This is the tenth in a series of articles from the National Center for Excellence in Primary Care Research (NCEPCR) in the Agency for Healthcare Research and Quality (AHRQ). This series introduces sets of tools and resources designed to help your practice.

An important part of self-management (last month’s article) is medication management, often augmented by the use of a portal and always cognizant of the importance of medication reconciliation and drug interactions. These latter issues can be addressed with health information technology (health IT), which will be discussed the next two columns. This month, we examine some of AHRQ’s other tools and resources to assist with medication management.

ahrq.gov/programs/index.html

Dr. Ganiats is director of the National Center for Excellence in Primary Care Research at AHRQ, Rockville, Md.

This is the tenth in a series of articles from the National Center for Excellence in Primary Care Research (NCEPCR) in the Agency for Healthcare Research and Quality (AHRQ). This series introduces sets of tools and resources designed to help your practice.

An important part of self-management (last month’s article) is medication management, often augmented by the use of a portal and always cognizant of the importance of medication reconciliation and drug interactions. These latter issues can be addressed with health information technology (health IT), which will be discussed the next two columns. This month, we examine some of AHRQ’s other tools and resources to assist with medication management.

ahrq.gov/programs/index.html

Dr. Ganiats is director of the National Center for Excellence in Primary Care Research at AHRQ, Rockville, Md.

This is the tenth in a series of articles from the National Center for Excellence in Primary Care Research (NCEPCR) in the Agency for Healthcare Research and Quality (AHRQ). This series introduces sets of tools and resources designed to help your practice.

An important part of self-management (last month’s article) is medication management, often augmented by the use of a portal and always cognizant of the importance of medication reconciliation and drug interactions. These latter issues can be addressed with health information technology (health IT), which will be discussed the next two columns. This month, we examine some of AHRQ’s other tools and resources to assist with medication management.

ahrq.gov/programs/index.html

Dr. Ganiats is director of the National Center for Excellence in Primary Care Research at AHRQ, Rockville, Md.

ABSTRACT

Standard 2-dimensional (2-D) computed tomography (CT) scans of the shoulder are often aligned to the plane of the body as opposed to the plane of the scapula, which may challenge the ability to accurately measure glenoid width and glenoid bone loss (GBL). The purpose of this study is to determine the effect of sagittal rotation of the glenoid on axial anterior-posterior (AP) glenoid width measurements in the setting of anterior GBL.

Forty-three CT scans from consecutive patients with anterior GBL (minimum 10%) were reformatted utilizing open-source DICOM software (OsiriX MD). Patients were grouped according to extent of GBL: I, 10% to 14.9% (N = 12); II, 15% to 19.9% (N = 16); and III, >20% (N = 15). The uncorrected (UNCORR) and corrected (CORR) images were assessed in the axial plane at 5 standardized cuts and measured for AP glenoid width.

For groups I and III, UNCORR scans underestimated axial AP width (and thus overestimated anterior GBL) in cuts 1 and 2, while in cuts 3 to 5, the axial AP width was overestimated (GBL was underestimated). In Group II, axial AP width was underestimated (GBL was overestimated), while in cuts 2 to 5, the axial AP width was overestimated (GBL was underestimated). Overall, AP glenoid width was consistently underestimated in cut 1, the most caudal cut; while AP glenoid width was consistently overestimated in cuts 3 to 5, the more cephalad cuts.

UNCORR 2-D CT scans inaccurately estimated glenoid width and the degree of anterior GBL. This data suggests that corrected 2D CT scans or a 3-dimensional (3-D) reconstruction can help in accurately defining the anterior GBL in patients with shoulder instability.

The treatment of glenohumeral instability has substantially evolved over the past several decades. The understanding of glenoid bone loss (GBL), in particular, has advanced to such a level that we utilize the quantification of GBL for surgical decision-making. Unrecognized and/or untreated GBL is associated with recurrent instability, pain, and disability. Controversy exists, however, regarding the precise amount of anterior GBL that is significant enough to warrant surgical treatment. While historically, 25%^1,2 of anterior GBL was thought to be the critical number required to warrant osseous augmentation, studies that are more recent have highlighted the need to perform osseous glenoid reconstruction with lesser degrees of GBL, particularly in the contact athlete.^3-9 As small differences in the amount of GBL can change surgical decision-making from an all-soft tissue repair to an osseous reconstruction, it is paramount that we have accurate, valid, and reproducible methods for calculating GBL.

Continue to: Historically, plain radiographs...

Computed tomography (CT) of the shoulder has become the most commonly utilized imaging modality in the evaluation of patients with shoulder instability associated with GBL. Standard 2-dimensional (2-D) CT scans of the shoulder are often aligned to the plane of the body as opposed to the plane of the scapula/glenoid, as standard protocols often fail to account for the anterior sagittal rotation of the scapula/glenoid, similar to the disadvantage of standard radiographs. While 3-dimensional (3-D) CT reconstructions eliminate the effect of gantry angles, and thus allow for an en face view of the glenoid, 3-D reconstructions are not always available, and cannot always be measured.^12-14 Thus, improved methodology for utilizing standard 2D scans is warranted, as the ability to correctly align the axial CT scan to the axis of the glenoid may allow for more accurate GBL measurements, which will ultimately impact surgical decision-making. Recently, Gross and colleagues¹⁵ reported the effect of sagittal rotation of the glenoid on axial measurements of anterior-posterior (AP) glenoid width and glenoid version in normal glenoids, without bone loss, and found that the mean angle of correction needed to align the sagittal plane was 20.1° ± 1.2° of rotation. To the authors’ knowledge, this same methodology has not been applied to patients with clinically meaningful anterior GBL. Given that the average glenoid width in human shoulders is 24.4 mm ± 2.9 mm,¹⁶ 1 mm of glenoid bone loss (GBL) corresponds to approximately 4% of the glenoid width, and thus even subtle differences in the interpretation of GBL may have substantial clinical implications. Therefore, the purpose of this study is to determine the effect of sagittal rotation of the glenoid on axial AP glenoid width measurements in the setting of clinically significant anterior GBL.

METHODS

This study was approved by Massachusetts General Hospital Institutional Review Board. A retrospective review of consecutive patients with a diagnosis of anterior shoulder instability between 2009 and 2013 was conducted. Inclusion criteria comprised patients with a minimum of 10% anterior GBL, an available CT scan of the affected shoulder, and no history of prior ipsilateral surgeries. Exclusion criteria comprised evidence of degenerative changes to the glenoid and/or humeral head, as well as prior ipsilateral shoulder surgery. Sixty consecutive patients were originally identified as having anterior shoulder instability, and 17 were excluded based on the inclusion/exclusion criteria, leaving 43 patients (43 shoulders) available for inclusion. Shoulder CT scans from all 43 patients were reformatted utilizing open-source DICOM software (OsiriX MD, version 2.5.1 65-bit) multi-planar reconstruction (MPR).

CT PROTOCOL

All patients underwent a standard glenohumeral CT scan using a Siemens Sensation 64 Scanner (Siemens), a 64-detector scanner. Scans were acquired with 0.6 mm of collimation, 140 kV, and 300 mA-seconds. Slice thickness was set to 2 mm. All patient information was de-identified for analysis.

The uncorrected (UNCORR) scans were defined as the default orientation on the scanner. In the UNCORR scans, the axial, coronal, and sagittal views were oriented relative to the scanner gantry table, as opposed to the anatomy of the glenoid. The corrected (CORR) CT scans were aligned in all 3 planes relative to the glenoid face, and thus the cuts were perpendicular to the long axis of the glenoid.¹⁵ This resulted in sagittal cuts perpendicular to the 12-o’clock to 6-o’clock axis in the sagittal plane (Figure 1).

Continue to: In a de-identified fashion...

IMAGE ANALYSIS AND REFORMATTING

In a de-identified fashion, all CT scans were imported and analyzed using open-source Digital Imaging and Communications in Medicine (DICOM) software (OsiriX MD, version 2.5.1 64-bit). By following a previously developed method, CT scans were reformatted using OsiriX MPR. The OsiriX software has an MPR function that allows simultaneous manipulation of 2-D CT scans in 3 orthogonal planes: axial, sagittal, and coronal. In the MPR mode, the alternation of 1 plane directly affects the orientation of the remaining 2 planes. Thus, by using an MPR, one can analyze the impact that a default CT scan performed relative to the gantry of the table, UNCORR, has on the axial images.

First, the en face view was obtained via a 2-step process: alignment of the axial plane to account for the scapular angle, followed by alignment of the coronal plane to adjust for the glenoid inclination.¹⁵ These 2 adjustments provided a true en face sagittal glenoid view. The final adjustment step was a sagittal en face rotation of the glenoid such that the superior and inferior glenoid tubercles were placed on the 12-o’clock to 6-o’clock axis (CORR scan). Previous studies have identified a central longitudinal axis that was used in this method to align the supraglenoid tubercle with the 12-o’clock to 6-o’clock axis on the glenoid face.^15,17,18 The standard error of mean was 1.21^°. This new CORR view resulted in axial cuts through the glenoid that were oriented perpendicular to the 12-o’clock to 6-o’clock axis. The UNCORR and CORR images were assessed in the axial plane at 5 standardized cuts and measured for AP glenoid width by 2 independent observers in a blinded, randomized fashion. When the measured AP width of the UNCORR scan was less than that measured on the CORR scan, the AP width of the glenoid was considered underestimated, and the degree of GBL was considered overestimated (Figure 2).

SCAPULAR ANGLE

Scapular angle measurements were performed on the axial view as the angle between a line through the long axis of the body of the scapula, and a line parallel to the CT gantry table.^15,19 Subsequently, the axial plane was aligned to the glenoid surface.

CORONAL INCLINATION

Coronal inclination measurements were performed on the sagittal view as the angle between a line tangential to the face of the glenoid and a line perpendicular to the CT gantry table. Positive values represented superior inclination, while negative values represented inferior glenoid inclination.¹⁵

SAGITTAL ROTATION

Sagittal rotation measurements were performed using the built-in angle measurement tool in OsiriX in the sagittal plane since the degree of rotation required aligning the long axis of the glenoid to the 12-o’clock to 6-o’clock axis. The amount of rotation was defined as the rotation angle.¹⁵

Continue to: Similarly, as described by Gross...

GLENOID WIDTH

Similarly, as described by Gross and colleagues,¹⁵ the sagittal en face view was divided via 5 cuts, throughout a superimposed best-fit circle that closely represents the glenoid.^9,15,20 For both the UNCORR and CORR, glenoid width (AP distance) was measured on the axial image at the widest point from AP cortex across the glenoid face.

PATIENT GROUPS

Utilizing the en face 3-D CT reconstruction view of the glenoid as the gold standard, patients were placed into 1 of 3 groups according to the degree of anterior GBL measured via the surface method.^9,20 The groups were as follows:

I. 10% to 14.9% (N = 12)

II. 15% to 19.9% (N = 16)

III. >20% (N = 15)

STATISTICAL METHODS

Paired t-tests were used to compare all measurements between CORR and UNCORR scans for each of the 5 cuts. A P-value of .05 was used as the threshold for statistical significance in 2-tailed comparisons. Mean and standard errors are presented with standard deviations throughout the study. For interobserver reliability, the measurements between the observers, the intraclass correlation coefficient was calculated. All statistics were performed with SPSS (Version 22).

RESULTS

The study cohort was comprised of 19 left shoulders (44%) and 24 right shoulders (56%), including 36 male patients (84%) and 7 female patients (16%). The average age was 27.8 years (range, 21-40 years). The variability in measured difference, with respect to AP width, was 1.05 mm. The UNCORR CT scans required a mean correction for coronal inclination of 7.0° ± 5.8° (range, -8°-6°). The UNCORR CT scans required a mean correction for scapular angle of 30.2° ± 8.0° (range, 15°-49°). The mean angle of sagittal rotation required to align the glenoid face with the 12-o’clock to 6-o’clock axis was 24.2° ± 5.1 ° (range, 13°-30°). These results are summarized in Table 1. 

For all measurements, the intraclass correlation coefficient for independent observers for all cuts within the 3 groups was r >.900 in all cases.

On an optimized CT scan, over 5 standardized cuts across a best-fit circle of the inferior glenoid, there was a statistically significant absolute mean difference of 12.6% in axial AP glenoid width (2.86 mm ± 2.00 mm, P =.016) when compared with the UNCORR scan. This corresponds to a 3% to 21% error in measurement of the AP width of the glenoid.

Continue to: For the entire cohort...

