws or cemented femoral components was decided intraoperatively by the surgeon.

The cohort’s acetabular components were either elliptic modular or hemispheric modular. The elliptic modular component used was the Peripheral Self-Locking (PSL) implant (Stryker Howmedica Osteonics), and the hemispheric modular components used were either the Trident implant (Stryker Howmedica Osteonics) or the ZTT-II implant (DePuy Synthes). Elliptic acetabular components have a peripheral flare, in contrast to true hemispheric acetabular components. Ten elliptic modular and 6 hemispheric modular components were implanted. In all cases, the difference between the final reamer used to prepare the acetabular bed and the true largest external diameter of the impacted shell was 2 mm or less.

The cohort’s 16 femoral components consisted of 8 Secur-Fit uncemented components (Stryker Howmedica Osteonics), 3 Accolade uncemented components (Stryker Howmedica Osteonics), 3 Omnifit EON cemented components (Stryker Howmedica Osteonics), and 2 S-ROM uncemented components (DePuy Synthes).

After surgery, all patients were followed up according to individual surgeon protocol for radiographic and physical examination.

Data on IAF incidence were obtained from a hospital database and were confirmed with electronic medical record (EMR) documentation. Also obtained were IAF causes and locations recorded in operative notes. For fractures identified after surgery, location was obtained from the immediate postoperative radiograph. Fracture management (eg, supplemental screw fixation, fracture reduction and fixation, bone grafting, acetabular component revision, protected weight-bearing) was determined from EMR documentation.

Results

Sixteen patients sustained an IAF in primary THA. All IAFs occurred in cases involving cementless acetabular components. The institution’s incidence of IAF with use of cementless components was 0.0007%.

Table.

Of the 5 IAFs (31%) identified during surgery, 4 were noted during impaction of the acetabular component, and 1 was noted during reaming. Eighty percent of these IAFs occurred directly posterior, and 60% were addressed at time of index procedure secondary to acetabular component instability. The other 11 fractures (69%) were identified on standard postoperative anteroposterior pelvis radiographs obtained in the postanesthesia care unit (PACU). Details of component characteristics, fracture location, immediate treatment, and weight-bearing precautions for all 16 patients are listed in the Table.

Figure 1.
The radiographs of patients 4 and 9, who were initially treated with observation, are presented in Figures 1A-1C and 2A-2C.
Figure 2.

There were additional complications. One patient sustained an intraoperative proximal femur fracture, which was addressed at the index THA with application of a cerclage wire and reinsertion of the femoral component; no further surgical intervention was required, and the femur fracture healed uneventfully. Another patient had a postoperative ileus that required nasogastric tube decompression and monitoring in the intensive care unit; the ileus resolved spontaneously. A third patient, initially treated with bone grafting and cemented cup insertion, was diagnosed with a periprosthetic joint infection 3 weeks after the index THA and was treated with explantation of all components and girdlestone resection arthroplasty; 1 month after the resection arthroplasty, a persistently draining wound was treated with irrigation and débridement. There were no other medical complications, thromboembolic events, or dislocations.

One to 7 weeks after surgery, patients returned for initial follow-up, and radiographs were obtained for component stability assessment. Three patients presented with gross acetabular instability, and revisions were performed. Standard clinical follow-up continued for all patients per individual surgeon protocol. Mean follow-up was 4 years.

Discussion

IAF is an uncommon complication of THA. The rarity of IAFs makes it difficult to obtain a cohort large enough to study the problem. Given the increasing incidence of primary THAs and the almost ubiquitous use of press-fit acetabular components, surgeons who perform THAs undoubtedly will encounter IAFs in their own practice. In this article, we report our institution’s experience with periprosthetic IAFs and provide a framework for making decisions regarding these complications.

Anatomical locations of IAFs have been associated with variable outcomes. In a 2015 series, Laflamme and colleagues6 found posterior column stability a crucial factor in implant stability. Fractures with posterior column instability had a 67% failure rate, and patients with an intact posterior column reliably had osteointegration occur without further intervention.6 In our series, fractures that violated the posterior column had similar results. All these fractures required further operative intervention, either at the index procedure or in the early postoperative period. Loss of posterior column stability prevents secure fixation of the acetabular component, thereby preventing successful hip reconstruction. One posterior column fracture in our series was not recognized until after surgery, on a PACU radiograph, and 1 posterior column fracture was fully appreciated only after postoperative computed tomography (CT) was obtained during immediate hospitalization after the index procedure. In both cases, conservative management was unsuccessful. Revision arthroplasty (and in 1 case late posterior column fixation) was performed to achieve adequate reconstruction. There were no failures after posterior column fixation. In cases of posterior wall or column fracture, we recommend early aggressive treatment, preferably at the time of index arthroplasty, to prevent catastrophic failure.

Most commonly, periprosthetic IAFs go unnoticed until initial postoperative radiographs are examined.6 Eleven of the 16 IAFs in our series were first recognized on radiographs obtained in the PACU. Surgeons thus have difficult decisions to make. The literature has little discussion on managing early postoperative periprosthetic IAFs. Most recent studies, which consist of small series and case reports, have focused on late and often traumatic IAFs.7-9 These were initially classified by Peterson and Lewallen10 as type I, which are stable radiographically (no movement relative to previous radiographs) and do not produce pain with minor movement of the extremity, or type II, which are unstable radiographically (gross displacement of component) or produce pain with any hip motion. Type I fractures were more common and were often managed with protected weight-bearing and observation. The authors concluded that, in type I fractures, retaining the original acetabular component is difficult; however, when these fractures are treated appropriately, a functional prosthesis can be salvaged, and fracture union can be expected.

Less common are acetabular fractures detected during surgery, as in our study. In an outcome series, Haidukewych and colleagues3 reported on 21 periprosthetic acetabular fractures, all recognized during surgery and managed according to perceived stability of the component. All fractures healed uneventfully, and there were no other complications.

These studies provide a framework for addressing IAFs noticed in the early postoperative period. The diagnostic dilemma presented by these fractures was first discussed by Laflamme and colleagues.6 Nine of the 32 fractures in their series were classified as so-called type III fractures, recognized only after the early postoperative period. Additional radiographs (eg, Judet views) or CT scans were crucial in determining acetabular component stability, given the known poor outcomes associated with posterior column fracture. In our series, only 1 patient had CT performed after intraoperative recognition of fracture, and the extent of the fracture was not readily apparent on the patient’s postoperative radiograph. Given the successful recognition and treatment of these fractures in the early postoperative period in our series,

it is difficult to recommend advanced imaging for all periprosthetic IAFs. Perhaps this success is attributable to our almost universal use of screws for acetabular component fixation. Of the 11 patients with fractures recognized during the postoperative period, 8 had supplemental screw fixation at time of index surgery. If there is a question of fixation during component insertion, we recommend scrutinizing the acetabular rim for fracture and placing supplemental screw fixation. Screws placed for acetabular component fixation provide initial stability and may prevent early component failure in the setting of unrecognized medial or anterior fracture. In addition, when component stability is in question after impaction, we recommend using finger palpation to evaluate the sciatic notch for cortical step-off from an otherwise unrecognized fracture. Protected weight-bearing in the postoperative period may be left to the discretion of the surgeon, and the decision should be based on intraoperative stability of the acetabular component.

In our series, there was a disproportionate representation of fractures associated with elliptic acetabular components. All 5 of the fractures recognized during surgery and 5 of the 11 recognized after surgery occurred with elliptic components. The association between elliptic cup design and periprosthetic IAF was identified earlier, by Haidukewych and colleagues.3 Their series showed a statistically significant increase in fracture incidence with impaction of an elliptic cup into a bed prepared with a hemispheric reamer. In the present series, 75% of our acetabular components were impacted into a bed underreamed by 1 mm to 2 mm. It is typical of many surgeons at our institution to underream by 1 mm to 2 mm regardless of the type of component being implanted, though they show a growing trend to overream by only 1 mm with the PSL component, which has been both safe and reliable in preventing catastrophic posterior column fractures, especially with impaction of small (<50 mm) acetabular components. We have not observed early loosening or other evidence of failure with this technique. Cup impaction generates significant hoop stresses that can easily fracture sclerotic or otherwise poor-quality bone, and the dense bone around the acetabular rim experiences increased stress with impaction of elliptic components.2,11-15 Surgeons must understand the design traits of their components and be cognizant of the true difference between the diameter of the final reamer used and the real diameter of the acetabular component. We recommend having a difference of ≤1 mm to mitigate the risk of IAF occurring with cup insertion. With use of elliptic components, slight overreaming of the acetabular bed should be considered. More study is needed to better define these outcomes.

Study Limitations

Our study had several limitations, including the inherent biases of its retrospective design, small cohort size, and inclusion of multiple surgeons. Small cohort size is unavoidable given the low incidence of these injuries, and our study encompassed the experience of a high-volume hip arthroplasty service. There is the possibility that a subset of fractures may have persistently gone unrecognized, either during or after surgery, and the actual incidence of these complications may be higher. These outcomes represent our institutional experience addressing the complexities of these injuries. The lack of standardization in the management of these fractures in our series reflects the diagnostic dilemma they present, as well as the need for more study focused on their management and outcomes.

Conclusion

IAF, an uncommon complication of primary THA, most commonly occurs during component impaction. Acetabular component and surgical technique may influence the fracture rate. Intraoperative or prompt postoperative recognition of these fractures is crucial, as their location is associated with stability and outcome. Careful examination of postoperative radiographs, judicious use of advanced imaging, and close follow-up are needed to prevent early catastrophic failure. We argue against simply observing these unstable fractures and recommend early treatment with rigid fixation and, when necessary, acetabular component revision.

Take Home Points

  • IAF is an uncommon, but serious complication of primary THA.
  • Small (<50 mm) cups are at higher risk for causing IAF.
  • Prompt recognition is critical to prevent component migration and need for revision.
  • Posterior column integrity is cirtical to a successful outcome when IAF occurs.
  • Initial stable fixation, with or without intraoperative acetabular revision, is critical for successful outcome when IAF is identified.

Intraoperative acetabular fracture (IAF) is a rare complication of primary total hip arthroplasty (THA).1-3 IAFs commonly occur with impaction of the acetabular component. Studies have found that underreaming of the acetabulum and impaction of relatively large, elliptic, or monoblock components may increase the risk of IAFs.2-5 There is a paucity of literature on risk factors, treatment strategies, and outcomes of this potentially devastating complication.

In this article, we report on the incidence of IAF in primary THA at our high-volume institution and present strategies for managing and preventing this rare fracture.

Materials and Methods

Between 1997 and 2015, more than 20 fellowship-trained arthroplasty surgeons performed 21,519 primary THAs at our institution. After obtaining Institutional Review Board approval for this study, we retrospectively searched the hospital database and identified 16 patients (16 hips) who sustained an IAF in primary THA. Mean age of the cohort (13 women, 3 men) at time of surgery was 70 years (range, 42-89 years). Of the 16 patients, 13 had a preoperative diagnosis of osteoarthritis, 2 had posttraumatic arthritis, and 1 had rheumatoid arthritis. A posterolateral approach was used with 14 patients and a modified anterolateral approach with the other 2. Surgical technique and implant selection varied among surgeons. Thirteen THAs were performed with an all-press-fit technique and 3 with a hybrid technique (uncemented acetabular component, cemented femoral component). In 9 cases, the acetabular component underwent supplemental screw fixation. Whether to use acetabular component screws or cemented femoral components was decided intraoperatively by the surgeon.

The cohort’s acetabular components were either elliptic modular or hemispheric modular. The elliptic modular component used was the Peripheral Self-Locking (PSL) implant (Stryker Howmedica Osteonics), and the hemispheric modular components used were either the Trident implant (Stryker Howmedica Osteonics) or the ZTT-II implant (DePuy Synthes). Elliptic acetabular components have a peripheral flare, in contrast to true hemispheric acetabular components. Ten elliptic modular and 6 hemispheric modular components were implanted. In all cases, the difference between the final reamer used to prepare the acetabular bed and the true largest external diameter of the impacted shell was 2 mm or less.

The cohort’s 16 femoral components consisted of 8 Secur-Fit uncemented components (Stryker Howmedica Osteonics), 3 Accolade uncemented components (Stryker Howmedica Osteonics), 3 Omnifit EON cemented components (Stryker Howmedica Osteonics), and 2 S-ROM uncemented components (DePuy Synthes).

After surgery, all patients were followed up according to individual surgeon protocol for radiographic and physical examination.

Data on IAF incidence were obtained from a hospital database and were confirmed with electronic medical record (EMR) documentation. Also obtained were IAF causes and locations recorded in operative notes. For fractures identified after surgery, location was obtained from the immediate postoperative radiograph. Fracture management (eg, supplemental screw fixation, fracture reduction and fixation, bone grafting, acetabular component revision, protected weight-bearing) was determined from EMR documentation.

Results

Sixteen patients sustained an IAF in primary THA. All IAFs occurred in cases involving cementless acetabular components. The institution’s incidence of IAF with use of cementless components was 0.0007%.

Table.

Of the 5 IAFs (31%) identified during surgery, 4 were noted during impaction of the acetabular component, and 1 was noted during reaming. Eighty percent of these IAFs occurred directly posterior, and 60% were addressed at time of index procedure secondary to acetabular component instability. The other 11 fractures (69%) were identified on standard postoperative anteroposterior pelvis radiographs obtained in the postanesthesia care unit (PACU). Details of component characteristics, fracture location, immediate treatment, and weight-bearing precautions for all 16 patients are listed in the Table.

Figure 1.
The radiographs of patients 4 and 9, who were initially treated with observation, are presented in Figures 1A-1C and 2A-2C.
Figure 2.

There were additional complications. One patient sustained an intraoperative proximal femur fracture, which was addressed at the index THA with application of a cerclage wire and reinsertion of the femoral component; no further surgical intervention was required, and the femur fracture healed uneventfully. Another patient had a postoperative ileus that required nasogastric tube decompression and monitoring in the intensive care unit; the ileus resolved spontaneously. A third patient, initially treated with bone grafting and cemented cup insertion, was diagnosed with a periprosthetic joint infection 3 weeks after the index THA and was treated with explantation of all components and girdlestone resection arthroplasty; 1 month after the resection arthroplasty, a persistently draining wound was treated with irrigation and débridement. There were no other medical complications, thromboembolic events, or dislocations.

One to 7 weeks after surgery, patients returned for initial follow-up, and radiographs were obtained for component stability assessment. Three patients presented with gross acetabular instability, and revisions were performed. Standard clinical follow-up continued for all patients per individual surgeon protocol. Mean follow-up was 4 years.

Discussion

IAF is an uncommon complication of THA. The rarity of IAFs makes it difficult to obtain a cohort large enough to study the problem. Given the increasing incidence of primary THAs and the almost ubiquitous use of press-fit acetabular components, surgeons who perform THAs undoubtedly will encounter IAFs in their own practice. In this article, we report our institution’s experience with periprosthetic IAFs and provide a framework for making decisions regarding these complications.

Anatomical locations of IAFs have been associated with variable outcomes. In a 2015 series, Laflamme and colleagues6 found posterior column stability a crucial factor in implant stability. Fractures with posterior column instability had a 67% failure rate, and patients with an intact posterior column reliably had osteointegration occur without further intervention.6 In our series, fractures that violated the posterior column had similar results. All these fractures required further operative intervention, either at the index procedure or in the early postoperative period. Loss of posterior column stability prevents secure fixation of the acetabular component, thereby preventing successful hip reconstruction. One posterior column fracture in our series was not recognized until after surgery, on a PACU radiograph, and 1 posterior column fracture was fully appreciated only after postoperative computed tomography (CT) was obtained during immediate hospitalization after the index procedure. In both cases, conservative management was unsuccessful. Revision arthroplasty (and in 1 case late posterior column fixation) was performed to achieve adequate reconstruction. There were no failures after posterior column fixation. In cases of posterior wall or column fracture, we recommend early aggressive treatment, preferably at the time of index arthroplasty, to prevent catastrophic failure.

Most commonly, periprosthetic IAFs go unnoticed until initial postoperative radiographs are examined.6 Eleven of the 16 IAFs in our series were first recognized on radiographs obtained in the PACU. Surgeons thus have difficult decisions to make. The literature has little discussion on managing early postoperative periprosthetic IAFs. Most recent studies, which consist of small series and case reports, have focused on late and often traumatic IAFs.7-9 These were initially classified by Peterson and Lewallen10 as type I, which are stable radiographically (no movement relative to previous radiographs) and do not produce pain with minor movement of the extremity, or type II, which are unstable radiographically (gross displacement of component) or produce pain with any hip motion. Type I fractures were more common and were often managed with protected weight-bearing and observation. The authors concluded that, in type I fractures, retaining the original acetabular component is difficult; however, when these fractures are treated appropriately, a functional prosthesis can be salvaged, and fracture union can be expected.

Less common are acetabular fractures detected during surgery, as in our study. In an outcome series, Haidukewych and colleagues3 reported on 21 periprosthetic acetabular fractures, all recognized during surgery and managed according to perceived stability of the component. All fractures healed uneventfully, and there were no other complications.

These studies provide a framework for addressing IAFs noticed in the early postoperative period. The diagnostic dilemma presented by these fractures was first discussed by Laflamme and colleagues.6 Nine of the 32 fractures in their series were classified as so-called type III fractures, recognized only after the early postoperative period. Additional radiographs (eg, Judet views) or CT scans were crucial in determining acetabular component stability, given the known poor outcomes associated with posterior column fracture. In our series, only 1 patient had CT performed after intraoperative recognition of fracture, and the extent of the fracture was not readily apparent on the patient’s postoperative radiograph. Given the successful recognition and treatment of these fractures in the early postoperative period in our series,

it is difficult to recommend advanced imaging for all periprosthetic IAFs. Perhaps this success is attributable to our almost universal use of screws for acetabular component fixation. Of the 11 patients with fractures recognized during the postoperative period, 8 had supplemental screw fixation at time of index surgery. If there is a question of fixation during component insertion, we recommend scrutinizing the acetabular rim for fracture and placing supplemental screw fixation. Screws placed for acetabular component fixation provide initial stability and may prevent early component failure in the setting of unrecognized medial or anterior fracture. In addition, when component stability is in question after impaction, we recommend using finger palpation to evaluate the sciatic notch for cortical step-off from an otherwise unrecognized fracture. Protected weight-bearing in the postoperative period may be left to the discretion of the surgeon, and the decision should be based on intraoperative stability of the acetabular component.

In our series, there was a disproportionate representation of fractures associated with elliptic acetabular components. All 5 of the fractures recognized during surgery and 5 of the 11 recognized after surgery occurred with elliptic components. The association between elliptic cup design and periprosthetic IAF was identified earlier, by Haidukewych and colleagues.3 Their series showed a statistically significant increase in fracture incidence with impaction of an elliptic cup into a bed prepared with a hemispheric reamer. In the present series, 75% of our acetabular components were impacted into a bed underreamed by 1 mm to 2 mm. It is typical of many surgeons at our institution to underream by 1 mm to 2 mm regardless of the type of component being implanted, though they show a growing trend to overream by only 1 mm with the PSL component, which has been both safe and reliable in preventing catastrophic posterior column fractures, especially with impaction of small (<50 mm) acetabular components. We have not observed early loosening or other evidence of failure with this technique. Cup impaction generates significant hoop stresses that can easily fracture sclerotic or otherwise poor-quality bone, and the dense bone around the acetabular rim experiences increased stress with impaction of elliptic components.2,11-15 Surgeons must understand the design traits of their components and be cognizant of the true difference between the diameter of the final reamer used and the real diameter of the acetabular component. We recommend having a difference of ≤1 mm to mitigate the risk of IAF occurring with cup insertion. With use of elliptic components, slight overreaming of the acetabular bed should be considered. More study is needed to better define these outcomes.

Study Limitations

Our study had several limitations, including the inherent biases of its retrospective design, small cohort size, and inclusion of multiple surgeons. Small cohort size is unavoidable given the low incidence of these injuries, and our study encompassed the experience of a high-volume hip arthroplasty service. There is the possibility that a subset of fractures may have persistently gone unrecognized, either during or after surgery, and the actual incidence of these complications may be higher. These outcomes represent our institutional experience addressing the complexities of these injuries. The lack of standardization in the management of these fractures in our series reflects the diagnostic dilemma they present, as well as the need for more study focused on their management and outcomes.

Conclusion

IAF, an uncommon complication of primary THA, most commonly occurs during component impaction. Acetabular component and surgical technique may influence the fracture rate. Intraoperative or prompt postoperative recognition of these fractures is crucial, as their location is associated with stability and outcome. Careful examination of postoperative radiographs, judicious use of advanced imaging, and close follow-up are needed to prevent early catastrophic failure. We argue against simply observing these unstable fractures and recommend early treatment with rigid fixation and, when necessary, acetabular component revision.

References

1. Sharkey PF, Hozack WJ, Callaghan JJ, et al. Acetabular fractures associated with cementless acetabular cup insertion: a report of 13 cases. J Arthroplasty.1999;14(4):426-431.

2. Kim YS, Callaghan JJ, Ahn PB, Brown TD. Fracture of the acetabulum during insertion of an oversized hemispherical component. J Bone Joint Surg Am. 1995;77(1):111-117.

3. Haidukewych GJ, Jacofsky DJ, Hanssen AD, Lewallen DG. Intraoperative fractures of the acetabulum during primary total hip arthroplasty. J Bone Joint Surg Am. 2006;88(9):1952-1956.

4. Curtis MJ, Jinnah RH, Wilson VD, Hungerford DS. The initial stability of uncemented acetabular components. J Bone Joint Surg Br. 1992;74(3):372-376.

5. Lachiewicz PF, Suh PB, Gilbert JA. In vitro initial fixation of porous-coated acetabular total hip components. A biomechanical and comparative study. J Arthroplasty. 1989;4(3):201-205.

6. Laflamme GY, Belzile EL, Fernandes JC, Vendittoli PA, Hébert-Davies J. Periprosthetic fractures of the acetabulum during component insertion: posterior column stability
is crucial. J Arthroplasty. 2015;30(2):265-269.

7. Desai G, Reis MD. Early postoperative acetabular discontinuity after total hip arthroplasty. J Arthroplasty. 2011;26(8):1570.e17-e19.

8. Gelalis ID, Politis AN, Arnaoutoglou CM, Georgakopoulos N, Mitsiou D, Xenakis TA. Traumatic periprosthetic acetabular fracture treated by acute one-stage revision arthroplasty. A case report and review of the literature. Injury. 2010;41(4):421-424.

9. Gras F, Marintschev I, Klos K, Fujak A, Mückley T, Hofmann GO. Navigated percutaneous screw fixation of a periprosthetic acetabular fracture. J Arthroplasty. 2010;25(7):1169.e1-e4.

10. Peterson CA, Lewallen DG. Periprosthetic fracture of the acetabulum after total hip arthroplasty. J Bone Joint Surg Am. 1996;78(8):1206-1213.

11. Hansen TM, Koenman JB, Headley AK. 3-D FEM analysis of interface fixation of acetabular implants. Trans Orthop Res Soc. 1992;17:400.

12. Yerby SA, Taylor JK, Murzic WJ. Acetabular component interface: press-fit fixation. Trans Orthop Res Soc. 1992;17:384.

13. Callaghan JJ. The clinical results and basic science of total hip arthroplasty with porous-coated prostheses. J Bone Joint Surg Am. 1993;75(2):299-310.

14. Cheng SL, Binnington AG, Bragdon CR, Jasty M, Harris WH, Davey JR. The effect of sizing mismatch on bone ingrowth into uncemented porous coated acetabular components: an in vivo canine study. Trans Orthop Res Soc. 1990;15:442.

15. Morscher E, Bereiter H, Lampert C, Cementless press-fit cup: principles, experimental data, and three-year follow-up study. Clin Orthop Relat Res. 1989;(249):12-20.

References

1. Sharkey PF, Hozack WJ, Callaghan JJ, et al. Acetabular fractures associated with cementless acetabular cup insertion: a report of 13 cases. J Arthroplasty.1999;14(4):426-431.

2. Kim YS, Callaghan JJ, Ahn PB, Brown TD. Fracture of the acetabulum during insertion of an oversized hemispherical component. J Bone Joint Surg Am. 1995;77(1):111-117.

3. Haidukewych GJ, Jacofsky DJ, Hanssen AD, Lewallen DG. Intraoperative fractures of the acetabulum during primary total hip arthroplasty. J Bone Joint Surg Am. 2006;88(9):1952-1956.

4. Curtis MJ, Jinnah RH, Wilson VD, Hungerford DS. The initial stability of uncemented acetabular components. J Bone Joint Surg Br. 1992;74(3):372-376.

5. Lachiewicz PF, Suh PB, Gilbert JA. In vitro initial fixation of porous-coated acetabular total hip components. A biomechanical and comparative study. J Arthroplasty. 1989;4(3):201-205.

6. Laflamme GY, Belzile EL, Fernandes JC, Vendittoli PA, Hébert-Davies J. Periprosthetic fractures of the acetabulum during component insertion: posterior column stability
is crucial. J Arthroplasty. 2015;30(2):265-269.

7. Desai G, Reis MD. Early postoperative acetabular discontinuity after total hip arthroplasty. J Arthroplasty. 2011;26(8):1570.e17-e19.

8. Gelalis ID, Politis AN, Arnaoutoglou CM, Georgakopoulos N, Mitsiou D, Xenakis TA. Traumatic periprosthetic acetabular fracture treated by acute one-stage revision arthroplasty. A case report and review of the literature. Injury. 2010;41(4):421-424.

9. Gras F, Marintschev I, Klos K, Fujak A, Mückley T, Hofmann GO. Navigated percutaneous screw fixation of a periprosthetic acetabular fracture. J Arthroplasty. 2010;25(7):1169.e1-e4.

10. Peterson CA, Lewallen DG. Periprosthetic fracture of the acetabulum after total hip arthroplasty. J Bone Joint Surg Am. 1996;78(8):1206-1213.

11. Hansen TM, Koenman JB, Headley AK. 3-D FEM analysis of interface fixation of acetabular implants. Trans Orthop Res Soc. 1992;17:400.

12. Yerby SA, Taylor JK, Murzic WJ. Acetabular component interface: press-fit fixation. Trans Orthop Res Soc. 1992;17:384.

13. Callaghan JJ. The clinical results and basic science of total hip arthroplasty with porous-coated prostheses. J Bone Joint Surg Am. 1993;75(2):299-310.

14. Cheng SL, Binnington AG, Bragdon CR, Jasty M, Harris WH, Davey JR. The effect of sizing mismatch on bone ingrowth into uncemented porous coated acetabular components: an in vivo canine study. Trans Orthop Res Soc. 1990;15:442.

15. Morscher E, Bereiter H, Lampert C, Cementless press-fit cup: principles, experimental data, and three-year follow-up study. Clin Orthop Relat Res. 1989;(249):12-20.

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Comparison of Lateral Retinaculum Release and Lengthening in the Treatment of Patellofemoral Disorders

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Take-Home Points

  • Understanding the indications for treatment is essential.
  • Identifying the superficial (oblique fibers) and deep layers (transverse fibers) of the LR is very important and can lengthen the LR by as much as 20 mm.
  • Open procedures reduce the risk of hematomas and related pain.
  • The goal is to obtain 1 or 2 patellar quadrants of medial and lateral patellar glide in extensino and a neutral patella.
  • If the Z-plasty is combined with the MPFL reconstruction or tibial tubercle transfer, the LR is set to length after the tubercle transfer and before the MPFL reconstruction (to avoid overconstraint).

Anterior knee pain is a common clinical problem that can be challenging to correct, in large part because of multiple causative factors, including structural/anatomical, functional, alignment, and neuroperception/pain pathway factors. One difficult aspect of anatomical assessment is judging the soft-tissue balance between the medial restraints (medial patellofemoral ligament [MPFL]; medial quadriceps tendon to femoral ligament; medial patellotibial and patellomeniscal ligaments) and the lateral restraints (lateral retinaculum [LR] specifically). Both LR tightness and patellar instability can be interpreted as anterior knee pain. Differentiating these entities is one of the most difficult clinical challenges in orthopedics.

LR release (LRR) has been found to improve patellar mobility and tracking.1 In the absence of clearly defined guidelines, the procedure quickly gained in popularity because of its technical simplicity and the enticing "one tool fits all" treatment approach suggested in early reviews. Injudicious use of LRR, alone or in combination with other procedures, led to iatrogenic instability and chronic pain. LR lengthening (LRL) was introduced to address LR tightness while maintaining lateral soft-tissue integrity and avoiding some of the severe complications of LRR.2

Today, isolated use of LRR/LRL is recommended only for treatment of LR tightness and pain secondary to lateral patellar hypercompression.3 It can also be used as an adjunct treatment in the setting of patellofemoral instability. LRR/LRL should never be used as primary treatment for patellofemoral instability.

In this review of treatments for LR tightness and patellofemoral disorders, we compare the use of LRR and LRL.

Discussion

LR procedures are indicated for LR tightness, which is assessed by taking a history, performing a physical examination, and obtaining diagnostic imaging. Decisions should be based on all findings considered together and never on imaging findings alone.

Physical Examination

The physical examination should include assessment of limb alignment, patellar mobility, muscle balance, and dynamic patellar tracking.

Limb Alignment. Abnormal valgus, rotational deformities, and increased Q-angle are associated with LR tightness. Valgus alignment can be assessed on standing inspection; rotational deformities with increased hip anteversion by hip motion with the patient in the prone position (increased hip internal rotation, decreased hip external rotation); and Q-angle on weight-bearing standing examination and with the patient flexing and extending the knee while seated.

Patellar Mobility. The patellar glide and tilt tests provide the most direct evaluations of LR tightness. Medial displacement of <1 quadrant is consistent with tightness, and displacement of >3 quadrants is consistent with laxity. In full extension, the patellar glide test evaluates only the soft-tissue restraints; at 30° flexion, it also evaluates patellofemoral engagement. The patellar tilt test measures the lifting of the lateral edge of the patella. With normal elevation being 0° to 20°, lack of patellar tilt means the LR is tight, and tilt of >20° means it is loose. MPFL patency can be examined with the Lachman test; the examiner rapidly moves the patella laterally while feeling for the characteristic hard endpoint of lateral translation.

Muscle Balance. The tone, strength, and tightness of the core (abdomen, dorsal, and hip muscles) and lower extremities (quadriceps, hamstrings, gastrocnemius) should be evaluated.

Dynamic Patellar Tracking. The J-sign is the course (shaped like an inverted J) that the patella takes when it is medialized into the trochlea from its laterally displaced resting position as the knee goes from full extension to flexion. The J-sign can be associated with LR tightness, trochlear dysplasia, and patella alta.

Imaging

Although we cannot provide a comprehensive review of the imaging literature, the following radiologic examinations should be used to assess the patellofemoral joint.

30° Lateral Radiograph.  Increased tilt is seen when the lateral facet is not anterior to the patellar ridge. Also evaluated are trochlear anatomy, patellar height, and other factors involved in patellofemoral disorders.

30° Flexed Axial (Merchant) Radiograph. Patellar tilt, subluxation, and trochlear dysplasia are evaluated. Images obtained with progressive flexion can be very useful in verifying patellar tilt reduction. Lack of reduction during early flexion suggests LR tightness.4

Alignment Axial Radiographs (Scanogram). Valgus alignment is assessed with this full-length, standing, long-leg examination.

Computed Tomography/Magnetic Resonance Imaging. Many parameters of patellar alignment have been described. Basic assessment should include evaluation of patellar tilt, angle by the line across posterior condyles and a line through the greatest patellar width (>20° indicates abnormality and LR tightness) and tibial tubercle-trochlear groove distance (computed tomography or magnetic resonance imaging scan of the knee is used to measure this distance, and to confirm a significant amount in light of complex patellofemoral malalignment5).

Indications

Lateral compression syndrome with LR tightness is often successfully treated with isolated LRR, and results are reproducible and predictable.6 Surgical intervention for patellofemoral pain should be undertaken only after failed extensive nonoperative treatment with physical therapy and bracing/taping. Patients with LR tightness on preoperative examination, lateral patellar tilt on imaging, and normal Q-angle can obtain satisfactory results with this procedure. Patellar subluxation or dislocation history, high Q-angle (>20°), grade 3 or 4 chondral injury, and patellofemoral arthritis are associated with poorer outcomes when the procedure is performed in isolation.6International Patellofemoral Study Group members agreed that LRR/LRL is a valid treatment option when indicated, but it is rarely performed in isolation and constitutes only 1% to 2% of surgeries performed by this group of experts.7 When lateral compression syndrome progresses to arthritis, LRR/LRL can be performed with lateral patella facetectomy for maximal improvement.4 In the setting of patellofemoral instability, LRR/LRL can be combined with proximal and/or distal realignment surgery if the LR is tight. The LR is the last line of defense limiting lateral translation in the setting of an incompetent MPFL. Isolated LRR/LRL in the setting of instability further destabilizes the patella and worsens the instability. Therefore, LRR/LRL
is a poor surgical option as an isolated procedure for this condition and should be used only as an adjunct in cases of patellofemoral instability with LR tightness that does not allow the patella to be centralized into the trochlea.8 LRR/LRL can also be performed to improve patellar tracking in patello­femoral arthroplasty and total knee arthroplasty.