For groups I (10%-14.9% GBL) and III (>20% GBL), the UNCORR scans underestimated the axial AP width (and thus overestimated anterior GBL) in cuts 1 and 2, while in cuts 3 to 5, the axial AP width was overestimated (GBL was underestimated) (Tables 2, 3). In Group II (15%-19.9% GBL), the axial AP width was underestimated (GBL was overestimated), while in cuts 2 to 5, the axial AP width was overestimated (GBL was underestimated). Overall, AP glenoid width was consistently underestimated in cut 1, the most caudal cut, while AP glenoid width was consistently overestimated in cuts 3 to 5, the more cephalad cuts.

Abbreviations: AP, anterior-posterior; GBL, glenoid bone loss.

Abbreviations: AP, anterior-posterior; CORR, corrected; UNCORR, uncorrected.

DISCUSSION

The principle findings of this study demonstrate that UNCORR conventional 2-D CT scans inaccurately estimate glenoid width as well as inaccurately quantify the degree of anterior GBL. Underestimations of GBL may lead to insufficient treatment of clinically meaningful GBL, thereby increasing the risk of instability recurrence; whereas overestimations of GBL may lead to unnecessary treatment, subjecting patients to increased surgical morbidity. Therefore, the authors recommend correcting the orientation of the scapula in cases wherein clinical decisions are entirely based on 2-D CT, or using alternative methods for quantifying GBL, specifically in the form of 3-D reconstructions.

The use of axial imaging, with CT scans and/or magnetic resonance imaging, is growing in popularity for evaluation of both glenoid anatomy and GBL. Nevertheless, despite our improved ability to critically evaluate the glenoid using these advanced imaging modalities, the images themselves require scrutiny by clinicians to determine if the images accurately depict the true anatomy of the glenoid. As demonstrated by Gross and colleagues,¹⁵ conventional 2D CT scan protocols are not optimized to the anatomy of the glenohumeral joint, even in patients without GBL. Due to the alignment of the image relative to the plane of the scapula as opposed to the plane of the glenoid, UNCORR scans result in significantly different measurements of glenoid version (2.0° ± 0.1°) and AP glenoid width (1.2 mm  ± 0.42 mm) compared with corrected scans, requiring an average 20.1° ± 1.2° of correction to align the sagittal plane. In the present study involving the patients with GBL, we also found that conventional, UNCORR 2-D CT scan protocols inaccurately estimate glenoid width and the degree of anterior GBL. In particular, AP glenoid width was consistently underestimated in the more caudal cuts, while AP glenoid width was consistently overestimated in the more cephalad cuts. Thus, anterior GBL was overestimated (AP glenoid width was underestimated) in the more caudal cuts, whereas anterior GBL was underestimated in the more cranial cuts (AP glenoid width was overestimated). Given that approximately 1 mm of glenoid bone corresponds to approximately 4% of glenoid width,¹⁶ even subtle differences in the interpretation of GBL may lead to gross overestimation/underestimation of bone loss, with significant clinical implications.

In the anterior instability patient population, clinical decision-making is often based on the degree of GBL as determined by advanced imaging modalities. In addition to other patient-specific factors, including age, gender, activity level, type of sport, and number of prior dislocations and/or prior surgeries, the quantity of GBL will often determine which surgical procedure needs to be performed. Typically, patients with >20% to 25% anterior GBL are indicated for a glenoid reconstruction procedure, most commonly via the Latarjet procedure (coracoid transfer).^21-27 The Latarjet procedure remains an excellent technique for appropriately indicated patients, with historically good clinical outcomes and low recurrence rates. Complications associated with the Latarjet procedure, however, are not uncommon, including devastating neuropraxia of the axillary and musculocutaneous nerves, and occasionally permanent neurologic deficits.²⁸ Thus, it is critical to avoid overtreating patients with recurrent instability and GBL. As demonstrated by this study, depending on the cranial-to-caudal location on the glenoid, current 2-D CT techniques may underestimate AP glenoid width, resulting in an overestimation of GBL, potentially leading to the decision to proceed with glenoid bone reconstruction when such a procedure is not required. On the contrary, overestimation of AP glenoid width, which occurs in the more cephalad cuts of the glenoid, is perhaps more worrisome, as the resulting underestimation of GBL may lead to inadequate treatment of patients with recurrent instability. Certainly, one of the main risk factors for failed soft tissue shoulder stabilization is a failure to address GBL. If clinical decisions are made based on UNCORR 2-D CT scans, which are often inaccurate with respect to AP glenoid width by an average 2.86 mm ± 2.00 mm (equivalent to 12.6% ± 6.9% GBL) as determined in this study, patients who truly require osseous glenoid reconstructions may be indicated for only soft tissue stabilization, based on the underestimation of GBL.

Continue to: The current gold standard...

LIMITATIONS

This study has limitations, such as the relatively small sample size and the selection bias by the reviewers with potential differences in interobserver reliability. Further, minor modifications during the reformatting process may be found with each attempt to manipulate the images and may result in minor, insignificant differences in AP width measurements. Performing 1 or more additional CT scans on the same cohort of patients would have been helpful; however, due to the increased risk of radiation exposure, this was not performed. Performing CT scans on cadaveric specimens with GBL and applying the study methodology would also have been helpful to provide independent verification of our clinical findings; however, specimens were not available for this study. Another limitation of this study is that we did not compare our findings with the findings of glenoid width, and bone loss, as determined using the circle method, which is commonly utilized when 3-D reconstructions are available. In this study, the purpose was to utilize only the 2-D reformatted images, with the assumption that 3-D reconstructions are not always available, and cannot always be measured. To minimize selection bias, the investigators measured the correction effects within groups of patients with similar degrees of GBL (10%-14.9%, 15%-19.9%, and >20%). In addition, not all the selected patients showed degenerative glenoid changes or irregular glenoid shape indicating previous bone augmentation.

CONCLUSIONS

UNCORR 2D CT scans inaccurately estimate glenoid width and the degree of anterior GBL. The clinical implications of these findings are profound and suggest corrected 2D CT scans or 3D reconstruction allow measurements to be taken in the axis of the glenoid to accurately define the anatomy and quantity of anterior GBL in patients with shoulder instability.

ABSTRACT

Standard 2-dimensional (2-D) computed tomography (CT) scans of the shoulder are often aligned to the plane of the body as opposed to the plane of the scapula, which may challenge the ability to accurately measure glenoid width and glenoid bone loss (GBL). The purpose of this study is to determine the effect of sagittal rotation of the glenoid on axial anterior-posterior (AP) glenoid width measurements in the setting of anterior GBL.

Forty-three CT scans from consecutive patients with anterior GBL (minimum 10%) were reformatted utilizing open-source DICOM software (OsiriX MD). Patients were grouped according to extent of GBL: I, 10% to 14.9% (N = 12); II, 15% to 19.9% (N = 16); and III, >20% (N = 15). The uncorrected (UNCORR) and corrected (CORR) images were assessed in the axial plane at 5 standardized cuts and measured for AP glenoid width.

For groups I and III, UNCORR scans underestimated axial AP width (and thus overestimated anterior GBL) in cuts 1 and 2, while in cuts 3 to 5, the axial AP width was overestimated (GBL was underestimated). In Group II, axial AP width was underestimated (GBL was overestimated), while in cuts 2 to 5, the axial AP width was overestimated (GBL was underestimated). Overall, AP glenoid width was consistently underestimated in cut 1, the most caudal cut; while AP glenoid width was consistently overestimated in cuts 3 to 5, the more cephalad cuts.

UNCORR 2-D CT scans inaccurately estimated glenoid width and the degree of anterior GBL. This data suggests that corrected 2D CT scans or a 3-dimensional (3-D) reconstruction can help in accurately defining the anterior GBL in patients with shoulder instability.

The treatment of glenohumeral instability has substantially evolved over the past several decades. The understanding of glenoid bone loss (GBL), in particular, has advanced to such a level that we utilize the quantification of GBL for surgical decision-making. Unrecognized and/or untreated GBL is associated with recurrent instability, pain, and disability. Controversy exists, however, regarding the precise amount of anterior GBL that is significant enough to warrant surgical treatment. While historically, 25%^1,2 of anterior GBL was thought to be the critical number required to warrant osseous augmentation, studies that are more recent have highlighted the need to perform osseous glenoid reconstruction with lesser degrees of GBL, particularly in the contact athlete.^3-9 As small differences in the amount of GBL can change surgical decision-making from an all-soft tissue repair to an osseous reconstruction, it is paramount that we have accurate, valid, and reproducible methods for calculating GBL.

Continue to: Historically, plain radiographs...

Computed tomography (CT) of the shoulder has become the most commonly utilized imaging modality in the evaluation of patients with shoulder instability associated with GBL. Standard 2-dimensional (2-D) CT scans of the shoulder are often aligned to the plane of the body as opposed to the plane of the scapula/glenoid, as standard protocols often fail to account for the anterior sagittal rotation of the scapula/glenoid, similar to the disadvantage of standard radiographs. While 3-dimensional (3-D) CT reconstructions eliminate the effect of gantry angles, and thus allow for an en face view of the glenoid, 3-D reconstructions are not always available, and cannot always be measured.^12-14 Thus, improved methodology for utilizing standard 2D scans is warranted, as the ability to correctly align the axial CT scan to the axis of the glenoid may allow for more accurate GBL measurements, which will ultimately impact surgical decision-making. Recently, Gross and colleagues¹⁵ reported the effect of sagittal rotation of the glenoid on axial measurements of anterior-posterior (AP) glenoid width and glenoid version in normal glenoids, without bone loss, and found that the mean angle of correction needed to align the sagittal plane was 20.1° ± 1.2° of rotation. To the authors’ knowledge, this same methodology has not been applied to patients with clinically meaningful anterior GBL. Given that the average glenoid width in human shoulders is 24.4 mm ± 2.9 mm,¹⁶ 1 mm of glenoid bone loss (GBL) corresponds to approximately 4% of the glenoid width, and thus even subtle differences in the interpretation of GBL may have substantial clinical implications. Therefore, the purpose of this study is to determine the effect of sagittal rotation of the glenoid on axial AP glenoid width measurements in the setting of clinically significant anterior GBL.

METHODS

This study was approved by Massachusetts General Hospital Institutional Review Board. A retrospective review of consecutive patients with a diagnosis of anterior shoulder instability between 2009 and 2013 was conducted. Inclusion criteria comprised patients with a minimum of 10% anterior GBL, an available CT scan of the affected shoulder, and no history of prior ipsilateral surgeries. Exclusion criteria comprised evidence of degenerative changes to the glenoid and/or humeral head, as well as prior ipsilateral shoulder surgery. Sixty consecutive patients were originally identified as having anterior shoulder instability, and 17 were excluded based on the inclusion/exclusion criteria, leaving 43 patients (43 shoulders) available for inclusion. Shoulder CT scans from all 43 patients were reformatted utilizing open-source DICOM software (OsiriX MD, version 2.5.1 65-bit) multi-planar reconstruction (MPR).

CT PROTOCOL

All patients underwent a standard glenohumeral CT scan using a Siemens Sensation 64 Scanner (Siemens), a 64-detector scanner. Scans were acquired with 0.6 mm of collimation, 140 kV, and 300 mA-seconds. Slice thickness was set to 2 mm. All patient information was de-identified for analysis.

The uncorrected (UNCORR) scans were defined as the default orientation on the scanner. In the UNCORR scans, the axial, coronal, and sagittal views were oriented relative to the scanner gantry table, as opposed to the anatomy of the glenoid. The corrected (CORR) CT scans were aligned in all 3 planes relative to the glenoid face, and thus the cuts were perpendicular to the long axis of the glenoid.¹⁵ This resulted in sagittal cuts perpendicular to the 12-o’clock to 6-o’clock axis in the sagittal plane (Figure 1).

Continue to: In a de-identified fashion...

IMAGE ANALYSIS AND REFORMATTING

In a de-identified fashion, all CT scans were imported and analyzed using open-source Digital Imaging and Communications in Medicine (DICOM) software (OsiriX MD, version 2.5.1 64-bit). By following a previously developed method, CT scans were reformatted using OsiriX MPR. The OsiriX software has an MPR function that allows simultaneous manipulation of 2-D CT scans in 3 orthogonal planes: axial, sagittal, and coronal. In the MPR mode, the alternation of 1 plane directly affects the orientation of the remaining 2 planes. Thus, by using an MPR, one can analyze the impact that a default CT scan performed relative to the gantry of the table, UNCORR, has on the axial images.

First, the en face view was obtained via a 2-step process: alignment of the axial plane to account for the scapular angle, followed by alignment of the coronal plane to adjust for the glenoid inclination.¹⁵ These 2 adjustments provided a true en face sagittal glenoid view. The final adjustment step was a sagittal en face rotation of the glenoid such that the superior and inferior glenoid tubercles were placed on the 12-o’clock to 6-o’clock axis (CORR scan). Previous studies have identified a central longitudinal axis that was used in this method to align the supraglenoid tubercle with the 12-o’clock to 6-o’clock axis on the glenoid face.^15,17,18 The standard error of mean was 1.21^°. This new CORR view resulted in axial cuts through the glenoid that were oriented perpendicular to the 12-o’clock to 6-o’clock axis. The UNCORR and CORR images were assessed in the axial plane at 5 standardized cuts and measured for AP glenoid width by 2 independent observers in a blinded, randomized fashion. When the measured AP width of the UNCORR scan was less than that measured on the CORR scan, the AP width of the glenoid was considered underestimated, and the degree of GBL was considered overestimated (Figure 2).

SCAPULAR ANGLE

Scapular angle measurements were performed on the axial view as the angle between a line through the long axis of the body of the scapula, and a line parallel to the CT gantry table.^15,19 Subsequently, the axial plane was aligned to the glenoid surface.

CORONAL INCLINATION

Coronal inclination measurements were performed on the sagittal view as the angle between a line tangential to the face of the glenoid and a line perpendicular to the CT gantry table. Positive values represented superior inclination, while negative values represented inferior glenoid inclination.¹⁵

SAGITTAL ROTATION

Sagittal rotation measurements were performed using the built-in angle measurement tool in OsiriX in the sagittal plane since the degree of rotation required aligning the long axis of the glenoid to the 12-o’clock to 6-o’clock axis. The amount of rotation was defined as the rotation angle.¹⁵

Continue to: Similarly, as described by Gross...

GLENOID WIDTH

Similarly, as described by Gross and colleagues,¹⁵ the sagittal en face view was divided via 5 cuts, throughout a superimposed best-fit circle that closely represents the glenoid.^9,15,20 For both the UNCORR and CORR, glenoid width (AP distance) was measured on the axial image at the widest point from AP cortex across the glenoid face.

PATIENT GROUPS

Utilizing the en face 3-D CT reconstruction view of the glenoid as the gold standard, patients were placed into 1 of 3 groups according to the degree of anterior GBL measured via the surface method.^9,20 The groups were as follows:

I. 10% to 14.9% (N = 12)

II. 15% to 19.9% (N = 16)

III. >20% (N = 15)

STATISTICAL METHODS

Paired t-tests were used to compare all measurements between CORR and UNCORR scans for each of the 5 cuts. A P-value of .05 was used as the threshold for statistical significance in 2-tailed comparisons. Mean and standard errors are presented with standard deviations throughout the study. For interobserver reliability, the measurements between the observers, the intraclass correlation coefficient was calculated. All statistics were performed with SPSS (Version 22).

RESULTS

The study cohort was comprised of 19 left shoulders (44%) and 24 right shoulders (56%), including 36 male patients (84%) and 7 female patients (16%). The average age was 27.8 years (range, 21-40 years). The variability in measured difference, with respect to AP width, was 1.05 mm. The UNCORR CT scans required a mean correction for coronal inclination of 7.0° ± 5.8° (range, -8°-6°). The UNCORR CT scans required a mean correction for scapular angle of 30.2° ± 8.0° (range, 15°-49°). The mean angle of sagittal rotation required to align the glenoid face with the 12-o’clock to 6-o’clock axis was 24.2° ± 5.1 ° (range, 13°-30°). These results are summarized in Table 1. 

For all measurements, the intraclass correlation coefficient for independent observers for all cuts within the 3 groups was r >.900 in all cases.

On an optimized CT scan, over 5 standardized cuts across a best-fit circle of the inferior glenoid, there was a statistically significant absolute mean difference of 12.6% in axial AP glenoid width (2.86 mm ± 2.00 mm, P =.016) when compared with the UNCORR scan. This corresponds to a 3% to 21% error in measurement of the AP width of the glenoid.

Continue to: For the entire cohort...

For groups I (10%-14.9% GBL) and III (>20% GBL), the UNCORR scans underestimated the axial AP width (and thus overestimated anterior GBL) in cuts 1 and 2, while in cuts 3 to 5, the axial AP width was overestimated (GBL was underestimated) (Tables 2, 3). In Group II (15%-19.9% GBL), the axial AP width was underestimated (GBL was overestimated), while in cuts 2 to 5, the axial AP width was overestimated (GBL was underestimated). Overall, AP glenoid width was consistently underestimated in cut 1, the most caudal cut, while AP glenoid width was consistently overestimated in cuts 3 to 5, the more cephalad cuts.

Abbreviations: AP, anterior-posterior; GBL, glenoid bone loss.

Abbreviations: AP, anterior-posterior; CORR, corrected; UNCORR, uncorrected.

DISCUSSION

The principle findings of this study demonstrate that UNCORR conventional 2-D CT scans inaccurately estimate glenoid width as well as inaccurately quantify the degree of anterior GBL. Underestimations of GBL may lead to insufficient treatment of clinically meaningful GBL, thereby increasing the risk of instability recurrence; whereas overestimations of GBL may lead to unnecessary treatment, subjecting patients to increased surgical morbidity. Therefore, the authors recommend correcting the orientation of the scapula in cases wherein clinical decisions are entirely based on 2-D CT, or using alternative methods for quantifying GBL, specifically in the form of 3-D reconstructions.

The use of axial imaging, with CT scans and/or magnetic resonance imaging, is growing in popularity for evaluation of both glenoid anatomy and GBL. Nevertheless, despite our improved ability to critically evaluate the glenoid using these advanced imaging modalities, the images themselves require scrutiny by clinicians to determine if the images accurately depict the true anatomy of the glenoid. As demonstrated by Gross and colleagues,¹⁵ conventional 2D CT scan protocols are not optimized to the anatomy of the glenohumeral joint, even in patients without GBL. Due to the alignment of the image relative to the plane of the scapula as opposed to the plane of the glenoid, UNCORR scans result in significantly different measurements of glenoid version (2.0° ± 0.1°) and AP glenoid width (1.2 mm  ± 0.42 mm) compared with corrected scans, requiring an average 20.1° ± 1.2° of correction to align the sagittal plane. In the present study involving the patients with GBL, we also found that conventional, UNCORR 2-D CT scan protocols inaccurately estimate glenoid width and the degree of anterior GBL. In particular, AP glenoid width was consistently underestimated in the more caudal cuts, while AP glenoid width was consistently overestimated in the more cephalad cuts. Thus, anterior GBL was overestimated (AP glenoid width was underestimated) in the more caudal cuts, whereas anterior GBL was underestimated in the more cranial cuts (AP glenoid width was overestimated). Given that approximately 1 mm of glenoid bone corresponds to approximately 4% of glenoid width,¹⁶ even subtle differences in the interpretation of GBL may lead to gross overestimation/underestimation of bone loss, with significant clinical implications.

In the anterior instability patient population, clinical decision-making is often based on the degree of GBL as determined by advanced imaging modalities. In addition to other patient-specific factors, including age, gender, activity level, type of sport, and number of prior dislocations and/or prior surgeries, the quantity of GBL will often determine which surgical procedure needs to be performed. Typically, patients with >20% to 25% anterior GBL are indicated for a glenoid reconstruction procedure, most commonly via the Latarjet procedure (coracoid transfer).^21-27 The Latarjet procedure remains an excellent technique for appropriately indicated patients, with historically good clinical outcomes and low recurrence rates. Complications associated with the Latarjet procedure, however, are not uncommon, including devastating neuropraxia of the axillary and musculocutaneous nerves, and occasionally permanent neurologic deficits.²⁸ Thus, it is critical to avoid overtreating patients with recurrent instability and GBL. As demonstrated by this study, depending on the cranial-to-caudal location on the glenoid, current 2-D CT techniques may underestimate AP glenoid width, resulting in an overestimation of GBL, potentially leading to the decision to proceed with glenoid bone reconstruction when such a procedure is not required. On the contrary, overestimation of AP glenoid width, which occurs in the more cephalad cuts of the glenoid, is perhaps more worrisome, as the resulting underestimation of GBL may lead to inadequate treatment of patients with recurrent instability. Certainly, one of the main risk factors for failed soft tissue shoulder stabilization is a failure to address GBL. If clinical decisions are made based on UNCORR 2-D CT scans, which are often inaccurate with respect to AP glenoid width by an average 2.86 mm ± 2.00 mm (equivalent to 12.6% ± 6.9% GBL) as determined in this study, patients who truly require osseous glenoid reconstructions may be indicated for only soft tissue stabilization, based on the underestimation of GBL.

Continue to: The current gold standard...

LIMITATIONS

This study has limitations, such as the relatively small sample size and the selection bias by the reviewers with potential differences in interobserver reliability. Further, minor modifications during the reformatting process may be found with each attempt to manipulate the images and may result in minor, insignificant differences in AP width measurements. Performing 1 or more additional CT scans on the same cohort of patients would have been helpful; however, due to the increased risk of radiation exposure, this was not performed. Performing CT scans on cadaveric specimens with GBL and applying the study methodology would also have been helpful to provide independent verification of our clinical findings; however, specimens were not available for this study. Another limitation of this study is that we did not compare our findings with the findings of glenoid width, and bone loss, as determined using the circle method, which is commonly utilized when 3-D reconstructions are available. In this study, the purpose was to utilize only the 2-D reformatted images, with the assumption that 3-D reconstructions are not always available, and cannot always be measured. To minimize selection bias, the investigators measured the correction effects within groups of patients with similar degrees of GBL (10%-14.9%, 15%-19.9%, and >20%). In addition, not all the selected patients showed degenerative glenoid changes or irregular glenoid shape indicating previous bone augmentation.

CONCLUSIONS

UNCORR 2D CT scans inaccurately estimate glenoid width and the degree of anterior GBL. The clinical implications of these findings are profound and suggest corrected 2D CT scans or 3D reconstruction allow measurements to be taken in the axis of the glenoid to accurately define the anatomy and quantity of anterior GBL in patients with shoulder instability.

ABSTRACT

Standard 2-dimensional (2-D) computed tomography (CT) scans of the shoulder are often aligned to the plane of the body as opposed to the plane of the scapula, which may challenge the ability to accurately measure glenoid width and glenoid bone loss (GBL). The purpose of this study is to determine the effect of sagittal rotation of the glenoid on axial anterior-posterior (AP) glenoid width measurements in the setting of anterior GBL.

Forty-three CT scans from consecutive patients with anterior GBL (minimum 10%) were reformatted utilizing open-source DICOM software (OsiriX MD). Patients were grouped according to extent of GBL: I, 10% to 14.9% (N = 12); II, 15% to 19.9% (N = 16); and III, >20% (N = 15). The uncorrected (UNCORR) and corrected (CORR) images were assessed in the axial plane at 5 standardized cuts and measured for AP glenoid width.

For groups I and III, UNCORR scans underestimated axial AP width (and thus overestimated anterior GBL) in cuts 1 and 2, while in cuts 3 to 5, the axial AP width was overestimated (GBL was underestimated). In Group II, axial AP width was underestimated (GBL was overestimated), while in cuts 2 to 5, the axial AP width was overestimated (GBL was underestimated). Overall, AP glenoid width was consistently underestimated in cut 1, the most caudal cut; while AP glenoid width was consistently overestimated in cuts 3 to 5, the more cephalad cuts.

UNCORR 2-D CT scans inaccurately estimated glenoid width and the degree of anterior GBL. This data suggests that corrected 2D CT scans or a 3-dimensional (3-D) reconstruction can help in accurately defining the anterior GBL in patients with shoulder instability.

The treatment of glenohumeral instability has substantially evolved over the past several decades. The understanding of glenoid bone loss (GBL), in particular, has advanced to such a level that we utilize the quantification of GBL for surgical decision-making. Unrecognized and/or untreated GBL is associated with recurrent instability, pain, and disability. Controversy exists, however, regarding the precise amount of anterior GBL that is significant enough to warrant surgical treatment. While historically, 25%^1,2 of anterior GBL was thought to be the critical number required to warrant osseous augmentation, studies that are more recent have highlighted the need to perform osseous glenoid reconstruction with lesser degrees of GBL, particularly in the contact athlete.^3-9 As small differences in the amount of GBL can change surgical decision-making from an all-soft tissue repair to an osseous reconstruction, it is paramount that we have accurate, valid, and reproducible methods for calculating GBL.