Lateral Retinaculum Release Versus Lengthening

LRR was first described for the treatment of patellar instability in 1891.9 It was also used for the treatment of lateral patellar hypercompression syndrome associated with LR tightness that led to lateral patellar tracking, joint overload, degeneration, and anterior knee pain.10 Metcalf10 further popularized the procedure by describing a minimally invasive arthroscopic version. However, the arthroscopic technique is as aggressive as the open technique and may be performed with less control, potentially making its results more variable. As proximal and distal releases are performed from the "inside out," more capsule and muscle disruption is needed to release the more superficial layers.

Z-plasty lengthening of the LR was described as an alternative for maintaining lateral patellar soft-tissue integrity while reducing the tension of the lateral tissue restraints.3 This is our preferred method.

Performing LRL instead of LRR avoids iatrogenic medial patellar instability, avoids overrelease and muscle injury, and improves soft-tissue balance.3 Open release or lengthening reduces inadvertent injury to the lateral superior/inferior geniculate arteries and allows direct hemostasis. Two prospective randomized studies found functional knee outcomes and return to athletic activities were improved more after LRL than LRR.11,12 These procedures had similar rates of postoperative knee stiffness, decreased muscle mass, and decreased strength. Each prospective study used an extensive LRR technique for LRR cases (various authors have recommended performing the release until the patella is perpendicular to the trochlea), which may have affected outcomes. In any case, with lengthening, the surgeon is less likely to excessively disrupt the lateral tissues.

Lateral Retinaculum Release.  LRR can be openly performed by lateral parapatellar incision,1 a mini-open percutaneous technique, or arthroscopy. For these open techniques, incisions of various sizes have been used to access the LR and incise it about 1 cm lateral to the patella starting at the distal end of the vastus lateralis and extending distally until patellar tilt reduction is sufficient. If tightness in deep flexion persists, the LRR can be extended distally to the tibial tubercle. Open techniques have the advantage of sparing the joint capsule. All-arthroscopic techniques involve using electrocautery to cut through the capsule and access the LR.

Lateral Retinaculum Lengthening. 

The LR is sharply divided into a superficial layer of superficial oblique fibers from the anterior iliotibial band and a deep layer of transverse fibers from the femur. For LRR, these 2 layers must be identified separate from the articular capsule.13

Figure 1.
Figure 1 illustrates the anatomy and the essential steps of the procedure. The fascia lata is carefully removed over the lateral patella, releasing some lateral tension and helping in the identification of the superficial and deep layers. The proximal lateral soft tissues of the patella are exposed, and the outer oblique layer of the LR is incised near the lateral border of the patella (Figure 2).
Figure 2.
The incision begins around the level of the proximal patellar pole and extends distally to the inferior patellar pole. The superficial oblique fibers of the LR are sharply dissected from the deep transverse fibers and are elevated as dissection is carried posteriorly to the posterior-most extent of the retinacular envelope, usually 1 cm to 2 cm (Figure 3). T
Figure 3.
he deep transverse fibers are then incised longitudinally (Figure 4). In many cases, a capsule that adheres to the deep layer can be separated from it. In cases with combined tibial tubercle transfers, the capsule is incised in order to mobilize the patella medially or distally.
Figure 4.
Then, the knee is moved through its full range of motion, positioned in 30° flexion, and engaged into the trochlear groove. The length of both the MPFL and the LR can then be adjusted. The cut edges of the superior oblique and deep transverse fibers are then sutured together with absorbable suture, and the appropriate amount of lengthening is performed to remove excess tension in lateral structures while maintaining lateral soft-tissue integrity (Figure 5).
Figure 5.
Neither the MPFL nor the LR is tensioned; rather, their lengths are adjusted, as they act as checkreins guiding the patella. If this procedure is performed with tibial tubercle transfer (medial and/or distal) or MPFL reconstruction, tubercle fixation is done first; next, MPFL length and then LR length are set.

Complications

Complications of performing LRR/LRL to change the lateral restraint include medial patellar instability, increased lateral pain, repair failure, recurrent lateral instability, quadriceps weakness and atrophy, postoperative hemarthrosis, knee stiffness, wound complications, and thermal skin injury.7 These complications often result from poor surgical technique and too aggressive release. Although recommended patellar tilt historically has varied from 45° to 90°, the current goal is to normalize the tight soft-tissue restraints without creating secondary instability.

The most significant complication of LRR is medial patellar instability caused by muscle atrophy and loss of soft-tissue restraint.14 Medial instability can be difficult to diagnose and should be considered in any patient with patellofemoral pain, popping, or patellar instability after LRR.15 A positive medial subluxation test or medial patellar apprehension test suggests medial instability.

Medial patellar instability usually requires surgical treatment. Direct LR repair, lateral soft-tissue reconstruction, and other procedures can be used to restore lateral restraint.15 However, these are salvage techniques, and patients often remain significantly limited by pain or instability. Therefore, the LR must be carefully addressed and preferably should undergo lengthening rather than release.

References

1. Merchant AC, Mercer RL. Lateral release of the patella. A preliminary report. Clin Orthop Relat Res. 1974;(103):40-45.

2. Ceder LC, Larson RL. Z-plasty lateral retinacular release for the treatment of patellar compression syndrome. Clin Orthop Relat Res. 1979;(144):110-113.

3. Biedert R. Lateral patellar hypercompression, tilt and mild lateral subluxation. In: Biedert R, ed. Patellofemoral Disorders. Chichester, England: Wiley; 2004:161-166.

4. Hinckel BB, Arendt EA. Lateral retinaculum lengthening or release. Oper Tech Sports Med. 2015;23(2):100-106.

5. Seitlinger G, Scheurecker G, Högler R, Labey L, Innocenti B, Hofmann S. Tibial tubercle–posterior cruciate ligament distance: a new measurement to define the position of the tibial tubercle in patients with patellar dislocation. Am J Sports Med. 2012;40(5):1119-1125.

6. Lattermann C, Toth J, Bach BR Jr. The role of lateral retinacular release in the treatment of patellar instability. Sports Med Arthrosc. 2007;15(2):57-60.

7. Fithian DC, Paxton EW, Post WR, Panni AS; International Patellofemoral Study Group. Lateral retinacular release: a survey of the International Patellofemoral Study Group. Arthroscopy. 2004;20(5):463-468.

8. Christoforakis J, Bull AM, Strachan RK, Shymkiw R, Senavongse W, Amis AA. Effects of lateral retinacular release on the lateral stability of the patella. Knee Surg Sports Traumatol Arthrosc. 2006;14(3):273-277.

9. Pollard B. Old dislocation of patella by intra-articular operation. Lancet. 1891;(988):17-22.

10. Metcalf RW. An arthroscopic method for lateral release of subluxating or dislocating patella. Clin Orthop Relat Res. 1982;167:9-18.

11. Pagenstert G, Wolf N, Bachmann M, et al. Open lateral patellar retinacular lengthening versus open retinacular release in lateral patellar hypercompression syndrome: a prospective double-blinded comparative study on complications and outcome. Arthroscopy. 2012;28(6):788-797.

12. O’Neill DB. Open lateral retinacular lengthening compared with arthroscopic release. A prospective, randomized outcome study. J Bone Joint Surg Am. 1997;79(12):1759-1769.

13. Merican AM, Amis AA. Anatomy of the lateral retinaculum of the knee. J Bone Joint Surg Br. 2008;90(4):527-534.

14. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.

15. McCarthy MA, Bollier MJ. Medial patella subluxation: diagnosis and treatment. Iowa Orthop J. 2015;35:26-33.

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Take-Home Points

  • Understanding the indications for treatment is essential.
  • Identifying the superficial (oblique fibers) and deep layers (transverse fibers) of the LR is very important and can lengthen the LR by as much as 20 mm.
  • Open procedures reduce the risk of hematomas and related pain.
  • The goal is to obtain 1 or 2 patellar quadrants of medial and lateral patellar glide in extensino and a neutral patella.
  • If the Z-plasty is combined with the MPFL reconstruction or tibial tubercle transfer, the LR is set to length after the tubercle transfer and before the MPFL reconstruction (to avoid overconstraint).

Anterior knee pain is a common clinical problem that can be challenging to correct, in large part because of multiple causative factors, including structural/anatomical, functional, alignment, and neuroperception/pain pathway factors. One difficult aspect of anatomical assessment is judging the soft-tissue balance between the medial restraints (medial patellofemoral ligament [MPFL]; medial quadriceps tendon to femoral ligament; medial patellotibial and patellomeniscal ligaments) and the lateral restraints (lateral retinaculum [LR] specifically). Both LR tightness and patellar instability can be interpreted as anterior knee pain. Differentiating these entities is one of the most difficult clinical challenges in orthopedics.

LR release (LRR) has been found to improve patellar mobility and tracking.1 In the absence of clearly defined guidelines, the procedure quickly gained in popularity because of its technical simplicity and the enticing "one tool fits all" treatment approach suggested in early reviews. Injudicious use of LRR, alone or in combination with other procedures, led to iatrogenic instability and chronic pain. LR lengthening (LRL) was introduced to address LR tightness while maintaining lateral soft-tissue integrity and avoiding some of the severe complications of LRR.2

Today, isolated use of LRR/LRL is recommended only for treatment of LR tightness and pain secondary to lateral patellar hypercompression.3 It can also be used as an adjunct treatment in the setting of patellofemoral instability. LRR/LRL should never be used as primary treatment for patellofemoral instability.

In this review of treatments for LR tightness and patellofemoral disorders, we compare the use of LRR and LRL.

Discussion

LR procedures are indicated for LR tightness, which is assessed by taking a history, performing a physical examination, and obtaining diagnostic imaging. Decisions should be based on all findings considered together and never on imaging findings alone.

Physical Examination

The physical examination should include assessment of limb alignment, patellar mobility, muscle balance, and dynamic patellar tracking.

Limb Alignment. Abnormal valgus, rotational deformities, and increased Q-angle are associated with LR tightness. Valgus alignment can be assessed on standing inspection; rotational deformities with increased hip anteversion by hip motion with the patient in the prone position (increased hip internal rotation, decreased hip external rotation); and Q-angle on weight-bearing standing examination and with the patient flexing and extending the knee while seated.

Patellar Mobility. The patellar glide and tilt tests provide the most direct evaluations of LR tightness. Medial displacement of <1 quadrant is consistent with tightness, and displacement of >3 quadrants is consistent with laxity. In full extension, the patellar glide test evaluates only the soft-tissue restraints; at 30° flexion, it also evaluates patellofemoral engagement. The patellar tilt test measures the lifting of the lateral edge of the patella. With normal elevation being 0° to 20°, lack of patellar tilt means the LR is tight, and tilt of >20° means it is loose. MPFL patency can be examined with the Lachman test; the examiner rapidly moves the patella laterally while feeling for the characteristic hard endpoint of lateral translation.

Muscle Balance. The tone, strength, and tightness of the core (abdomen, dorsal, and hip muscles) and lower extremities (quadriceps, hamstrings, gastrocnemius) should be evaluated.

Dynamic Patellar Tracking. The J-sign is the course (shaped like an inverted J) that the patella takes when it is medialized into the trochlea from its laterally displaced resting position as the knee goes from full extension to flexion. The J-sign can be associated with LR tightness, trochlear dysplasia, and patella alta.

Imaging

Although we cannot provide a comprehensive review of the imaging literature, the following radiologic examinations should be used to assess the patellofemoral joint.

30° Lateral Radiograph.  Increased tilt is seen when the lateral facet is not anterior to the patellar ridge. Also evaluated are trochlear anatomy, patellar height, and other factors involved in patellofemoral disorders.

30° Flexed Axial (Merchant) Radiograph. Patellar tilt, subluxation, and trochlear dysplasia are evaluated. Images obtained with progressive flexion can be very useful in verifying patellar tilt reduction. Lack of reduction during early flexion suggests LR tightness.4

Alignment Axial Radiographs (Scanogram). Valgus alignment is assessed with this full-length, standing, long-leg examination.

Computed Tomography/Magnetic Resonance Imaging. Many parameters of patellar alignment have been described. Basic assessment should include evaluation of patellar tilt, angle by the line across posterior condyles and a line through the greatest patellar width (>20° indicates abnormality and LR tightness) and tibial tubercle-trochlear groove distance (computed tomography or magnetic resonance imaging scan of the knee is used to measure this distance, and to confirm a significant amount in light of complex patellofemoral malalignment5).

Indications

Lateral compression syndrome with LR tightness is often successfully treated with isolated LRR, and results are reproducible and predictable.6 Surgical intervention for patellofemoral pain should be undertaken only after failed extensive nonoperative treatment with physical therapy and bracing/taping. Patients with LR tightness on preoperative examination, lateral patellar tilt on imaging, and normal Q-angle can obtain satisfactory results with this procedure. Patellar subluxation or dislocation history, high Q-angle (>20°), grade 3 or 4 chondral injury, and patellofemoral arthritis are associated with poorer outcomes when the procedure is performed in isolation.6International Patellofemoral Study Group members agreed that LRR/LRL is a valid treatment option when indicated, but it is rarely performed in isolation and constitutes only 1% to 2% of surgeries performed by this group of experts.7 When lateral compression syndrome progresses to arthritis, LRR/LRL can be performed with lateral patella facetectomy for maximal improvement.4 In the setting of patellofemoral instability, LRR/LRL can be combined with proximal and/or distal realignment surgery if the LR is tight. The LR is the last line of defense limiting lateral translation in the setting of an incompetent MPFL. Isolated LRR/LRL in the setting of instability further destabilizes the patella and worsens the instability. Therefore, LRR/LRL
is a poor surgical option as an isolated procedure for this condition and should be used only as an adjunct in cases of patellofemoral instability with LR tightness that does not allow the patella to be centralized into the trochlea.8 LRR/LRL can also be performed to improve patellar tracking in patello­femoral arthroplasty and total knee arthroplasty.

Lateral Retinaculum Release Versus Lengthening

LRR was first described for the treatment of patellar instability in 1891.9 It was also used for the treatment of lateral patellar hypercompression syndrome associated with LR tightness that led to lateral patellar tracking, joint overload, degeneration, and anterior knee pain.10 Metcalf10 further popularized the procedure by describing a minimally invasive arthroscopic version. However, the arthroscopic technique is as aggressive as the open technique and may be performed with less control, potentially making its results more variable. As proximal and distal releases are performed from the "inside out," more capsule and muscle disruption is needed to release the more superficial layers.

Z-plasty lengthening of the LR was described as an alternative for maintaining lateral patellar soft-tissue integrity while reducing the tension of the lateral tissue restraints.3 This is our preferred method.

Performing LRL instead of LRR avoids iatrogenic medial patellar instability, avoids overrelease and muscle injury, and improves soft-tissue balance.3 Open release or lengthening reduces inadvertent injury to the lateral superior/inferior geniculate arteries and allows direct hemostasis. Two prospective randomized studies found functional knee outcomes and return to athletic activities were improved more after LRL than LRR.11,12 These procedures had similar rates of postoperative knee stiffness, decreased muscle mass, and decreased strength. Each prospective study used an extensive LRR technique for LRR cases (various authors have recommended performing the release until the patella is perpendicular to the trochlea), which may have affected outcomes. In any case, with lengthening, the surgeon is less likely to excessively disrupt the lateral tissues.

Lateral Retinaculum Release.  LRR can be openly performed by lateral parapatellar incision,1 a mini-open percutaneous technique, or arthroscopy. For these open techniques, incisions of various sizes have been used to access the LR and incise it about 1 cm lateral to the patella starting at the distal end of the vastus lateralis and extending distally until patellar tilt reduction is sufficient. If tightness in deep flexion persists, the LRR can be extended distally to the tibial tubercle. Open techniques have the advantage of sparing the joint capsule. All-arthroscopic techniques involve using electrocautery to cut through the capsule and access the LR.

Lateral Retinaculum Lengthening. 

The LR is sharply divided into a superficial layer of superficial oblique fibers from the anterior iliotibial band and a deep layer of transverse fibers from the femur. For LRR, these 2 layers must be identified separate from the articular capsule.13

Figure 1.
Figure 1 illustrates the anatomy and the essential steps of the procedure. The fascia lata is carefully removed over the lateral patella, releasing some lateral tension and helping in the identification of the superficial and deep layers. The proximal lateral soft tissues of the patella are exposed, and the outer oblique layer of the LR is incised near the lateral border of the patella (Figure 2).
Figure 2.
The incision begins around the level of the proximal patellar pole and extends distally to the inferior patellar pole. The superficial oblique fibers of the LR are sharply dissected from the deep transverse fibers and are elevated as dissection is carried posteriorly to the posterior-most extent of the retinacular envelope, usually 1 cm to 2 cm (Figure 3). T
Figure 3.
he deep transverse fibers are then incised longitudinally (Figure 4). In many cases, a capsule that adheres to the deep layer can be separated from it. In cases with combined tibial tubercle transfers, the capsule is incised in order to mobilize the patella medially or distally.
Figure 4.
Then, the knee is moved through its full range of motion, positioned in 30° flexion, and engaged into the trochlear groove. The length of both the MPFL and the LR can then be adjusted. The cut edges of the superior oblique and deep transverse fibers are then sutured together with absorbable suture, and the appropriate amount of lengthening is performed to remove excess tension in lateral structures while maintaining lateral soft-tissue integrity (Figure 5).
Figure 5.
Neither the MPFL nor the LR is tensioned; rather, their lengths are adjusted, as they act as checkreins guiding the patella. If this procedure is performed with tibial tubercle transfer (medial and/or distal) or MPFL reconstruction, tubercle fixation is done first; next, MPFL length and then LR length are set.

Complications

Complications of performing LRR/LRL to change the lateral restraint include medial patellar instability, increased lateral pain, repair failure, recurrent lateral instability, quadriceps weakness and atrophy, postoperative hemarthrosis, knee stiffness, wound complications, and thermal skin injury.7 These complications often result from poor surgical technique and too aggressive release. Although recommended patellar tilt historically has varied from 45° to 90°, the current goal is to normalize the tight soft-tissue restraints without creating secondary instability.

The most significant complication of LRR is medial patellar instability caused by muscle atrophy and loss of soft-tissue restraint.14 Medial instability can be difficult to diagnose and should be considered in any patient with patellofemoral pain, popping, or patellar instability after LRR.15 A positive medial subluxation test or medial patellar apprehension test suggests medial instability.

Medial patellar instability usually requires surgical treatment. Direct LR repair, lateral soft-tissue reconstruction, and other procedures can be used to restore lateral restraint.15 However, these are salvage techniques, and patients often remain significantly limited by pain or instability. Therefore, the LR must be carefully addressed and preferably should undergo lengthening rather than release.

Take-Home Points

  • Understanding the indications for treatment is essential.
  • Identifying the superficial (oblique fibers) and deep layers (transverse fibers) of the LR is very important and can lengthen the LR by as much as 20 mm.
  • Open procedures reduce the risk of hematomas and related pain.
  • The goal is to obtain 1 or 2 patellar quadrants of medial and lateral patellar glide in extensino and a neutral patella.
  • If the Z-plasty is combined with the MPFL reconstruction or tibial tubercle transfer, the LR is set to length after the tubercle transfer and before the MPFL reconstruction (to avoid overconstraint).

Anterior knee pain is a common clinical problem that can be challenging to correct, in large part because of multiple causative factors, including structural/anatomical, functional, alignment, and neuroperception/pain pathway factors. One difficult aspect of anatomical assessment is judging the soft-tissue balance between the medial restraints (medial patellofemoral ligament [MPFL]; medial quadriceps tendon to femoral ligament; medial patellotibial and patellomeniscal ligaments) and the lateral restraints (lateral retinaculum [LR] specifically). Both LR tightness and patellar instability can be interpreted as anterior knee pain. Differentiating these entities is one of the most difficult clinical challenges in orthopedics.

LR release (LRR) has been found to improve patellar mobility and tracking.1 In the absence of clearly defined guidelines, the procedure quickly gained in popularity because of its technical simplicity and the enticing "one tool fits all" treatment approach suggested in early reviews. Injudicious use of LRR, alone or in combination with other procedures, led to iatrogenic instability and chronic pain. LR lengthening (LRL) was introduced to address LR tightness while maintaining lateral soft-tissue integrity and avoiding some of the severe complications of LRR.2

Today, isolated use of LRR/LRL is recommended only for treatment of LR tightness and pain secondary to lateral patellar hypercompression.3 It can also be used as an adjunct treatment in the setting of patellofemoral instability. LRR/LRL should never be used as primary treatment for patellofemoral instability.

In this review of treatments for LR tightness and patellofemoral disorders, we compare the use of LRR and LRL.

Discussion

LR procedures are indicated for LR tightness, which is assessed by taking a history, performing a physical examination, and obtaining diagnostic imaging. Decisions should be based on all findings considered together and never on imaging findings alone.

Physical Examination

The physical examination should include assessment of limb alignment, patellar mobility, muscle balance, and dynamic patellar tracking.

Limb Alignment. Abnormal valgus, rotational deformities, and increased Q-angle are associated with LR tightness. Valgus alignment can be assessed on standing inspection; rotational deformities with increased hip anteversion by hip motion with the patient in the prone position (increased hip internal rotation, decreased hip external rotation); and Q-angle on weight-bearing standing examination and with the patient flexing and extending the knee while seated.

Patellar Mobility. The patellar glide and tilt tests provide the most direct evaluations of LR tightness. Medial displacement of <1 quadrant is consistent with tightness, and displacement of >3 quadrants is consistent with laxity. In full extension, the patellar glide test evaluates only the soft-tissue restraints; at 30° flexion, it also evaluates patellofemoral engagement. The patellar tilt test measures the lifting of the lateral edge of the patella. With normal elevation being 0° to 20°, lack of patellar tilt means the LR is tight, and tilt of >20° means it is loose. MPFL patency can be examined with the Lachman test; the examiner rapidly moves the patella laterally while feeling for the characteristic hard endpoint of lateral translation.

Muscle Balance. The tone, strength, and tightness of the core (abdomen, dorsal, and hip muscles) and lower extremities (quadriceps, hamstrings, gastrocnemius) should be evaluated.

Dynamic Patellar Tracking. The J-sign is the course (shaped like an inverted J) that the patella takes when it is medialized into the trochlea from its laterally displaced resting position as the knee goes from full extension to flexion. The J-sign can be associated with LR tightness, trochlear dysplasia, and patella alta.

Imaging

Although we cannot provide a comprehensive review of the imaging literature, the following radiologic examinations should be used to assess the patellofemoral joint.

30° Lateral Radiograph.  Increased tilt is seen when the lateral facet is not anterior to the patellar ridge. Also evaluated are trochlear anatomy, patellar height, and other factors involved in patellofemoral disorders.

30° Flexed Axial (Merchant) Radiograph. Patellar tilt, subluxation, and trochlear dysplasia are evaluated. Images obtained with progressive flexion can be very useful in verifying patellar tilt reduction. Lack of reduction during early flexion suggests LR tightness.4

Alignment Axial Radiographs (Scanogram). Valgus alignment is assessed with this full-length, standing, long-leg examination.

Computed Tomography/Magnetic Resonance Imaging. Many parameters of patellar alignment have been described. Basic assessment should include evaluation of patellar tilt, angle by the line across posterior condyles and a line through the greatest patellar width (>20° indicates abnormality and LR tightness) and tibial tubercle-trochlear groove distance (computed tomography or magnetic resonance imaging scan of the knee is used to measure this distance, and to confirm a significant amount in light of complex patellofemoral malalignment5).

Indications

Lateral compression syndrome with LR tightness is often successfully treated with isolated LRR, and results are reproducible and predictable.6 Surgical intervention for patellofemoral pain should be undertaken only after failed extensive nonoperative treatment with physical therapy and bracing/taping. Patients with LR tightness on preoperative examination, lateral patellar tilt on imaging, and normal Q-angle can obtain satisfactory results with this procedure. Patellar subluxation or dislocation history, high Q-angle (>20°), grade 3 or 4 chondral injury, and patellofemoral arthritis are associated with poorer outcomes when the procedure is performed in isolation.6International Patellofemoral Study Group members agreed that LRR/LRL is a valid treatment option when indicated, but it is rarely performed in isolation and constitutes only 1% to 2% of surgeries performed by this group of experts.7 When lateral compression syndrome progresses to arthritis, LRR/LRL can be performed with lateral patella facetectomy for maximal improvement.4 In the setting of patellofemoral instability, LRR/LRL can be combined with proximal and/or distal realignment surgery if the LR is tight. The LR is the last line of defense limiting lateral translation in the setting of an incompetent MPFL. Isolated LRR/LRL in the setting of instability further destabilizes the patella and worsens the instability. Therefore, LRR/LRL
is a poor surgical option as an isolated procedure for this condition and should be used only as an adjunct in cases of patellofemoral instability with LR tightness that does not allow the patella to be centralized into the trochlea.8 LRR/LRL can also be performed to improve patellar tracking in patello­femoral arthroplasty and total knee arthroplasty.

Lateral Retinaculum Release Versus Lengthening

LRR was first described for the treatment of patellar instability in 1891.9 It was also used for the treatment of lateral patellar hypercompression syndrome associated with LR tightness that led to lateral patellar tracking, joint overload, degeneration, and anterior knee pain.10 Metcalf10 further popularized the procedure by describing a minimally invasive arthroscopic version. However, the arthroscopic technique is as aggressive as the open technique and may be performed with less control, potentially making its results more variable. As proximal and distal releases are performed from the "inside out," more capsule and muscle disruption is needed to release the more superficial layers.

Z-plasty lengthening of the LR was described as an alternative for maintaining lateral patellar soft-tissue integrity while reducing the tension of the lateral tissue restraints.3 This is our preferred method.

Performing LRL instead of LRR avoids iatrogenic medial patellar instability, avoids overrelease and muscle injury, and improves soft-tissue balance.3 Open release or lengthening reduces inadvertent injury to the lateral superior/inferior geniculate arteries and allows direct hemostasis. Two prospective randomized studies found functional knee outcomes and return to athletic activities were improved more after LRL than LRR.11,12 These procedures had similar rates of postoperative knee stiffness, decreased muscle mass, and decreased strength. Each prospective study used an extensive LRR technique for LRR cases (various authors have recommended performing the release until the patella is perpendicular to the trochlea), which may have affected outcomes. In any case, with lengthening, the surgeon is less likely to excessively disrupt the lateral tissues.

Lateral Retinaculum Release.  LRR can be openly performed by lateral parapatellar incision,1 a mini-open percutaneous technique, or arthroscopy. For these open techniques, incisions of various sizes have been used to access the LR and incise it about 1 cm lateral to the patella starting at the distal end of the vastus lateralis and extending distally until patellar tilt reduction is sufficient. If tightness in deep flexion persists, the LRR can be extended distally to the tibial tubercle. Open techniques have the advantage of sparing the joint capsule. All-arthroscopic techniques involve using electrocautery to cut through the capsule and access the LR.

Lateral Retinaculum Lengthening. 

The LR is sharply divided into a superficial layer of superficial oblique fibers from the anterior iliotibial band and a deep layer of transverse fibers from the femur. For LRR, these 2 layers must be identified separate from the articular capsule.13

Figure 1.
Figure 1 illustrates the anatomy and the essential steps of the procedure. The fascia lata is carefully removed over the lateral patella, releasing some lateral tension and helping in the identification of the superficial and deep layers. The proximal lateral soft tissues of the patella are exposed, and the outer oblique layer of the LR is incised near the lateral border of the patella (Figure 2).
Figure 2.
The incision begins around the level of the proximal patellar pole and extends distally to the inferior patellar pole. The superficial oblique fibers of the LR are sharply dissected from the deep transverse fibers and are elevated as dissection is carried posteriorly to the posterior-most extent of the retinacular envelope, usually 1 cm to 2 cm (Figure 3). T
Figure 3.
he deep transverse fibers are then incised longitudinally (Figure 4). In many cases, a capsule that adheres to the deep layer can be separated from it. In cases with combined tibial tubercle transfers, the capsule is incised in order to mobilize the patella medially or distally.
Figure 4.
Then, the knee is moved through its full range of motion, positioned in 30° flexion, and engaged into the trochlear groove. The length of both the MPFL and the LR can then be adjusted. The cut edges of the superior oblique and deep transverse fibers are then sutured together with absorbable suture, and the appropriate amount of lengthening is performed to remove excess tension in lateral structures while maintaining lateral soft-tissue integrity (Figure 5).
Figure 5.
Neither the MPFL nor the LR is tensioned; rather, their lengths are adjusted, as they act as checkreins guiding the patella. If this procedure is performed with tibial tubercle transfer (medial and/or distal) or MPFL reconstruction, tubercle fixation is done first; next, MPFL length and then LR length are set.

Complications

Complications of performing LRR/LRL to change the lateral restraint include medial patellar instability, increased lateral pain, repair failure, recurrent lateral instability, quadriceps weakness and atrophy, postoperative hemarthrosis, knee stiffness, wound complications, and thermal skin injury.7 These complications often result from poor surgical technique and too aggressive release. Although recommended patellar tilt historically has varied from 45° to 90°, the current goal is to normalize the tight soft-tissue restraints without creating secondary instability.

The most significant complication of LRR is medial patellar instability caused by muscle atrophy and loss of soft-tissue restraint.14 Medial instability can be difficult to diagnose and should be considered in any patient with patellofemoral pain, popping, or patellar instability after LRR.15 A positive medial subluxation test or medial patellar apprehension test suggests medial instability.

Medial patellar instability usually requires surgical treatment. Direct LR repair, lateral soft-tissue reconstruction, and other procedures can be used to restore lateral restraint.15 However, these are salvage techniques, and patients often remain significantly limited by pain or instability. Therefore, the LR must be carefully addressed and preferably should undergo lengthening rather than release.

References

1. Merchant AC, Mercer RL. Lateral release of the patella. A preliminary report. Clin Orthop Relat Res. 1974;(103):40-45.

2. Ceder LC, Larson RL. Z-plasty lateral retinacular release for the treatment of patellar compression syndrome. Clin Orthop Relat Res. 1979;(144):110-113.

3. Biedert R. Lateral patellar hypercompression, tilt and mild lateral subluxation. In: Biedert R, ed. Patellofemoral Disorders. Chichester, England: Wiley; 2004:161-166.

4. Hinckel BB, Arendt EA. Lateral retinaculum lengthening or release. Oper Tech Sports Med. 2015;23(2):100-106.

5. Seitlinger G, Scheurecker G, Högler R, Labey L, Innocenti B, Hofmann S. Tibial tubercle–posterior cruciate ligament distance: a new measurement to define the position of the tibial tubercle in patients with patellar dislocation. Am J Sports Med. 2012;40(5):1119-1125.

6. Lattermann C, Toth J, Bach BR Jr. The role of lateral retinacular release in the treatment of patellar instability. Sports Med Arthrosc. 2007;15(2):57-60.

7. Fithian DC, Paxton EW, Post WR, Panni AS; International Patellofemoral Study Group. Lateral retinacular release: a survey of the International Patellofemoral Study Group. Arthroscopy. 2004;20(5):463-468.

8. Christoforakis J, Bull AM, Strachan RK, Shymkiw R, Senavongse W, Amis AA. Effects of lateral retinacular release on the lateral stability of the patella. Knee Surg Sports Traumatol Arthrosc. 2006;14(3):273-277.

9. Pollard B. Old dislocation of patella by intra-articular operation. Lancet. 1891;(988):17-22.

10. Metcalf RW. An arthroscopic method for lateral release of subluxating or dislocating patella. Clin Orthop Relat Res. 1982;167:9-18.

11. Pagenstert G, Wolf N, Bachmann M, et al. Open lateral patellar retinacular lengthening versus open retinacular release in lateral patellar hypercompression syndrome: a prospective double-blinded comparative study on complications and outcome. Arthroscopy. 2012;28(6):788-797.

12. O’Neill DB. Open lateral retinacular lengthening compared with arthroscopic release. A prospective, randomized outcome study. J Bone Joint Surg Am. 1997;79(12):1759-1769.

13. Merican AM, Amis AA. Anatomy of the lateral retinaculum of the knee. J Bone Joint Surg Br. 2008;90(4):527-534.

14. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.

15. McCarthy MA, Bollier MJ. Medial patella subluxation: diagnosis and treatment. Iowa Orthop J. 2015;35:26-33.

References

1. Merchant AC, Mercer RL. Lateral release of the patella. A preliminary report. Clin Orthop Relat Res. 1974;(103):40-45.

2. Ceder LC, Larson RL. Z-plasty lateral retinacular release for the treatment of patellar compression syndrome. Clin Orthop Relat Res. 1979;(144):110-113.

3. Biedert R. Lateral patellar hypercompression, tilt and mild lateral subluxation. In: Biedert R, ed. Patellofemoral Disorders. Chichester, England: Wiley; 2004:161-166.

4. Hinckel BB, Arendt EA. Lateral retinaculum lengthening or release. Oper Tech Sports Med. 2015;23(2):100-106.

5. Seitlinger G, Scheurecker G, Högler R, Labey L, Innocenti B, Hofmann S. Tibial tubercle–posterior cruciate ligament distance: a new measurement to define the position of the tibial tubercle in patients with patellar dislocation. Am J Sports Med. 2012;40(5):1119-1125.

6. Lattermann C, Toth J, Bach BR Jr. The role of lateral retinacular release in the treatment of patellar instability. Sports Med Arthrosc. 2007;15(2):57-60.

7. Fithian DC, Paxton EW, Post WR, Panni AS; International Patellofemoral Study Group. Lateral retinacular release: a survey of the International Patellofemoral Study Group. Arthroscopy. 2004;20(5):463-468.

8. Christoforakis J, Bull AM, Strachan RK, Shymkiw R, Senavongse W, Amis AA. Effects of lateral retinacular release on the lateral stability of the patella. Knee Surg Sports Traumatol Arthrosc. 2006;14(3):273-277.

9. Pollard B. Old dislocation of patella by intra-articular operation. Lancet. 1891;(988):17-22.

10. Metcalf RW. An arthroscopic method for lateral release of subluxating or dislocating patella. Clin Orthop Relat Res. 1982;167:9-18.

11. Pagenstert G, Wolf N, Bachmann M, et al. Open lateral patellar retinacular lengthening versus open retinacular release in lateral patellar hypercompression syndrome: a prospective double-blinded comparative study on complications and outcome. Arthroscopy. 2012;28(6):788-797.

12. O’Neill DB. Open lateral retinacular lengthening compared with arthroscopic release. A prospective, randomized outcome study. J Bone Joint Surg Am. 1997;79(12):1759-1769.

13. Merican AM, Amis AA. Anatomy of the lateral retinaculum of the knee. J Bone Joint Surg Br. 2008;90(4):527-534.

14. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.

15. McCarthy MA, Bollier MJ. Medial patella subluxation: diagnosis and treatment. Iowa Orthop J. 2015;35:26-33.

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Patella Alta Sees You, Do You See It?

Article Type
Changed
Thu, 09/19/2019 - 13:21

Take-Home Points

  • The decision to adda TTDO to an MPFL reconstruction is dependent on patellar height as assessed with the CDI, as well as multiple other patient and anatomical factors.

  • TTDOs that include a complete detachment of the tibial tubercle (as required for distalization) have increased risk of nonunion and hardware failure.

  • Poor surgical technique (failure to make a flat osteotomy cut, cortical only bone block, poor bony apposition of the detached bone block- particularly at the location of any transverse plane cut, and failure to minimize thermal damage through copious irrigation) can increase nonunion risk.

  • Postoperative rehabilitation should include a 6-week period of limited weight-bearing.

  • Reconstruction of the MPFL should be performed after any TTO is performed.

Patellar instability is the result of numerous anatomical factors, including trochlear dysplasia,1,2 patella alta,2-4 and increased tibial tubercle-trochlear groove (TT-TG) or tibial tubercle-posterior cruciate ligament distance.2,5 Of all the factors, TT-TG distance and the medial patellofemoral ligament (MPFL) have received the ost attention. Patellar height remains a crucial yet underappreciated contributor that is amenable to surgical correction with tibial tubercle distalization osteotomy (TTDO). The obvious question is how severe patella alta must be to require surgical correction. In other words, when is patella alta so severe that isolated MPFL reconstruction is insufficient to restore patellar stability?

The indications for TTDO are not completely clear and depend on multiple factors. Patient factors, physical examination findings, and radiographic measures must be considered. In general, adding TTDO to MPFL reconstruction should be considered when the degree of patella alta exceeds 1.4 on the Caton-Deschamps Index (CDI). Presence of trochlear dysplasia, patellar maltracking (J-sign), lateral patellar apprehension that persists at higher flexion angles, and decreased patellotrochlear articular cartilage contact on sagittal magnetic resonance imaging may drive the decision to proceed with TTDO when the CDI is lower.

Why You Need To Know About Patella Alta

Recurrent lateral patellar dislocation is a debilitating knee condition that often involves young, active patients and significantly affects their quality of life. The MPFL is a primary restraint to lateral patellar dislocation, and an MPFL injury is a key contributor to loss of patellar stability. MPFL reconstruction is increasingly being performed to treat recurrent lateral patellar instability.6 Patellar instability is the result of numerous anatomical factors, including trochlear dysplasia,1,2 patella alta,2-4 and increased TT-TG distance.2,5 This review focuses on patella alta.

The classic teaching of the Lyon School of Knee Surgery in France, the menu à la carte, is that patella alta exceeding 1.2 on the CDI is an indication for TTDO.2 Although this teaching is an excellent guide for normal anatomy, we must keep in mind that the classic surgical menu does not consider the influence of MPFL reconstruction, as development of the menu predated this surgical option. At that time, the proximal soft-tissue procedures included vastus medialis obliquus plasty and advancement, which are performed to balance soft tissues and treat patellar tilt. These procedures and MPFL reconstruction have different functions, and the difference may be important. Furthermore, performing TTDO alongside MPFL reconstruction significantly increases the risk of complications and alters the rehabilitation protocol. However, significant untreated patella alta has been implicated as a cause of failure of isolated MPFL reconstruction.7 Establishing when MPFL reconstruction alone is sufficient is therefore crucial in avoiding the increased morbidity associated with the addition of TTDO.

Discussion

Above a certain degree of patella alta, isolated MPFL reconstruction fails to restore patellar stability. What remains unknown is the appropriate CDI cutoff (1.4) and whether the same cutoff can be used for all patients. In 2013, Wagner and colleagues8 assessed the influence of patella alta on isolated MPFL reconstruction outcomes and found no significant difference, though their study did not include many patients with significant alta and was underpowered. In 2014, Feller and colleagues9 reported on a series of patients who were successfully treated with isolated MPFL reconstruction despite patella alta significantly exceeding the traditional CDI cutoff of 1.2. Their indication for performing the isolated procedure was normal patellar tracking—in particular, absence of the J-sign. Further analysis of these patients revealed a preponderance of relatively normal TT-TG distances and low-grade, if any, trochlear dysplasia in comparison with other patients treated with a combination of MPFL reconstruction and tibial tubercle osteotomy.

Together, the work of Wagner and colleagues8 and Feller and colleagues9 suggests the historical use of the CDI of 1.2 as a hard and fast indication for adding TTDO is aggressive. In fact, it is probably the case that there really is no single CDI cutoff that is an appropriate indication for adding TTDO in all patients with instability. This decision is, and should be, influenced by a multitude of other factors, including other anatomical factors, physical examination findings, patient factors, and, of course, patient preference.

An interesting idea to consider in treating patellar instability is the interplay of patella alta and trochlear dysplasia. Patella alta is theorized as contributing to patellar instability in part by delaying entry of the patella into the TG as the knee flexes, therefore requiring less force to laterally displace

the patella.10 Similarly, in the setting of trochlear dysplasia, a shallow TG leads to less bony constraint of the patella, particularly in the groove’s superior portions, which are more involved in lower grade dysplasia. Because trochlear dysplasia and patella alta decrease patellar stability by similar mechanisms, they clearly interact, and a patient with both is at higher risk for instability than a patient who exhibits either in isolation.11 Therefore, trochlear dysplasia, particularly higher grade, may be an indication for adding TTDO at lower CDI.

Other imaging and physical examination factors can provide additional insight into the process of patellar engagement into the trochlea in each patient. The patellotrochlear index (PTI) directly measures the relationship between the patella and the trochlea, rather than relative to the tibia, as with other measures of patellar height.12[[{"fid":"201853","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]":""}}}]]The PTI is correlated with tibia-based measures of height, but the correlation is not perfect. Lower degrees of overlap between the patella and the trochlea (PTI <0.15) and significant functional patella alta may warrant adding TTDO in cases of borderline CDI (1.2-1.4). Figures 1A, 1B and 2A, 2B show the imaging of 2 patients with relatively similar patellar height (assessed with CDI) but quite different degrees of overlap between the patella and trochlea. [[{"fid":"201854","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]":""}}}]]The patient with less overlap is more likely to have delayed patellar engagement and symptomatic patella alta and thus may be a poorer candidate for isolated MPFL reconstruction. For additional information, please refer to the work by Roland Biedert, MD, who has proposed trochlear lengthening in these situations.13

Physical examination (even in the era of advance imaging) continues to provide useful insight into whether to add TTDO. One physical examination test that can help in understanding patellar-
trochlear dynamics is the patellar apprehension and relief test. Patellar apprehension has been widely discussed, but equally important is the degree of knee flexion above which apprehension dissipates. As patella alta and trochlear dysplasia become more severe, more knee flexion is required to relieve apprehension. Apprehension that is relieved at 30° to 40° of flexion suggests that patellar stability stands a good chance of being restored with isolated MPFL reconstruction, whereas persistent instability >45° or especially 60° of knee flexion suggests that there is significant patella alta, trochlear dysplasia, or both and that TTDO should be added. A large J-sign during knee flexion and extension provides further evidence that entry of the patella into the TG is delayed, typically because of patella alta, trochlear dysplasia, or both, and possibly tight lateral structures or a lateralized tibial tubercle. This sign is another clue that isolated MPFL reconstruction may be insufficient to completely restore patellar stability.

References

1. Dejour H, Walch G, Neyret P, Adeleine P. Dysplasia of the femoral trochlea [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1990;76(1):45-54.

2. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.

3. Geenen E, Molenaers G, Martens M. Patella alta in patellofemoral instability. Acta Orthop Belg. 1989;55(3):387-393.

4. Simmons E Jr, Cameron JC. Patella alta and recurrent dislocation of the patella. Clin Orthop Relat Res. 1992;(274):265-269.

5. Goutallier D, Bernageau J, Lecudonnec B. The measurement of the tibial tuberosity. Patella groove distanced technique and results (author’s transl) [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1978;64(5):423-428.

6. Feller JA, Lind M, Nelson J, Diduch DR, Arendt E. Repair and reconstruction of the medial patellofemoral ligament for treatment of lateral patellar dislocations. In: Scott WN, ed. Insall & Scott—Surgery of the Knee. 5th ed. Philadelphia, PA: Churchill Livingstone; 2011:677-687.

7. Thaunat M, Erasmus PJ. Recurrent patellar dislocation after medial patellofemoral ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2008;16(1):40-43.

8. Wagner D, Pfalzer F, Hingelbaum S, Huth J, Mauch F, Bauer G. The influence of risk factors on clinical outcomes following anatomical medial patellofemoral ligament (MPFL) reconstruction using the gracilis tendon. Knee Surg Sports Traumatol Arthrosc. 2013;21(2):318-324.

9. Feller JA, Richmond AK, Wasiak J. Medial patellofemoral ligament reconstruction as an isolated or combined procedure for recurrent patellar instability. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2470-2476.

10. Ward SR, Terk MR, Powers CM. Patella alta: association
with patellofemoral alignment and changes in contact area during weight-bearing. J Bone Joint Surg Am. 2007;89(8):
1749-1755.

11. Lewallen L, McIntosh A, Dahm D. First-time patellofemoral dislocation: risk factors for recurrent instability. J Knee Surg. 2015;28(4):303-309

12. Biedert RM, Albrecht S. The patellotrochlear index: a new index for assessing patellar height. Knee Surg Sports Traumatol Arthrosc. 2006;14(8):707-712.

13. Biedert RM. Trochlear lengthening osteotomy with or without elevation of the lateral trochlear facet. In: Zaffagnini S, Dejour D, Arendt EA, eds. Patellofemoral Pain, Instability, and Arthritis. Germany: Springer-Verlag Berlin Heidelberg; 2010:
209-215.

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Take-Home Points

  • The decision to adda TTDO to an MPFL reconstruction is dependent on patellar height as assessed with the CDI, as well as multiple other patient and anatomical factors.

  • TTDOs that include a complete detachment of the tibial tubercle (as required for distalization) have increased risk of nonunion and hardware failure.

  • Poor surgical technique (failure to make a flat osteotomy cut, cortical only bone block, poor bony apposition of the detached bone block- particularly at the location of any transverse plane cut, and failure to minimize thermal damage through copious irrigation) can increase nonunion risk.

  • Postoperative rehabilitation should include a 6-week period of limited weight-bearing.

  • Reconstruction of the MPFL should be performed after any TTO is performed.

Patellar instability is the result of numerous anatomical factors, including trochlear dysplasia,1,2 patella alta,2-4 and increased tibial tubercle-trochlear groove (TT-TG) or tibial tubercle-posterior cruciate ligament distance.2,5 Of all the factors, TT-TG distance and the medial patellofemoral ligament (MPFL) have received the ost attention. Patellar height remains a crucial yet underappreciated contributor that is amenable to surgical correction with tibial tubercle distalization osteotomy (TTDO). The obvious question is how severe patella alta must be to require surgical correction. In other words, when is patella alta so severe that isolated MPFL reconstruction is insufficient to restore patellar stability?

The indications for TTDO are not completely clear and depend on multiple factors. Patient factors, physical examination findings, and radiographic measures must be considered. In general, adding TTDO to MPFL reconstruction should be considered when the degree of patella alta exceeds 1.4 on the Caton-Deschamps Index (CDI). Presence of trochlear dysplasia, patellar maltracking (J-sign), lateral patellar apprehension that persists at higher flexion angles, and decreased patellotrochlear articular cartilage contact on sagittal magnetic resonance imaging may drive the decision to proceed with TTDO when the CDI is lower.

Why You Need To Know About Patella Alta

Recurrent lateral patellar dislocation is a debilitating knee condition that often involves young, active patients and significantly affects their quality of life. The MPFL is a primary restraint to lateral patellar dislocation, and an MPFL injury is a key contributor to loss of patellar stability. MPFL reconstruction is increasingly being performed to treat recurrent lateral patellar instability.6 Patellar instability is the result of numerous anatomical factors, including trochlear dysplasia,1,2 patella alta,2-4 and increased TT-TG distance.2,5 This review focuses on patella alta.

The classic teaching of the Lyon School of Knee Surgery in France, the menu à la carte, is that patella alta exceeding 1.2 on the CDI is an indication for TTDO.2 Although this teaching is an excellent guide for normal anatomy, we must keep in mind that the classic surgical menu does not consider the influence of MPFL reconstruction, as development of the menu predated this surgical option. At that time, the proximal soft-tissue procedures included vastus medialis obliquus plasty and advancement, which are performed to balance soft tissues and treat patellar tilt. These procedures and MPFL reconstruction have different functions, and the difference may be important. Furthermore, performing TTDO alongside MPFL reconstruction significantly increases the risk of complications and alters the rehabilitation protocol. However, significant untreated patella alta has been implicated as a cause of failure of isolated MPFL reconstruction.7 Establishing when MPFL reconstruction alone is sufficient is therefore crucial in avoiding the increased morbidity associated with the addition of TTDO.

Discussion

Above a certain degree of patella alta, isolated MPFL reconstruction fails to restore patellar stability. What remains unknown is the appropriate CDI cutoff (1.4) and whether the same cutoff can be used for all patients. In 2013, Wagner and colleagues8 assessed the influence of patella alta on isolated MPFL reconstruction outcomes and found no significant difference, though their study did not include many patients with significant alta and was underpowered. In 2014, Feller and colleagues9 reported on a series of patients who were successfully treated with isolated MPFL reconstruction despite patella alta significantly exceeding the traditional CDI cutoff of 1.2. Their indication for performing the isolated procedure was normal patellar tracking—in particular, absence of the J-sign. Further analysis of these patients revealed a preponderance of relatively normal TT-TG distances and low-grade, if any, trochlear dysplasia in comparison with other patients treated with a combination of MPFL reconstruction and tibial tubercle osteotomy.

Together, the work of Wagner and colleagues8 and Feller and colleagues9 suggests the historical use of the CDI of 1.2 as a hard and fast indication for adding TTDO is aggressive. In fact, it is probably the case that there really is no single CDI cutoff that is an appropriate indication for adding TTDO in all patients with instability. This decision is, and should be, influenced by a multitude of other factors, including other anatomical factors, physical examination findings, patient factors, and, of course, patient preference.

An interesting idea to consider in treating patellar instability is the interplay of patella alta and trochlear dysplasia. Patella alta is theorized as contributing to patellar instability in part by delaying entry of the patella into the TG as the knee flexes, therefore requiring less force to laterally displace

the patella.10 Similarly, in the setting of trochlear dysplasia, a shallow TG leads to less bony constraint of the patella, particularly in the groove’s superior portions, which are more involved in lower grade dysplasia. Because trochlear dysplasia and patella alta decrease patellar stability by similar mechanisms, they clearly interact, and a patient with both is at higher risk for instability than a patient who exhibits either in isolation.11 Therefore, trochlear dysplasia, particularly higher grade, may be an indication for adding TTDO at lower CDI.

Other imaging and physical examination factors can provide additional insight into the process of patellar engagement into the trochlea in each patient. The patellotrochlear index (PTI) directly measures the relationship between the patella and the trochlea, rather than relative to the tibia, as with other measures of patellar height.12[[{"fid":"201853","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]":""}}}]]The PTI is correlated with tibia-based measures of height, but the correlation is not perfect. Lower degrees of overlap between the patella and the trochlea (PTI <0.15) and significant functional patella alta may warrant adding TTDO in cases of borderline CDI (1.2-1.4). Figures 1A, 1B and 2A, 2B show the imaging of 2 patients with relatively similar patellar height (assessed with CDI) but quite different degrees of overlap between the patella and trochlea. [[{"fid":"201854","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]":""}}}]]The patient with less overlap is more likely to have delayed patellar engagement and symptomatic patella alta and thus may be a poorer candidate for isolated MPFL reconstruction. For additional information, please refer to the work by Roland Biedert, MD, who has proposed trochlear lengthening in these situations.13

Physical examination (even in the era of advance imaging) continues to provide useful insight into whether to add TTDO. One physical examination test that can help in understanding patellar-
trochlear dynamics is the patellar apprehension and relief test. Patellar apprehension has been widely discussed, but equally important is the degree of knee flexion above which apprehension dissipates. As patella alta and trochlear dysplasia become more severe, more knee flexion is required to relieve apprehension. Apprehension that is relieved at 30° to 40° of flexion suggests that patellar stability stands a good chance of being restored with isolated MPFL reconstruction, whereas persistent instability >45° or especially 60° of knee flexion suggests that there is significant patella alta, trochlear dysplasia, or both and that TTDO should be added. A large J-sign during knee flexion and extension provides further evidence that entry of the patella into the TG is delayed, typically because of patella alta, trochlear dysplasia, or both, and possibly tight lateral structures or a lateralized tibial tubercle. This sign is another clue that isolated MPFL reconstruction may be insufficient to completely restore patellar stability.

Take-Home Points

  • The decision to adda TTDO to an MPFL reconstruction is dependent on patellar height as assessed with the CDI, as well as multiple other patient and anatomical factors.

  • TTDOs that include a complete detachment of the tibial tubercle (as required for distalization) have increased risk of nonunion and hardware failure.

  • Poor surgical technique (failure to make a flat osteotomy cut, cortical only bone block, poor bony apposition of the detached bone block- particularly at the location of any transverse plane cut, and failure to minimize thermal damage through copious irrigation) can increase nonunion risk.

  • Postoperative rehabilitation should include a 6-week period of limited weight-bearing.

  • Reconstruction of the MPFL should be performed after any TTO is performed.

Patellar instability is the result of numerous anatomical factors, including trochlear dysplasia,1,2 patella alta,2-4 and increased tibial tubercle-trochlear groove (TT-TG) or tibial tubercle-posterior cruciate ligament distance.2,5 Of all the factors, TT-TG distance and the medial patellofemoral ligament (MPFL) have received the ost attention. Patellar height remains a crucial yet underappreciated contributor that is amenable to surgical correction with tibial tubercle distalization osteotomy (TTDO). The obvious question is how severe patella alta must be to require surgical correction. In other words, when is patella alta so severe that isolated MPFL reconstruction is insufficient to restore patellar stability?

The indications for TTDO are not completely clear and depend on multiple factors. Patient factors, physical examination findings, and radiographic measures must be considered. In general, adding TTDO to MPFL reconstruction should be considered when the degree of patella alta exceeds 1.4 on the Caton-Deschamps Index (CDI). Presence of trochlear dysplasia, patellar maltracking (J-sign), lateral patellar apprehension that persists at higher flexion angles, and decreased patellotrochlear articular cartilage contact on sagittal magnetic resonance imaging may drive the decision to proceed with TTDO when the CDI is lower.

Why You Need To Know About Patella Alta

Recurrent lateral patellar dislocation is a debilitating knee condition that often involves young, active patients and significantly affects their quality of life. The MPFL is a primary restraint to lateral patellar dislocation, and an MPFL injury is a key contributor to loss of patellar stability. MPFL reconstruction is increasingly being performed to treat recurrent lateral patellar instability.6 Patellar instability is the result of numerous anatomical factors, including trochlear dysplasia,1,2 patella alta,2-4 and increased TT-TG distance.2,5 This review focuses on patella alta.

The classic teaching of the Lyon School of Knee Surgery in France, the menu à la carte, is that patella alta exceeding 1.2 on the CDI is an indication for TTDO.2 Although this teaching is an excellent guide for normal anatomy, we must keep in mind that the classic surgical menu does not consider the influence of MPFL reconstruction, as development of the menu predated this surgical option. At that time, the proximal soft-tissue procedures included vastus medialis obliquus plasty and advancement, which are performed to balance soft tissues and treat patellar tilt. These procedures and MPFL reconstruction have different functions, and the difference may be important. Furthermore, performing TTDO alongside MPFL reconstruction significantly increases the risk of complications and alters the rehabilitation protocol. However, significant untreated patella alta has been implicated as a cause of failure of isolated MPFL reconstruction.7 Establishing when MPFL reconstruction alone is sufficient is therefore crucial in avoiding the increased morbidity associated with the addition of TTDO.

Discussion

Above a certain degree of patella alta, isolated MPFL reconstruction fails to restore patellar stability. What remains unknown is the appropriate CDI cutoff (1.4) and whether the same cutoff can be used for all patients. In 2013, Wagner and colleagues8 assessed the influence of patella alta on isolated MPFL reconstruction outcomes and found no significant difference, though their study did not include many patients with significant alta and was underpowered. In 2014, Feller and colleagues9 reported on a series of patients who were successfully treated with isolated MPFL reconstruction despite patella alta significantly exceeding the traditional CDI cutoff of 1.2. Their indication for performing the isolated procedure was normal patellar tracking—in particular, absence of the J-sign. Further analysis of these patients revealed a preponderance of relatively normal TT-TG distances and low-grade, if any, trochlear dysplasia in comparison with other patients treated with a combination of MPFL reconstruction and tibial tubercle osteotomy.

Together, the work of Wagner and colleagues8 and Feller and colleagues9 suggests the historical use of the CDI of 1.2 as a hard and fast indication for adding TTDO is aggressive. In fact, it is probably the case that there really is no single CDI cutoff that is an appropriate indication for adding TTDO in all patients with instability. This decision is, and should be, influenced by a multitude of other factors, including other anatomical factors, physical examination findings, patient factors, and, of course, patient preference.

An interesting idea to consider in treating patellar instability is the interplay of patella alta and trochlear dysplasia. Patella alta is theorized as contributing to patellar instability in part by delaying entry of the patella into the TG as the knee flexes, therefore requiring less force to laterally displace

the patella.10 Similarly, in the setting of trochlear dysplasia, a shallow TG leads to less bony constraint of the patella, particularly in the groove’s superior portions, which are more involved in lower grade dysplasia. Because trochlear dysplasia and patella alta decrease patellar stability by similar mechanisms, they clearly interact, and a patient with both is at higher risk for instability than a patient who exhibits either in isolation.11 Therefore, trochlear dysplasia, particularly higher grade, may be an indication for adding TTDO at lower CDI.

Other imaging and physical examination factors can provide additional insight into the process of patellar engagement into the trochlea in each patient. The patellotrochlear index (PTI) directly measures the relationship between the patella and the trochlea, rather than relative to the tibia, as with other measures of patellar height.12[[{"fid":"201853","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]":""}}}]]The PTI is correlated with tibia-based measures of height, but the correlation is not perfect. Lower degrees of overlap between the patella and the trochlea (PTI <0.15) and significant functional patella alta may warrant adding TTDO in cases of borderline CDI (1.2-1.4). Figures 1A, 1B and 2A, 2B show the imaging of 2 patients with relatively similar patellar height (assessed with CDI) but quite different degrees of overlap between the patella and trochlea. [[{"fid":"201854","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]":""}}}]]The patient with less overlap is more likely to have delayed patellar engagement and symptomatic patella alta and thus may be a poorer candidate for isolated MPFL reconstruction. For additional information, please refer to the work by Roland Biedert, MD, who has proposed trochlear lengthening in these situations.13

Physical examination (even in the era of advance imaging) continues to provide useful insight into whether to add TTDO. One physical examination test that can help in understanding patellar-
trochlear dynamics is the patellar apprehension and relief test. Patellar apprehension has been widely discussed, but equally important is the degree of knee flexion above which apprehension dissipates. As patella alta and trochlear dysplasia become more severe, more knee flexion is required to relieve apprehension. Apprehension that is relieved at 30° to 40° of flexion suggests that patellar stability stands a good chance of being restored with isolated MPFL reconstruction, whereas persistent instability >45° or especially 60° of knee flexion suggests that there is significant patella alta, trochlear dysplasia, or both and that TTDO should be added. A large J-sign during knee flexion and extension provides further evidence that entry of the patella into the TG is delayed, typically because of patella alta, trochlear dysplasia, or both, and possibly tight lateral structures or a lateralized tibial tubercle. This sign is another clue that isolated MPFL reconstruction may be insufficient to completely restore patellar stability.

References

1. Dejour H, Walch G, Neyret P, Adeleine P. Dysplasia of the femoral trochlea [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1990;76(1):45-54.

2. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.

3. Geenen E, Molenaers G, Martens M. Patella alta in patellofemoral instability. Acta Orthop Belg. 1989;55(3):387-393.

4. Simmons E Jr, Cameron JC. Patella alta and recurrent dislocation of the patella. Clin Orthop Relat Res. 1992;(274):265-269.

5. Goutallier D, Bernageau J, Lecudonnec B. The measurement of the tibial tuberosity. Patella groove distanced technique and results (author’s transl) [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1978;64(5):423-428.

6. Feller JA, Lind M, Nelson J, Diduch DR, Arendt E. Repair and reconstruction of the medial patellofemoral ligament for treatment of lateral patellar dislocations. In: Scott WN, ed. Insall & Scott—Surgery of the Knee. 5th ed. Philadelphia, PA: Churchill Livingstone; 2011:677-687.

7. Thaunat M, Erasmus PJ. Recurrent patellar dislocation after medial patellofemoral ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2008;16(1):40-43.

8. Wagner D, Pfalzer F, Hingelbaum S, Huth J, Mauch F, Bauer G. The influence of risk factors on clinical outcomes following anatomical medial patellofemoral ligament (MPFL) reconstruction using the gracilis tendon. Knee Surg Sports Traumatol Arthrosc. 2013;21(2):318-324.

9. Feller JA, Richmond AK, Wasiak J. Medial patellofemoral ligament reconstruction as an isolated or combined procedure for recurrent patellar instability. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2470-2476.

10. Ward SR, Terk MR, Powers CM. Patella alta: association
with patellofemoral alignment and changes in contact area during weight-bearing. J Bone Joint Surg Am. 2007;89(8):
1749-1755.

11. Lewallen L, McIntosh A, Dahm D. First-time patellofemoral dislocation: risk factors for recurrent instability. J Knee Surg. 2015;28(4):303-309

12. Biedert RM, Albrecht S. The patellotrochlear index: a new index for assessing patellar height. Knee Surg Sports Traumatol Arthrosc. 2006;14(8):707-712.

13. Biedert RM. Trochlear lengthening osteotomy with or without elevation of the lateral trochlear facet. In: Zaffagnini S, Dejour D, Arendt EA, eds. Patellofemoral Pain, Instability, and Arthritis. Germany: Springer-Verlag Berlin Heidelberg; 2010:
209-215.

References

1. Dejour H, Walch G, Neyret P, Adeleine P. Dysplasia of the femoral trochlea [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1990;76(1):45-54.

2. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.

3. Geenen E, Molenaers G, Martens M. Patella alta in patellofemoral instability. Acta Orthop Belg. 1989;55(3):387-393.

4. Simmons E Jr, Cameron JC. Patella alta and recurrent dislocation of the patella. Clin Orthop Relat Res. 1992;(274):265-269.

5. Goutallier D, Bernageau J, Lecudonnec B. The measurement of the tibial tuberosity. Patella groove distanced technique and results (author’s transl) [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1978;64(5):423-428.

6. Feller JA, Lind M, Nelson J, Diduch DR, Arendt E. Repair and reconstruction of the medial patellofemoral ligament for treatment of lateral patellar dislocations. In: Scott WN, ed. Insall & Scott—Surgery of the Knee. 5th ed. Philadelphia, PA: Churchill Livingstone; 2011:677-687.

7. Thaunat M, Erasmus PJ. Recurrent patellar dislocation after medial patellofemoral ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2008;16(1):40-43.

8. Wagner D, Pfalzer F, Hingelbaum S, Huth J, Mauch F, Bauer G. The influence of risk factors on clinical outcomes following anatomical medial patellofemoral ligament (MPFL) reconstruction using the gracilis tendon. Knee Surg Sports Traumatol Arthrosc. 2013;21(2):318-324.

9. Feller JA, Richmond AK, Wasiak J. Medial patellofemoral ligament reconstruction as an isolated or combined procedure for recurrent patellar instability. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2470-2476.

10. Ward SR, Terk MR, Powers CM. Patella alta: association
with patellofemoral alignment and changes in contact area during weight-bearing. J Bone Joint Surg Am. 2007;89(8):
1749-1755.

11. Lewallen L, McIntosh A, Dahm D. First-time patellofemoral dislocation: risk factors for recurrent instability. J Knee Surg. 2015;28(4):303-309

12. Biedert RM, Albrecht S. The patellotrochlear index: a new index for assessing patellar height. Knee Surg Sports Traumatol Arthrosc. 2006;14(8):707-712.

13. Biedert RM. Trochlear lengthening osteotomy with or without elevation of the lateral trochlear facet. In: Zaffagnini S, Dejour D, Arendt EA, eds. Patellofemoral Pain, Instability, and Arthritis. Germany: Springer-Verlag Berlin Heidelberg; 2010:
209-215.

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Cartilage Restoration in the Patellofemoral Joint

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Take-Home Points

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

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

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

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

Etiology

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

Patellar Instability

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

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

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

Chronic Maltracking Without Instability

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

Direct Trauma

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

Repetitive Microtrauma

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

Idiopathic

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

History and Physical Examination

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

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

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

Imaging

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

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

Treatment

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

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

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

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

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

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

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

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

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

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

Fragment Fixation

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

MFx

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

ACI and Matrix-Induced ACI

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

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

OAT

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

Figure 3.

OCA

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

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

Experimental and Emerging Technologies

Biocartilage

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

Fresh and Viable OCA

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

Bone Marrow Aspirate Concentrate Implantation

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

Particulated Juvenile Allograft Cartilage

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

Rehabilitation After Surgery

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

Conclusion

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Take-Home Points

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

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

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

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

Etiology

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

Patellar Instability

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

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

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

Chronic Maltracking Without Instability

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

Direct Trauma

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

Repetitive Microtrauma

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

Idiopathic

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

History and Physical Examination

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

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

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

Imaging

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

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

Treatment

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

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

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

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

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

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

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

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

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

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

Fragment Fixation

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

MFx

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

ACI and Matrix-Induced ACI

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

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

OAT

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

Figure 3.