Continue to: Historically, plain radiographs...

Computed tomography (CT) of the shoulder has become the most commonly utilized imaging modality in the evaluation of patients with shoulder instability associated with GBL. Standard 2-dimensional (2-D) CT scans of the shoulder are often aligned to the plane of the body as opposed to the plane of the scapula/glenoid, as standard protocols often fail to account for the anterior sagittal rotation of the scapula/glenoid, similar to the disadvantage of standard radiographs. While 3-dimensional (3-D) CT reconstructions eliminate the effect of gantry angles, and thus allow for an en face view of the glenoid, 3-D reconstructions are not always available, and cannot always be measured.^12-14 Thus, improved methodology for utilizing standard 2D scans is warranted, as the ability to correctly align the axial CT scan to the axis of the glenoid may allow for more accurate GBL measurements, which will ultimately impact surgical decision-making. Recently, Gross and colleagues¹⁵ reported the effect of sagittal rotation of the glenoid on axial measurements of anterior-posterior (AP) glenoid width and glenoid version in normal glenoids, without bone loss, and found that the mean angle of correction needed to align the sagittal plane was 20.1° ± 1.2° of rotation. To the authors’ knowledge, this same methodology has not been applied to patients with clinically meaningful anterior GBL. Given that the average glenoid width in human shoulders is 24.4 mm ± 2.9 mm,¹⁶ 1 mm of glenoid bone loss (GBL) corresponds to approximately 4% of the glenoid width, and thus even subtle differences in the interpretation of GBL may have substantial clinical implications. Therefore, the purpose of this study is to determine the effect of sagittal rotation of the glenoid on axial AP glenoid width measurements in the setting of clinically significant anterior GBL.

METHODS

This study was approved by Massachusetts General Hospital Institutional Review Board. A retrospective review of consecutive patients with a diagnosis of anterior shoulder instability between 2009 and 2013 was conducted. Inclusion criteria comprised patients with a minimum of 10% anterior GBL, an available CT scan of the affected shoulder, and no history of prior ipsilateral surgeries. Exclusion criteria comprised evidence of degenerative changes to the glenoid and/or humeral head, as well as prior ipsilateral shoulder surgery. Sixty consecutive patients were originally identified as having anterior shoulder instability, and 17 were excluded based on the inclusion/exclusion criteria, leaving 43 patients (43 shoulders) available for inclusion. Shoulder CT scans from all 43 patients were reformatted utilizing open-source DICOM software (OsiriX MD, version 2.5.1 65-bit) multi-planar reconstruction (MPR).

CT PROTOCOL

All patients underwent a standard glenohumeral CT scan using a Siemens Sensation 64 Scanner (Siemens), a 64-detector scanner. Scans were acquired with 0.6 mm of collimation, 140 kV, and 300 mA-seconds. Slice thickness was set to 2 mm. All patient information was de-identified for analysis.

The uncorrected (UNCORR) scans were defined as the default orientation on the scanner. In the UNCORR scans, the axial, coronal, and sagittal views were oriented relative to the scanner gantry table, as opposed to the anatomy of the glenoid. The corrected (CORR) CT scans were aligned in all 3 planes relative to the glenoid face, and thus the cuts were perpendicular to the long axis of the glenoid.¹⁵ This resulted in sagittal cuts perpendicular to the 12-o’clock to 6-o’clock axis in the sagittal plane (Figure 1).

Continue to: In a de-identified fashion...

IMAGE ANALYSIS AND REFORMATTING

In a de-identified fashion, all CT scans were imported and analyzed using open-source Digital Imaging and Communications in Medicine (DICOM) software (OsiriX MD, version 2.5.1 64-bit). By following a previously developed method, CT scans were reformatted using OsiriX MPR. The OsiriX software has an MPR function that allows simultaneous manipulation of 2-D CT scans in 3 orthogonal planes: axial, sagittal, and coronal. In the MPR mode, the alternation of 1 plane directly affects the orientation of the remaining 2 planes. Thus, by using an MPR, one can analyze the impact that a default CT scan performed relative to the gantry of the table, UNCORR, has on the axial images.

First, the en face view was obtained via a 2-step process: alignment of the axial plane to account for the scapular angle, followed by alignment of the coronal plane to adjust for the glenoid inclination.¹⁵ These 2 adjustments provided a true en face sagittal glenoid view. The final adjustment step was a sagittal en face rotation of the glenoid such that the superior and inferior glenoid tubercles were placed on the 12-o’clock to 6-o’clock axis (CORR scan). Previous studies have identified a central longitudinal axis that was used in this method to align the supraglenoid tubercle with the 12-o’clock to 6-o’clock axis on the glenoid face.^15,17,18 The standard error of mean was 1.21^°. This new CORR view resulted in axial cuts through the glenoid that were oriented perpendicular to the 12-o’clock to 6-o’clock axis. The UNCORR and CORR images were assessed in the axial plane at 5 standardized cuts and measured for AP glenoid width by 2 independent observers in a blinded, randomized fashion. When the measured AP width of the UNCORR scan was less than that measured on the CORR scan, the AP width of the glenoid was considered underestimated, and the degree of GBL was considered overestimated (Figure 2).

SCAPULAR ANGLE

Scapular angle measurements were performed on the axial view as the angle between a line through the long axis of the body of the scapula, and a line parallel to the CT gantry table.^15,19 Subsequently, the axial plane was aligned to the glenoid surface.

CORONAL INCLINATION

Coronal inclination measurements were performed on the sagittal view as the angle between a line tangential to the face of the glenoid and a line perpendicular to the CT gantry table. Positive values represented superior inclination, while negative values represented inferior glenoid inclination.¹⁵

SAGITTAL ROTATION

Sagittal rotation measurements were performed using the built-in angle measurement tool in OsiriX in the sagittal plane since the degree of rotation required aligning the long axis of the glenoid to the 12-o’clock to 6-o’clock axis. The amount of rotation was defined as the rotation angle.¹⁵

Continue to: Similarly, as described by Gross...

GLENOID WIDTH

Similarly, as described by Gross and colleagues,¹⁵ the sagittal en face view was divided via 5 cuts, throughout a superimposed best-fit circle that closely represents the glenoid.^9,15,20 For both the UNCORR and CORR, glenoid width (AP distance) was measured on the axial image at the widest point from AP cortex across the glenoid face.

PATIENT GROUPS

Utilizing the en face 3-D CT reconstruction view of the glenoid as the gold standard, patients were placed into 1 of 3 groups according to the degree of anterior GBL measured via the surface method.^9,20 The groups were as follows:

I. 10% to 14.9% (N = 12)

II. 15% to 19.9% (N = 16)

III. >20% (N = 15)

STATISTICAL METHODS

Paired t-tests were used to compare all measurements between CORR and UNCORR scans for each of the 5 cuts. A P-value of .05 was used as the threshold for statistical significance in 2-tailed comparisons. Mean and standard errors are presented with standard deviations throughout the study. For interobserver reliability, the measurements between the observers, the intraclass correlation coefficient was calculated. All statistics were performed with SPSS (Version 22).

RESULTS

The study cohort was comprised of 19 left shoulders (44%) and 24 right shoulders (56%), including 36 male patients (84%) and 7 female patients (16%). The average age was 27.8 years (range, 21-40 years). The variability in measured difference, with respect to AP width, was 1.05 mm. The UNCORR CT scans required a mean correction for coronal inclination of 7.0° ± 5.8° (range, -8°-6°). The UNCORR CT scans required a mean correction for scapular angle of 30.2° ± 8.0° (range, 15°-49°). The mean angle of sagittal rotation required to align the glenoid face with the 12-o’clock to 6-o’clock axis was 24.2° ± 5.1 ° (range, 13°-30°). These results are summarized in Table 1. 

For all measurements, the intraclass correlation coefficient for independent observers for all cuts within the 3 groups was r >.900 in all cases.

On an optimized CT scan, over 5 standardized cuts across a best-fit circle of the inferior glenoid, there was a statistically significant absolute mean difference of 12.6% in axial AP glenoid width (2.86 mm ± 2.00 mm, P =.016) when compared with the UNCORR scan. This corresponds to a 3% to 21% error in measurement of the AP width of the glenoid.

Continue to: For the entire cohort...

For groups I (10%-14.9% GBL) and III (>20% GBL), the UNCORR scans underestimated the axial AP width (and thus overestimated anterior GBL) in cuts 1 and 2, while in cuts 3 to 5, the axial AP width was overestimated (GBL was underestimated) (Tables 2, 3). In Group II (15%-19.9% GBL), the axial AP width was underestimated (GBL was overestimated), while in cuts 2 to 5, the axial AP width was overestimated (GBL was underestimated). Overall, AP glenoid width was consistently underestimated in cut 1, the most caudal cut, while AP glenoid width was consistently overestimated in cuts 3 to 5, the more cephalad cuts.

Abbreviations: AP, anterior-posterior; GBL, glenoid bone loss.

Abbreviations: AP, anterior-posterior; CORR, corrected; UNCORR, uncorrected.

DISCUSSION

The principle findings of this study demonstrate that UNCORR conventional 2-D CT scans inaccurately estimate glenoid width as well as inaccurately quantify the degree of anterior GBL. Underestimations of GBL may lead to insufficient treatment of clinically meaningful GBL, thereby increasing the risk of instability recurrence; whereas overestimations of GBL may lead to unnecessary treatment, subjecting patients to increased surgical morbidity. Therefore, the authors recommend correcting the orientation of the scapula in cases wherein clinical decisions are entirely based on 2-D CT, or using alternative methods for quantifying GBL, specifically in the form of 3-D reconstructions.

The use of axial imaging, with CT scans and/or magnetic resonance imaging, is growing in popularity for evaluation of both glenoid anatomy and GBL. Nevertheless, despite our improved ability to critically evaluate the glenoid using these advanced imaging modalities, the images themselves require scrutiny by clinicians to determine if the images accurately depict the true anatomy of the glenoid. As demonstrated by Gross and colleagues,¹⁵ conventional 2D CT scan protocols are not optimized to the anatomy of the glenohumeral joint, even in patients without GBL. Due to the alignment of the image relative to the plane of the scapula as opposed to the plane of the glenoid, UNCORR scans result in significantly different measurements of glenoid version (2.0° ± 0.1°) and AP glenoid width (1.2 mm  ± 0.42 mm) compared with corrected scans, requiring an average 20.1° ± 1.2° of correction to align the sagittal plane. In the present study involving the patients with GBL, we also found that conventional, UNCORR 2-D CT scan protocols inaccurately estimate glenoid width and the degree of anterior GBL. In particular, AP glenoid width was consistently underestimated in the more caudal cuts, while AP glenoid width was consistently overestimated in the more cephalad cuts. Thus, anterior GBL was overestimated (AP glenoid width was underestimated) in the more caudal cuts, whereas anterior GBL was underestimated in the more cranial cuts (AP glenoid width was overestimated). Given that approximately 1 mm of glenoid bone corresponds to approximately 4% of glenoid width,¹⁶ even subtle differences in the interpretation of GBL may lead to gross overestimation/underestimation of bone loss, with significant clinical implications.

In the anterior instability patient population, clinical decision-making is often based on the degree of GBL as determined by advanced imaging modalities. In addition to other patient-specific factors, including age, gender, activity level, type of sport, and number of prior dislocations and/or prior surgeries, the quantity of GBL will often determine which surgical procedure needs to be performed. Typically, patients with >20% to 25% anterior GBL are indicated for a glenoid reconstruction procedure, most commonly via the Latarjet procedure (coracoid transfer).^21-27 The Latarjet procedure remains an excellent technique for appropriately indicated patients, with historically good clinical outcomes and low recurrence rates. Complications associated with the Latarjet procedure, however, are not uncommon, including devastating neuropraxia of the axillary and musculocutaneous nerves, and occasionally permanent neurologic deficits.²⁸ Thus, it is critical to avoid overtreating patients with recurrent instability and GBL. As demonstrated by this study, depending on the cranial-to-caudal location on the glenoid, current 2-D CT techniques may underestimate AP glenoid width, resulting in an overestimation of GBL, potentially leading to the decision to proceed with glenoid bone reconstruction when such a procedure is not required. On the contrary, overestimation of AP glenoid width, which occurs in the more cephalad cuts of the glenoid, is perhaps more worrisome, as the resulting underestimation of GBL may lead to inadequate treatment of patients with recurrent instability. Certainly, one of the main risk factors for failed soft tissue shoulder stabilization is a failure to address GBL. If clinical decisions are made based on UNCORR 2-D CT scans, which are often inaccurate with respect to AP glenoid width by an average 2.86 mm ± 2.00 mm (equivalent to 12.6% ± 6.9% GBL) as determined in this study, patients who truly require osseous glenoid reconstructions may be indicated for only soft tissue stabilization, based on the underestimation of GBL.