OCA

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

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

Experimental and Emerging Technologies

Biocartilage

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

Fresh and Viable OCA

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

Bone Marrow Aspirate Concentrate Implantation

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

Particulated Juvenile Allograft Cartilage

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

Rehabilitation After Surgery

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

Conclusion

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

Take-Home Points

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

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

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

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

Etiology

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

Patellar Instability

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

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

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

Chronic Maltracking Without Instability

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

Direct Trauma

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

Repetitive Microtrauma

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

Idiopathic

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

History and Physical Examination

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

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

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

Imaging

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

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

Treatment

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

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

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

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

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

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

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

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

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

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

Fragment Fixation

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

MFx

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

ACI and Matrix-Induced ACI

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

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

OAT

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

Figure 3.

OCA

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

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

Experimental and Emerging Technologies

Biocartilage

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

Fresh and Viable OCA

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

Bone Marrow Aspirate Concentrate Implantation

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

Particulated Juvenile Allograft Cartilage

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

Rehabilitation After Surgery

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

Conclusion

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Thu, 09/19/2019 - 13:21

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Prediction tool for mortality after respiratory compromise

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Background: Scoring systems exist to predict outcomes following cardiac arrest. There is currently no reliable model to predict outcome of patients who have survived acute respiratory compromise (ARC).

Study Design: A retrospective cohort study.

Setting: Get with the Guidelines Resuscitation (GWTG-R) is an online medical registry that tracks ARC data from more than 300 hospitals.

Synopsis: Using the GWTG-R database of ARC, researchers identified 13,193 cases of ARC to study the variables affecting prognosis. They randomized the group into derivation (75% of patients) and validation (25% of patients) cohorts and used c-statistics to create the prognostic scoring system. The greatest predictors of in-hospital mortality were age greater than 80 years, hypotension in the four hours preceding the ARC event, and the need for intubation.

This scoring system did not take into account any comorbidities (such as organ failure) that occurred shortly after the ARC event, although these likely affect mortality.

Bottom Line: Predicting in-hospital mortality for survivors of ARC events may help clinical prognostication. Such tools could also facilitate comparisons between hospitals and guide quality improvement projects.

Citation: Moskowitz A, Anderson LW, Karlsson M, et. al. Predicting in-hospital mortality for initial survivors of acute respiratory compromise (ARC) events: Development and validation of the ARC score. Resuscitation. 2017 Jun;115:5-10.

Dr. Suman is clinical instructor of medicine in the University of Kentucky division of hospital medicine.
 

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Background: Scoring systems exist to predict outcomes following cardiac arrest. There is currently no reliable model to predict outcome of patients who have survived acute respiratory compromise (ARC).

Study Design: A retrospective cohort study.

Setting: Get with the Guidelines Resuscitation (GWTG-R) is an online medical registry that tracks ARC data from more than 300 hospitals.

Synopsis: Using the GWTG-R database of ARC, researchers identified 13,193 cases of ARC to study the variables affecting prognosis. They randomized the group into derivation (75% of patients) and validation (25% of patients) cohorts and used c-statistics to create the prognostic scoring system. The greatest predictors of in-hospital mortality were age greater than 80 years, hypotension in the four hours preceding the ARC event, and the need for intubation.

This scoring system did not take into account any comorbidities (such as organ failure) that occurred shortly after the ARC event, although these likely affect mortality.

Bottom Line: Predicting in-hospital mortality for survivors of ARC events may help clinical prognostication. Such tools could also facilitate comparisons between hospitals and guide quality improvement projects.

Citation: Moskowitz A, Anderson LW, Karlsson M, et. al. Predicting in-hospital mortality for initial survivors of acute respiratory compromise (ARC) events: Development and validation of the ARC score. Resuscitation. 2017 Jun;115:5-10.

Dr. Suman is clinical instructor of medicine in the University of Kentucky division of hospital medicine.
 

Background: Scoring systems exist to predict outcomes following cardiac arrest. There is currently no reliable model to predict outcome of patients who have survived acute respiratory compromise (ARC).

Study Design: A retrospective cohort study.

Setting: Get with the Guidelines Resuscitation (GWTG-R) is an online medical registry that tracks ARC data from more than 300 hospitals.

Synopsis: Using the GWTG-R database of ARC, researchers identified 13,193 cases of ARC to study the variables affecting prognosis. They randomized the group into derivation (75% of patients) and validation (25% of patients) cohorts and used c-statistics to create the prognostic scoring system. The greatest predictors of in-hospital mortality were age greater than 80 years, hypotension in the four hours preceding the ARC event, and the need for intubation.

This scoring system did not take into account any comorbidities (such as organ failure) that occurred shortly after the ARC event, although these likely affect mortality.

Bottom Line: Predicting in-hospital mortality for survivors of ARC events may help clinical prognostication. Such tools could also facilitate comparisons between hospitals and guide quality improvement projects.

Citation: Moskowitz A, Anderson LW, Karlsson M, et. al. Predicting in-hospital mortality for initial survivors of acute respiratory compromise (ARC) events: Development and validation of the ARC score. Resuscitation. 2017 Jun;115:5-10.

Dr. Suman is clinical instructor of medicine in the University of Kentucky division of hospital medicine.
 

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External cephalic version: How to increase the chances for success

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External cephalic version: How to increase the chances for success

About 3% to 4% of all fetuses at term are in breech presentation. Since 2000, when Hannah and colleagues reported finding that vaginal delivery of breech-presenting babies was riskier than cesarean delivery,1 most breech-presenting neonates in the United States have been delivered abdominally2—despite subsequent questioning of some of that study’s conclusions.

Each year in the United States, approximately 4 million babies are born, and fetal malpresentation accounts for 110,000 to 150,000 cesarean deliveries. In fact, about 15% of all cesarean deliveries in the United States are for breech presentation or transverse lie; in England the percentage is 10%.3 Fortunately, the repopularized technique of external cephalic version (ECV), in which the clinician externally rotates a breech- or transverse-lying fetus to a vertex position (FIGURE), along with the facilitating tools of tocolysis and neuraxial analgesia/anesthesia, is helping to reduce the number of breech presentations in fetuses at term and thus the number of cesarean deliveries and their sequelae—placenta accreta, prolonged recovery, and cesarean deliveries in subsequent pregnancies.

Reluctance to perform ECV is unfounded

In the United States, the practice of offering ECV to women who present with their fetus in breech presentation at term varies tremendously. It is routine at some institutions but not even offered at others.

Many ObGyns are reluctant to perform ECV. Cited reasons include the potential for injury to the fetus and mother (and related liability concerns), the ease of elective cesarean delivery, the variable success rate of ECV (35% to 86%),4 and the pain that women often have with the procedure. According to the literature, however, these concerns either are unfounded or can be mitigated with use of current techniques. Multiple studies have found that the risk of ECV to the fetus and mother is minimal, and that tocolysis and neuraxial anesthesia can facilitate the success of ECV and relieve the pain associated with the procedure.

 

Related article:
2017 Update on obstetrics

 

Indications for ECV

The indications for ECV include breech, oblique, or transverse lie presentation after 36 weeks’ gestation and the mother’s desire to avoid cesarean delivery. A clinician skilled in ECV and a facility where emergency cesarean delivery is possible are essential.

There are several instances in which ECV should not be attempted.

Contraindications include:

  • concerns about fetal status, including nonreactive nonstress test, biophysical profile score <6/8, severe intrauterine growth restriction, decreased end-diastolic umbilical blood flow
  • placenta previa
  • multifetal gestation before delivery of first twin
  • severe oligohydramnios
  • severe preeclampsia
  • significant fetal anomaly
  • known malformation of uterus
  • breech with hyperextended head or arms above shoulders, as seen on ultrasonography.

More controversial contraindications include prior uterine incision, maternal obesity (body mass index >40 kg/m2), ruptured membranes, and fetal macrosomia.

 

Read about timing, success rates, risk factors, alternate approaches for ECV

 

 

Optimal timing for the ECV procedure

Current practice is to wait until 36 to 37 weeks to perform ECV, as most fetuses spontaneously move into vertex presentation by 36 weeks’ gestation. This time frame has several advantages: Many unnecessary attempts at ECV are avoided; only 8% of fetuses in breech presentation after 36 weeks spontaneously change to vertex5; many fetuses revert to breech if ECV is performed too early; and prematurity generally is not an issue in the rare case that immediate delivery is required during or just after attempted ECV.

ECV during labor. Performing ECV during labor appears to pose no increased risk to mother or fetus if membranes are intact and there are no other contraindications to the procedure. Some clinicians perform ECV only during labor. The advantages are that the fetus has had every chance to move into vertex presentation on its own, the equipment used to continuously monitor the fetus during ECV is in place, and cesarean delivery and anesthesia are immediately available in the event ECV is unsuccessful.

The major disadvantage of waiting until labor is that the increased size of the fetus makes ECV more difficult. In addition, the membranes may have already ruptured, and the breech may have descended deeply into the pelvis.

 

Related article:
For the management of labor, patience is a virtue

 

Success rates in breech-to-vertex conversions

In 2016, the American College of Obstetricians and Gynecologists (ACOG) reported an average ECV success rate of 58% (range, 16% to 100%).6 ACOG noted that, with transverse lie, the success rate was significantly higher. Other studies have found a wide range of rates: 58% in 1,308 patients in a Cochrane review by Hofmeyr and colleagues7; 47% in a study by Beuckens and colleagues8; and 63.1% for primiparas and 82.7% for multiparas in a study by Tong Leung and colleagues.9 These rates were affected by whether ECV was performed with or without tocolysis, with or without intravenous analgesia, and with or without neuraxial analgesia/anesthesia (TABLE).

Likelihood of vaginal delivery after successful ECV

The rate of vaginal delivery after successful ECV is roughly half that of fetuses that were never in breech presentation.10 In successful ECV cases, dystocia and nonreassuring fetal heart rate patterns are the major indications for cesarean delivery. Some experts have speculated that the factors leading to near-term breech presentation—such as an unengaged presenting part or a mother’s smaller pelvis—also may be risk factors for dystocia in labor. Despite this, the rate of vaginal delivery of successfully verted babies has been reported to be as high as 80%.10

As might be expected, post-ECV vaginal deliveries are more common in multiparous than in primiparous women.

 
Risks of ECV: Generally low and manageable

Although multiple problems may occur with ECV, generally they are rare and reversible. For instance, Grootscholten and colleagues found a stillbirth and placental abruption rate of only 0.25% in a large group of patients who underwent ECV.11 Similarly, the rate of emergency cesarean delivery was 0.35%. In addition, Hofmeyr and Kulier, in their Cochrane Data Review of 2015, found no significant differences in the Apgar scores and pH’s of babies in the ECV group compared with babies in breech presentation whose mothers did not undergo ECV.7 Results of other studies have confirmed the safety of ECV.12,13

One significant risk of ECV attempts is fetal-to-maternal blood transfer. Boucher and colleagues found that 2.4% of 1,244 women who underwent ECV had a positive Kleihauer-Betke test result, and, in one-third of the positive cases, more than 1 mL of fetal blood was found in maternal circulation.14 This risk can be minimized by administering Rho (D) immune globulin to all Rh-negative mothers after the procedure.

Even these small risks, however, should not be considered in isolation. The infrequent complications of ECV must be compared with what can occur with breech-presenting fetuses during labor or cesarean delivery: complications of breech vaginal delivery, cord prolapse, difficulties with cesarean delivery, and maternal operative complications related to present and future cesarean deliveries.

Alternative approaches to converting breech presentation of unproven efficacy

Over the years, attempts have been made to address breech presentations with measures short of ECV. There is little evidence that these measures work, or work consistently.

  • Observation. After 36 weeks’ gestation, only 8% of fetuses in breech presentationspontaneously move into vertex presentation.5
  • Maternal positioning. There is no good evidence that such maneuvers are effective in changing fetal presentation.15
  • Moxibustion and acupuncture. Moxibustion is inhalation of smoke from burning herbal compounds. In formal studies using controls, these techniques did not consistently increase the rate of movement from breech to vertex presentation.16–18 Likewise, studies with the use of acupuncture have not shown consistent success in changing fetal presentation.19

 

Read about various methods to facilitate ECV success

 

 

Methods to facilitate ECV success

Two techniques that can facilitate ECV success are tocolysis, which relaxes the uterus, and neuraxial analgesia/anesthesia, which relaxes anterior abdominal wall muscles and reduces or relieves ECV-associated pain.

Tocolysis

In tocolysis, a medication is administered to reduce myometrial activity and to relax the uterine muscle so that it stretches more easily around the fetus during repositioning. Tocolytic medications originally were studied for their use in decreasing myometrial tone during preterm labor.

Tocolysis clearly is effective in increasing ECV success rates. Reviewing the results of 4 randomized trials, Cluver showed a 1.38 risk ratio for successful ECV when terbutaline was used versus when there was no tocolysis. The risk ratio for cesarean delivery was 0.82.20 Fernandez, in a study of 103 women divided into terbutaline versus placebo groups, had a 52% success rate for ECV with the terbutaline group versus only a 27% success rate with the placebo group.21

Tocolytic medications include terbutaline, nifedipine, and nitroglycerin.

Tocolysis most often involves the use of β2-adrenergic receptor agonists, particularly terbutaline (despite the boxed safety warning in its prescribing information). A 0.25-mg dose of terbutaline is given subcutaneously 15 to 30 minutes before ECV. Clinicians have successfully used β2-adrenergic receptor agonists in the treatment of patients in preterm labor, and there are more data on this class of medications than on other agents used to facilitate ECV.

Although nifedipine is as effective as terbutaline in the temporary treatment of preterm uterine contractions, several studies have found this calcium channel blocker less effective than terbutaline in facilitating ECV.22,23

The uterus-relaxing effect of nitroglycerin was once thought to make this medication appropriate for facilitating ECV, but multiple studies have found success rates unimproved. In some cases, the drug performed more poorly than placebo.24 Moreover, nitroglycerin is associated with a fairly high rate of adverse effects, such as headaches and blood pressure changes.

Neuraxial analgesia/anesthesia

Over the past 2 decades, there has been a resurgence in the use of neuraxial analgesia/anesthesia in ECV. This technique is more effective than others in improving ECV success rates, it reduces maternal discomfort, and it is very safe. Specifically, it relaxes the maternal abdominal wall muscles and thereby facilitates ECV. Another benefit is that the anesthesia is in place and available for use should emergency cesarean delivery be needed during or after attempted ECV. Neuraxial anesthesia, which includes spinal, epidural, and combined spinal-epidural techniques, is almost always used with tocolysis.

The major complications of neuraxial analgesia/anesthesia are maternal hypotension and fetal bradycardia. Each is dose related and usually transient.

In the past, there was concern that using regional anesthesia to control pain would reduce a patient’s natural warning symptoms and result in a clinician applying excessive force, thus increasing the chances of fetal and maternal injury and even fetal death. However, multiple studies have found that ECV complication rates are not increased with use of neuraxial methods.

Higher doses of neuraxial anesthesia produce higher ECV success rates. This dose-dependent relationship is almost surely attributable to the fact that, although lower dose neuraxial analgesia can relieve the pain associated with ECV, an anesthetic dose is needed to relax the abdominal wall muscles and facilitate fetus repositioning.

The literature is clear: ECV success rates are significantly increased with the use of neuraxial techniques, with anesthesia having higher success rates than analgesia. Reviewing the results of 6 controlled trials in which a total of 508 patients underwent ECV with tocolysis, Goetzinger and colleagues found that the chance of ECV success was almost 60% higher in the 253 patients who received regional anesthesia than in the 255 patients who received intravenous or no analgesia.25 Moreover, only 48.4% of the regional anesthesia patients as compared with 59.3% of patients who did not have regional anesthesia underwent cesarean delivery, roughly a 20% decrease. Pain scores were consistently lower in the regional anesthesia group. Multiple other studies have reported similar results.

Although the use of neuraxial anesthesia increases the ECV success rate, and decreases the cesarean delivery rate for breech presentation by 5% to 15%,25 some groups of obstetrics professionals, noting that the decreased cesarean delivery rate does not meet the formal criterion for statistical significance, have expressed reservations about recommending regional anesthesia for ECV. Thus, despite the positive results obtained with neuraxial anesthesia, neither the literature nor authoritative professional organizations definitively recommend the use of neuraxial anesthesia in facilitating ECV.

This lack of official recommendation, however, overlooks an important point: While the cesarean delivery percentage decrease that occurs with the use of neuraxial anesthesia may not be statistically significant, the promise of a pain-free procedure will encourage more women to undergo ECV. If the procedure population increases, then the average ECV success rate of roughly 60%6 applies to a larger base of patients, reducing the total number of cesarean deliveries for breech presentation. As only a small percentage of the 110,000 to 150,000 women with breech presentation at 36 weeks currently elects to undergo ECV, any increase in the number of women who proceed with attempts at fetal repositioning once procedural pain is no longer an issue will accordingly reduce the number of cesarean deliveries for the indication of malpresentation.

 

Related article:
Nitrous oxide for labor pain

 

Overarching goal: Reduce cesarean delivery rate and associated risks

In the United States, increasing the use of ECV in cases of breech-presenting fetuses would reduce the cesarean delivery rate by about 10%, thereby reducing recovery time for cesarean deliveries, minimizing the risks associated with these deliveries (current and future), and providing the health care system with a major cost savings.

Tocolysis and the use of neuraxial anesthesia each increases the ECV success rate and each is remarkably safe within the context of a well-defined protocol. Reducing the pain associated with ECV by administering neuraxial anesthesia will increase the number of women electing to undergo the procedure and ultimately will reduce the number of cesarean deliveries performed for the indication of breech presentation.

 

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

References
  1. Hannah ME, Hannah WJ, Hewson SA, Hodnett ED, Saigal S, Willan AR. Planned cesarean section versus planned vaginal birth for breech presentation at term: a randomised multicentre trial. Term Breech Trial Collaborative Group. Lancet. 2000;356(9239):1375–1383.
  2. Weiniger CF, Lyell DJ, Tsen LC, et al. Maternal outcomes of term breech presentation delivery: impact of successful external cephalic version in a nationwide sample of delivery admissions in the United States. BMC Pregnancy Childbirth. 2016;16(1):150.
  3. Eller DP, Van Dorsten JP. Breech presentation. Curr Opin Obstet Gynecol.1993;5(5)664–668.
  4. Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics. 24th ed. New York, NY: McGraw Hill; 2014:570.
  5. Westgren M, Edvall H, Nordstrom L, Svalenius E, Ranstam J. Spontaneous cephalic version of breech presentation in the last trimester. Br J Obstet Gynaecol. 1985;92(1):19–22.
  6. External cephalic version. ACOG Practice Bulletin No. 161. American College of Obstetricians and Gynecologists. Washington, DC: ACOG; 2016.
  7. Hofmeyr GJ, Kulier R, West HM. External cephalic version for breech presentation at term. Cochrane Database Syst Rev. 2015;(4):CD000083.
  8. Beuckens A, Rijnders M, Verburgt-Doeleman GH, Rijninks-van Driel GC, Thorpe J, Hutton EK. An observational study of the success and complications of 2546 external cephalic versions in low-risk pregnant women performed by trained midwives. BJOG. 2016;123(3):415–423.
  9. Tong Leung VK, Suen SS, Singh Sahota D, Lau TK, Yeung Leung T. External cephalic version does not increase the risk of intra-uterine death: a 17-year experience and literature review. J Matern Fetal Neonatal Med. 2012;25(9):1774–1778.
  10. de Hundt M, Velzel J, de Groot CJ, Mol BW, Kok M. Mode of delivery after successful external cephalic version: a systematic review and meta-analysis. Obstet Gynecol. 2014;123(6):1327–1334.
  11. Grootscholten K, Kok M, Oei SG, Mol BW, van der Post JA. External cephalic version–related risks: a meta-analysis. Obstet Gynecol. 2008;112(5):1143–1151.
  12. Collaris RJ, Oei SG. External cephalic version: a safe procedure? A systematic review of version-related risk. Acta Obstet Gynecol Scand. 2004;83(6):511–518.
  13. Khaw KS, Lee SW, Ngan Kee WD, et al. Randomized trial of anesthetic interventions in external cephalic version for breech presentation. Br J Anaesth. 2015;114(6):944–950.
  14. Boucher M, Marquette GP, Varin J, Champagne J, Bujold E. Fetomaternal hemorrhage during external cephalic version. Obstet Gynecol. 2008;112(1):79–84.
  15. Hofmeyr GJ, Kulier R. Cephalic version by postural management for breech presentation. Cochrane Database Syst Rev. 2012;(10):CD00051.
  16. Coulon C, Poleszczuk M, Paty-Montaigne MH, et al. Version of breech fetuses by moxibustion with acupuncture: a randomized controlled trial. Obstet Gynecol. 2014;124(1):32–39.
  17. Bue L, Lauszus FF. Moxibustion did not have an effect in a randomised clinical trial for version of breech position. Dan Med J. 2016;63(2):pii:A5199.
  18. Coyle ME, Smith CA, Peat B. Cephalic version by moxibustion for breech presentation. Cochrane Database Syst Rev. 2012;(5):CD003928.
  19. Sananes N, Roth GE, Aissi GA, et al. Acupuncture version of breech presentation: a randomized sham-controlled single-blinded trial. Eur J Obstet Gynecol Reprod Biol. 2016;204:24–30.
  20. Cluver C, Gyte GM, Sinclair M, Dowswell T, Hofmeyr G. Interventions for helping to turn breech babies to head first presentation when using external cephalic version. Cochrane Database Syst Rev. 2015;(2):CD000184.
  21. Fernandez CO, Bloom SL, Smulian JC, Ananth CV, Wendel GD Jr. A randomized placebo-controlled evaluation of terbutaline for external cephalic version. Obstet Gynecol. 1997;90(5):775–779.
  22. Mohamed Ismail NA, Ibrahim M, Mohd Naim N, Mahdy ZA, Jamil MA, Mohd Razi ZR. Nifedipine versus terbutaline for tocolysis in external cephalic version. Int J Gynaecol Obstet. 2008;102(3):263–266.
  23. Kok M, Bais J, van Lith J, et al. Nifedipine as a uterine relaxant for external cephalic version: a meta-analysis. Am J Obstet Gynecol. 2008;112(2 pt 1):271–276.
  24. Bujold E, Boucher M, Rinfred D, Berman S, Ferreira E, Marquette GP. Sublingual nitroglycerin versus placebo as a tocolytic for external cephalic version: a randomized controlled trial in parous women. Am J Obstet Gynecol. 2003;189(4):1070–1073.
  25. Goetzinger KR, Harper LM, Tuuli MG, Macones GA, Colditz GA. Effect of regional anesthesia on the success of external cephalic version: a systematic review and meta-analysis. Obstet Gynecol. 2011;118(5):1137–1144.
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About 3% to 4% of all fetuses at term are in breech presentation. Since 2000, when Hannah and colleagues reported finding that vaginal delivery of breech-presenting babies was riskier than cesarean delivery,1 most breech-presenting neonates in the United States have been delivered abdominally2—despite subsequent questioning of some of that study’s conclusions.

Each year in the United States, approximately 4 million babies are born, and fetal malpresentation accounts for 110,000 to 150,000 cesarean deliveries. In fact, about 15% of all cesarean deliveries in the United States are for breech presentation or transverse lie; in England the percentage is 10%.3 Fortunately, the repopularized technique of external cephalic version (ECV), in which the clinician externally rotates a breech- or transverse-lying fetus to a vertex position (FIGURE), along with the facilitating tools of tocolysis and neuraxial analgesia/anesthesia, is helping to reduce the number of breech presentations in fetuses at term and thus the number of cesarean deliveries and their sequelae—placenta accreta, prolonged recovery, and cesarean deliveries in subsequent pregnancies.

Reluctance to perform ECV is unfounded

In the United States, the practice of offering ECV to women who present with their fetus in breech presentation at term varies tremendously. It is routine at some institutions but not even offered at others.

Many ObGyns are reluctant to perform ECV. Cited reasons include the potential for injury to the fetus and mother (and related liability concerns), the ease of elective cesarean delivery, the variable success rate of ECV (35% to 86%),4 and the pain that women often have with the procedure. According to the literature, however, these concerns either are unfounded or can be mitigated with use of current techniques. Multiple studies have found that the risk of ECV to the fetus and mother is minimal, and that tocolysis and neuraxial anesthesia can facilitate the success of ECV and relieve the pain associated with the procedure.

 

Related article:
2017 Update on obstetrics

 

Indications for ECV

The indications for ECV include breech, oblique, or transverse lie presentation after 36 weeks’ gestation and the mother’s desire to avoid cesarean delivery. A clinician skilled in ECV and a facility where emergency cesarean delivery is possible are essential.

There are several instances in which ECV should not be attempted.

Contraindications include:

  • concerns about fetal status, including nonreactive nonstress test, biophysical profile score <6/8, severe intrauterine growth restriction, decreased end-diastolic umbilical blood flow
  • placenta previa
  • multifetal gestation before delivery of first twin
  • severe oligohydramnios
  • severe preeclampsia
  • significant fetal anomaly
  • known malformation of uterus
  • breech with hyperextended head or arms above shoulders, as seen on ultrasonography.

More controversial contraindications include prior uterine incision, maternal obesity (body mass index >40 kg/m2), ruptured membranes, and fetal macrosomia.

 

Read about timing, success rates, risk factors, alternate approaches for ECV

 

 

Optimal timing for the ECV procedure

Current practice is to wait until 36 to 37 weeks to perform ECV, as most fetuses spontaneously move into vertex presentation by 36 weeks’ gestation. This time frame has several advantages: Many unnecessary attempts at ECV are avoided; only 8% of fetuses in breech presentation after 36 weeks spontaneously change to vertex5; many fetuses revert to breech if ECV is performed too early; and prematurity generally is not an issue in the rare case that immediate delivery is required during or just after attempted ECV.

ECV during labor. Performing ECV during labor appears to pose no increased risk to mother or fetus if membranes are intact and there are no other contraindications to the procedure. Some clinicians perform ECV only during labor. The advantages are that the fetus has had every chance to move into vertex presentation on its own, the equipment used to continuously monitor the fetus during ECV is in place, and cesarean delivery and anesthesia are immediately available in the event ECV is unsuccessful.

The major disadvantage of waiting until labor is that the increased size of the fetus makes ECV more difficult. In addition, the membranes may have already ruptured, and the breech may have descended deeply into the pelvis.

 

Related article:
For the management of labor, patience is a virtue

 

Success rates in breech-to-vertex conversions

In 2016, the American College of Obstetricians and Gynecologists (ACOG) reported an average ECV success rate of 58% (range, 16% to 100%).6 ACOG noted that, with transverse lie, the success rate was significantly higher. Other studies have found a wide range of rates: 58% in 1,308 patients in a Cochrane review by Hofmeyr and colleagues7; 47% in a study by Beuckens and colleagues8; and 63.1% for primiparas and 82.7% for multiparas in a study by Tong Leung and colleagues.9 These rates were affected by whether ECV was performed with or without tocolysis, with or without intravenous analgesia, and with or without neuraxial analgesia/anesthesia (TABLE).

Likelihood of vaginal delivery after successful ECV

The rate of vaginal delivery after successful ECV is roughly half that of fetuses that were never in breech presentation.10 In successful ECV cases, dystocia and nonreassuring fetal heart rate patterns are the major indications for cesarean delivery. Some experts have speculated that the factors leading to near-term breech presentation—such as an unengaged presenting part or a mother’s smaller pelvis—also may be risk factors for dystocia in labor. Despite this, the rate of vaginal delivery of successfully verted babies has been reported to be as high as 80%.10

As might be expected, post-ECV vaginal deliveries are more common in multiparous than in primiparous women.

 
Risks of ECV: Generally low and manageable

Although multiple problems may occur with ECV, generally they are rare and reversible. For instance, Grootscholten and colleagues found a stillbirth and placental abruption rate of only 0.25% in a large group of patients who underwent ECV.11 Similarly, the rate of emergency cesarean delivery was 0.35%. In addition, Hofmeyr and Kulier, in their Cochrane Data Review of 2015, found no significant differences in the Apgar scores and pH’s of babies in the ECV group compared with babies in breech presentation whose mothers did not undergo ECV.7 Results of other studies have confirmed the safety of ECV.12,13

One significant risk of ECV attempts is fetal-to-maternal blood transfer. Boucher and colleagues found that 2.4% of 1,244 women who underwent ECV had a positive Kleihauer-Betke test result, and, in one-third of the positive cases, more than 1 mL of fetal blood was found in maternal circulation.14 This risk can be minimized by administering Rho (D) immune globulin to all Rh-negative mothers after the procedure.

Even these small risks, however, should not be considered in isolation. The infrequent complications of ECV must be compared with what can occur with breech-presenting fetuses during labor or cesarean delivery: complications of breech vaginal delivery, cord prolapse, difficulties with cesarean delivery, and maternal operative complications related to present and future cesarean deliveries.

Alternative approaches to converting breech presentation of unproven efficacy

Over the years, attempts have been made to address breech presentations with measures short of ECV. There is little evidence that these measures work, or work consistently.

  • Observation. After 36 weeks’ gestation, only 8% of fetuses in breech presentationspontaneously move into vertex presentation.5
  • Maternal positioning. There is no good evidence that such maneuvers are effective in changing fetal presentation.15
  • Moxibustion and acupuncture. Moxibustion is inhalation of smoke from burning herbal compounds. In formal studies using controls, these techniques did not consistently increase the rate of movement from breech to vertex presentation.16–18 Likewise, studies with the use of acupuncture have not shown consistent success in changing fetal presentation.19

 

Read about various methods to facilitate ECV success

 

 

Methods to facilitate ECV success

Two techniques that can facilitate ECV success are tocolysis, which relaxes the uterus, and neuraxial analgesia/anesthesia, which relaxes anterior abdominal wall muscles and reduces or relieves ECV-associated pain.

Tocolysis

In tocolysis, a medication is administered to reduce myometrial activity and to relax the uterine muscle so that it stretches more easily around the fetus during repositioning. Tocolytic medications originally were studied for their use in decreasing myometrial tone during preterm labor.

Tocolysis clearly is effective in increasing ECV success rates. Reviewing the results of 4 randomized trials, Cluver showed a 1.38 risk ratio for successful ECV when terbutaline was used versus when there was no tocolysis. The risk ratio for cesarean delivery was 0.82.20 Fernandez, in a study of 103 women divided into terbutaline versus placebo groups, had a 52% success rate for ECV with the terbutaline group versus only a 27% success rate with the placebo group.21

Tocolytic medications include terbutaline, nifedipine, and nitroglycerin.

Tocolysis most often involves the use of β2-adrenergic receptor agonists, particularly terbutaline (despite the boxed safety warning in its prescribing information). A 0.25-mg dose of terbutaline is given subcutaneously 15 to 30 minutes before ECV. Clinicians have successfully used β2-adrenergic receptor agonists in the treatment of patients in preterm labor, and there are more data on this class of medications than on other agents used to facilitate ECV.

Although nifedipine is as effective as terbutaline in the temporary treatment of preterm uterine contractions, several studies have found this calcium channel blocker less effective than terbutaline in facilitating ECV.22,23

The uterus-relaxing effect of nitroglycerin was once thought to make this medication appropriate for facilitating ECV, but multiple studies have found success rates unimproved. In some cases, the drug performed more poorly than placebo.24 Moreover, nitroglycerin is associated with a fairly high rate of adverse effects, such as headaches and blood pressure changes.

Neuraxial analgesia/anesthesia

Over the past 2 decades, there has been a resurgence in the use of neuraxial analgesia/anesthesia in ECV. This technique is more effective than others in improving ECV success rates, it reduces maternal discomfort, and it is very safe. Specifically, it relaxes the maternal abdominal wall muscles and thereby facilitates ECV. Another benefit is that the anesthesia is in place and available for use should emergency cesarean delivery be needed during or after attempted ECV. Neuraxial anesthesia, which includes spinal, epidural, and combined spinal-epidural techniques, is almost always used with tocolysis.

The major complications of neuraxial analgesia/anesthesia are maternal hypotension and fetal bradycardia. Each is dose related and usually transient.

In the past, there was concern that using regional anesthesia to control pain would reduce a patient’s natural warning symptoms and result in a clinician applying excessive force, thus increasing the chances of fetal and maternal injury and even fetal death. However, multiple studies have found that ECV complication rates are not increased with use of neuraxial methods.

Higher doses of neuraxial anesthesia produce higher ECV success rates. This dose-dependent relationship is almost surely attributable to the fact that, although lower dose neuraxial analgesia can relieve the pain associated with ECV, an anesthetic dose is needed to relax the abdominal wall muscles and facilitate fetus repositioning.

The literature is clear: ECV success rates are significantly increased with the use of neuraxial techniques, with anesthesia having higher success rates than analgesia. Reviewing the results of 6 controlled trials in which a total of 508 patients underwent ECV with tocolysis, Goetzinger and colleagues found that the chance of ECV success was almost 60% higher in the 253 patients who received regional anesthesia than in the 255 patients who received intravenous or no analgesia.25 Moreover, only 48.4% of the regional anesthesia patients as compared with 59.3% of patients who did not have regional anesthesia underwent cesarean delivery, roughly a 20% decrease. Pain scores were consistently lower in the regional anesthesia group. Multiple other studies have reported similar results.

Although the use of neuraxial anesthesia increases the ECV success rate, and decreases the cesarean delivery rate for breech presentation by 5% to 15%,25 some groups of obstetrics professionals, noting that the decreased cesarean delivery rate does not meet the formal criterion for statistical significance, have expressed reservations about recommending regional anesthesia for ECV. Thus, despite the positive results obtained with neuraxial anesthesia, neither the literature nor authoritative professional organizations definitively recommend the use of neuraxial anesthesia in facilitating ECV.

This lack of official recommendation, however, overlooks an important point: While the cesarean delivery percentage decrease that occurs with the use of neuraxial anesthesia may not be statistically significant, the promise of a pain-free procedure will encourage more women to undergo ECV. If the procedure population increases, then the average ECV success rate of roughly 60%6 applies to a larger base of patients, reducing the total number of cesarean deliveries for breech presentation. As only a small percentage of the 110,000 to 150,000 women with breech presentation at 36 weeks currently elects to undergo ECV, any increase in the number of women who proceed with attempts at fetal repositioning once procedural pain is no longer an issue will accordingly reduce the number of cesarean deliveries for the indication of malpresentation.

 

Related article:
Nitrous oxide for labor pain

 

Overarching goal: Reduce cesarean delivery rate and associated risks

In the United States, increasing the use of ECV in cases of breech-presenting fetuses would reduce the cesarean delivery rate by about 10%, thereby reducing recovery time for cesarean deliveries, minimizing the risks associated with these deliveries (current and future), and providing the health care system with a major cost savings.

Tocolysis and the use of neuraxial anesthesia each increases the ECV success rate and each is remarkably safe within the context of a well-defined protocol. Reducing the pain associated with ECV by administering neuraxial anesthesia will increase the number of women electing to undergo the procedure and ultimately will reduce the number of cesarean deliveries performed for the indication of breech presentation.

 

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

About 3% to 4% of all fetuses at term are in breech presentation. Since 2000, when Hannah and colleagues reported finding that vaginal delivery of breech-presenting babies was riskier than cesarean delivery,1 most breech-presenting neonates in the United States have been delivered abdominally2—despite subsequent questioning of some of that study’s conclusions.

Each year in the United States, approximately 4 million babies are born, and fetal malpresentation accounts for 110,000 to 150,000 cesarean deliveries. In fact, about 15% of all cesarean deliveries in the United States are for breech presentation or transverse lie; in England the percentage is 10%.3 Fortunately, the repopularized technique of external cephalic version (ECV), in which the clinician externally rotates a breech- or transverse-lying fetus to a vertex position (FIGURE), along with the facilitating tools of tocolysis and neuraxial analgesia/anesthesia, is helping to reduce the number of breech presentations in fetuses at term and thus the number of cesarean deliveries and their sequelae—placenta accreta, prolonged recovery, and cesarean deliveries in subsequent pregnancies.

Reluctance to perform ECV is unfounded

In the United States, the practice of offering ECV to women who present with their fetus in breech presentation at term varies tremendously. It is routine at some institutions but not even offered at others.

Many ObGyns are reluctant to perform ECV. Cited reasons include the potential for injury to the fetus and mother (and related liability concerns), the ease of elective cesarean delivery, the variable success rate of ECV (35% to 86%),4 and the pain that women often have with the procedure. According to the literature, however, these concerns either are unfounded or can be mitigated with use of current techniques. Multiple studies have found that the risk of ECV to the fetus and mother is minimal, and that tocolysis and neuraxial anesthesia can facilitate the success of ECV and relieve the pain associated with the procedure.

 

Related article:
2017 Update on obstetrics

 

Indications for ECV

The indications for ECV include breech, oblique, or transverse lie presentation after 36 weeks’ gestation and the mother’s desire to avoid cesarean delivery. A clinician skilled in ECV and a facility where emergency cesarean delivery is possible are essential.

There are several instances in which ECV should not be attempted.

Contraindications include:

  • concerns about fetal status, including nonreactive nonstress test, biophysical profile score <6/8, severe intrauterine growth restriction, decreased end-diastolic umbilical blood flow
  • placenta previa
  • multifetal gestation before delivery of first twin
  • severe oligohydramnios
  • severe preeclampsia
  • significant fetal anomaly
  • known malformation of uterus
  • breech with hyperextended head or arms above shoulders, as seen on ultrasonography.

More controversial contraindications include prior uterine incision, maternal obesity (body mass index >40 kg/m2), ruptured membranes, and fetal macrosomia.

 

Read about timing, success rates, risk factors, alternate approaches for ECV

 

 

Optimal timing for the ECV procedure

Current practice is to wait until 36 to 37 weeks to perform ECV, as most fetuses spontaneously move into vertex presentation by 36 weeks’ gestation. This time frame has several advantages: Many unnecessary attempts at ECV are avoided; only 8% of fetuses in breech presentation after 36 weeks spontaneously change to vertex5; many fetuses revert to breech if ECV is performed too early; and prematurity generally is not an issue in the rare case that immediate delivery is required during or just after attempted ECV.

ECV during labor. Performing ECV during labor appears to pose no increased risk to mother or fetus if membranes are intact and there are no other contraindications to the procedure. Some clinicians perform ECV only during labor. The advantages are that the fetus has had every chance to move into vertex presentation on its own, the equipment used to continuously monitor the fetus during ECV is in place, and cesarean delivery and anesthesia are immediately available in the event ECV is unsuccessful.

The major disadvantage of waiting until labor is that the increased size of the fetus makes ECV more difficult. In addition, the membranes may have already ruptured, and the breech may have descended deeply into the pelvis.

 

Related article:
For the management of labor, patience is a virtue

 

Success rates in breech-to-vertex conversions

In 2016, the American College of Obstetricians and Gynecologists (ACOG) reported an average ECV success rate of 58% (range, 16% to 100%).6 ACOG noted that, with transverse lie, the success rate was significantly higher. Other studies have found a wide range of rates: 58% in 1,308 patients in a Cochrane review by Hofmeyr and colleagues7; 47% in a study by Beuckens and colleagues8; and 63.1% for primiparas and 82.7% for multiparas in a study by Tong Leung and colleagues.9 These rates were affected by whether ECV was performed with or without tocolysis, with or without intravenous analgesia, and with or without neuraxial analgesia/anesthesia (TABLE).

Likelihood of vaginal delivery after successful ECV

The rate of vaginal delivery after successful ECV is roughly half that of fetuses that were never in breech presentation.10 In successful ECV cases, dystocia and nonreassuring fetal heart rate patterns are the major indications for cesarean delivery. Some experts have speculated that the factors leading to near-term breech presentation—such as an unengaged presenting part or a mother’s smaller pelvis—also may be risk factors for dystocia in labor. Despite this, the rate of vaginal delivery of successfully verted babies has been reported to be as high as 80%.10

As might be expected, post-ECV vaginal deliveries are more common in multiparous than in primiparous women.

 
Risks of ECV: Generally low and manageable

Although multiple problems may occur with ECV, generally they are rare and reversible. For instance, Grootscholten and colleagues found a stillbirth and placental abruption rate of only 0.25% in a large group of patients who underwent ECV.11 Similarly, the rate of emergency cesarean delivery was 0.35%. In addition, Hofmeyr and Kulier, in their Cochrane Data Review of 2015, found no significant differences in the Apgar scores and pH’s of babies in the ECV group compared with babies in breech presentation whose mothers did not undergo ECV.7 Results of other studies have confirmed the safety of ECV.12,13

One significant risk of ECV attempts is fetal-to-maternal blood transfer. Boucher and colleagues found that 2.4% of 1,244 women who underwent ECV had a positive Kleihauer-Betke test result, and, in one-third of the positive cases, more than 1 mL of fetal blood was found in maternal circulation.14 This risk can be minimized by administering Rho (D) immune globulin to all Rh-negative mothers after the procedure.

Even these small risks, however, should not be considered in isolation. The infrequent complications of ECV must be compared with what can occur with breech-presenting fetuses during labor or cesarean delivery: complications of breech vaginal delivery, cord prolapse, difficulties with cesarean delivery, and maternal operative complications related to present and future cesarean deliveries.

Alternative approaches to converting breech presentation of unproven efficacy

Over the years, attempts have been made to address breech presentations with measures short of ECV. There is little evidence that these measures work, or work consistently.

  • Observation. After 36 weeks’ gestation, only 8% of fetuses in breech presentationspontaneously move into vertex presentation.5
  • Maternal positioning. There is no good evidence that such maneuvers are effective in changing fetal presentation.15
  • Moxibustion and acupuncture. Moxibustion is inhalation of smoke from burning herbal compounds. In formal studies using controls, these techniques did not consistently increase the rate of movement from breech to vertex presentation.16–18 Likewise, studies with the use of acupuncture have not shown consistent success in changing fetal presentation.19

 

Read about various methods to facilitate ECV success

 

 

Methods to facilitate ECV success

Two techniques that can facilitate ECV success are tocolysis, which relaxes the uterus, and neuraxial analgesia/anesthesia, which relaxes anterior abdominal wall muscles and reduces or relieves ECV-associated pain.

Tocolysis

In tocolysis, a medication is administered to reduce myometrial activity and to relax the uterine muscle so that it stretches more easily around the fetus during repositioning. Tocolytic medications originally were studied for their use in decreasing myometrial tone during preterm labor.

Tocolysis clearly is effective in increasing ECV success rates. Reviewing the results of 4 randomized trials, Cluver showed a 1.38 risk ratio for successful ECV when terbutaline was used versus when there was no tocolysis. The risk ratio for cesarean delivery was 0.82.20 Fernandez, in a study of 103 women divided into terbutaline versus placebo groups, had a 52% success rate for ECV with the terbutaline group versus only a 27% success rate with the placebo group.21

Tocolytic medications include terbutaline, nifedipine, and nitroglycerin.

Tocolysis most often involves the use of β2-adrenergic receptor agonists, particularly terbutaline (despite the boxed safety warning in its prescribing information). A 0.25-mg dose of terbutaline is given subcutaneously 15 to 30 minutes before ECV. Clinicians have successfully used β2-adrenergic receptor agonists in the treatment of patients in preterm labor, and there are more data on this class of medications than on other agents used to facilitate ECV.

Although nifedipine is as effective as terbutaline in the temporary treatment of preterm uterine contractions, several studies have found this calcium channel blocker less effective than terbutaline in facilitating ECV.22,23

The uterus-relaxing effect of nitroglycerin was once thought to make this medication appropriate for facilitating ECV, but multiple studies have found success rates unimproved. In some cases, the drug performed more poorly than placebo.24 Moreover, nitroglycerin is associated with a fairly high rate of adverse effects, such as headaches and blood pressure changes.

Neuraxial analgesia/anesthesia

Over the past 2 decades, there has been a resurgence in the use of neuraxial analgesia/anesthesia in ECV. This technique is more effective than others in improving ECV success rates, it reduces maternal discomfort, and it is very safe. Specifically, it relaxes the maternal abdominal wall muscles and thereby facilitates ECV. Another benefit is that the anesthesia is in place and available for use should emergency cesarean delivery be needed during or after attempted ECV. Neuraxial anesthesia, which includes spinal, epidural, and combined spinal-epidural techniques, is almost always used with tocolysis.

The major complications of neuraxial analgesia/anesthesia are maternal hypotension and fetal bradycardia. Each is dose related and usually transient.

In the past, there was concern that using regional anesthesia to control pain would reduce a patient’s natural warning symptoms and result in a clinician applying excessive force, thus increasing the chances of fetal and maternal injury and even fetal death. However, multiple studies have found that ECV complication rates are not increased with use of neuraxial methods.

Higher doses of neuraxial anesthesia produce higher ECV success rates. This dose-dependent relationship is almost surely attributable to the fact that, although lower dose neuraxial analgesia can relieve the pain associated with ECV, an anesthetic dose is needed to relax the abdominal wall muscles and facilitate fetus repositioning.

The literature is clear: ECV success rates are significantly increased with the use of neuraxial techniques, with anesthesia having higher success rates than analgesia. Reviewing the results of 6 controlled trials in which a total of 508 patients underwent ECV with tocolysis, Goetzinger and colleagues found that the chance of ECV success was almost 60% higher in the 253 patients who received regional anesthesia than in the 255 patients who received intravenous or no analgesia.25 Moreover, only 48.4% of the regional anesthesia patients as compared with 59.3% of patients who did not have regional anesthesia underwent cesarean delivery, roughly a 20% decrease. Pain scores were consistently lower in the regional anesthesia group. Multiple other studies have reported similar results.

Although the use of neuraxial anesthesia increases the ECV success rate, and decreases the cesarean delivery rate for breech presentation by 5% to 15%,25 some groups of obstetrics professionals, noting that the decreased cesarean delivery rate does not meet the formal criterion for statistical significance, have expressed reservations about recommending regional anesthesia for ECV. Thus, despite the positive results obtained with neuraxial anesthesia, neither the literature nor authoritative professional organizations definitively recommend the use of neuraxial anesthesia in facilitating ECV.

This lack of official recommendation, however, overlooks an important point: While the cesarean delivery percentage decrease that occurs with the use of neuraxial anesthesia may not be statistically significant, the promise of a pain-free procedure will encourage more women to undergo ECV. If the procedure population increases, then the average ECV success rate of roughly 60%6 applies to a larger base of patients, reducing the total number of cesarean deliveries for breech presentation. As only a small percentage of the 110,000 to 150,000 women with breech presentation at 36 weeks currently elects to undergo ECV, any increase in the number of women who proceed with attempts at fetal repositioning once procedural pain is no longer an issue will accordingly reduce the number of cesarean deliveries for the indication of malpresentation.

 

Related article:
Nitrous oxide for labor pain

 

Overarching goal: Reduce cesarean delivery rate and associated risks

In the United States, increasing the use of ECV in cases of breech-presenting fetuses would reduce the cesarean delivery rate by about 10%, thereby reducing recovery time for cesarean deliveries, minimizing the risks associated with these deliveries (current and future), and providing the health care system with a major cost savings.

Tocolysis and the use of neuraxial anesthesia each increases the ECV success rate and each is remarkably safe within the context of a well-defined protocol. Reducing the pain associated with ECV by administering neuraxial anesthesia will increase the number of women electing to undergo the procedure and ultimately will reduce the number of cesarean deliveries performed for the indication of breech presentation.

 

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

References
  1. Hannah ME, Hannah WJ, Hewson SA, Hodnett ED, Saigal S, Willan AR. Planned cesarean section versus planned vaginal birth for breech presentation at term: a randomised multicentre trial. Term Breech Trial Collaborative Group. Lancet. 2000;356(9239):1375–1383.
  2. Weiniger CF, Lyell DJ, Tsen LC, et al. Maternal outcomes of term breech presentation delivery: impact of successful external cephalic version in a nationwide sample of delivery admissions in the United States. BMC Pregnancy Childbirth. 2016;16(1):150.
  3. Eller DP, Van Dorsten JP. Breech presentation. Curr Opin Obstet Gynecol.1993;5(5)664–668.
  4. Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics. 24th ed. New York, NY: McGraw Hill; 2014:570.
  5. Westgren M, Edvall H, Nordstrom L, Svalenius E, Ranstam J. Spontaneous cephalic version of breech presentation in the last trimester. Br J Obstet Gynaecol. 1985;92(1):19–22.
  6. External cephalic version. ACOG Practice Bulletin No. 161. American College of Obstetricians and Gynecologists. Washington, DC: ACOG; 2016.
  7. Hofmeyr GJ, Kulier R, West HM. External cephalic version for breech presentation at term. Cochrane Database Syst Rev. 2015;(4):CD000083.
  8. Beuckens A, Rijnders M, Verburgt-Doeleman GH, Rijninks-van Driel GC, Thorpe J, Hutton EK. An observational study of the success and complications of 2546 external cephalic versions in low-risk pregnant women performed by trained midwives. BJOG. 2016;123(3):415–423.
  9. Tong Leung VK, Suen SS, Singh Sahota D, Lau TK, Yeung Leung T. External cephalic version does not increase the risk of intra-uterine death: a 17-year experience and literature review. J Matern Fetal Neonatal Med. 2012;25(9):1774–1778.
  10. de Hundt M, Velzel J, de Groot CJ, Mol BW, Kok M. Mode of delivery after successful external cephalic version: a systematic review and meta-analysis. Obstet Gynecol. 2014;123(6):1327–1334.
  11. Grootscholten K, Kok M, Oei SG, Mol BW, van der Post JA. External cephalic version–related risks: a meta-analysis. Obstet Gynecol. 2008;112(5):1143–1151.
  12. Collaris RJ, Oei SG. External cephalic version: a safe procedure? A systematic review of version-related risk. Acta Obstet Gynecol Scand. 2004;83(6):511–518.
  13. Khaw KS, Lee SW, Ngan Kee WD, et al. Randomized trial of anesthetic interventions in external cephalic version for breech presentation. Br J Anaesth. 2015;114(6):944–950.
  14. Boucher M, Marquette GP, Varin J, Champagne J, Bujold E. Fetomaternal hemorrhage during external cephalic version. Obstet Gynecol. 2008;112(1):79–84.
  15. Hofmeyr GJ, Kulier R. Cephalic version by postural management for breech presentation. Cochrane Database Syst Rev. 2012;(10):CD00051.
  16. Coulon C, Poleszczuk M, Paty-Montaigne MH, et al. Version of breech fetuses by moxibustion with acupuncture: a randomized controlled trial. Obstet Gynecol. 2014;124(1):32–39.
  17. Bue L, Lauszus FF. Moxibustion did not have an effect in a randomised clinical trial for version of breech position. Dan Med J. 2016;63(2):pii:A5199.
  18. Coyle ME, Smith CA, Peat B. Cephalic version by moxibustion for breech presentation. Cochrane Database Syst Rev. 2012;(5):CD003928.
  19. Sananes N, Roth GE, Aissi GA, et al. Acupuncture version of breech presentation: a randomized sham-controlled single-blinded trial. Eur J Obstet Gynecol Reprod Biol. 2016;204:24–30.
  20. Cluver C, Gyte GM, Sinclair M, Dowswell T, Hofmeyr G. Interventions for helping to turn breech babies to head first presentation when using external cephalic version. Cochrane Database Syst Rev. 2015;(2):CD000184.
  21. Fernandez CO, Bloom SL, Smulian JC, Ananth CV, Wendel GD Jr. A randomized placebo-controlled evaluation of terbutaline for external cephalic version. Obstet Gynecol. 1997;90(5):775–779.
  22. Mohamed Ismail NA, Ibrahim M, Mohd Naim N, Mahdy ZA, Jamil MA, Mohd Razi ZR. Nifedipine versus terbutaline for tocolysis in external cephalic version. Int J Gynaecol Obstet. 2008;102(3):263–266.
  23. Kok M, Bais J, van Lith J, et al. Nifedipine as a uterine relaxant for external cephalic version: a meta-analysis. Am J Obstet Gynecol. 2008;112(2 pt 1):271–276.
  24. Bujold E, Boucher M, Rinfred D, Berman S, Ferreira E, Marquette GP. Sublingual nitroglycerin versus placebo as a tocolytic for external cephalic version: a randomized controlled trial in parous women. Am J Obstet Gynecol. 2003;189(4):1070–1073.
  25. Goetzinger KR, Harper LM, Tuuli MG, Macones GA, Colditz GA. Effect of regional anesthesia on the success of external cephalic version: a systematic review and meta-analysis. Obstet Gynecol. 2011;118(5):1137–1144.
References
  1. Hannah ME, Hannah WJ, Hewson SA, Hodnett ED, Saigal S, Willan AR. Planned cesarean section versus planned vaginal birth for breech presentation at term: a randomised multicentre trial. Term Breech Trial Collaborative Group. Lancet. 2000;356(9239):1375–1383.
  2. Weiniger CF, Lyell DJ, Tsen LC, et al. Maternal outcomes of term breech presentation delivery: impact of successful external cephalic version in a nationwide sample of delivery admissions in the United States. BMC Pregnancy Childbirth. 2016;16(1):150.
  3. Eller DP, Van Dorsten JP. Breech presentation. Curr Opin Obstet Gynecol.1993;5(5)664–668.
  4. Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics. 24th ed. New York, NY: McGraw Hill; 2014:570.
  5. Westgren M, Edvall H, Nordstrom L, Svalenius E, Ranstam J. Spontaneous cephalic version of breech presentation in the last trimester. Br J Obstet Gynaecol. 1985;92(1):19–22.
  6. External cephalic version. ACOG Practice Bulletin No. 161. American College of Obstetricians and Gynecologists. Washington, DC: ACOG; 2016.
  7. Hofmeyr GJ, Kulier R, West HM. External cephalic version for breech presentation at term. Cochrane Database Syst Rev. 2015;(4):CD000083.
  8. Beuckens A, Rijnders M, Verburgt-Doeleman GH, Rijninks-van Driel GC, Thorpe J, Hutton EK. An observational study of the success and complications of 2546 external cephalic versions in low-risk pregnant women performed by trained midwives. BJOG. 2016;123(3):415–423.
  9. Tong Leung VK, Suen SS, Singh Sahota D, Lau TK, Yeung Leung T. External cephalic version does not increase the risk of intra-uterine death: a 17-year experience and literature review. J Matern Fetal Neonatal Med. 2012;25(9):1774–1778.
  10. de Hundt M, Velzel J, de Groot CJ, Mol BW, Kok M. Mode of delivery after successful external cephalic version: a systematic review and meta-analysis. Obstet Gynecol. 2014;123(6):1327–1334.
  11. Grootscholten K, Kok M, Oei SG, Mol BW, van der Post JA. External cephalic version–related risks: a meta-analysis. Obstet Gynecol. 2008;112(5):1143–1151.
  12. Collaris RJ, Oei SG. External cephalic version: a safe procedure? A systematic review of version-related risk. Acta Obstet Gynecol Scand. 2004;83(6):511–518.
  13. Khaw KS, Lee SW, Ngan Kee WD, et al. Randomized trial of anesthetic interventions in external cephalic version for breech presentation. Br J Anaesth. 2015;114(6):944–950.
  14. Boucher M, Marquette GP, Varin J, Champagne J, Bujold E. Fetomaternal hemorrhage during external cephalic version. Obstet Gynecol. 2008;112(1):79–84.
  15. Hofmeyr GJ, Kulier R. Cephalic version by postural management for breech presentation. Cochrane Database Syst Rev. 2012;(10):CD00051.
  16. Coulon C, Poleszczuk M, Paty-Montaigne MH, et al. Version of breech fetuses by moxibustion with acupuncture: a randomized controlled trial. Obstet Gynecol. 2014;124(1):32–39.
  17. Bue L, Lauszus FF. Moxibustion did not have an effect in a randomised clinical trial for version of breech position. Dan Med J. 2016;63(2):pii:A5199.
  18. Coyle ME, Smith CA, Peat B. Cephalic version by moxibustion for breech presentation. Cochrane Database Syst Rev. 2012;(5):CD003928.
  19. Sananes N, Roth GE, Aissi GA, et al. Acupuncture version of breech presentation: a randomized sham-controlled single-blinded trial. Eur J Obstet Gynecol Reprod Biol. 2016;204:24–30.
  20. Cluver C, Gyte GM, Sinclair M, Dowswell T, Hofmeyr G. Interventions for helping to turn breech babies to head first presentation when using external cephalic version. Cochrane Database Syst Rev. 2015;(2):CD000184.
  21. Fernandez CO, Bloom SL, Smulian JC, Ananth CV, Wendel GD Jr. A randomized placebo-controlled evaluation of terbutaline for external cephalic version. Obstet Gynecol. 1997;90(5):775–779.
  22. Mohamed Ismail NA, Ibrahim M, Mohd Naim N, Mahdy ZA, Jamil MA, Mohd Razi ZR. Nifedipine versus terbutaline for tocolysis in external cephalic version. Int J Gynaecol Obstet. 2008;102(3):263–266.
  23. Kok M, Bais J, van Lith J, et al. Nifedipine as a uterine relaxant for external cephalic version: a meta-analysis. Am J Obstet Gynecol. 2008;112(2 pt 1):271–276.
  24. Bujold E, Boucher M, Rinfred D, Berman S, Ferreira E, Marquette GP. Sublingual nitroglycerin versus placebo as a tocolytic for external cephalic version: a randomized controlled trial in parous women. Am J Obstet Gynecol. 2003;189(4):1070–1073.
  25. Goetzinger KR, Harper LM, Tuuli MG, Macones GA, Colditz GA. Effect of regional anesthesia on the success of external cephalic version: a systematic review and meta-analysis. Obstet Gynecol. 2011;118(5):1137–1144.
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  • Current practice is to wait until 36 to 37 weeks of gestation to perform ECV, since most fetuses spontaneously move into vertex presentation by 36 weeks
  • Tocolysis, which relaxes the uterus, and neuraxial analgesia/anesthesia, which relaxes anterior abdominal wall muscles and reduces ECV-associated pain, can facilitate ECV success
  • Several studies have found that nifedipine is less effective than terbutaline in facilitating ECV
  • Higher doses of neuraxial anesthesia produce higher ECV success rates, possibly because the higher anesthetic dose relaxes the abdominal wall muscles and facilitates fetus repositioning
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A minimally invasive treatment for early GI cancers

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A minimally invasive treatment for early GI cancers

The treatment of early esophageal, gastric, and colorectal cancer is changing.1 For many years, surgery was the mainstay of treatment for early-stage gastrointestinal cancer. Unfortunately, surgery leads to significant loss of function of the organ, resulting in increased morbidity and decreased quality of life.2

Endoscopic techniques, particularly endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD), have been developed and are widely used in Japan, where gastrointestinal cancer is more common than in the West. This article reviews the indications, complications, and outcomes of ESD for early gastrointestinal neoplasms, so that readers will recognize the subset of patients who would benefit from ESD in a Western setting.

ENDOSCOPIC MUCOSAL RESECTION AND SUBMUCOSAL DISSECTION

Since the first therapeutic polypectomy was performed in Japan in 1974, several endoscopic techniques for tumor resection have been developed.3

EMR, one of the most successful and widely used techniques, involves elevating the lesion either with submucosal injection of a solution or with cap suction, and then removing it with a snare.4 Most lesions smaller than 20 mm can be removed in one piece (en bloc).5 Larger lesions are removed in multiple pieces (ie, piecemeal). Unfortunately, some fibrotic lesions, which are usually difficult to lift, cannot be completely removed by EMR.

ESD was first performed in the late 1990s with the aim of overcoming the limitations of EMR in resecting large or fibrotic tumors en bloc.6,7 Since then, ESD technique has been standardized and training centers have been created, especially in Asia, where it is widely used for treatment of early gastric cancer.3,8–10 Since 2012 it has been covered by the Japanese National Health Insurance for treatment of early gastric cancer, and since 2014 for treatment of colorectal malignant tumors measuring 2 to 5 cm.11

Adoption of ESD has been slow in Western countries, where many patients are still referred for surgery or undergo EMR for removal of superficial neoplasms. Reasons for this slow adoption are that gastric cancer is much less common in Western countries, and also that ESD demands a high level of technical skill, is difficult to learn, and is expensive.3,12,13 However, small groups of Western endoscopists have become interested and are advocating it, first studying it on their own and then training in a Japanese center and learning from experts performing the procedure.

Therefore, in a Western setting, ESD should be performed in specialized endoscopy centers and offered to selected patients.1  

CANDIDATES SHOULD HAVE EARLY-STAGE, SUPERFICIAL TUMORS

Ideal candidates for endoscopic resection are patients who have early cancer with a negligible risk of lymph node metastasis, such as cancer limited to the mucosa (stage T1a).7 Therefore, to determine the best treatment for a patient with a newly diagnosed gastrointestinal neoplasm, it is mandatory to estimate the depth of invasion.

The depth of invasion is directly correlated with lymph node involvement, which is ultimately the main predictive factor for long-term adverse outcomes of gastrointestinal tumors.4,14–17 Accurate multidisciplinary preprocedure estimations are mandatory, as incorrect evaluations may result in inappropriate therapy and residual cancer.18

Other factors that have been used to predict lymph node involvement include tumor size, macroscopic appearance, histologic differentiation, and lymphatic and vascular involvement.19 Some of these factors can be assessed by special endoscopic techniques (chromoendoscopy and narrow-band imaging with magnifying endoscopy) that allow accurate real-time estimation of the depth of invasion of the lesion.5,17,20–27 Evaluation of microsurface and microvascular arrangements is especially useful for determining the feasibility of ESD in gastric tumors, evaluation of intracapillary loops is useful in esophageal lesions, and assessment of mucosal pit patterns is useful for colorectal lesions.21–29

Endoscopic ultrasonography is another tool that has been used to estimate the depth of the tumor. Although it can differentiate between definite intramucosal and definite submucosal invasive cancers, its ability to confirm minute submucosal invasion is limited. Its use as the sole tumor staging modality is not encouraged, and it should always be used in conjunction with endoscopic evaluation.18

Though the aforementioned factors help stratify patients, pathologic staging is the best predictor of lymph node metastasis. ESD provides adequate specimens for accurate pathologic evaluation, as it removes lesions en bloc.30

All patients found to have risk factors for lymph node metastasis on endoscopic, ultrasonographic, or pathologic analysis should be referred for surgical evaluation.9,19,31,32

ENDOSCOPIC SUBMUCOSAL DISSECTION

Before the procedure, the patient’s physicians need to do the following:

Determine the best type of intervention (EMR, ESD, ablation, surgery) for the specific lesion.3 A multidisciplinary approach is encouraged, with involvement of the internist, gastroenterologist, and surgeon.

Plan for anesthesia, additional consultations, pre- and postprocedural hospital admission, and need for special equipment.33

During the procedure

Figure 1. Endoscopic submucosal dissection, a minimally invasive treatment for early-stage cancers of the gastrointestinal system, involves the following steps: (A) marking the circumference of the tumor, (B) lifting the tumor by injecting saline or another inert substance beneath it, (C) cutting around the outside of the tumor margin, and (D) dissecting and removing the tumor.
The main steps of ESD are circumferential marking of the lesion, submucosal injection, circumferential incision, and submucosal dissection (Figure 1). The endoscopist must do the following:

Define the lateral extent of the lesion using magnification chromoendoscopy or narrow-band imaging. In the stomach, a biopsy sample should be taken from the worst-looking segment and from normal-looking mucosa. Multiple biopsies should be avoided to prevent subsequent fibrosis.33 In the colon, biopsy should be avoided.34

Identify and circumferentially mark the target lesion. Cautery or argon plasma coagulation can be used for making markings at a distance of 5 to 10 mm from the edges.33 This is done to recognize the borders of the lesion, because they can become distorted after submucosal injection.14 This step is unnecessary in colorectal cases, as tumor margins can be adequately visualized after chromoendoscopy.16,35

Lift the lesion by injecting saline, 0.5% hyaluronate, or glycerin to create a submucosal fluid cushion.19,33

Perform a circumferential incision lateral to the mucosal margins to allow for a normal tissue margin.33 Partial incision is performed for esophageal and colorectal ESD to avoid fluid leakage from the submucosal layer, achieving a sustained submucosal lift and safer dissection.16

Submucosal dissection. The submucosal layer is dissected with an electrocautery knife until the lesion is completely removed. Dissection should be done carefully to keep the submucosal plane.33 Hemoclips or hemostat forceps can be used to control visible bleeding. The resected specimen is then stretched and fixed to a board using small pins for further histopathologic evaluation.35

Postprocedural monitoring.  All patients should be admitted for overnight observation. Those who undergo gastric ESD should receive high-dose acid suppression, and the next day they can be started on a liquid diet.19

 

 

STOMACH CANCER

Indications for ESD for stomach cancer in the East

The incidence of gastric cancer is higher in Japan and Korea, where widespread screening programs have led to early identification and early treatment of this disease.36

Pathology studies37 of samples from patients with gastric cancer identified the following as risk factors for lymph node metastasis, which would make ESD unsuitable:

  • Undifferentiated type
  • Tumors larger than 2 cm
  • Lymphatic or venous involvement
  • Submucosal invasion
  • Ulcerative change.