Continue to: The current gold standard...

LIMITATIONS

This study has limitations, such as the relatively small sample size and the selection bias by the reviewers with potential differences in interobserver reliability. Further, minor modifications during the reformatting process may be found with each attempt to manipulate the images and may result in minor, insignificant differences in AP width measurements. Performing 1 or more additional CT scans on the same cohort of patients would have been helpful; however, due to the increased risk of radiation exposure, this was not performed. Performing CT scans on cadaveric specimens with GBL and applying the study methodology would also have been helpful to provide independent verification of our clinical findings; however, specimens were not available for this study. Another limitation of this study is that we did not compare our findings with the findings of glenoid width, and bone loss, as determined using the circle method, which is commonly utilized when 3-D reconstructions are available. In this study, the purpose was to utilize only the 2-D reformatted images, with the assumption that 3-D reconstructions are not always available, and cannot always be measured. To minimize selection bias, the investigators measured the correction effects within groups of patients with similar degrees of GBL (10%-14.9%, 15%-19.9%, and >20%). In addition, not all the selected patients showed degenerative glenoid changes or irregular glenoid shape indicating previous bone augmentation.

CONCLUSIONS

UNCORR 2D CT scans inaccurately estimate glenoid width and the degree of anterior GBL. The clinical implications of these findings are profound and suggest corrected 2D CT scans or 3D reconstruction allow measurements to be taken in the axis of the glenoid to accurately define the anatomy and quantity of anterior GBL in patients with shoulder instability.

BOSTON – New ways for implanted cardiac rhythm devices to work without need for transvenous leads are in clinical testing, reflecting a keen interest in getting leads out of the vascular space and potentially cutting risks for infections, pneumothorax, hematoma, and the possible need for future lead extraction.

Leads are “the Achilles heel” of pacemakers and defibrillators; “there are too many places where the wire can break,” John D. Day, MD, said in an interview during the annual scientific sessions of the Heart Rhythm Society. Eliminating transvenous leads, or any type of lead for that matter, “solves a lot of problems” that currently occur with implanted cardiac devices, said Dr. Day, a cardiac electrophysiologist with Intermountain Health in Murray, Utah.

Mitchel L. Zoler/MDedge News

Mitchel L. Zoler/MDedge News

[email protected]

On Twitter @mitchelzoler

SOURCE: Boersma L et al. Heart Rhythm 2018, Abstract B-LBCT03-03; Chinitz L et al. Heart Rhythm 2018, Abstract B-LBCT03-04.

BOSTON – New ways for implanted cardiac rhythm devices to work without need for transvenous leads are in clinical testing, reflecting a keen interest in getting leads out of the vascular space and potentially cutting risks for infections, pneumothorax, hematoma, and the possible need for future lead extraction.

Leads are “the Achilles heel” of pacemakers and defibrillators; “there are too many places where the wire can break,” John D. Day, MD, said in an interview during the annual scientific sessions of the Heart Rhythm Society. Eliminating transvenous leads, or any type of lead for that matter, “solves a lot of problems” that currently occur with implanted cardiac devices, said Dr. Day, a cardiac electrophysiologist with Intermountain Health in Murray, Utah.

Mitchel L. Zoler/MDedge News

Mitchel L. Zoler/MDedge News

[email protected]

On Twitter @mitchelzoler

SOURCE: Boersma L et al. Heart Rhythm 2018, Abstract B-LBCT03-03; Chinitz L et al. Heart Rhythm 2018, Abstract B-LBCT03-04.

BOSTON – New ways for implanted cardiac rhythm devices to work without need for transvenous leads are in clinical testing, reflecting a keen interest in getting leads out of the vascular space and potentially cutting risks for infections, pneumothorax, hematoma, and the possible need for future lead extraction.

Leads are “the Achilles heel” of pacemakers and defibrillators; “there are too many places where the wire can break,” John D. Day, MD, said in an interview during the annual scientific sessions of the Heart Rhythm Society. Eliminating transvenous leads, or any type of lead for that matter, “solves a lot of problems” that currently occur with implanted cardiac devices, said Dr. Day, a cardiac electrophysiologist with Intermountain Health in Murray, Utah.

Mitchel L. Zoler/MDedge News

Mitchel L. Zoler/MDedge News

[email protected]

On Twitter @mitchelzoler

SOURCE: Boersma L et al. Heart Rhythm 2018, Abstract B-LBCT03-03; Chinitz L et al. Heart Rhythm 2018, Abstract B-LBCT03-04.

Clothes moths are common pests found inside buildings such as homes, stores, and museums. The most common species of importance include the webbing clothes moth (Tineola bisselliella)(Figure) and the casemaking clothes moth (Tineola pellionella). Both species target textiles such as wool, rugs, feathers, felts, hair, furs, and even grains.^1,2 They avoid synthetics and plant materials such as cottons.¹

Characteristics

Adult clothes moths extend 7 to 8 mm and are a golden (T bisselliella) to brown (T pellionella) color with fringed wings and a tuft on their heads.^1,3 Adults do not eat; females die within a few days of laying eggs, while males live approximately 1 month. Once laid, eggs hatch within 4 to 10 days.^1,3 The larvae (caterpillars) incur damage to clothes and other household goods. Fully mature larvae are 12- to 13-mm long, and the Tineola species have white- to cream-colored bodies with brown heads. The webbing clothes moth larva lacks ocelli (eyes), while the casemaking moth larva has a singular ocellus.¹

Transmission

An infestation is evidenced by woolen items that have furrows or holes in them. Pheromone traps also can expose an active infestation.³ The webbing moth larvae can be found beneath a self-spun silken mat on the food source that offers the insect protection and camouflage while it eats; the mat collects frass (feces) and clothes particles.^1,3,4 The casemaking moth larvae drag around a portable silken bag that takes on the color of the fabric being eaten and serves as a refuge when disturbed.^1,3,4 Both adult and larval stages prefer low light conditions. The total time of development from caterpillar to adult varies depending on the temperature and humidity of the environment, but most clothes moths complete their life cycle within 1 to 3 months.¹

Management of an Infestation

Multiple infestation treatment options exist should a patient present with a clothes moth infestation. Infested clothing articles or small blankets and rugs can be dry-cleaned or laundered. Any items not in use should be laundered before being sealed in airtight storage containers. Mothball vapor at appropriate concentrations is lethal to the moths, and when possible, clothing should be stored with mothballs or flakes at the concentration recommended by the manufacturer.⁴ Individuals should avoid application of household insecticides to clothing or bedding, which may be poisonous to people.^1,4 Freezing, heating, and dry ice fumigation techniques also can be used to treat infested products.³ Cedarwood usually is insufficient to deter an infestation, as the oil vapor rarely reaches an effective concentration to repel or harm the insects.^3,4 Strict housekeeping with attention to vacuuming carpets, baseboards, closets, and laundering all linens and furniture covers can further reduce an infestation.⁴ Clothes items can be set in the sunlight and brushed to help loosen the pests, as they dislike direct light and may fall from the garments.³ Dust insecticides also can be used per the manufacturer label to treat crevices and baseboards in an active area of infestation that may otherwise be difficult to clean.³ If an extensive infestation exists or larger items are infested, then a professional pest control agency should be employed for proper eradication.

Conclusion

Understanding the life cycle and basic biology of clothes moths and other common household pests will help the clinician identify an infestation and counsel patients if an insect is a true ectoparasite. Clothes moth larvae are not parasites but can be found on clothing and can be confused with myiasis or true parasites.

Clothes moths are common pests found inside buildings such as homes, stores, and museums. The most common species of importance include the webbing clothes moth (Tineola bisselliella)(Figure) and the casemaking clothes moth (Tineola pellionella). Both species target textiles such as wool, rugs, feathers, felts, hair, furs, and even grains.^1,2 They avoid synthetics and plant materials such as cottons.¹

Characteristics

Adult clothes moths extend 7 to 8 mm and are a golden (T bisselliella) to brown (T pellionella) color with fringed wings and a tuft on their heads.^1,3 Adults do not eat; females die within a few days of laying eggs, while males live approximately 1 month. Once laid, eggs hatch within 4 to 10 days.^1,3 The larvae (caterpillars) incur damage to clothes and other household goods. Fully mature larvae are 12- to 13-mm long, and the Tineola species have white- to cream-colored bodies with brown heads. The webbing clothes moth larva lacks ocelli (eyes), while the casemaking moth larva has a singular ocellus.¹

Transmission

An infestation is evidenced by woolen items that have furrows or holes in them. Pheromone traps also can expose an active infestation.³ The webbing moth larvae can be found beneath a self-spun silken mat on the food source that offers the insect protection and camouflage while it eats; the mat collects frass (feces) and clothes particles.^1,3,4 The casemaking moth larvae drag around a portable silken bag that takes on the color of the fabric being eaten and serves as a refuge when disturbed.^1,3,4 Both adult and larval stages prefer low light conditions. The total time of development from caterpillar to adult varies depending on the temperature and humidity of the environment, but most clothes moths complete their life cycle within 1 to 3 months.¹

Management of an Infestation

Multiple infestation treatment options exist should a patient present with a clothes moth infestation. Infested clothing articles or small blankets and rugs can be dry-cleaned or laundered. Any items not in use should be laundered before being sealed in airtight storage containers. Mothball vapor at appropriate concentrations is lethal to the moths, and when possible, clothing should be stored with mothballs or flakes at the concentration recommended by the manufacturer.⁴ Individuals should avoid application of household insecticides to clothing or bedding, which may be poisonous to people.^1,4 Freezing, heating, and dry ice fumigation techniques also can be used to treat infested products.³ Cedarwood usually is insufficient to deter an infestation, as the oil vapor rarely reaches an effective concentration to repel or harm the insects.^3,4 Strict housekeeping with attention to vacuuming carpets, baseboards, closets, and laundering all linens and furniture covers can further reduce an infestation.⁴ Clothes items can be set in the sunlight and brushed to help loosen the pests, as they dislike direct light and may fall from the garments.³ Dust insecticides also can be used per the manufacturer label to treat crevices and baseboards in an active area of infestation that may otherwise be difficult to clean.³ If an extensive infestation exists or larger items are infested, then a professional pest control agency should be employed for proper eradication.

Conclusion

Understanding the life cycle and basic biology of clothes moths and other common household pests will help the clinician identify an infestation and counsel patients if an insect is a true ectoparasite. Clothes moth larvae are not parasites but can be found on clothing and can be confused with myiasis or true parasites.

Clothes moths are common pests found inside buildings such as homes, stores, and museums. The most common species of importance include the webbing clothes moth (Tineola bisselliella)(Figure) and the casemaking clothes moth (Tineola pellionella). Both species target textiles such as wool, rugs, feathers, felts, hair, furs, and even grains.^1,2 They avoid synthetics and plant materials such as cottons.¹

Characteristics

Adult clothes moths extend 7 to 8 mm and are a golden (T bisselliella) to brown (T pellionella) color with fringed wings and a tuft on their heads.^1,3 Adults do not eat; females die within a few days of laying eggs, while males live approximately 1 month. Once laid, eggs hatch within 4 to 10 days.^1,3 The larvae (caterpillars) incur damage to clothes and other household goods. Fully mature larvae are 12- to 13-mm long, and the Tineola species have white- to cream-colored bodies with brown heads. The webbing clothes moth larva lacks ocelli (eyes), while the casemaking moth larva has a singular ocellus.¹

Transmission

An infestation is evidenced by woolen items that have furrows or holes in them. Pheromone traps also can expose an active infestation.³ The webbing moth larvae can be found beneath a self-spun silken mat on the food source that offers the insect protection and camouflage while it eats; the mat collects frass (feces) and clothes particles.^1,3,4 The casemaking moth larvae drag around a portable silken bag that takes on the color of the fabric being eaten and serves as a refuge when disturbed.^1,3,4 Both adult and larval stages prefer low light conditions. The total time of development from caterpillar to adult varies depending on the temperature and humidity of the environment, but most clothes moths complete their life cycle within 1 to 3 months.¹

Management of an Infestation

Multiple infestation treatment options exist should a patient present with a clothes moth infestation. Infested clothing articles or small blankets and rugs can be dry-cleaned or laundered. Any items not in use should be laundered before being sealed in airtight storage containers. Mothball vapor at appropriate concentrations is lethal to the moths, and when possible, clothing should be stored with mothballs or flakes at the concentration recommended by the manufacturer.⁴ Individuals should avoid application of household insecticides to clothing or bedding, which may be poisonous to people.^1,4 Freezing, heating, and dry ice fumigation techniques also can be used to treat infested products.³ Cedarwood usually is insufficient to deter an infestation, as the oil vapor rarely reaches an effective concentration to repel or harm the insects.^3,4 Strict housekeeping with attention to vacuuming carpets, baseboards, closets, and laundering all linens and furniture covers can further reduce an infestation.⁴ Clothes items can be set in the sunlight and brushed to help loosen the pests, as they dislike direct light and may fall from the garments.³ Dust insecticides also can be used per the manufacturer label to treat crevices and baseboards in an active area of infestation that may otherwise be difficult to clean.³ If an extensive infestation exists or larger items are infested, then a professional pest control agency should be employed for proper eradication.