Based on these findings, the situations in which there was no risk of lymph node involvement (ie, when none of the above factors are present) were accepted as absolute indications for endoscopic resection of early gastric cancer.38 Further histologic studies identified a subset of patients with lesions with very low risk of lymph node metastasis, which outweighed the risk of surgery. Based on these findings, expanded criteria for gastric ESD were proposed,39,40 and the Japanese gastric cancer treatment guidelines now include these expanded preoperative indications9,17 (Table 1).

Treatment algorithm based on the histopathologic evaluation after resection of early gastric tumors.
Based on information from the Japanese Gastric Cancer Association, reference 9.
Figure 2. Treatment algorithm based on the histopathologic evaluation after resection of early gastric tumors.

The Japanese Gastric Cancer Association has proposed a treatment algorithm based on the histopathologic evaluation after resection (Figure 2).9

Outcomes

In the largest series of patients who underwent curative ESD for early gastric cancer, the 5-year survival rate was 92.6%, the 5-year disease-specific survival rate was 99.9%, and the 5-year relative survival rate was 105%.41

Similarly, in a Japanese population-based survival analysis, the relative 5-year survival rate for localized gastric cancer was 94.4%.42 Rates of en bloc resection and complete resection with ESD are higher than those with EMR, resulting in a lower risk of local recurrence in selected patients who undergo ESD.8,43,44

Although rare, local recurrence after curative gastric ESD has been reported.45 The annual incidence of local recurrence has been estimated to be 0.84%.46

ESD entails a shorter hospital stay and requires fewer resources than surgery, resulting in lower medical costs (Table 2).44 Additionally, as endoscopic resection is associated with less morbidity, fewer procedure-related adverse events, and fewer complications, ESD could be used as the standard treatment for early gastric cancer.47,48

The Western perspective on endoscopic submucosal dissection for gastric cancer

Since the prevalence of gastric cancer in Western countries is significantly lower than in Japan and Korea, local data and experience are scarce. However, experts performing ESD in the West have adopted the indications of the Japan Gastroenterological Endoscopy Society. The European Society of Gastrointestinal Endoscopy recommends ESD for excision of most superficial gastric neoplasms, with EMR being preferred only in lesions smaller than 15 mm, Paris classification 0 or IIA.5,32

Patients with gastric lesions measuring 15 mm or larger should undergo high-quality endoscopy, preferably chromoendoscopy, to evaluate the mucosal patterns and determine the depth of invasion. If superficial involvement is confirmed, other imaging techniques are not routinely recommended.5 A surgery consult is also recommended.

ESOPHAGEAL CANCER

Indications for ESD for esophageal cancer in the East

Due to the success of ESD for early gastric cancer, this technique is now also used for superficial esophageal neoplasms.19,49 It should be done in a specialized center, as it is more technically difficult than gastric ESD: the esophageal lumen is narrow, the wall is thin, and the esophagus moves with respiration and heartbeat.50 A multidisciplinary approach including an endoscopist, a surgeon, and a pathologist is highly recommended for evaluation and treatment.

EMR is preferred for removal of mucosal cancer, in view of its safety profile and success rates. ESD can be considered in cases of lesions larger than 15 mm, poorly lifting tumors, and those with the possibility of submucosal invasion (Table 3).5,45,49,51

Circumference involvement is critical when determining eligible candidates, as a defect involving more than three-fourths of the esophageal circumference can lead to esophageal strictures.52 Controlled prospective studies have shown promising results from giving intralesional and oral steroids to prevent stricture after ESD, which could potentially overcome this size limitation.53,54

Outcomes for esophageal cancer

ESD has been shown to be safe and effective, achieving en bloc resection in 85% to 100% of patients.19,51 Its advantages over EMR include en bloc resection, complete resection, and high curative rates, resulting in higher recurrence-free survival.2,55,56 Although the incidence of complications such as bleeding, perforation, and stricture formation are higher with ESD, patients usually recover uneventfully.2,19,20

ESD in the esophagus: The Western perspective

As data on the efficacy of EMR vs ESD for the treatment of Barrett esophagus with adenocarcinoma are limited, EMR is the gold standard endoscopic technique for removal of visible esophageal dysplastic lesions.5,51,57 ESD can be considered for tumors larger than 15 mm, for poorly lifting lesions, and if there is suspicion of submucosal invasion.5

Patients should be evaluated by an experienced endoscopist, using an advanced imaging technique such as narrow-band imaging or chromoendoscopy. If suspicious features are found, endoscopic ultrasonography should be considered to confirm submucosal invasion or lymph node involvement.5

 

 

COLORECTAL CANCER

Indications for ESD for colorectal cancer in the East

Colon cancer is one of the leading causes of cancer-related deaths worldwide.58 Since ESD has been found to be effective and safe in treating gastric cancer, it has also been used to remove large colorectal tumors.59 However, ESD is not universally accepted in the treatment of colorectal neoplasms due to its greater technical difficulty, longer procedural time, and higher risk of perforating the thinner colonic wall compared with EMR.21,60

According to the Japanese Society of Gastroenterology, ESD should be reserved for lesions that are not amenable to snare removal (> 20 mm in size, intramucosal tumors with fibrosis, localized lesions that result from chronic inflammation, and local residual carcinoma) (Tables 4 and 5).21,61 Colorectal ESD should be performed only by a trained endoscopist.11

Outcomes for colorectal cancer

Piecemeal resection is one of the predictors of recurrence after endoscopic removal of colorectal cancer.62 Therefore, the cumulative rates of en bloc resection and curative resection are higher and the recurrence rate is lower for en bloc ESD than for EMR.62–65 Complication rates and procedural time are higher for ESD than for EMR.59,66

Tumor size of 50 mm or larger is a risk factor for complications, while a high procedure volume at the center is a protective factor.60

Endoscopic treatment of colorectal cancer: The Western perspective

EMR is the gold standard for removal of superficial colorectal lesions. However, ESD can be considered if there is suspicion of superficial submucosal invasion, especially for lesions larger than 20 mm that cannot be resected en bloc by EMR.32 ESD can also be used for fibrotic lesions not amenable to complete EMR removal, or as a salvage procedure after recurrence after EMR.67 Proper selection of cases is critical.1

Patients who have a superficial colonic lesion should be evaluated by means of high-definition endoscopy and chromoendoscopy to assess the mucosal pattern and establish feasibility of endoscopic resection. If submucosal invasion is suspected, staging with endoscopic ultrasonography or magnetic resonance imaging should be considered.5

FOLLOW-UP AFTER ESD

Endoscopic surveillance after the procedure is recommended, given the persistent risk of metachronous cancer after curative ESD due to its organ-sparing quality.68 Surveillance endoscopy aims to achieve early detection and subsequent endoscopic resection of metachronous lesions.

Histopathologic evaluation assessing the presence of malignant cells in the margins of a resected sample is mandatory for determining the next step in treatment. If margins are negative, follow-up endoscopy can be done every 6 to 12 months. If margins are positive, the approach includes surgery, reattempting ESD or endoscopic surveillance in 3 or 6 months.3,32 Although the surveillance strategy varies according to individual risk of metachronous cancer, it should be continued indefinitely.68

COMPLICATIONS OF ESD

The most common procedure-related complications of ESD are bleeding, perforation, and stricture. Most intraprocedural adverse events can be managed endoscopically.69

Bleeding

Most bleeding occurs during the procedure or early after it and can be controlled with electrocautery.49,69 No episodes of massive bleeding, defined as causing clinical symptoms and requiring transfusion or surgery, have been reported.20,43,55

In gastric ESD, delayed bleeding rates have ranged from 0 to 15.6%.69 Bleeding may be prevented with endoscopic coagulation of visible vessels after dissection has been completed and by proton pump inhibitor therapy.70,71 Excessive coagulation should be avoided to lower the risk of perforation.33

In colorectal ESD the bleeding rate has been reported to be 2.2%; applying coagulation to an area where a blood vessel is suspected before cutting (precoagulation) may prevent subsequent bleeding.21

Perforation

For gastric ESD, perforation rates range from 1.2% to 5.2%.69 Esophageal perforation rates can be up to 4%.49 In colorectal ESD, perforation rates have been reported to be 1.6% to 6.6%.60,72

Although most of the cases were successfully managed with conservative treatment, some required emergency surgery.60,73

Strictures

In a case series of 532 patients undergoing gastric ESD, stricture was reported in 5 patients, all of whom presented with obstructive symptoms.74 Risk factors for post-ESD gastric stenosis are a mucosal defect with a circumferential extent of more than three-fourths or a longitudinal extent of more than 5 cm.75

Strictures are common after esophageal ESD, with rates ranging from 2% to 26%. The risk is higher when longer segments are removed or circumferential resection is performed. As previously mentioned, this complication may be reduced with ingestion or injection of steroids  after the procedure.53,54

Surprisingly, ESD of large colorectal lesions involving more than three-fourths of the circumference of the rectum is rarely complicated by stenosis.76

 

 

LIMITATIONS OF ESD

ESD requires a high level of technical skill, is time-consuming, and has a higher rate of complications than conventional endoscopic resection. A standardized ESD training system is needed, as the procedure is more difficult than EMR. Training in porcine models has been shown to confer competency in ESD in a Western setting.13,16,33

Colorectal ESD is an even more challenging procedure, given the potential for complications related to its anatomy. Training centers in Japan usually have their trainees first master gastric ESD, then assist in more than 20 colorectal ESDs conducted by experienced endoscopists, and accomplish 30 cases before performing the procedure safely and independently.

As the incidence of gastric cancer is low in Western countries, trainees may also begin with lower rectal lesions, which are easier to remove.77 Incorporation of ESD in the West would require a clear treatment algorithm. It is a complex procedure, with higher rates of complications, a prolonged learning curve, and prolonged procedure time. Therefore, it should be performed in specialized centers and under the special situations discussed here to ensure that the benefits for the patients outweigh the risks.

VALUE OF ENDOSCOPIC SUBMUCOSAL DISSECTION

The optimal method for resecting gastrointestinal neoplasms should be safe, cost-effective, and quick and should also completely remove the lesion. The best treatment strategy takes into account the characteristics of the lesion and the comorbidities and wishes of the patient. Internists should be aware of the multiple options available to achieve the best outcome for the patient.1

Endoscopic resection of superficial gastrointestinal neoplasms, including EMR and ESD, has been a subject of increasing interest due to its minimally invasive and potentially curative character. However, cancer can recur after endoscopic resection because the procedure is organ-sparing.

ESD allows resection of early gastrointestinal tumors with a minimally invasive technique. It can achieve higher curative resection rates and lower recurrence rates compared with EMR. Compared with surgery, ESD leads to less morbidity, fewer procedure-related complications, and lower medical costs. Indications should be rigorously followed to achieve successful treatments in selected patients.

Multiple variables have to be taken into account when deciding which treatment is best, such as tumor characteristics, the patient’s baseline condition, physician expertise, and hospital resources.48 Less-invasive treatments may improve the prognosis of patients. No matter the approach, patients should be treated in specialized treatment centers.

Internal medicine physicians should be aware of the advances in treatments for early gastrointestinal cancer so appropriate options can be considered.

References
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  28. Sato H, Inoue H, Ikeda H, et al. Utility of intrapapillary capillary loops seen on magnifying narrow-band imaging in estimating invasive depth of esophageal squamous cell carcinoma. Endoscopy 2015; 8:122–128.
  29. Muto M, Yao K, Kaise M, et al. Magnifying endoscopy simple diagnostic algorithm for early gastric cancer (MESDA-G). Dig Endosc 2016; 28:379–393.
  30. Waddell T, Verheij M, Allum W, Cunningham D, Cervantes A, Arnold D; European Society for Medical Oncology (ESMO); European Society of Surgical Oncology (ESSO); European Society of Radiotherapy and Oncology (ESTRO). Gastric cancer: ESMO-ESSO-ESTRO clinical practice guidelines for diagnosis, treatment and follow-up. Ann Oncol 2013; 24(suppl 6):vi57–vi63.
  31. Kuwano H, Nishimura Y, Ohtsu A, et al. Guidelines for diagnosis and treatment of carcinoma of the esophagus. April 2007 edition: part I - Edited by the Japan Esophageal Society. Esophagus 2008; 5:61–73.
  32. Tanaka S, Kashida H, Saito Y, et al. JGES guidelines for colorectal endoscopic submucosal dissection/endoscopic mucosal resection. Dig Endosc 2015; 27:417–434.
  33. Gotoda T, Ho KY, Soetikno R, Kaltenbach T, Draganov P. Gastric ESD: current status and future directions of devices and training. Gastrointest Endosc Clin North Am 2014; 24:213–233.
  34. Saito Y, Sakamoto T, Nakajima T, Matsuda T. Colorectal ESD: current indications and latest technical advances. Gastrointest Endosc Clin N Am 2014; 24:245–255.
  35. Saito Y, Otake Y, Sakamoto T, et al. Indications for and technical aspects of colorectal endoscopic submucosal dissection. Gut Liver 2013; 7:263–269.
  36. Saragoni L. Upgrading the definition of early gastric cancer: better staging means more appropriate treatment. Cancer Biol Med 2015; 12:355–361.
  37. Tsujitani S, Oka S, Saito H, et al. Less invasive surgery for early gastric cancer based on the low probability of lymph node metastasis. Surgery 1999; 125:148–154.
  38. Soetikno RM, Gotoda T, Nakanishi Y, Soehendra N. Endoscopic mucosal resection. Gastrointest Endosc 2003; 57:567–579.
  39. Hirasawa T, Gotoda T, Miyata S, et al. Incidence of lymph node metastasis and the feasibility of endoscopic resection for undifferentiated-type early gastric cancer. Gastric Cancer 2009; 12:148–152.
  40. Gotoda T, Yanagisawa A, Sasako M, et al. Incidence of lymph node metastasis from early gastric cancer: estimation with a large number of cases at two large centers. Gastric Cancer 2000; 3:219–225.
  41. Suzuki H, Oda I, Abe S, et al. High rate of 5-year survival among patients with early gastric cancer undergoing curative endoscopic submucosal dissection. Gastric Cancer 2016; 19:198–205.
  42. Matsuda T, Ajiki W, Marugame T, Ioka A, Tsukuma H, Sobue T; Research Group of Population-Based Cancer Registries of Japan. Population-based survival of cancer patients diagnosed between 1993 and 1999 in Japan: a chronological and international comparative study. Jpn J Clin Oncol 2011; 41:40–51.
  43. Ahn JY, Jung HY, Choi KD, et al. Endoscopic and oncologic outcomes after endoscopic resection for early gastric cancer: 1370 cases of absolute and extended indications. Gastrointest Endosc 2011; 74:485–493.
  44. Kim Y, Kim YW, Choi IJ, et al. Cost comparison between surgical treatments and endoscopic submucosal dissection in patients with early gastric cancer in Korea. Gut Liver 2015; 9:174–180.
  45. Abe S, Oda I, Nakajima T, et al. A case of local recurrence and distant metastasis following curative endoscopic submucosal dissection of early gastric cancer. Gastric Cancer 2015; 18:188–192.
  46. Hahn KY, Park JC, Kim EH, et al. Incidence and impact of scheduled endoscopic surveillance on recurrence after curative endoscopic resection for early gastric cancer. Gastrointest Endosc 2016; 84:628–638.e1.
  47. Wang S, Zhang Z, Liu M, Li S, Jiang C. Endoscopic resection compared with gastrectomy to treat early gastric cancer: a systematic review and meta-analysis. PLoS One 2015; 10:e0144774.
  48. Kondo A, de Moura EG, Bernardo WM, et al. Endoscopy vs surgery in the treatment of early gastric cancer: systematic review. World J Gastroenterol 2015; 21:13177–13187.
  49. Kothari S, Kaul V. Endoscopic mucosal resection and endoscopic submucosal dissection for endoscopic therapy of Barrett’s esophagus-related neoplasia. Gastroenterol Clin North Am 2015; 44:317–335.
  50. Yamashita T, Zeniya A, Ishii H, et al. Endoscopic mucosal resection using a cap-fitted panendoscope and endoscopic submucosal dissection as optimal endoscopic procedures for superficial esophageal carcinoma. Surg Endosc 2011; 25:2541–2546.
  51. Kagemoto K, Oka S, Tanaka S, et al. Clinical outcomes of endoscopic submucosal dissection for superficial Barrett’s adenocarcinoma. Gastrointest Endosc 2014; 80:239–245.
  52. Katada C, Muto M, Manabe T, Boku N, Ohtsu A, Yoshida S. Esophageal stenosis after endoscopic mucosal resection of superficial esophageal lesions. Gastrointest Endosc 2003; 57:165–169.
  53. Hanaoka N, Ishihara R, Takeuchi Y, et al. 1139: A single session of intralesional steroid injection to prevent esophageal stricture after endoscopic submucosal dissection for esophageal squamous cell carcinoma. Gastrointest Endosc 2012; 75(suppl):AB175.
  54. Yamaguchi N, Isomoto H, Nakayama T, et al. Usefulness of oral prednisolone in the treatment of esophageal stricture after endoscopic submucosal dissection for superficial esophageal squamous cell carcinoma. Gastrointest Endosc 2011; 73:1115–1121.
  55. Ono S, Fujishiro M, Niimi K, et al. Long-term outcomes of endoscopic submucosal dissection for superficial esophageal squamous cell neoplasms. Gastrointest Endosc 2009; 70:860–866.
  56. Katada C, Muto M, Manabe T, Ohtsu A, Yoshida S. Local recurrence of squamous-cell carcinoma of the esophagus after EMR. Gastrointest Endosc 2005; 61:219–225.
  57. Hirasawa K, Kokawa A, Oka H, et al. Superficial adenocarcinoma of the esophagogastric junction: long-term results of endoscopic submucosal dissection. Gastrointest Endosc 2010; 72:960–966.
  58. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011; 61:69–90.
  59. Nakajima T, Saito Y, Tanaka S, et al. Current status of endoscopic resection strategy for large, early colorectal neoplasia in Japan. Surg Endosc 2013; 27:3262–3770.
  60. Saito Y, Uraoka T, Yamaguchi Y, et al. A prospective, multicenter study of 1111 colorectal endoscopic submucosal dissections (with video). Gastrointest Endosc 2010; 72:1217–1225.
  61. Tanaka S, Saitoh Y, Matsuda T, et al; Japanese Society of Gastroenterology. Evidence-based clinical practice guidelines for management of colorectal polyps. J Gastroenterol 2015; 50:252–260.
  62. Oka S, Tanaka S, Saito Y, et al; Colorectal Endoscopic Resection Standardization Implementation Working Group of the Japanese Society for Cancer of the Colon and Rectum, Tokyo, Japan. Local recurrence after endoscopic resection for large colorectal neoplasia: a multicenter prospective study in Japan. Am J Gastroenterol 2015; 110:697–707.
  63. Saito Y, Fukuzawa M, Matsuda T, et al. Clinical outcome of endoscopic submucosal dissection versus endoscopic mucosal resection of large colorectal tumors as determined by curative resection. Surg Endosc 2010; 24:343–352.
  64. Makazu M, Sakamoto T, So E, et al. Relationship between indeterminate or positive lateral margin and local recurrence after endoscopic resection of colorectal polyps. Endosc Int Open 2015; 3:E252–E257.
  65. Belderbos TD, Leenders M, Moons LM, Siersema PD. Local recurrence after endoscopic mucosal resection of nonpedunculated colorectal lesions: systematic review and meta-analysis. Endoscopy 2014; 46:388–402.
  66. Fujiya M, Tanaka K, Dokoshi T, et al. Efficacy and adverse events of EMR and endoscopic submucosal dissection for the treatment of colon neoplasms: a meta-analysis of studies comparing EMR and endoscopic submucosal dissection. Gastrointest Endosc 2015; 81:583–595.
  67. Rahmi G, Tanaka S, Ohara Y, et al. Efficacy of endoscopic submucosal dissection for residual or recurrent superficial colorectal tumors after endoscopic mucosal resection. J Dig Dis 2015; 16:14–21.
  68. Abe S, Oda I, Suzuki H, et al. Long-term surveillance and treatment outcomes of metachronous gastric cancer occurring after curative endoscopic submucosal dissection. Endoscopy 2015; 47:1113–1118.
  69. Oda I, Suzuki H, Nonaka S, Yoshinaga S. Complications of gastric endoscopic submucosal dissection. Dig Endosc 2013; 25(suppl 1):71–78.
  70. Takizawa K, Oda I, Gotoda T, et al. Routine coagulation of visible vessels may prevent delayed bleeding after endoscopic submucosal dissection—an analysis of risk factors. Endoscopy 2008; 40:179–183.
  71. Uedo N, Takeuchi Y, Yamada T, et al. Effect of a proton pump inhibitor or an H2-receptor antagonist on prevention of bleeding from ulcer after endoscopic submucosal dissection of early gastric cancer: a prospective randomized controlled trial. Am J Gastroenterol 2007; 102:1610–1616.
  72. Hayashi N, Tanaka S, Nishiyama S, et al. Predictors of incomplete resection and perforation associated with endoscopic submucosal dissection for colorectal tumors. Gastrointest Endosc 2014; 79:427–435.
  73. Suzuki H, Oda I, Sekiguchi M, et al. Management and associated factors of delayed perforation after gastric endoscopic submucosal dissection. World J Gastroenterol 2015; 21:12635–12643.
  74. Tsunada S, Ogata S, Mannen K, et al. Case series of endoscopic balloon dilation to treat a stricture caused by circumferential resection of the gastric antrum by endoscopic submucosal dissection. Gastrointest Endosc 2008; 67:979–983.
  75. Coda S, Oda I, Gotoda T, Yokoi C, Kikuchi T, Ono H. Risk factors for cardiac and pyloric stenosis after endoscopic submucosal dissection, and efficacy of endoscopic balloon dilation treatment. Endoscopy 2009; 41:421–426.
  76. Abe S, Sakamoto T, Takamaru H, et al. Stenosis rates after endoscopic submucosal dissection of large rectal tumors involving greater than three quarters of the luminal circumference. Surg Endosc 2016; 30:5459–5464.
  77. Sakamoto T, Saito Y, Fukunaga S, Nakajima T, Matsuda T. Learning curve associated with colorectal endoscopic submucosal dissection for endoscopists experienced in gastric endoscopic submucosal dissection. Dis Colon Rectum 2011; 54:1307–1312.
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Lady Katherine Mejía-Pérez, MD
Department of Internal Medicine, Cleveland Clinic

Seiichiro Abe, MD
Endoscopy Division, National Cancer Center Hospital,  Tokyo, Japan

Tyler Stevens, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Mansour A. Parsi, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic

Sunguk N. Jang, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic

Ichiro Oda, MD
Endoscopy Division, National Cancer Center Hospital, Tokyo, Japan

John J. Vargo, MD, MPH
Chairman, Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Yutaka Saito, MD, PhD
Endoscopy Division, National Cancer Center Hospital, Tokyo, Japan

Amit Bhatt, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Clinical Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Amit Bhatt, MD, Department of Gastroenterology and Hepatology, Digestive Disease Institute, A30, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; [email protected]

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Cleveland Clinic Journal of Medicine - 84(9)
Publications
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707-717
Legacy Keywords
gastric cancer, stomach cancer, GI cancer, colorectal cancer, esophageal cancer, adenocarcinoma, Barrett esophagus, endoscopic submucosal dissection, ESD, endoscopic mucosal resection, EMR, endoscopy, colonoscopy, Lady Katherine Mejia-Perez, Seiichiro Abe, Tyler Stevens, Mansour Parsi, Sunguk Jang, Ichiro Oda, John Vargo, Yutaka Saito, Amit Bhatt
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Author and Disclosure Information

Lady Katherine Mejía-Pérez, MD
Department of Internal Medicine, Cleveland Clinic

Seiichiro Abe, MD
Endoscopy Division, National Cancer Center Hospital,  Tokyo, Japan

Tyler Stevens, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Mansour A. Parsi, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic

Sunguk N. Jang, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic

Ichiro Oda, MD
Endoscopy Division, National Cancer Center Hospital, Tokyo, Japan

John J. Vargo, MD, MPH
Chairman, Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Yutaka Saito, MD, PhD
Endoscopy Division, National Cancer Center Hospital, Tokyo, Japan

Amit Bhatt, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Clinical Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Amit Bhatt, MD, Department of Gastroenterology and Hepatology, Digestive Disease Institute, A30, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; [email protected]

Author and Disclosure Information

Lady Katherine Mejía-Pérez, MD
Department of Internal Medicine, Cleveland Clinic

Seiichiro Abe, MD
Endoscopy Division, National Cancer Center Hospital,  Tokyo, Japan

Tyler Stevens, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Mansour A. Parsi, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic

Sunguk N. Jang, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic

Ichiro Oda, MD
Endoscopy Division, National Cancer Center Hospital, Tokyo, Japan

John J. Vargo, MD, MPH
Chairman, Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Yutaka Saito, MD, PhD
Endoscopy Division, National Cancer Center Hospital, Tokyo, Japan

Amit Bhatt, MD
Department of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic; Clinical Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Amit Bhatt, MD, Department of Gastroenterology and Hepatology, Digestive Disease Institute, A30, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; [email protected]

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Related Articles

The treatment of early esophageal, gastric, and colorectal cancer is changing.1 For many years, surgery was the mainstay of treatment for early-stage gastrointestinal cancer. Unfortunately, surgery leads to significant loss of function of the organ, resulting in increased morbidity and decreased quality of life.2

Endoscopic techniques, particularly endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD), have been developed and are widely used in Japan, where gastrointestinal cancer is more common than in the West. This article reviews the indications, complications, and outcomes of ESD for early gastrointestinal neoplasms, so that readers will recognize the subset of patients who would benefit from ESD in a Western setting.

ENDOSCOPIC MUCOSAL RESECTION AND SUBMUCOSAL DISSECTION

Since the first therapeutic polypectomy was performed in Japan in 1974, several endoscopic techniques for tumor resection have been developed.3

EMR, one of the most successful and widely used techniques, involves elevating the lesion either with submucosal injection of a solution or with cap suction, and then removing it with a snare.4 Most lesions smaller than 20 mm can be removed in one piece (en bloc).5 Larger lesions are removed in multiple pieces (ie, piecemeal). Unfortunately, some fibrotic lesions, which are usually difficult to lift, cannot be completely removed by EMR.

ESD was first performed in the late 1990s with the aim of overcoming the limitations of EMR in resecting large or fibrotic tumors en bloc.6,7 Since then, ESD technique has been standardized and training centers have been created, especially in Asia, where it is widely used for treatment of early gastric cancer.3,8–10 Since 2012 it has been covered by the Japanese National Health Insurance for treatment of early gastric cancer, and since 2014 for treatment of colorectal malignant tumors measuring 2 to 5 cm.11

Adoption of ESD has been slow in Western countries, where many patients are still referred for surgery or undergo EMR for removal of superficial neoplasms. Reasons for this slow adoption are that gastric cancer is much less common in Western countries, and also that ESD demands a high level of technical skill, is difficult to learn, and is expensive.3,12,13 However, small groups of Western endoscopists have become interested and are advocating it, first studying it on their own and then training in a Japanese center and learning from experts performing the procedure.

Therefore, in a Western setting, ESD should be performed in specialized endoscopy centers and offered to selected patients.1  

CANDIDATES SHOULD HAVE EARLY-STAGE, SUPERFICIAL TUMORS

Ideal candidates for endoscopic resection are patients who have early cancer with a negligible risk of lymph node metastasis, such as cancer limited to the mucosa (stage T1a).7 Therefore, to determine the best treatment for a patient with a newly diagnosed gastrointestinal neoplasm, it is mandatory to estimate the depth of invasion.

The depth of invasion is directly correlated with lymph node involvement, which is ultimately the main predictive factor for long-term adverse outcomes of gastrointestinal tumors.4,14–17 Accurate multidisciplinary preprocedure estimations are mandatory, as incorrect evaluations may result in inappropriate therapy and residual cancer.18

Other factors that have been used to predict lymph node involvement include tumor size, macroscopic appearance, histologic differentiation, and lymphatic and vascular involvement.19 Some of these factors can be assessed by special endoscopic techniques (chromoendoscopy and narrow-band imaging with magnifying endoscopy) that allow accurate real-time estimation of the depth of invasion of the lesion.5,17,20–27 Evaluation of microsurface and microvascular arrangements is especially useful for determining the feasibility of ESD in gastric tumors, evaluation of intracapillary loops is useful in esophageal lesions, and assessment of mucosal pit patterns is useful for colorectal lesions.21–29

Endoscopic ultrasonography is another tool that has been used to estimate the depth of the tumor. Although it can differentiate between definite intramucosal and definite submucosal invasive cancers, its ability to confirm minute submucosal invasion is limited. Its use as the sole tumor staging modality is not encouraged, and it should always be used in conjunction with endoscopic evaluation.18

Though the aforementioned factors help stratify patients, pathologic staging is the best predictor of lymph node metastasis. ESD provides adequate specimens for accurate pathologic evaluation, as it removes lesions en bloc.30

All patients found to have risk factors for lymph node metastasis on endoscopic, ultrasonographic, or pathologic analysis should be referred for surgical evaluation.9,19,31,32

ENDOSCOPIC SUBMUCOSAL DISSECTION

Before the procedure, the patient’s physicians need to do the following:

Determine the best type of intervention (EMR, ESD, ablation, surgery) for the specific lesion.3 A multidisciplinary approach is encouraged, with involvement of the internist, gastroenterologist, and surgeon.

Plan for anesthesia, additional consultations, pre- and postprocedural hospital admission, and need for special equipment.33

During the procedure

Figure 1. Endoscopic submucosal dissection, a minimally invasive treatment for early-stage cancers of the gastrointestinal system, involves the following steps: (A) marking the circumference of the tumor, (B) lifting the tumor by injecting saline or another inert substance beneath it, (C) cutting around the outside of the tumor margin, and (D) dissecting and removing the tumor.
The main steps of ESD are circumferential marking of the lesion, submucosal injection, circumferential incision, and submucosal dissection (Figure 1). The endoscopist must do the following:

Define the lateral extent of the lesion using magnification chromoendoscopy or narrow-band imaging. In the stomach, a biopsy sample should be taken from the worst-looking segment and from normal-looking mucosa. Multiple biopsies should be avoided to prevent subsequent fibrosis.33 In the colon, biopsy should be avoided.34

Identify and circumferentially mark the target lesion. Cautery or argon plasma coagulation can be used for making markings at a distance of 5 to 10 mm from the edges.33 This is done to recognize the borders of the lesion, because they can become distorted after submucosal injection.14 This step is unnecessary in colorectal cases, as tumor margins can be adequately visualized after chromoendoscopy.16,35

Lift the lesion by injecting saline, 0.5% hyaluronate, or glycerin to create a submucosal fluid cushion.19,33

Perform a circumferential incision lateral to the mucosal margins to allow for a normal tissue margin.33 Partial incision is performed for esophageal and colorectal ESD to avoid fluid leakage from the submucosal layer, achieving a sustained submucosal lift and safer dissection.16

Submucosal dissection. The submucosal layer is dissected with an electrocautery knife until the lesion is completely removed. Dissection should be done carefully to keep the submucosal plane.33 Hemoclips or hemostat forceps can be used to control visible bleeding. The resected specimen is then stretched and fixed to a board using small pins for further histopathologic evaluation.35

Postprocedural monitoring.  All patients should be admitted for overnight observation. Those who undergo gastric ESD should receive high-dose acid suppression, and the next day they can be started on a liquid diet.19

 

 

STOMACH CANCER

Indications for ESD for stomach cancer in the East

The incidence of gastric cancer is higher in Japan and Korea, where widespread screening programs have led to early identification and early treatment of this disease.36

Pathology studies37 of samples from patients with gastric cancer identified the following as risk factors for lymph node metastasis, which would make ESD unsuitable:

  • Undifferentiated type
  • Tumors larger than 2 cm
  • Lymphatic or venous involvement
  • Submucosal invasion
  • Ulcerative change.