Conclusion

Understanding the life cycle and basic biology of clothes moths and other common household pests will help the clinician identify an infestation and counsel patients if an insect is a true ectoparasite. Clothes moth larvae are not parasites but can be found on clothing and can be confused with myiasis or true parasites.

On February 23, 2018, Anthem Insurance Companies, Inc, announced the reversal of its proposed policy to reduce reimbursement for evaluation and management (E/M) services billed using modifier -25.¹ This win for physicians was the result of a broad-based, multipronged advocacy campaign, and the American Academy of Dermatology Association (AADA) was critical to this victory.

Dermatology Took the Lead in Opposing Policy That Would Reduce Reimbursement

Dermatology was the first to trumpet the dangers of modifier -25 reduction policies and explain why other specialty societies should care. The AADA took the lead in assembling a coalition of physician groups to oppose the proposed policy by sharing language for opposition letters and meeting talking points with many societies outside of dermatology as well as producing the first draft for the American Medical Association (AMA) House of Delegates’ resolution that spurred action against Anthem’s proposed policy.² Members of the AADA attended numerous conference calls and in-person meetings with health insurance officials to urge them to reverse the policy and helped coordinate opposition from state and national specialty societies. The influence and advocacy of the AMA was critical in reversing the proposed policy, but dermatology started the opposition and organized the players to bring the fight against Anthem.

AADA Continues to Fight

Despite the victory against Anthem, challenges to fair reimbursement of modifier -25 claims are ongoing. Two insurers recently announced implementation of new modifier -25 reduction policies.^3,4 Moreover, 4 other insurers have existing modifier -25 reduction policies in place.^5-8 The AADA has engaged, and will continue engaging, each of these insurers with the message that the ability to perform procedures and distinct E/M services on the same day is integral to efficient, patient-centered care of dermatologic diseases. The AADA argues that insurers’ rationale (overlapping indirect practice expenses) for payment reduction is improper and that appropriately documented modifier -25 claims should be reimbursed at 100% of allowable charges.

In addition to the existing insurer policies affecting modifier -25, Anthem has announced that it plans to conduct audits of modifier -25 claims with recoupments of inappropriate charges.¹ Some Medicare Administrative Contractors also have cited modifier -25 as an area of concern and issued guidelines for reporting modifier -25, which frequently precede audits.⁹ The AADA is concerned that if Anthem follows through with its aggressive audits to recoup money, which can result in substantial take-backs, and finds a high error rate in modifier -25 claims, it also may consider revisiting its reduction policy. Moreover, it is likely that other insurers will use failed modifier -25 audits as an excuse to continue, expand, or adopt modifier -25 reduction policies. It is clear that blanket reduction in payment is much easier and less expensive for insurers than auditing medical records and not paying those who abuse modifier -25. As long as insurers are under financial pressure, modifier -25 will be a tempting target for reducing health care costs.

How to Use Modifier -25 Correctly

In addition to opposing inappropriate reimbursement of modifier -25, the AADA is committed to educating its members and insurers on the correct use and documentation of modifier -25. In December 2017, Mollie A. MacCormack, MD (Nashua, New Hampshire), and I led an educational webinar on modifier -25 for more than 1100 attendees.¹⁰ We discussed the performance standards and documentation requirements of modifier -25. It was clear that dermatologists were interested not only in the correct coding of modifier -25 claims but also avoiding the consequences of audits.

My peers frequently ask, “What can we [dermatologists] do to prepare for potential modifier -25 audits?” My advice is always, “Physician audit thyself.” I recommend self-auditing to make sure you and your practice are in compliance with modifier -25 documentation requirements. In a March 2017 Cutis column on modifier -25, I discussed what constitutes separate and distinct E/M services and what is included in a procedure’s global surgical package.¹¹ A self-audit is as simple as pulling 10 to 20 medical records in which a same-day procedure and E/M service were billed. Cross out any information in the note included in the procedure’s global surgical package including history associated with establishing the diagnosis, physical examination of the procedure area(s), and discussion of treatment options. If complete documentation for an E/M is still present after removing the procedure and associated evaluation, you have passed the self-audit. If not, consider changing your coding to better reflect the documentation in your records. In my experience, insurance auditors are not physicians and often are not even medical professionals. Clear documentation and clear existence of a separate, distinct, and medically necessary E/M service is needed to succeed in a modifier -25 audit.

Final Thoughts

Dermatologists should rejoice that Anthem decided to rescind its modifier -25 policy. If this policy had gone into effect, the modifier -25 reduction would likely have spread to most other insurers as industry standard. This victory certainly shows what can be accomplished when organized medicine works together. Your state dermatology and medical societies, national societies, and the AMA collaborated on a critical existential threat to cost-effective and efficient patient care and won. These organizations deserve your membership and support as well as your thanks; however, our celebration must be short-lived, as there still are other insurers with modifier -25 reductions in place, and audits have been promised. We must continue to focus on proper use and documentation of modifier -25. This effort will not only help dermatologists decrease the risk of large recoupments from audits but also help the AADA continue to oppose inappropriate payment policies.

On February 23, 2018, Anthem Insurance Companies, Inc, announced the reversal of its proposed policy to reduce reimbursement for evaluation and management (E/M) services billed using modifier -25.¹ This win for physicians was the result of a broad-based, multipronged advocacy campaign, and the American Academy of Dermatology Association (AADA) was critical to this victory.

Dermatology Took the Lead in Opposing Policy That Would Reduce Reimbursement

Dermatology was the first to trumpet the dangers of modifier -25 reduction policies and explain why other specialty societies should care. The AADA took the lead in assembling a coalition of physician groups to oppose the proposed policy by sharing language for opposition letters and meeting talking points with many societies outside of dermatology as well as producing the first draft for the American Medical Association (AMA) House of Delegates’ resolution that spurred action against Anthem’s proposed policy.² Members of the AADA attended numerous conference calls and in-person meetings with health insurance officials to urge them to reverse the policy and helped coordinate opposition from state and national specialty societies. The influence and advocacy of the AMA was critical in reversing the proposed policy, but dermatology started the opposition and organized the players to bring the fight against Anthem.

AADA Continues to Fight

Despite the victory against Anthem, challenges to fair reimbursement of modifier -25 claims are ongoing. Two insurers recently announced implementation of new modifier -25 reduction policies.^3,4 Moreover, 4 other insurers have existing modifier -25 reduction policies in place.^5-8 The AADA has engaged, and will continue engaging, each of these insurers with the message that the ability to perform procedures and distinct E/M services on the same day is integral to efficient, patient-centered care of dermatologic diseases. The AADA argues that insurers’ rationale (overlapping indirect practice expenses) for payment reduction is improper and that appropriately documented modifier -25 claims should be reimbursed at 100% of allowable charges.

In addition to the existing insurer policies affecting modifier -25, Anthem has announced that it plans to conduct audits of modifier -25 claims with recoupments of inappropriate charges.¹ Some Medicare Administrative Contractors also have cited modifier -25 as an area of concern and issued guidelines for reporting modifier -25, which frequently precede audits.⁹ The AADA is concerned that if Anthem follows through with its aggressive audits to recoup money, which can result in substantial take-backs, and finds a high error rate in modifier -25 claims, it also may consider revisiting its reduction policy. Moreover, it is likely that other insurers will use failed modifier -25 audits as an excuse to continue, expand, or adopt modifier -25 reduction policies. It is clear that blanket reduction in payment is much easier and less expensive for insurers than auditing medical records and not paying those who abuse modifier -25. As long as insurers are under financial pressure, modifier -25 will be a tempting target for reducing health care costs.

How to Use Modifier -25 Correctly

In addition to opposing inappropriate reimbursement of modifier -25, the AADA is committed to educating its members and insurers on the correct use and documentation of modifier -25. In December 2017, Mollie A. MacCormack, MD (Nashua, New Hampshire), and I led an educational webinar on modifier -25 for more than 1100 attendees.¹⁰ We discussed the performance standards and documentation requirements of modifier -25. It was clear that dermatologists were interested not only in the correct coding of modifier -25 claims but also avoiding the consequences of audits.

My peers frequently ask, “What can we [dermatologists] do to prepare for potential modifier -25 audits?” My advice is always, “Physician audit thyself.” I recommend self-auditing to make sure you and your practice are in compliance with modifier -25 documentation requirements. In a March 2017 Cutis column on modifier -25, I discussed what constitutes separate and distinct E/M services and what is included in a procedure’s global surgical package.¹¹ A self-audit is as simple as pulling 10 to 20 medical records in which a same-day procedure and E/M service were billed. Cross out any information in the note included in the procedure’s global surgical package including history associated with establishing the diagnosis, physical examination of the procedure area(s), and discussion of treatment options. If complete documentation for an E/M is still present after removing the procedure and associated evaluation, you have passed the self-audit. If not, consider changing your coding to better reflect the documentation in your records. In my experience, insurance auditors are not physicians and often are not even medical professionals. Clear documentation and clear existence of a separate, distinct, and medically necessary E/M service is needed to succeed in a modifier -25 audit.

Final Thoughts

Dermatologists should rejoice that Anthem decided to rescind its modifier -25 policy. If this policy had gone into effect, the modifier -25 reduction would likely have spread to most other insurers as industry standard. This victory certainly shows what can be accomplished when organized medicine works together. Your state dermatology and medical societies, national societies, and the AMA collaborated on a critical existential threat to cost-effective and efficient patient care and won. These organizations deserve your membership and support as well as your thanks; however, our celebration must be short-lived, as there still are other insurers with modifier -25 reductions in place, and audits have been promised. We must continue to focus on proper use and documentation of modifier -25. This effort will not only help dermatologists decrease the risk of large recoupments from audits but also help the AADA continue to oppose inappropriate payment policies.

On February 23, 2018, Anthem Insurance Companies, Inc, announced the reversal of its proposed policy to reduce reimbursement for evaluation and management (E/M) services billed using modifier -25.¹ This win for physicians was the result of a broad-based, multipronged advocacy campaign, and the American Academy of Dermatology Association (AADA) was critical to this victory.

Dermatology Took the Lead in Opposing Policy That Would Reduce Reimbursement

Dermatology was the first to trumpet the dangers of modifier -25 reduction policies and explain why other specialty societies should care. The AADA took the lead in assembling a coalition of physician groups to oppose the proposed policy by sharing language for opposition letters and meeting talking points with many societies outside of dermatology as well as producing the first draft for the American Medical Association (AMA) House of Delegates’ resolution that spurred action against Anthem’s proposed policy.² Members of the AADA attended numerous conference calls and in-person meetings with health insurance officials to urge them to reverse the policy and helped coordinate opposition from state and national specialty societies. The influence and advocacy of the AMA was critical in reversing the proposed policy, but dermatology started the opposition and organized the players to bring the fight against Anthem.

AADA Continues to Fight

Despite the victory against Anthem, challenges to fair reimbursement of modifier -25 claims are ongoing. Two insurers recently announced implementation of new modifier -25 reduction policies.^3,4 Moreover, 4 other insurers have existing modifier -25 reduction policies in place.^5-8 The AADA has engaged, and will continue engaging, each of these insurers with the message that the ability to perform procedures and distinct E/M services on the same day is integral to efficient, patient-centered care of dermatologic diseases. The AADA argues that insurers’ rationale (overlapping indirect practice expenses) for payment reduction is improper and that appropriately documented modifier -25 claims should be reimbursed at 100% of allowable charges.