Based on these findings, the situations in which there was no risk of lymph node involvement (ie, when none of the above factors are present) were accepted as absolute indications for endoscopic resection of early gastric cancer.38 Further histologic studies identified a subset of patients with lesions with very low risk of lymph node metastasis, which outweighed the risk of surgery. Based on these findings, expanded criteria for gastric ESD were proposed,39,40 and the Japanese gastric cancer treatment guidelines now include these expanded preoperative indications9,17 (Table 1).

Treatment algorithm based on the histopathologic evaluation after resection of early gastric tumors.
Based on information from the Japanese Gastric Cancer Association, reference 9.
Figure 2. Treatment algorithm based on the histopathologic evaluation after resection of early gastric tumors.

The Japanese Gastric Cancer Association has proposed a treatment algorithm based on the histopathologic evaluation after resection (Figure 2).9

Outcomes

In the largest series of patients who underwent curative ESD for early gastric cancer, the 5-year survival rate was 92.6%, the 5-year disease-specific survival rate was 99.9%, and the 5-year relative survival rate was 105%.41

Similarly, in a Japanese population-based survival analysis, the relative 5-year survival rate for localized gastric cancer was 94.4%.42 Rates of en bloc resection and complete resection with ESD are higher than those with EMR, resulting in a lower risk of local recurrence in selected patients who undergo ESD.8,43,44

Although rare, local recurrence after curative gastric ESD has been reported.45 The annual incidence of local recurrence has been estimated to be 0.84%.46

ESD entails a shorter hospital stay and requires fewer resources than surgery, resulting in lower medical costs (Table 2).44 Additionally, as endoscopic resection is associated with less morbidity, fewer procedure-related adverse events, and fewer complications, ESD could be used as the standard treatment for early gastric cancer.47,48

The Western perspective on endoscopic submucosal dissection for gastric cancer

Since the prevalence of gastric cancer in Western countries is significantly lower than in Japan and Korea, local data and experience are scarce. However, experts performing ESD in the West have adopted the indications of the Japan Gastroenterological Endoscopy Society. The European Society of Gastrointestinal Endoscopy recommends ESD for excision of most superficial gastric neoplasms, with EMR being preferred only in lesions smaller than 15 mm, Paris classification 0 or IIA.5,32

Patients with gastric lesions measuring 15 mm or larger should undergo high-quality endoscopy, preferably chromoendoscopy, to evaluate the mucosal patterns and determine the depth of invasion. If superficial involvement is confirmed, other imaging techniques are not routinely recommended.5 A surgery consult is also recommended.

ESOPHAGEAL CANCER

Indications for ESD for esophageal cancer in the East

Due to the success of ESD for early gastric cancer, this technique is now also used for superficial esophageal neoplasms.19,49 It should be done in a specialized center, as it is more technically difficult than gastric ESD: the esophageal lumen is narrow, the wall is thin, and the esophagus moves with respiration and heartbeat.50 A multidisciplinary approach including an endoscopist, a surgeon, and a pathologist is highly recommended for evaluation and treatment.

EMR is preferred for removal of mucosal cancer, in view of its safety profile and success rates. ESD can be considered in cases of lesions larger than 15 mm, poorly lifting tumors, and those with the possibility of submucosal invasion (Table 3).5,45,49,51

Circumference involvement is critical when determining eligible candidates, as a defect involving more than three-fourths of the esophageal circumference can lead to esophageal strictures.52 Controlled prospective studies have shown promising results from giving intralesional and oral steroids to prevent stricture after ESD, which could potentially overcome this size limitation.53,54

Outcomes for esophageal cancer

ESD has been shown to be safe and effective, achieving en bloc resection in 85% to 100% of patients.19,51 Its advantages over EMR include en bloc resection, complete resection, and high curative rates, resulting in higher recurrence-free survival.2,55,56 Although the incidence of complications such as bleeding, perforation, and stricture formation are higher with ESD, patients usually recover uneventfully.2,19,20

ESD in the esophagus: The Western perspective

As data on the efficacy of EMR vs ESD for the treatment of Barrett esophagus with adenocarcinoma are limited, EMR is the gold standard endoscopic technique for removal of visible esophageal dysplastic lesions.5,51,57 ESD can be considered for tumors larger than 15 mm, for poorly lifting lesions, and if there is suspicion of submucosal invasion.5

Patients should be evaluated by an experienced endoscopist, using an advanced imaging technique such as narrow-band imaging or chromoendoscopy. If suspicious features are found, endoscopic ultrasonography should be considered to confirm submucosal invasion or lymph node involvement.5

 

 

COLORECTAL CANCER

Indications for ESD for colorectal cancer in the East

Colon cancer is one of the leading causes of cancer-related deaths worldwide.58 Since ESD has been found to be effective and safe in treating gastric cancer, it has also been used to remove large colorectal tumors.59 However, ESD is not universally accepted in the treatment of colorectal neoplasms due to its greater technical difficulty, longer procedural time, and higher risk of perforating the thinner colonic wall compared with EMR.21,60

According to the Japanese Society of Gastroenterology, ESD should be reserved for lesions that are not amenable to snare removal (> 20 mm in size, intramucosal tumors with fibrosis, localized lesions that result from chronic inflammation, and local residual carcinoma) (Tables 4 and 5).21,61 Colorectal ESD should be performed only by a trained endoscopist.11

Outcomes for colorectal cancer

Piecemeal resection is one of the predictors of recurrence after endoscopic removal of colorectal cancer.62 Therefore, the cumulative rates of en bloc resection and curative resection are higher and the recurrence rate is lower for en bloc ESD than for EMR.62–65 Complication rates and procedural time are higher for ESD than for EMR.59,66

Tumor size of 50 mm or larger is a risk factor for complications, while a high procedure volume at the center is a protective factor.60

Endoscopic treatment of colorectal cancer: The Western perspective

EMR is the gold standard for removal of superficial colorectal lesions. However, ESD can be considered if there is suspicion of superficial submucosal invasion, especially for lesions larger than 20 mm that cannot be resected en bloc by EMR.32 ESD can also be used for fibrotic lesions not amenable to complete EMR removal, or as a salvage procedure after recurrence after EMR.67 Proper selection of cases is critical.1

Patients who have a superficial colonic lesion should be evaluated by means of high-definition endoscopy and chromoendoscopy to assess the mucosal pattern and establish feasibility of endoscopic resection. If submucosal invasion is suspected, staging with endoscopic ultrasonography or magnetic resonance imaging should be considered.5

FOLLOW-UP AFTER ESD

Endoscopic surveillance after the procedure is recommended, given the persistent risk of metachronous cancer after curative ESD due to its organ-sparing quality.68 Surveillance endoscopy aims to achieve early detection and subsequent endoscopic resection of metachronous lesions.

Histopathologic evaluation assessing the presence of malignant cells in the margins of a resected sample is mandatory for determining the next step in treatment. If margins are negative, follow-up endoscopy can be done every 6 to 12 months. If margins are positive, the approach includes surgery, reattempting ESD or endoscopic surveillance in 3 or 6 months.3,32 Although the surveillance strategy varies according to individual risk of metachronous cancer, it should be continued indefinitely.68

COMPLICATIONS OF ESD

The most common procedure-related complications of ESD are bleeding, perforation, and stricture. Most intraprocedural adverse events can be managed endoscopically.69

Bleeding

Most bleeding occurs during the procedure or early after it and can be controlled with electrocautery.49,69 No episodes of massive bleeding, defined as causing clinical symptoms and requiring transfusion or surgery, have been reported.20,43,55

In gastric ESD, delayed bleeding rates have ranged from 0 to 15.6%.69 Bleeding may be prevented with endoscopic coagulation of visible vessels after dissection has been completed and by proton pump inhibitor therapy.70,71 Excessive coagulation should be avoided to lower the risk of perforation.33

In colorectal ESD the bleeding rate has been reported to be 2.2%; applying coagulation to an area where a blood vessel is suspected before cutting (precoagulation) may prevent subsequent bleeding.21

Perforation

For gastric ESD, perforation rates range from 1.2% to 5.2%.69 Esophageal perforation rates can be up to 4%.49 In colorectal ESD, perforation rates have been reported to be 1.6% to 6.6%.60,72

Although most of the cases were successfully managed with conservative treatment, some required emergency surgery.60,73

Strictures

In a case series of 532 patients undergoing gastric ESD, stricture was reported in 5 patients, all of whom presented with obstructive symptoms.74 Risk factors for post-ESD gastric stenosis are a mucosal defect with a circumferential extent of more than three-fourths or a longitudinal extent of more than 5 cm.75

Strictures are common after esophageal ESD, with rates ranging from 2% to 26%. The risk is higher when longer segments are removed or circumferential resection is performed. As previously mentioned, this complication may be reduced with ingestion or injection of steroids  after the procedure.53,54

Surprisingly, ESD of large colorectal lesions involving more than three-fourths of the circumference of the rectum is rarely complicated by stenosis.76

 

 

LIMITATIONS OF ESD

ESD requires a high level of technical skill, is time-consuming, and has a higher rate of complications than conventional endoscopic resection. A standardized ESD training system is needed, as the procedure is more difficult than EMR. Training in porcine models has been shown to confer competency in ESD in a Western setting.13,16,33

Colorectal ESD is an even more challenging procedure, given the potential for complications related to its anatomy. Training centers in Japan usually have their trainees first master gastric ESD, then assist in more than 20 colorectal ESDs conducted by experienced endoscopists, and accomplish 30 cases before performing the procedure safely and independently.

As the incidence of gastric cancer is low in Western countries, trainees may also begin with lower rectal lesions, which are easier to remove.77 Incorporation of ESD in the West would require a clear treatment algorithm. It is a complex procedure, with higher rates of complications, a prolonged learning curve, and prolonged procedure time. Therefore, it should be performed in specialized centers and under the special situations discussed here to ensure that the benefits for the patients outweigh the risks.

VALUE OF ENDOSCOPIC SUBMUCOSAL DISSECTION

The optimal method for resecting gastrointestinal neoplasms should be safe, cost-effective, and quick and should also completely remove the lesion. The best treatment strategy takes into account the characteristics of the lesion and the comorbidities and wishes of the patient. Internists should be aware of the multiple options available to achieve the best outcome for the patient.1

Endoscopic resection of superficial gastrointestinal neoplasms, including EMR and ESD, has been a subject of increasing interest due to its minimally invasive and potentially curative character. However, cancer can recur after endoscopic resection because the procedure is organ-sparing.

ESD allows resection of early gastrointestinal tumors with a minimally invasive technique. It can achieve higher curative resection rates and lower recurrence rates compared with EMR. Compared with surgery, ESD leads to less morbidity, fewer procedure-related complications, and lower medical costs. Indications should be rigorously followed to achieve successful treatments in selected patients.

Multiple variables have to be taken into account when deciding which treatment is best, such as tumor characteristics, the patient’s baseline condition, physician expertise, and hospital resources.48 Less-invasive treatments may improve the prognosis of patients. No matter the approach, patients should be treated in specialized treatment centers.

Internal medicine physicians should be aware of the advances in treatments for early gastrointestinal cancer so appropriate options can be considered.

The treatment of early esophageal, gastric, and colorectal cancer is changing.1 For many years, surgery was the mainstay of treatment for early-stage gastrointestinal cancer. Unfortunately, surgery leads to significant loss of function of the organ, resulting in increased morbidity and decreased quality of life.2

Endoscopic techniques, particularly endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD), have been developed and are widely used in Japan, where gastrointestinal cancer is more common than in the West. This article reviews the indications, complications, and outcomes of ESD for early gastrointestinal neoplasms, so that readers will recognize the subset of patients who would benefit from ESD in a Western setting.

ENDOSCOPIC MUCOSAL RESECTION AND SUBMUCOSAL DISSECTION

Since the first therapeutic polypectomy was performed in Japan in 1974, several endoscopic techniques for tumor resection have been developed.3

EMR, one of the most successful and widely used techniques, involves elevating the lesion either with submucosal injection of a solution or with cap suction, and then removing it with a snare.4 Most lesions smaller than 20 mm can be removed in one piece (en bloc).5 Larger lesions are removed in multiple pieces (ie, piecemeal). Unfortunately, some fibrotic lesions, which are usually difficult to lift, cannot be completely removed by EMR.

ESD was first performed in the late 1990s with the aim of overcoming the limitations of EMR in resecting large or fibrotic tumors en bloc.6,7 Since then, ESD technique has been standardized and training centers have been created, especially in Asia, where it is widely used for treatment of early gastric cancer.3,8–10 Since 2012 it has been covered by the Japanese National Health Insurance for treatment of early gastric cancer, and since 2014 for treatment of colorectal malignant tumors measuring 2 to 5 cm.11

Adoption of ESD has been slow in Western countries, where many patients are still referred for surgery or undergo EMR for removal of superficial neoplasms. Reasons for this slow adoption are that gastric cancer is much less common in Western countries, and also that ESD demands a high level of technical skill, is difficult to learn, and is expensive.3,12,13 However, small groups of Western endoscopists have become interested and are advocating it, first studying it on their own and then training in a Japanese center and learning from experts performing the procedure.

Therefore, in a Western setting, ESD should be performed in specialized endoscopy centers and offered to selected patients.1  

CANDIDATES SHOULD HAVE EARLY-STAGE, SUPERFICIAL TUMORS

Ideal candidates for endoscopic resection are patients who have early cancer with a negligible risk of lymph node metastasis, such as cancer limited to the mucosa (stage T1a).7 Therefore, to determine the best treatment for a patient with a newly diagnosed gastrointestinal neoplasm, it is mandatory to estimate the depth of invasion.

The depth of invasion is directly correlated with lymph node involvement, which is ultimately the main predictive factor for long-term adverse outcomes of gastrointestinal tumors.4,14–17 Accurate multidisciplinary preprocedure estimations are mandatory, as incorrect evaluations may result in inappropriate therapy and residual cancer.18

Other factors that have been used to predict lymph node involvement include tumor size, macroscopic appearance, histologic differentiation, and lymphatic and vascular involvement.19 Some of these factors can be assessed by special endoscopic techniques (chromoendoscopy and narrow-band imaging with magnifying endoscopy) that allow accurate real-time estimation of the depth of invasion of the lesion.5,17,20–27 Evaluation of microsurface and microvascular arrangements is especially useful for determining the feasibility of ESD in gastric tumors, evaluation of intracapillary loops is useful in esophageal lesions, and assessment of mucosal pit patterns is useful for colorectal lesions.21–29

Endoscopic ultrasonography is another tool that has been used to estimate the depth of the tumor. Although it can differentiate between definite intramucosal and definite submucosal invasive cancers, its ability to confirm minute submucosal invasion is limited. Its use as the sole tumor staging modality is not encouraged, and it should always be used in conjunction with endoscopic evaluation.18

Though the aforementioned factors help stratify patients, pathologic staging is the best predictor of lymph node metastasis. ESD provides adequate specimens for accurate pathologic evaluation, as it removes lesions en bloc.30

All patients found to have risk factors for lymph node metastasis on endoscopic, ultrasonographic, or pathologic analysis should be referred for surgical evaluation.9,19,31,32

ENDOSCOPIC SUBMUCOSAL DISSECTION

Before the procedure, the patient’s physicians need to do the following:

Determine the best type of intervention (EMR, ESD, ablation, surgery) for the specific lesion.3 A multidisciplinary approach is encouraged, with involvement of the internist, gastroenterologist, and surgeon.

Plan for anesthesia, additional consultations, pre- and postprocedural hospital admission, and need for special equipment.33

During the procedure

Figure 1. Endoscopic submucosal dissection, a minimally invasive treatment for early-stage cancers of the gastrointestinal system, involves the following steps: (A) marking the circumference of the tumor, (B) lifting the tumor by injecting saline or another inert substance beneath it, (C) cutting around the outside of the tumor margin, and (D) dissecting and removing the tumor.
The main steps of ESD are circumferential marking of the lesion, submucosal injection, circumferential incision, and submucosal dissection (Figure 1). The endoscopist must do the following:

Define the lateral extent of the lesion using magnification chromoendoscopy or narrow-band imaging. In the stomach, a biopsy sample should be taken from the worst-looking segment and from normal-looking mucosa. Multiple biopsies should be avoided to prevent subsequent fibrosis.33 In the colon, biopsy should be avoided.34

Identify and circumferentially mark the target lesion. Cautery or argon plasma coagulation can be used for making markings at a distance of 5 to 10 mm from the edges.33 This is done to recognize the borders of the lesion, because they can become distorted after submucosal injection.14 This step is unnecessary in colorectal cases, as tumor margins can be adequately visualized after chromoendoscopy.16,35

Lift the lesion by injecting saline, 0.5% hyaluronate, or glycerin to create a submucosal fluid cushion.19,33

Perform a circumferential incision lateral to the mucosal margins to allow for a normal tissue margin.33 Partial incision is performed for esophageal and colorectal ESD to avoid fluid leakage from the submucosal layer, achieving a sustained submucosal lift and safer dissection.16

Submucosal dissection. The submucosal layer is dissected with an electrocautery knife until the lesion is completely removed. Dissection should be done carefully to keep the submucosal plane.33 Hemoclips or hemostat forceps can be used to control visible bleeding. The resected specimen is then stretched and fixed to a board using small pins for further histopathologic evaluation.35

Postprocedural monitoring.  All patients should be admitted for overnight observation. Those who undergo gastric ESD should receive high-dose acid suppression, and the next day they can be started on a liquid diet.19

 

 

STOMACH CANCER

Indications for ESD for stomach cancer in the East

The incidence of gastric cancer is higher in Japan and Korea, where widespread screening programs have led to early identification and early treatment of this disease.36

Pathology studies37 of samples from patients with gastric cancer identified the following as risk factors for lymph node metastasis, which would make ESD unsuitable:

  • Undifferentiated type
  • Tumors larger than 2 cm
  • Lymphatic or venous involvement
  • Submucosal invasion
  • Ulcerative change.

Based on these findings, the situations in which there was no risk of lymph node involvement (ie, when none of the above factors are present) were accepted as absolute indications for endoscopic resection of early gastric cancer.38 Further histologic studies identified a subset of patients with lesions with very low risk of lymph node metastasis, which outweighed the risk of surgery. Based on these findings, expanded criteria for gastric ESD were proposed,39,40 and the Japanese gastric cancer treatment guidelines now include these expanded preoperative indications9,17 (Table 1).

Treatment algorithm based on the histopathologic evaluation after resection of early gastric tumors.
Based on information from the Japanese Gastric Cancer Association, reference 9.
Figure 2. Treatment algorithm based on the histopathologic evaluation after resection of early gastric tumors.

The Japanese Gastric Cancer Association has proposed a treatment algorithm based on the histopathologic evaluation after resection (Figure 2).9

Outcomes

In the largest series of patients who underwent curative ESD for early gastric cancer, the 5-year survival rate was 92.6%, the 5-year disease-specific survival rate was 99.9%, and the 5-year relative survival rate was 105%.41

Similarly, in a Japanese population-based survival analysis, the relative 5-year survival rate for localized gastric cancer was 94.4%.42 Rates of en bloc resection and complete resection with ESD are higher than those with EMR, resulting in a lower risk of local recurrence in selected patients who undergo ESD.8,43,44

Although rare, local recurrence after curative gastric ESD has been reported.45 The annual incidence of local recurrence has been estimated to be 0.84%.46

ESD entails a shorter hospital stay and requires fewer resources than surgery, resulting in lower medical costs (Table 2).44 Additionally, as endoscopic resection is associated with less morbidity, fewer procedure-related adverse events, and fewer complications, ESD could be used as the standard treatment for early gastric cancer.47,48

The Western perspective on endoscopic submucosal dissection for gastric cancer

Since the prevalence of gastric cancer in Western countries is significantly lower than in Japan and Korea, local data and experience are scarce. However, experts performing ESD in the West have adopted the indications of the Japan Gastroenterological Endoscopy Society. The European Society of Gastrointestinal Endoscopy recommends ESD for excision of most superficial gastric neoplasms, with EMR being preferred only in lesions smaller than 15 mm, Paris classification 0 or IIA.5,32

Patients with gastric lesions measuring 15 mm or larger should undergo high-quality endoscopy, preferably chromoendoscopy, to evaluate the mucosal patterns and determine the depth of invasion. If superficial involvement is confirmed, other imaging techniques are not routinely recommended.5 A surgery consult is also recommended.

ESOPHAGEAL CANCER

Indications for ESD for esophageal cancer in the East

Due to the success of ESD for early gastric cancer, this technique is now also used for superficial esophageal neoplasms.19,49 It should be done in a specialized center, as it is more technically difficult than gastric ESD: the esophageal lumen is narrow, the wall is thin, and the esophagus moves with respiration and heartbeat.50 A multidisciplinary approach including an endoscopist, a surgeon, and a pathologist is highly recommended for evaluation and treatment.

EMR is preferred for removal of mucosal cancer, in view of its safety profile and success rates. ESD can be considered in cases of lesions larger than 15 mm, poorly lifting tumors, and those with the possibility of submucosal invasion (Table 3).5,45,49,51

Circumference involvement is critical when determining eligible candidates, as a defect involving more than three-fourths of the esophageal circumference can lead to esophageal strictures.52 Controlled prospective studies have shown promising results from giving intralesional and oral steroids to prevent stricture after ESD, which could potentially overcome this size limitation.53,54

Outcomes for esophageal cancer

ESD has been shown to be safe and effective, achieving en bloc resection in 85% to 100% of patients.19,51 Its advantages over EMR include en bloc resection, complete resection, and high curative rates, resulting in higher recurrence-free survival.2,55,56 Although the incidence of complications such as bleeding, perforation, and stricture formation are higher with ESD, patients usually recover uneventfully.2,19,20

ESD in the esophagus: The Western perspective

As data on the efficacy of EMR vs ESD for the treatment of Barrett esophagus with adenocarcinoma are limited, EMR is the gold standard endoscopic technique for removal of visible esophageal dysplastic lesions.5,51,57 ESD can be considered for tumors larger than 15 mm, for poorly lifting lesions, and if there is suspicion of submucosal invasion.5

Patients should be evaluated by an experienced endoscopist, using an advanced imaging technique such as narrow-band imaging or chromoendoscopy. If suspicious features are found, endoscopic ultrasonography should be considered to confirm submucosal invasion or lymph node involvement.5

 

 

COLORECTAL CANCER

Indications for ESD for colorectal cancer in the East

Colon cancer is one of the leading causes of cancer-related deaths worldwide.58 Since ESD has been found to be effective and safe in treating gastric cancer, it has also been used to remove large colorectal tumors.59 However, ESD is not universally accepted in the treatment of colorectal neoplasms due to its greater technical difficulty, longer procedural time, and higher risk of perforating the thinner colonic wall compared with EMR.21,60

According to the Japanese Society of Gastroenterology, ESD should be reserved for lesions that are not amenable to snare removal (> 20 mm in size, intramucosal tumors with fibrosis, localized lesions that result from chronic inflammation, and local residual carcinoma) (Tables 4 and 5).21,61 Colorectal ESD should be performed only by a trained endoscopist.11

Outcomes for colorectal cancer

Piecemeal resection is one of the predictors of recurrence after endoscopic removal of colorectal cancer.62 Therefore, the cumulative rates of en bloc resection and curative resection are higher and the recurrence rate is lower for en bloc ESD than for EMR.62–65 Complication rates and procedural time are higher for ESD than for EMR.59,66

Tumor size of 50 mm or larger is a risk factor for complications, while a high procedure volume at the center is a protective factor.60

Endoscopic treatment of colorectal cancer: The Western perspective

EMR is the gold standard for removal of superficial colorectal lesions. However, ESD can be considered if there is suspicion of superficial submucosal invasion, especially for lesions larger than 20 mm that cannot be resected en bloc by EMR.32 ESD can also be used for fibrotic lesions not amenable to complete EMR removal, or as a salvage procedure after recurrence after EMR.67 Proper selection of cases is critical.1

Patients who have a superficial colonic lesion should be evaluated by means of high-definition endoscopy and chromoendoscopy to assess the mucosal pattern and establish feasibility of endoscopic resection. If submucosal invasion is suspected, staging with endoscopic ultrasonography or magnetic resonance imaging should be considered.5

FOLLOW-UP AFTER ESD

Endoscopic surveillance after the procedure is recommended, given the persistent risk of metachronous cancer after curative ESD due to its organ-sparing quality.68 Surveillance endoscopy aims to achieve early detection and subsequent endoscopic resection of metachronous lesions.

Histopathologic evaluation assessing the presence of malignant cells in the margins of a resected sample is mandatory for determining the next step in treatment. If margins are negative, follow-up endoscopy can be done every 6 to 12 months. If margins are positive, the approach includes surgery, reattempting ESD or endoscopic surveillance in 3 or 6 months.3,32 Although the surveillance strategy varies according to individual risk of metachronous cancer, it should be continued indefinitely.68

COMPLICATIONS OF ESD

The most common procedure-related complications of ESD are bleeding, perforation, and stricture. Most intraprocedural adverse events can be managed endoscopically.69

Bleeding

Most bleeding occurs during the procedure or early after it and can be controlled with electrocautery.49,69 No episodes of massive bleeding, defined as causing clinical symptoms and requiring transfusion or surgery, have been reported.20,43,55

In gastric ESD, delayed bleeding rates have ranged from 0 to 15.6%.69 Bleeding may be prevented with endoscopic coagulation of visible vessels after dissection has been completed and by proton pump inhibitor therapy.70,71 Excessive coagulation should be avoided to lower the risk of perforation.33

In colorectal ESD the bleeding rate has been reported to be 2.2%; applying coagulation to an area where a blood vessel is suspected before cutting (precoagulation) may prevent subsequent bleeding.21

Perforation

For gastric ESD, perforation rates range from 1.2% to 5.2%.69 Esophageal perforation rates can be up to 4%.49 In colorectal ESD, perforation rates have been reported to be 1.6% to 6.6%.60,72

Although most of the cases were successfully managed with conservative treatment, some required emergency surgery.60,73

Strictures

In a case series of 532 patients undergoing gastric ESD, stricture was reported in 5 patients, all of whom presented with obstructive symptoms.74 Risk factors for post-ESD gastric stenosis are a mucosal defect with a circumferential extent of more than three-fourths or a longitudinal extent of more than 5 cm.75

Strictures are common after esophageal ESD, with rates ranging from 2% to 26%. The risk is higher when longer segments are removed or circumferential resection is performed. As previously mentioned, this complication may be reduced with ingestion or injection of steroids  after the procedure.53,54

Surprisingly, ESD of large colorectal lesions involving more than three-fourths of the circumference of the rectum is rarely complicated by stenosis.76

 

 

LIMITATIONS OF ESD

ESD requires a high level of technical skill, is time-consuming, and has a higher rate of complications than conventional endoscopic resection. A standardized ESD training system is needed, as the procedure is more difficult than EMR. Training in porcine models has been shown to confer competency in ESD in a Western setting.13,16,33

Colorectal ESD is an even more challenging procedure, given the potential for complications related to its anatomy. Training centers in Japan usually have their trainees first master gastric ESD, then assist in more than 20 colorectal ESDs conducted by experienced endoscopists, and accomplish 30 cases before performing the procedure safely and independently.

As the incidence of gastric cancer is low in Western countries, trainees may also begin with lower rectal lesions, which are easier to remove.77 Incorporation of ESD in the West would require a clear treatment algorithm. It is a complex procedure, with higher rates of complications, a prolonged learning curve, and prolonged procedure time. Therefore, it should be performed in specialized centers and under the special situations discussed here to ensure that the benefits for the patients outweigh the risks.

VALUE OF ENDOSCOPIC SUBMUCOSAL DISSECTION

The optimal method for resecting gastrointestinal neoplasms should be safe, cost-effective, and quick and should also completely remove the lesion. The best treatment strategy takes into account the characteristics of the lesion and the comorbidities and wishes of the patient. Internists should be aware of the multiple options available to achieve the best outcome for the patient.1

Endoscopic resection of superficial gastrointestinal neoplasms, including EMR and ESD, has been a subject of increasing interest due to its minimally invasive and potentially curative character. However, cancer can recur after endoscopic resection because the procedure is organ-sparing.

ESD allows resection of early gastrointestinal tumors with a minimally invasive technique. It can achieve higher curative resection rates and lower recurrence rates compared with EMR. Compared with surgery, ESD leads to less morbidity, fewer procedure-related complications, and lower medical costs. Indications should be rigorously followed to achieve successful treatments in selected patients.

Multiple variables have to be taken into account when deciding which treatment is best, such as tumor characteristics, the patient’s baseline condition, physician expertise, and hospital resources.48 Less-invasive treatments may improve the prognosis of patients. No matter the approach, patients should be treated in specialized treatment centers.

Internal medicine physicians should be aware of the advances in treatments for early gastrointestinal cancer so appropriate options can be considered.