In addition to the existing insurer policies affecting modifier -25, Anthem has announced that it plans to conduct audits of modifier -25 claims with recoupments of inappropriate charges.¹ Some Medicare Administrative Contractors also have cited modifier -25 as an area of concern and issued guidelines for reporting modifier -25, which frequently precede audits.⁹ The AADA is concerned that if Anthem follows through with its aggressive audits to recoup money, which can result in substantial take-backs, and finds a high error rate in modifier -25 claims, it also may consider revisiting its reduction policy. Moreover, it is likely that other insurers will use failed modifier -25 audits as an excuse to continue, expand, or adopt modifier -25 reduction policies. It is clear that blanket reduction in payment is much easier and less expensive for insurers than auditing medical records and not paying those who abuse modifier -25. As long as insurers are under financial pressure, modifier -25 will be a tempting target for reducing health care costs.

How to Use Modifier -25 Correctly

In addition to opposing inappropriate reimbursement of modifier -25, the AADA is committed to educating its members and insurers on the correct use and documentation of modifier -25. In December 2017, Mollie A. MacCormack, MD (Nashua, New Hampshire), and I led an educational webinar on modifier -25 for more than 1100 attendees.¹⁰ We discussed the performance standards and documentation requirements of modifier -25. It was clear that dermatologists were interested not only in the correct coding of modifier -25 claims but also avoiding the consequences of audits.

My peers frequently ask, “What can we [dermatologists] do to prepare for potential modifier -25 audits?” My advice is always, “Physician audit thyself.” I recommend self-auditing to make sure you and your practice are in compliance with modifier -25 documentation requirements. In a March 2017 Cutis column on modifier -25, I discussed what constitutes separate and distinct E/M services and what is included in a procedure’s global surgical package.¹¹ A self-audit is as simple as pulling 10 to 20 medical records in which a same-day procedure and E/M service were billed. Cross out any information in the note included in the procedure’s global surgical package including history associated with establishing the diagnosis, physical examination of the procedure area(s), and discussion of treatment options. If complete documentation for an E/M is still present after removing the procedure and associated evaluation, you have passed the self-audit. If not, consider changing your coding to better reflect the documentation in your records. In my experience, insurance auditors are not physicians and often are not even medical professionals. Clear documentation and clear existence of a separate, distinct, and medically necessary E/M service is needed to succeed in a modifier -25 audit.

Final Thoughts

Dermatologists should rejoice that Anthem decided to rescind its modifier -25 policy. If this policy had gone into effect, the modifier -25 reduction would likely have spread to most other insurers as industry standard. This victory certainly shows what can be accomplished when organized medicine works together. Your state dermatology and medical societies, national societies, and the AMA collaborated on a critical existential threat to cost-effective and efficient patient care and won. These organizations deserve your membership and support as well as your thanks; however, our celebration must be short-lived, as there still are other insurers with modifier -25 reductions in place, and audits have been promised. We must continue to focus on proper use and documentation of modifier -25. This effort will not only help dermatologists decrease the risk of large recoupments from audits but also help the AADA continue to oppose inappropriate payment policies.

It has been said that “extraordinary claims require extraordinary evidence.”¹ In the pursuit of evidence-based medicine, we are encouraged to follow a similar standard, with an emphasis on waiting for multiple studies with good-quality data and high levels of agreement before changing any aspect of our clinical practice. The ostensible purpose is that studies can be flawed, conclusions can be incorrect, or biases can be overlooked. In such cases, acting on questionable results could imperil patients. It is for this reason that so many review articles sometimes frustratingly seem to conclude that further evidence is needed.²

Based on this standard, recently published addendum guidelines from the National Institute of Allergy and Infectious Diseases for prevention of peanut allergy in the United States³ are somewhat striking in that they make fairly bold recommendations based on results from the 2015 Learning Early about Peanut Allergy (LEAP) study,⁴ a randomized trial evaluating early peanut introduction as a preventive strategy for peanut allergy. Of note, this study was not placebo controlled, was conducted at only 1 site in the United Kingdom, and only included 640 children, though the number of participants was admittedly large for this type of study.⁴ Arguably, the LEAP study alone does not provide enough evidence upon which to base what essentially amounts to an about-face in the official recommendations for prevention of peanut and other food allergies, which emphasized delayed introduction of high-risk foods, especially in high-risk individuals.^5-7 To better understand this shift, we need to briefly explore the context of the addendum guidelines.

As many as one-third of pediatric patients with atopic dermatitis (AD) have food allergies, thus diet often is invoked by patients and providers alike as an underlying cause of the disease.⁸ Many patients in my practice are so focused on potential food allergies that actual treatment of the affected skin is marginalized and often dismissed as a stopgap that does not address the root of the problem. A 2004 study of 100 children with AD found that diet was manipulated by the parents in 75% of patients in an attempt to manage the disease.⁹

Patients are not the only ones who consider food allergies to be a driving force in AD. The medical literature indicates that this theory has existed for centuries; for instance, with regard to the relationship between diet and AD, the author of an article from 1830 quipped, “There is probably no subject in which more deeply rooted convictions have been held . . . than the connection between diet and disease, both as regards the causation and treatment of the latter . . .”¹⁰ More apropos perhaps is a statement from the 2010 National Institute of Allergy and Infectious Diseases guidelines on food allergy management, which noted that while the expert group “does not mean to imply that AD results from [food allergies], the role of [food allergies] in the pathogenesis and severity of this condition remains controversial.”¹¹

Prior to the LEAP study, food allergy recommendations for clinical practice in the United Kingdom in 1998¹² and the United States in 2000¹³ recommended excluding allergenic foods (eg, peanuts, tree nuts, soy, milk, eggs) from the diet in infants with a family history of atopy until 3 years of age. However, those recommendations did not seem to be working, when in fact just the opposite was happening. From 1997 until the LEAP study was conducted in 2015, the prevalence of peanut allergy more than quadrupled and became the leading cause of anaphylaxis and death related to food allergy.¹⁴ Additionally, study after study concluded that elimination diets did not seem to help most patients with AD.¹⁵ As is required in good scientific thinking, when a hypothesis is proven false, other approaches must be considered.

The idea arose that perhaps delaying introduction of allergenic foods was the opposite of the answer.⁴ The LEAP study tested the notion that peanut allergies are rare in countries where peanuts are introduced early and if telling families to delay introduction of peanuts in infants might actually be causing development of a peanut allergy, and the tests bore fruit. It was found that giving infants peanut-containing foods resulted in a more than 80% reduction in peanut allergy at 5 years of age (P<.001).⁴ What was perhaps even more interesting was the connection between AD and peanut allergy. An important idea articulated in the LEAP study is in some ways revolutionary: Rather than foods causing AD, it could be that “early environmental exposure (through the skin) to peanut may account for early sensitization, whereas early oral exposure may lead to immune tolerance.”⁴ This concept—that impaired eczematous skin may actually lead to the development of food allergies—turns the whole thing upside down.

What do these updated guidelines actually suggest? The first guideline focuses on infants with severe AD, egg allergy, or both, who therefore are thought to be at the highest risk for developing peanut allergy.³ Because of the higher baseline risk in this subgroup, measurement of the peanut-specific IgE (peanut sIgE) level, skin prick testing (SPT), or both is strongly recommended before introducing peanut protein into the diet. This testing can be performed by qualified providers as a screening measure, but if positive (≥0.35 kU_A/L for peanut sIgE or >2 mm on the peanut SPT), referral to an allergy specialist is warranted. If these studies are negative, it is thought the likelihood of peanut allergy is low, and it is recommended that caregivers introduce age-appropriate peanut-containing foods (eg, peanut butter snack puffs, diluted peanut butter) as early as 4 to 6 months of age. The second guideline recommends that peanut-containing foods should be introduced into the diets of infants with mild or moderate AD at approximately 6 months of age without the need for prior screening via peanut sIgE or SPT. Lastly, the third guideline recommends that caregivers freely introduce peanut-containing foods together with other solid foods in infants without AD or food allergies in accordance with family preference.³

The results of the LEAP study are certainly exciting, and although the theoretical basis makes good scientific sense and the updated guidelines truly address an important and growing problem, there are several issues with this update that are worth considering. Given the constraints of the LEAP study, it certainly seems possible that the results will not be applicable to all populations or foods. More research is needed to ensure that this robust finding applies to other children and to explore the introduction of other allergenic foods, which the LEAP study investigators also emphasized.⁴

In fairness, the updated guidelines clearly state the quality of evidence of their recommendations and make it clear that expert opinion is playing a large role.³ For the first guideline regarding recommendations for those with severe AD and/or egg allergy, the quality of evidence is deemed moderate, while the contribution of expert opinion is listed as significant. For the second and third guidelines regarding recommendations for mild to moderate AD and those without AD, respectively, the quality of evidence is low and expert opinion is again listed as significant.³

Importantly, delineating severe AD from moderate disease—which is necessary because only severe AD warrants evaluation with peanut sIgE and/or SPT—can be difficult, as the distinction relies on a degree of subjectivity that may vary between specialists. Indeed, 2 publications suggest extending the definition of severe AD to include infants with early-onset AD (<3 months of age) and those with moderate AD not responding to treatment.^16,17

Despite these reservations, the updated guidelines represent a breakthrough in understanding in an area truly in need of advancement. Although the evidence may not be exactly extraordinary, the context for these developments and our deeper understanding suggest that we do indeed live in extraordinary times. 

It has been said that “extraordinary claims require extraordinary evidence.”¹ In the pursuit of evidence-based medicine, we are encouraged to follow a similar standard, with an emphasis on waiting for multiple studies with good-quality data and high levels of agreement before changing any aspect of our clinical practice. The ostensible purpose is that studies can be flawed, conclusions can be incorrect, or biases can be overlooked. In such cases, acting on questionable results could imperil patients. It is for this reason that so many review articles sometimes frustratingly seem to conclude that further evidence is needed.²

Based on this standard, recently published addendum guidelines from the National Institute of Allergy and Infectious Diseases for prevention of peanut allergy in the United States³ are somewhat striking in that they make fairly bold recommendations based on results from the 2015 Learning Early about Peanut Allergy (LEAP) study,⁴ a randomized trial evaluating early peanut introduction as a preventive strategy for peanut allergy. Of note, this study was not placebo controlled, was conducted at only 1 site in the United Kingdom, and only included 640 children, though the number of participants was admittedly large for this type of study.⁴ Arguably, the LEAP study alone does not provide enough evidence upon which to base what essentially amounts to an about-face in the official recommendations for prevention of peanut and other food allergies, which emphasized delayed introduction of high-risk foods, especially in high-risk individuals.^5-7 To better understand this shift, we need to briefly explore the context of the addendum guidelines.

As many as one-third of pediatric patients with atopic dermatitis (AD) have food allergies, thus diet often is invoked by patients and providers alike as an underlying cause of the disease.⁸ Many patients in my practice are so focused on potential food allergies that actual treatment of the affected skin is marginalized and often dismissed as a stopgap that does not address the root of the problem. A 2004 study of 100 children with AD found that diet was manipulated by the parents in 75% of patients in an attempt to manage the disease.⁹

Patients are not the only ones who consider food allergies to be a driving force in AD. The medical literature indicates that this theory has existed for centuries; for instance, with regard to the relationship between diet and AD, the author of an article from 1830 quipped, “There is probably no subject in which more deeply rooted convictions have been held . . . than the connection between diet and disease, both as regards the causation and treatment of the latter . . .”¹⁰ More apropos perhaps is a statement from the 2010 National Institute of Allergy and Infectious Diseases guidelines on food allergy management, which noted that while the expert group “does not mean to imply that AD results from [food allergies], the role of [food allergies] in the pathogenesis and severity of this condition remains controversial.”¹¹

Prior to the LEAP study, food allergy recommendations for clinical practice in the United Kingdom in 1998¹² and the United States in 2000¹³ recommended excluding allergenic foods (eg, peanuts, tree nuts, soy, milk, eggs) from the diet in infants with a family history of atopy until 3 years of age. However, those recommendations did not seem to be working, when in fact just the opposite was happening. From 1997 until the LEAP study was conducted in 2015, the prevalence of peanut allergy more than quadrupled and became the leading cause of anaphylaxis and death related to food allergy.¹⁴ Additionally, study after study concluded that elimination diets did not seem to help most patients with AD.¹⁵ As is required in good scientific thinking, when a hypothesis is proven false, other approaches must be considered.