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  57. Hirasawa K, Kokawa A, Oka H, et al. Superficial adenocarcinoma of the esophagogastric junction: long-term results of endoscopic submucosal dissection. Gastrointest Endosc 2010; 72:960–966.
  58. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011; 61:69–90.
  59. Nakajima T, Saito Y, Tanaka S, et al. Current status of endoscopic resection strategy for large, early colorectal neoplasia in Japan. Surg Endosc 2013; 27:3262–3770.
  60. Saito Y, Uraoka T, Yamaguchi Y, et al. A prospective, multicenter study of 1111 colorectal endoscopic submucosal dissections (with video). Gastrointest Endosc 2010; 72:1217–1225.
  61. Tanaka S, Saitoh Y, Matsuda T, et al; Japanese Society of Gastroenterology. Evidence-based clinical practice guidelines for management of colorectal polyps. J Gastroenterol 2015; 50:252–260.
  62. Oka S, Tanaka S, Saito Y, et al; Colorectal Endoscopic Resection Standardization Implementation Working Group of the Japanese Society for Cancer of the Colon and Rectum, Tokyo, Japan. Local recurrence after endoscopic resection for large colorectal neoplasia: a multicenter prospective study in Japan. Am J Gastroenterol 2015; 110:697–707.
  63. Saito Y, Fukuzawa M, Matsuda T, et al. Clinical outcome of endoscopic submucosal dissection versus endoscopic mucosal resection of large colorectal tumors as determined by curative resection. Surg Endosc 2010; 24:343–352.
  64. Makazu M, Sakamoto T, So E, et al. Relationship between indeterminate or positive lateral margin and local recurrence after endoscopic resection of colorectal polyps. Endosc Int Open 2015; 3:E252–E257.
  65. Belderbos TD, Leenders M, Moons LM, Siersema PD. Local recurrence after endoscopic mucosal resection of nonpedunculated colorectal lesions: systematic review and meta-analysis. Endoscopy 2014; 46:388–402.
  66. Fujiya M, Tanaka K, Dokoshi T, et al. Efficacy and adverse events of EMR and endoscopic submucosal dissection for the treatment of colon neoplasms: a meta-analysis of studies comparing EMR and endoscopic submucosal dissection. Gastrointest Endosc 2015; 81:583–595.
  67. Rahmi G, Tanaka S, Ohara Y, et al. Efficacy of endoscopic submucosal dissection for residual or recurrent superficial colorectal tumors after endoscopic mucosal resection. J Dig Dis 2015; 16:14–21.
  68. Abe S, Oda I, Suzuki H, et al. Long-term surveillance and treatment outcomes of metachronous gastric cancer occurring after curative endoscopic submucosal dissection. Endoscopy 2015; 47:1113–1118.
  69. Oda I, Suzuki H, Nonaka S, Yoshinaga S. Complications of gastric endoscopic submucosal dissection. Dig Endosc 2013; 25(suppl 1):71–78.
  70. Takizawa K, Oda I, Gotoda T, et al. Routine coagulation of visible vessels may prevent delayed bleeding after endoscopic submucosal dissection—an analysis of risk factors. Endoscopy 2008; 40:179–183.
  71. Uedo N, Takeuchi Y, Yamada T, et al. Effect of a proton pump inhibitor or an H2-receptor antagonist on prevention of bleeding from ulcer after endoscopic submucosal dissection of early gastric cancer: a prospective randomized controlled trial. Am J Gastroenterol 2007; 102:1610–1616.
  72. Hayashi N, Tanaka S, Nishiyama S, et al. Predictors of incomplete resection and perforation associated with endoscopic submucosal dissection for colorectal tumors. Gastrointest Endosc 2014; 79:427–435.
  73. Suzuki H, Oda I, Sekiguchi M, et al. Management and associated factors of delayed perforation after gastric endoscopic submucosal dissection. World J Gastroenterol 2015; 21:12635–12643.
  74. Tsunada S, Ogata S, Mannen K, et al. Case series of endoscopic balloon dilation to treat a stricture caused by circumferential resection of the gastric antrum by endoscopic submucosal dissection. Gastrointest Endosc 2008; 67:979–983.
  75. Coda S, Oda I, Gotoda T, Yokoi C, Kikuchi T, Ono H. Risk factors for cardiac and pyloric stenosis after endoscopic submucosal dissection, and efficacy of endoscopic balloon dilation treatment. Endoscopy 2009; 41:421–426.
  76. Abe S, Sakamoto T, Takamaru H, et al. Stenosis rates after endoscopic submucosal dissection of large rectal tumors involving greater than three quarters of the luminal circumference. Surg Endosc 2016; 30:5459–5464.
  77. Sakamoto T, Saito Y, Fukunaga S, Nakajima T, Matsuda T. Learning curve associated with colorectal endoscopic submucosal dissection for endoscopists experienced in gastric endoscopic submucosal dissection. Dis Colon Rectum 2011; 54:1307–1312.
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  14. Sano T, Sasako M, Kinoshita T, Maruyama K. Recurrence of early gastric cancer follow-up of 1475 patients and review of the Japanese literature. Cancer 1993; 72:3174–3178.
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  20. Higuchi K, Tanabe S, Azuma M, et al. A phase II study of endoscopic submucosal dissection for superficial esophageal neoplasms (KDOG 0901). Gastrointest Endosc 2013; 78:704–710.
  21. Sakamoto T, Mori G, Yamada M, et al. Endoscopic submucosal dissection for colorectal neoplasms: a review. World J Gastroenterol 2014; 20:16153–16158.
  22. Ohta A, Tominaga K, Sakai Y. Efficacy of magnifying colonoscopy for the diagnosis of colorectal neoplasia: comparison with histopathological findings. Dig Endosc 2004; 16:308–314.
  23. Katagiri A, Fu K, Sano Y, et al. Narrow band imaging with magnifying colonoscopy as diagnostic tool for predicting histology of early colorectal neoplasia. Aliment Pharmacol Ther 2008; 27:1269–1274.
  24. Fu KI, Kato S, Sano Y, et al. Staging of early colorectal cancers: magnifying colonoscopy versus endoscopic ultrasonography for estimation of depth of invasion. Dig Dis Sci 2008; 53:1886–1892.
  25. Uraoka T, Saito Y, Ikematsu H, Yamamoto K, Sano Y. Sano’s capillary pattern classification for narrow-band imaging of early colorectal lesions. Dig Endosc 2011; 23(suppl 1):112–115.
  26. Ikematsu H, Matsuda T, Emura F, et al. Efficacy of capillary pattern type IIIA/IIIB by magnifying narrow band imaging for estimating depth of invasion of early colorectal neoplasms. BMC Gastroenterol 2010;10:33.
  27. Matsuda T, Fujii T, Saito Y, et al. Efficacy of the invasive/non-invasive pattern by magnifying chromoendoscopy to estimate the depth of invasion of early colorectal neoplasms. Am J Gastroenterol 2008; 103:2700–2706.
  28. Sato H, Inoue H, Ikeda H, et al. Utility of intrapapillary capillary loops seen on magnifying narrow-band imaging in estimating invasive depth of esophageal squamous cell carcinoma. Endoscopy 2015; 8:122–128.
  29. Muto M, Yao K, Kaise M, et al. Magnifying endoscopy simple diagnostic algorithm for early gastric cancer (MESDA-G). Dig Endosc 2016; 28:379–393.
  30. Waddell T, Verheij M, Allum W, Cunningham D, Cervantes A, Arnold D; European Society for Medical Oncology (ESMO); European Society of Surgical Oncology (ESSO); European Society of Radiotherapy and Oncology (ESTRO). Gastric cancer: ESMO-ESSO-ESTRO clinical practice guidelines for diagnosis, treatment and follow-up. Ann Oncol 2013; 24(suppl 6):vi57–vi63.
  31. Kuwano H, Nishimura Y, Ohtsu A, et al. Guidelines for diagnosis and treatment of carcinoma of the esophagus. April 2007 edition: part I - Edited by the Japan Esophageal Society. Esophagus 2008; 5:61–73.
  32. Tanaka S, Kashida H, Saito Y, et al. JGES guidelines for colorectal endoscopic submucosal dissection/endoscopic mucosal resection. Dig Endosc 2015; 27:417–434.
  33. Gotoda T, Ho KY, Soetikno R, Kaltenbach T, Draganov P. Gastric ESD: current status and future directions of devices and training. Gastrointest Endosc Clin North Am 2014; 24:213–233.
  34. Saito Y, Sakamoto T, Nakajima T, Matsuda T. Colorectal ESD: current indications and latest technical advances. Gastrointest Endosc Clin N Am 2014; 24:245–255.
  35. Saito Y, Otake Y, Sakamoto T, et al. Indications for and technical aspects of colorectal endoscopic submucosal dissection. Gut Liver 2013; 7:263–269.
  36. Saragoni L. Upgrading the definition of early gastric cancer: better staging means more appropriate treatment. Cancer Biol Med 2015; 12:355–361.
  37. Tsujitani S, Oka S, Saito H, et al. Less invasive surgery for early gastric cancer based on the low probability of lymph node metastasis. Surgery 1999; 125:148–154.
  38. Soetikno RM, Gotoda T, Nakanishi Y, Soehendra N. Endoscopic mucosal resection. Gastrointest Endosc 2003; 57:567–579.
  39. Hirasawa T, Gotoda T, Miyata S, et al. Incidence of lymph node metastasis and the feasibility of endoscopic resection for undifferentiated-type early gastric cancer. Gastric Cancer 2009; 12:148–152.
  40. Gotoda T, Yanagisawa A, Sasako M, et al. Incidence of lymph node metastasis from early gastric cancer: estimation with a large number of cases at two large centers. Gastric Cancer 2000; 3:219–225.
  41. Suzuki H, Oda I, Abe S, et al. High rate of 5-year survival among patients with early gastric cancer undergoing curative endoscopic submucosal dissection. Gastric Cancer 2016; 19:198–205.
  42. Matsuda T, Ajiki W, Marugame T, Ioka A, Tsukuma H, Sobue T; Research Group of Population-Based Cancer Registries of Japan. Population-based survival of cancer patients diagnosed between 1993 and 1999 in Japan: a chronological and international comparative study. Jpn J Clin Oncol 2011; 41:40–51.
  43. Ahn JY, Jung HY, Choi KD, et al. Endoscopic and oncologic outcomes after endoscopic resection for early gastric cancer: 1370 cases of absolute and extended indications. Gastrointest Endosc 2011; 74:485–493.
  44. Kim Y, Kim YW, Choi IJ, et al. Cost comparison between surgical treatments and endoscopic submucosal dissection in patients with early gastric cancer in Korea. Gut Liver 2015; 9:174–180.
  45. Abe S, Oda I, Nakajima T, et al. A case of local recurrence and distant metastasis following curative endoscopic submucosal dissection of early gastric cancer. Gastric Cancer 2015; 18:188–192.
  46. Hahn KY, Park JC, Kim EH, et al. Incidence and impact of scheduled endoscopic surveillance on recurrence after curative endoscopic resection for early gastric cancer. Gastrointest Endosc 2016; 84:628–638.e1.
  47. Wang S, Zhang Z, Liu M, Li S, Jiang C. Endoscopic resection compared with gastrectomy to treat early gastric cancer: a systematic review and meta-analysis. PLoS One 2015; 10:e0144774.
  48. Kondo A, de Moura EG, Bernardo WM, et al. Endoscopy vs surgery in the treatment of early gastric cancer: systematic review. World J Gastroenterol 2015; 21:13177–13187.
  49. Kothari S, Kaul V. Endoscopic mucosal resection and endoscopic submucosal dissection for endoscopic therapy of Barrett’s esophagus-related neoplasia. Gastroenterol Clin North Am 2015; 44:317–335.
  50. Yamashita T, Zeniya A, Ishii H, et al. Endoscopic mucosal resection using a cap-fitted panendoscope and endoscopic submucosal dissection as optimal endoscopic procedures for superficial esophageal carcinoma. Surg Endosc 2011; 25:2541–2546.
  51. Kagemoto K, Oka S, Tanaka S, et al. Clinical outcomes of endoscopic submucosal dissection for superficial Barrett’s adenocarcinoma. Gastrointest Endosc 2014; 80:239–245.
  52. Katada C, Muto M, Manabe T, Boku N, Ohtsu A, Yoshida S. Esophageal stenosis after endoscopic mucosal resection of superficial esophageal lesions. Gastrointest Endosc 2003; 57:165–169.
  53. Hanaoka N, Ishihara R, Takeuchi Y, et al. 1139: A single session of intralesional steroid injection to prevent esophageal stricture after endoscopic submucosal dissection for esophageal squamous cell carcinoma. Gastrointest Endosc 2012; 75(suppl):AB175.
  54. Yamaguchi N, Isomoto H, Nakayama T, et al. Usefulness of oral prednisolone in the treatment of esophageal stricture after endoscopic submucosal dissection for superficial esophageal squamous cell carcinoma. Gastrointest Endosc 2011; 73:1115–1121.
  55. Ono S, Fujishiro M, Niimi K, et al. Long-term outcomes of endoscopic submucosal dissection for superficial esophageal squamous cell neoplasms. Gastrointest Endosc 2009; 70:860–866.
  56. Katada C, Muto M, Manabe T, Ohtsu A, Yoshida S. Local recurrence of squamous-cell carcinoma of the esophagus after EMR. Gastrointest Endosc 2005; 61:219–225.
  57. Hirasawa K, Kokawa A, Oka H, et al. Superficial adenocarcinoma of the esophagogastric junction: long-term results of endoscopic submucosal dissection. Gastrointest Endosc 2010; 72:960–966.
  58. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011; 61:69–90.
  59. Nakajima T, Saito Y, Tanaka S, et al. Current status of endoscopic resection strategy for large, early colorectal neoplasia in Japan. Surg Endosc 2013; 27:3262–3770.
  60. Saito Y, Uraoka T, Yamaguchi Y, et al. A prospective, multicenter study of 1111 colorectal endoscopic submucosal dissections (with video). Gastrointest Endosc 2010; 72:1217–1225.
  61. Tanaka S, Saitoh Y, Matsuda T, et al; Japanese Society of Gastroenterology. Evidence-based clinical practice guidelines for management of colorectal polyps. J Gastroenterol 2015; 50:252–260.
  62. Oka S, Tanaka S, Saito Y, et al; Colorectal Endoscopic Resection Standardization Implementation Working Group of the Japanese Society for Cancer of the Colon and Rectum, Tokyo, Japan. Local recurrence after endoscopic resection for large colorectal neoplasia: a multicenter prospective study in Japan. Am J Gastroenterol 2015; 110:697–707.
  63. Saito Y, Fukuzawa M, Matsuda T, et al. Clinical outcome of endoscopic submucosal dissection versus endoscopic mucosal resection of large colorectal tumors as determined by curative resection. Surg Endosc 2010; 24:343–352.
  64. Makazu M, Sakamoto T, So E, et al. Relationship between indeterminate or positive lateral margin and local recurrence after endoscopic resection of colorectal polyps. Endosc Int Open 2015; 3:E252–E257.
  65. Belderbos TD, Leenders M, Moons LM, Siersema PD. Local recurrence after endoscopic mucosal resection of nonpedunculated colorectal lesions: systematic review and meta-analysis. Endoscopy 2014; 46:388–402.
  66. Fujiya M, Tanaka K, Dokoshi T, et al. Efficacy and adverse events of EMR and endoscopic submucosal dissection for the treatment of colon neoplasms: a meta-analysis of studies comparing EMR and endoscopic submucosal dissection. Gastrointest Endosc 2015; 81:583–595.
  67. Rahmi G, Tanaka S, Ohara Y, et al. Efficacy of endoscopic submucosal dissection for residual or recurrent superficial colorectal tumors after endoscopic mucosal resection. J Dig Dis 2015; 16:14–21.
  68. Abe S, Oda I, Suzuki H, et al. Long-term surveillance and treatment outcomes of metachronous gastric cancer occurring after curative endoscopic submucosal dissection. Endoscopy 2015; 47:1113–1118.
  69. Oda I, Suzuki H, Nonaka S, Yoshinaga S. Complications of gastric endoscopic submucosal dissection. Dig Endosc 2013; 25(suppl 1):71–78.
  70. Takizawa K, Oda I, Gotoda T, et al. Routine coagulation of visible vessels may prevent delayed bleeding after endoscopic submucosal dissection—an analysis of risk factors. Endoscopy 2008; 40:179–183.
  71. Uedo N, Takeuchi Y, Yamada T, et al. Effect of a proton pump inhibitor or an H2-receptor antagonist on prevention of bleeding from ulcer after endoscopic submucosal dissection of early gastric cancer: a prospective randomized controlled trial. Am J Gastroenterol 2007; 102:1610–1616.
  72. Hayashi N, Tanaka S, Nishiyama S, et al. Predictors of incomplete resection and perforation associated with endoscopic submucosal dissection for colorectal tumors. Gastrointest Endosc 2014; 79:427–435.
  73. Suzuki H, Oda I, Sekiguchi M, et al. Management and associated factors of delayed perforation after gastric endoscopic submucosal dissection. World J Gastroenterol 2015; 21:12635–12643.
  74. Tsunada S, Ogata S, Mannen K, et al. Case series of endoscopic balloon dilation to treat a stricture caused by circumferential resection of the gastric antrum by endoscopic submucosal dissection. Gastrointest Endosc 2008; 67:979–983.
  75. Coda S, Oda I, Gotoda T, Yokoi C, Kikuchi T, Ono H. Risk factors for cardiac and pyloric stenosis after endoscopic submucosal dissection, and efficacy of endoscopic balloon dilation treatment. Endoscopy 2009; 41:421–426.
  76. Abe S, Sakamoto T, Takamaru H, et al. Stenosis rates after endoscopic submucosal dissection of large rectal tumors involving greater than three quarters of the luminal circumference. Surg Endosc 2016; 30:5459–5464.
  77. Sakamoto T, Saito Y, Fukunaga S, Nakajima T, Matsuda T. Learning curve associated with colorectal endoscopic submucosal dissection for endoscopists experienced in gastric endoscopic submucosal dissection. Dis Colon Rectum 2011; 54:1307–1312.
Issue
Cleveland Clinic Journal of Medicine - 84(9)
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Cleveland Clinic Journal of Medicine - 84(9)
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707-717
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707-717
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A minimally invasive treatment for early GI cancers
Display Headline
A minimally invasive treatment for early GI cancers
Legacy Keywords
gastric cancer, stomach cancer, GI cancer, colorectal cancer, esophageal cancer, adenocarcinoma, Barrett esophagus, endoscopic submucosal dissection, ESD, endoscopic mucosal resection, EMR, endoscopy, colonoscopy, Lady Katherine Mejia-Perez, Seiichiro Abe, Tyler Stevens, Mansour Parsi, Sunguk Jang, Ichiro Oda, John Vargo, Yutaka Saito, Amit Bhatt
Legacy Keywords
gastric cancer, stomach cancer, GI cancer, colorectal cancer, esophageal cancer, adenocarcinoma, Barrett esophagus, endoscopic submucosal dissection, ESD, endoscopic mucosal resection, EMR, endoscopy, colonoscopy, Lady Katherine Mejia-Perez, Seiichiro Abe, Tyler Stevens, Mansour Parsi, Sunguk Jang, Ichiro Oda, John Vargo, Yutaka Saito, Amit Bhatt
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KEY POINTS

  • ESD is a minimally invasive endoscopic technique with curative potential for patients with superficial GI neoplasia.
  • ESD preserves the integrity of the organ while achieving curative resection of large neoplasms.
  • ESD is indicated rather than surgery in patients with early GI lesions with a negligible risk of lymph node metastasis.
  • Complications of the procedure include bleeding, perforation, and stenosis. Most of these respond to endoscopic treatment.
  • Successful ESD requires supportive teamwork among internists, gastroenterologists, pathologists, and surgeons.
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Heartburn or heart attack? A mimic of MI

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Heartburn or heart attack? A mimic of MI

A 71-year-old man with a history of hypertension, 4 prior myocardial infarctions (MIs), and well-compensated ischemic cardiomyopathy presented to the emergency department after 2 episodes of sharp pain in the left upper abdomen and chest. The episodes lasted 1 to 2 minutes and were not relieved by rest. Their location was similar to that of the pain he experienced with his MIs. He could not identify any exacerbating or ameliorating factors. The pain had resolved without specific therapy before he arrived.

He reported polydipsia and constipation over the past 2 weeks and generalized muscle weakness and acute exacerbations of chronic back pain in the past 2 days. Neither he nor a friend who accompanied him noticed any confusion. He had been taking as many as 15 calcium carbonate tablets a day for 6 weeks to self-treat dyspepsia refractory to once-daily ranitidine, and hydrochlorothiazide for his hypertension for 3 weeks.

FURTHER EVALUATION, CARDIOLOGY CONSULT

On physical examination, he had diffuse weakness, dry mucous membranes, and an irregular heart rhythm.

Electrocardiography at presentation showed a corrected QT interval of 360 msec.
Figure 1. Electrocardiography at presentation showed a corrected QT interval of 360 msec. In addition to ST-segment elevations (blue arrows) and ST-segment depressions (blue diamonds), varying ectopic beats (red arrows) were present that were absent on previous studies.
Electrocardiography (ECG) (Figure 1) showed ST-segment elevation in leads V1, V2, V3, II, III, and aVF and ST-segment depression in leads I and aVL. The corrected QT interval was 360 ms, compared with 426 ms 4 months earlier (Figure 2).

Laboratory testing showed the following:

  • Troponin I 0.11 ng/mL (reference range ≤ 0.04); repeated, it was 0.12 ng/mL
  • Serum creatinine 3.4 mg/dL (0.44–1.27) (9 months earlier it had been 0.99 mg/dL)
  • Serum calcium 17.3 mg/dL (8.6–10.5)
  • Parathyroid hormone 9 pg/mL (12–88)
  • Serum bicarbonate 33 mmol/L (24–32); 2 weeks earlier, it had been 27 mmol/L.

An electrocardiogram 4 months earlier showed no ST-segment elevations or ST-segment depressions.
Figure 2. An electrocardiogram 4 months earlier showed no ST-segment elevations (blue arrows) or ST-segment depressions (blue diamonds).
A cardiology consult was ordered out of concern for ST-elevation MI (STEMI). The cardiology consult team did not recommend coronary angiography because the patient’s chest pain had resolved spontaneously, its presentation was atypical, and the results of laboratory studies indicated acute kidney injury, a relative contraindication to angiography.

DIAGNOSIS: MILK-ALKALI SYNDROME

The diagnosis, based on the presentation and the results of the workup, was milk-alkali syndrome complicated by recent hydrochlorothiazide use. This syndrome consists of the triad of hypercalcemia, metabolic alkalosis, and acute kidney injury, all due to excessive ingestion of calcium and alkali, usually calcium carbonate.

His hydrochlorothiazide and calcium carbonate were discontinued. He was given intravenous normal saline and subcutaneous calcitonin, and his serum calcium level came down to 11.5 mg/dL within the next 24 hours. His dyspepsia was treated with pantoprazole.

The patient had no further episodes of chest pain, and the cardiology consult team again recommended against coronary angiography. Repeat ECG after the hypercalcemia resolved showed results identical to those 4 months before his admission. Two months later, his serum calcium level was 9.4 mg/dL and his creatinine level was 1.24 mg/dL.

A MIMIC OF STEMI

In numerous reported cases, these electrocardiographic findings coupled with chest pain led to misdiagnosis of STEMI.1–3 While STEMI and occasionally hypercalcemia can cause ST elevation, hypercalcemia causes a significant shortening of the corrected QT interval that is not associated with STEMI.4,5

Ultimately, the diagnosis of MI involves clinical, laboratory, and ECG findings, and if a strong clinical suspicion for myocardial ischemia exists, STEMI cannot reliably be distinguished from hypercalcemia by ECG alone. It is nonetheless important to be aware of this complication of hypercalcemia to avoid unnecessary cardiac interventions.

References
  1. Ashizawa N, Arakawa S, Koide Y, Toda G, Seto S, Yano K. Hypercalcemia due to vitamin D intoxication with clinical features mimicking acute myocardial infarction. Intern Med 2003; 42:340–344.
  2. Nishi SP, Barbagelata NA, Atar S, Birnbaum Y, Tuero E. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. J Electrocardiol 2006; 39:298–300.
  3. Turnham S, Kilickap M, Kilinc S. ST segment elevation mimicking acute myocardial infarction in hypercalcemia. Heart 2005; 91:999.
  4. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hypercalcemia. Am J Cardiol 1979; 44:243–248.
  5. Ahmed R, Hashiba K. Reliability of QT intervals as indicators of clinical hypercalcemia. Clin Cardiol 1988; 11:395–400.
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Willis S. Bowman, MD
Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Amir Farid, MD
Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Paul Aronowitz, MD, FACP
Health Sciences Clinical Professor of Medicine, Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Address: Willis S. Bowman, MD, Department of Internal Medicine, University of California Davis Medical Center, 4150 V Street, Suite 3100, Sacramento, CA 95817; [email protected]

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Cleveland Clinic Journal of Medicine - 84(9)
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664-665
Legacy Keywords
milk alkali syndrome, heartburn, heart attack, myocardial infarction, STEMI, ST elevation, calcium, mimic, hypercalcemia, calcium carbonate, ECG, electrocardiography, GERD, gastroesophageal reflux disease, antacids, Willis Bowman, Amir Farid, Paul Aronowitz
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Willis S. Bowman, MD
Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Amir Farid, MD
Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Paul Aronowitz, MD, FACP
Health Sciences Clinical Professor of Medicine, Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Address: Willis S. Bowman, MD, Department of Internal Medicine, University of California Davis Medical Center, 4150 V Street, Suite 3100, Sacramento, CA 95817; [email protected]

Author and Disclosure Information

Willis S. Bowman, MD
Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Amir Farid, MD
Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Paul Aronowitz, MD, FACP
Health Sciences Clinical Professor of Medicine, Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA

Address: Willis S. Bowman, MD, Department of Internal Medicine, University of California Davis Medical Center, 4150 V Street, Suite 3100, Sacramento, CA 95817; [email protected]

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Related Articles

A 71-year-old man with a history of hypertension, 4 prior myocardial infarctions (MIs), and well-compensated ischemic cardiomyopathy presented to the emergency department after 2 episodes of sharp pain in the left upper abdomen and chest. The episodes lasted 1 to 2 minutes and were not relieved by rest. Their location was similar to that of the pain he experienced with his MIs. He could not identify any exacerbating or ameliorating factors. The pain had resolved without specific therapy before he arrived.

He reported polydipsia and constipation over the past 2 weeks and generalized muscle weakness and acute exacerbations of chronic back pain in the past 2 days. Neither he nor a friend who accompanied him noticed any confusion. He had been taking as many as 15 calcium carbonate tablets a day for 6 weeks to self-treat dyspepsia refractory to once-daily ranitidine, and hydrochlorothiazide for his hypertension for 3 weeks.

FURTHER EVALUATION, CARDIOLOGY CONSULT

On physical examination, he had diffuse weakness, dry mucous membranes, and an irregular heart rhythm.

Electrocardiography at presentation showed a corrected QT interval of 360 msec.
Figure 1. Electrocardiography at presentation showed a corrected QT interval of 360 msec. In addition to ST-segment elevations (blue arrows) and ST-segment depressions (blue diamonds), varying ectopic beats (red arrows) were present that were absent on previous studies.
Electrocardiography (ECG) (Figure 1) showed ST-segment elevation in leads V1, V2, V3, II, III, and aVF and ST-segment depression in leads I and aVL. The corrected QT interval was 360 ms, compared with 426 ms 4 months earlier (Figure 2).

Laboratory testing showed the following:

  • Troponin I 0.11 ng/mL (reference range ≤ 0.04); repeated, it was 0.12 ng/mL
  • Serum creatinine 3.4 mg/dL (0.44–1.27) (9 months earlier it had been 0.99 mg/dL)
  • Serum calcium 17.3 mg/dL (8.6–10.5)
  • Parathyroid hormone 9 pg/mL (12–88)
  • Serum bicarbonate 33 mmol/L (24–32); 2 weeks earlier, it had been 27 mmol/L.

An electrocardiogram 4 months earlier showed no ST-segment elevations or ST-segment depressions.
Figure 2. An electrocardiogram 4 months earlier showed no ST-segment elevations (blue arrows) or ST-segment depressions (blue diamonds).
A cardiology consult was ordered out of concern for ST-elevation MI (STEMI). The cardiology consult team did not recommend coronary angiography because the patient’s chest pain had resolved spontaneously, its presentation was atypical, and the results of laboratory studies indicated acute kidney injury, a relative contraindication to angiography.

DIAGNOSIS: MILK-ALKALI SYNDROME

The diagnosis, based on the presentation and the results of the workup, was milk-alkali syndrome complicated by recent hydrochlorothiazide use. This syndrome consists of the triad of hypercalcemia, metabolic alkalosis, and acute kidney injury, all due to excessive ingestion of calcium and alkali, usually calcium carbonate.

His hydrochlorothiazide and calcium carbonate were discontinued. He was given intravenous normal saline and subcutaneous calcitonin, and his serum calcium level came down to 11.5 mg/dL within the next 24 hours. His dyspepsia was treated with pantoprazole.

The patient had no further episodes of chest pain, and the cardiology consult team again recommended against coronary angiography. Repeat ECG after the hypercalcemia resolved showed results identical to those 4 months before his admission. Two months later, his serum calcium level was 9.4 mg/dL and his creatinine level was 1.24 mg/dL.

A MIMIC OF STEMI

In numerous reported cases, these electrocardiographic findings coupled with chest pain led to misdiagnosis of STEMI.1–3 While STEMI and occasionally hypercalcemia can cause ST elevation, hypercalcemia causes a significant shortening of the corrected QT interval that is not associated with STEMI.4,5

Ultimately, the diagnosis of MI involves clinical, laboratory, and ECG findings, and if a strong clinical suspicion for myocardial ischemia exists, STEMI cannot reliably be distinguished from hypercalcemia by ECG alone. It is nonetheless important to be aware of this complication of hypercalcemia to avoid unnecessary cardiac interventions.

A 71-year-old man with a history of hypertension, 4 prior myocardial infarctions (MIs), and well-compensated ischemic cardiomyopathy presented to the emergency department after 2 episodes of sharp pain in the left upper abdomen and chest. The episodes lasted 1 to 2 minutes and were not relieved by rest. Their location was similar to that of the pain he experienced with his MIs. He could not identify any exacerbating or ameliorating factors. The pain had resolved without specific therapy before he arrived.

He reported polydipsia and constipation over the past 2 weeks and generalized muscle weakness and acute exacerbations of chronic back pain in the past 2 days. Neither he nor a friend who accompanied him noticed any confusion. He had been taking as many as 15 calcium carbonate tablets a day for 6 weeks to self-treat dyspepsia refractory to once-daily ranitidine, and hydrochlorothiazide for his hypertension for 3 weeks.

FURTHER EVALUATION, CARDIOLOGY CONSULT

On physical examination, he had diffuse weakness, dry mucous membranes, and an irregular heart rhythm.

Electrocardiography at presentation showed a corrected QT interval of 360 msec.
Figure 1. Electrocardiography at presentation showed a corrected QT interval of 360 msec. In addition to ST-segment elevations (blue arrows) and ST-segment depressions (blue diamonds), varying ectopic beats (red arrows) were present that were absent on previous studies.
Electrocardiography (ECG) (Figure 1) showed ST-segment elevation in leads V1, V2, V3, II, III, and aVF and ST-segment depression in leads I and aVL. The corrected QT interval was 360 ms, compared with 426 ms 4 months earlier (Figure 2).

Laboratory testing showed the following:

  • Troponin I 0.11 ng/mL (reference range ≤ 0.04); repeated, it was 0.12 ng/mL
  • Serum creatinine 3.4 mg/dL (0.44–1.27) (9 months earlier it had been 0.99 mg/dL)
  • Serum calcium 17.3 mg/dL (8.6–10.5)
  • Parathyroid hormone 9 pg/mL (12–88)
  • Serum bicarbonate 33 mmol/L (24–32); 2 weeks earlier, it had been 27 mmol/L.

An electrocardiogram 4 months earlier showed no ST-segment elevations or ST-segment depressions.
Figure 2. An electrocardiogram 4 months earlier showed no ST-segment elevations (blue arrows) or ST-segment depressions (blue diamonds).
A cardiology consult was ordered out of concern for ST-elevation MI (STEMI). The cardiology consult team did not recommend coronary angiography because the patient’s chest pain had resolved spontaneously, its presentation was atypical, and the results of laboratory studies indicated acute kidney injury, a relative contraindication to angiography.

DIAGNOSIS: MILK-ALKALI SYNDROME

The diagnosis, based on the presentation and the results of the workup, was milk-alkali syndrome complicated by recent hydrochlorothiazide use. This syndrome consists of the triad of hypercalcemia, metabolic alkalosis, and acute kidney injury, all due to excessive ingestion of calcium and alkali, usually calcium carbonate.

His hydrochlorothiazide and calcium carbonate were discontinued. He was given intravenous normal saline and subcutaneous calcitonin, and his serum calcium level came down to 11.5 mg/dL within the next 24 hours. His dyspepsia was treated with pantoprazole.

The patient had no further episodes of chest pain, and the cardiology consult team again recommended against coronary angiography. Repeat ECG after the hypercalcemia resolved showed results identical to those 4 months before his admission. Two months later, his serum calcium level was 9.4 mg/dL and his creatinine level was 1.24 mg/dL.

A MIMIC OF STEMI

In numerous reported cases, these electrocardiographic findings coupled with chest pain led to misdiagnosis of STEMI.1–3 While STEMI and occasionally hypercalcemia can cause ST elevation, hypercalcemia causes a significant shortening of the corrected QT interval that is not associated with STEMI.4,5

Ultimately, the diagnosis of MI involves clinical, laboratory, and ECG findings, and if a strong clinical suspicion for myocardial ischemia exists, STEMI cannot reliably be distinguished from hypercalcemia by ECG alone. It is nonetheless important to be aware of this complication of hypercalcemia to avoid unnecessary cardiac interventions.

References
  1. Ashizawa N, Arakawa S, Koide Y, Toda G, Seto S, Yano K. Hypercalcemia due to vitamin D intoxication with clinical features mimicking acute myocardial infarction. Intern Med 2003; 42:340–344.
  2. Nishi SP, Barbagelata NA, Atar S, Birnbaum Y, Tuero E. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. J Electrocardiol 2006; 39:298–300.
  3. Turnham S, Kilickap M, Kilinc S. ST segment elevation mimicking acute myocardial infarction in hypercalcemia. Heart 2005; 91:999.
  4. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hypercalcemia. Am J Cardiol 1979; 44:243–248.
  5. Ahmed R, Hashiba K. Reliability of QT intervals as indicators of clinical hypercalcemia. Clin Cardiol 1988; 11:395–400.
References
  1. Ashizawa N, Arakawa S, Koide Y, Toda G, Seto S, Yano K. Hypercalcemia due to vitamin D intoxication with clinical features mimicking acute myocardial infarction. Intern Med 2003; 42:340–344.
  2. Nishi SP, Barbagelata NA, Atar S, Birnbaum Y, Tuero E. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. J Electrocardiol 2006; 39:298–300.
  3. Turnham S, Kilickap M, Kilinc S. ST segment elevation mimicking acute myocardial infarction in hypercalcemia. Heart 2005; 91:999.
  4. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hypercalcemia. Am J Cardiol 1979; 44:243–248.
  5. Ahmed R, Hashiba K. Reliability of QT intervals as indicators of clinical hypercalcemia. Clin Cardiol 1988; 11:395–400.
Issue
Cleveland Clinic Journal of Medicine - 84(9)
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Cleveland Clinic Journal of Medicine - 84(9)
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664-665
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664-665
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Heartburn or heart attack? A mimic of MI
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Heartburn or heart attack? A mimic of MI
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milk alkali syndrome, heartburn, heart attack, myocardial infarction, STEMI, ST elevation, calcium, mimic, hypercalcemia, calcium carbonate, ECG, electrocardiography, GERD, gastroesophageal reflux disease, antacids, Willis Bowman, Amir Farid, Paul Aronowitz
Legacy Keywords
milk alkali syndrome, heartburn, heart attack, myocardial infarction, STEMI, ST elevation, calcium, mimic, hypercalcemia, calcium carbonate, ECG, electrocardiography, GERD, gastroesophageal reflux disease, antacids, Willis Bowman, Amir Farid, Paul Aronowitz
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