The idea arose that perhaps delaying introduction of allergenic foods was the opposite of the answer.⁴ The LEAP study tested the notion that peanut allergies are rare in countries where peanuts are introduced early and if telling families to delay introduction of peanuts in infants might actually be causing development of a peanut allergy, and the tests bore fruit. It was found that giving infants peanut-containing foods resulted in a more than 80% reduction in peanut allergy at 5 years of age (P<.001).⁴ What was perhaps even more interesting was the connection between AD and peanut allergy. An important idea articulated in the LEAP study is in some ways revolutionary: Rather than foods causing AD, it could be that “early environmental exposure (through the skin) to peanut may account for early sensitization, whereas early oral exposure may lead to immune tolerance.”⁴ This concept—that impaired eczematous skin may actually lead to the development of food allergies—turns the whole thing upside down.

What do these updated guidelines actually suggest? The first guideline focuses on infants with severe AD, egg allergy, or both, who therefore are thought to be at the highest risk for developing peanut allergy.³ Because of the higher baseline risk in this subgroup, measurement of the peanut-specific IgE (peanut sIgE) level, skin prick testing (SPT), or both is strongly recommended before introducing peanut protein into the diet. This testing can be performed by qualified providers as a screening measure, but if positive (≥0.35 kU_A/L for peanut sIgE or >2 mm on the peanut SPT), referral to an allergy specialist is warranted. If these studies are negative, it is thought the likelihood of peanut allergy is low, and it is recommended that caregivers introduce age-appropriate peanut-containing foods (eg, peanut butter snack puffs, diluted peanut butter) as early as 4 to 6 months of age. The second guideline recommends that peanut-containing foods should be introduced into the diets of infants with mild or moderate AD at approximately 6 months of age without the need for prior screening via peanut sIgE or SPT. Lastly, the third guideline recommends that caregivers freely introduce peanut-containing foods together with other solid foods in infants without AD or food allergies in accordance with family preference.³

The results of the LEAP study are certainly exciting, and although the theoretical basis makes good scientific sense and the updated guidelines truly address an important and growing problem, there are several issues with this update that are worth considering. Given the constraints of the LEAP study, it certainly seems possible that the results will not be applicable to all populations or foods. More research is needed to ensure that this robust finding applies to other children and to explore the introduction of other allergenic foods, which the LEAP study investigators also emphasized.⁴

In fairness, the updated guidelines clearly state the quality of evidence of their recommendations and make it clear that expert opinion is playing a large role.³ For the first guideline regarding recommendations for those with severe AD and/or egg allergy, the quality of evidence is deemed moderate, while the contribution of expert opinion is listed as significant. For the second and third guidelines regarding recommendations for mild to moderate AD and those without AD, respectively, the quality of evidence is low and expert opinion is again listed as significant.³

Importantly, delineating severe AD from moderate disease—which is necessary because only severe AD warrants evaluation with peanut sIgE and/or SPT—can be difficult, as the distinction relies on a degree of subjectivity that may vary between specialists. Indeed, 2 publications suggest extending the definition of severe AD to include infants with early-onset AD (<3 months of age) and those with moderate AD not responding to treatment.^16,17

Despite these reservations, the updated guidelines represent a breakthrough in understanding in an area truly in need of advancement. Although the evidence may not be exactly extraordinary, the context for these developments and our deeper understanding suggest that we do indeed live in extraordinary times. 

It has been said that “extraordinary claims require extraordinary evidence.”¹ In the pursuit of evidence-based medicine, we are encouraged to follow a similar standard, with an emphasis on waiting for multiple studies with good-quality data and high levels of agreement before changing any aspect of our clinical practice. The ostensible purpose is that studies can be flawed, conclusions can be incorrect, or biases can be overlooked. In such cases, acting on questionable results could imperil patients. It is for this reason that so many review articles sometimes frustratingly seem to conclude that further evidence is needed.²

Based on this standard, recently published addendum guidelines from the National Institute of Allergy and Infectious Diseases for prevention of peanut allergy in the United States³ are somewhat striking in that they make fairly bold recommendations based on results from the 2015 Learning Early about Peanut Allergy (LEAP) study,⁴ a randomized trial evaluating early peanut introduction as a preventive strategy for peanut allergy. Of note, this study was not placebo controlled, was conducted at only 1 site in the United Kingdom, and only included 640 children, though the number of participants was admittedly large for this type of study.⁴ Arguably, the LEAP study alone does not provide enough evidence upon which to base what essentially amounts to an about-face in the official recommendations for prevention of peanut and other food allergies, which emphasized delayed introduction of high-risk foods, especially in high-risk individuals.^5-7 To better understand this shift, we need to briefly explore the context of the addendum guidelines.

As many as one-third of pediatric patients with atopic dermatitis (AD) have food allergies, thus diet often is invoked by patients and providers alike as an underlying cause of the disease.⁸ Many patients in my practice are so focused on potential food allergies that actual treatment of the affected skin is marginalized and often dismissed as a stopgap that does not address the root of the problem. A 2004 study of 100 children with AD found that diet was manipulated by the parents in 75% of patients in an attempt to manage the disease.⁹

Patients are not the only ones who consider food allergies to be a driving force in AD. The medical literature indicates that this theory has existed for centuries; for instance, with regard to the relationship between diet and AD, the author of an article from 1830 quipped, “There is probably no subject in which more deeply rooted convictions have been held . . . than the connection between diet and disease, both as regards the causation and treatment of the latter . . .”¹⁰ More apropos perhaps is a statement from the 2010 National Institute of Allergy and Infectious Diseases guidelines on food allergy management, which noted that while the expert group “does not mean to imply that AD results from [food allergies], the role of [food allergies] in the pathogenesis and severity of this condition remains controversial.”¹¹

Prior to the LEAP study, food allergy recommendations for clinical practice in the United Kingdom in 1998¹² and the United States in 2000¹³ recommended excluding allergenic foods (eg, peanuts, tree nuts, soy, milk, eggs) from the diet in infants with a family history of atopy until 3 years of age. However, those recommendations did not seem to be working, when in fact just the opposite was happening. From 1997 until the LEAP study was conducted in 2015, the prevalence of peanut allergy more than quadrupled and became the leading cause of anaphylaxis and death related to food allergy.¹⁴ Additionally, study after study concluded that elimination diets did not seem to help most patients with AD.¹⁵ As is required in good scientific thinking, when a hypothesis is proven false, other approaches must be considered.

The idea arose that perhaps delaying introduction of allergenic foods was the opposite of the answer.⁴ The LEAP study tested the notion that peanut allergies are rare in countries where peanuts are introduced early and if telling families to delay introduction of peanuts in infants might actually be causing development of a peanut allergy, and the tests bore fruit. It was found that giving infants peanut-containing foods resulted in a more than 80% reduction in peanut allergy at 5 years of age (P<.001).⁴ What was perhaps even more interesting was the connection between AD and peanut allergy. An important idea articulated in the LEAP study is in some ways revolutionary: Rather than foods causing AD, it could be that “early environmental exposure (through the skin) to peanut may account for early sensitization, whereas early oral exposure may lead to immune tolerance.”⁴ This concept—that impaired eczematous skin may actually lead to the development of food allergies—turns the whole thing upside down.

What do these updated guidelines actually suggest? The first guideline focuses on infants with severe AD, egg allergy, or both, who therefore are thought to be at the highest risk for developing peanut allergy.³ Because of the higher baseline risk in this subgroup, measurement of the peanut-specific IgE (peanut sIgE) level, skin prick testing (SPT), or both is strongly recommended before introducing peanut protein into the diet. This testing can be performed by qualified providers as a screening measure, but if positive (≥0.35 kU_A/L for peanut sIgE or >2 mm on the peanut SPT), referral to an allergy specialist is warranted. If these studies are negative, it is thought the likelihood of peanut allergy is low, and it is recommended that caregivers introduce age-appropriate peanut-containing foods (eg, peanut butter snack puffs, diluted peanut butter) as early as 4 to 6 months of age. The second guideline recommends that peanut-containing foods should be introduced into the diets of infants with mild or moderate AD at approximately 6 months of age without the need for prior screening via peanut sIgE or SPT. Lastly, the third guideline recommends that caregivers freely introduce peanut-containing foods together with other solid foods in infants without AD or food allergies in accordance with family preference.³

The results of the LEAP study are certainly exciting, and although the theoretical basis makes good scientific sense and the updated guidelines truly address an important and growing problem, there are several issues with this update that are worth considering. Given the constraints of the LEAP study, it certainly seems possible that the results will not be applicable to all populations or foods. More research is needed to ensure that this robust finding applies to other children and to explore the introduction of other allergenic foods, which the LEAP study investigators also emphasized.⁴

In fairness, the updated guidelines clearly state the quality of evidence of their recommendations and make it clear that expert opinion is playing a large role.³ For the first guideline regarding recommendations for those with severe AD and/or egg allergy, the quality of evidence is deemed moderate, while the contribution of expert opinion is listed as significant. For the second and third guidelines regarding recommendations for mild to moderate AD and those without AD, respectively, the quality of evidence is low and expert opinion is again listed as significant.³

Importantly, delineating severe AD from moderate disease—which is necessary because only severe AD warrants evaluation with peanut sIgE and/or SPT—can be difficult, as the distinction relies on a degree of subjectivity that may vary between specialists. Indeed, 2 publications suggest extending the definition of severe AD to include infants with early-onset AD (<3 months of age) and those with moderate AD not responding to treatment.^16,17

Despite these reservations, the updated guidelines represent a breakthrough in understanding in an area truly in need of advancement. Although the evidence may not be exactly extraordinary, the context for these developments and our deeper understanding suggest that we do indeed live in extraordinary times. 

SAN FRANCISCO – Long-term use of statins may protect against lethal forms of prostate cancer by altering the inflammatory profile of the tumor microenvironment, according to the results of a new genetic analysis of prostate cancers in men in the Health Professionals Follow Up Study.

A previous analysis from the Health Professionals Follow Up Study published in 2015 showed no difference in the risk of lethal prostate cancer for those who began using statins after diagnosis of their tumors.

Jim Kling/MDedge News

There was no association between lethality and ERG-positive or ERG-negative status. Those who used statins for more than 5 years were less likely to have a PTEN-null tumor (hazard ratio, 0.42; 95% confidence interval, 0.20-0.90) but not more likely to have a PTEN-positive tumor (HR, 1.18; 95% CI, 0.95-1.46).

Compared with never users, long-term statin users also were less likely to have advanced prostate cancer (multivariate analysis, HR, 0.62; 95% CI, 0.45-0.85) as well as lethal prostate cancer (HR, 0.52; 95% CI, 0.35-0.78).

The researchers conducted a gene set enrichment analysis in statin users and found an enrichment of T-cell, B-cell, and PI3K signaling in tumor-adjacent normal prostate tissue, as well as other changes. “We think maybe there’s a microenvironment inflammation component to the mechanism through which statins are associated with lower risk of lethal prostate cancer,” said Dr. Allott.

The molecular data could identify patient subgroups that could benefit from statins. Dr. Allott said that is the goal, but it will take time. “That’s more obviously translatable to the clinic, but we don’t yet have enough data in this cohort to look at that.”

SOURCE: Allott E et al. AUA 2018, Abstract MP21-01.

SAN FRANCISCO – Long-term use of statins may protect against lethal forms of prostate cancer by altering the inflammatory profile of the tumor microenvironment, according to the results of a new genetic analysis of prostate cancers in men in the Health Professionals Follow Up Study.

A previous analysis from the Health Professionals Follow Up Study published in 2015 showed no difference in the risk of lethal prostate cancer for those who began using statins after diagnosis of their tumors.

Jim Kling/MDedge News

There was no association between lethality and ERG-positive or ERG-negative status. Those who used statins for more than 5 years were less likely to have a PTEN-null tumor (hazard ratio, 0.42; 95% confidence interval, 0.20-0.90) but not more likely to have a PTEN-positive tumor (HR, 1.18; 95% CI, 0.95-1.46).

Compared with never users, long-term statin users also were less likely to have advanced prostate cancer (multivariate analysis, HR, 0.62; 95% CI, 0.45-0.85) as well as lethal prostate cancer (HR, 0.52; 95% CI, 0.35-0.78).

The researchers conducted a gene set enrichment analysis in statin users and found an enrichment of T-cell, B-cell, and PI3K signaling in tumor-adjacent normal prostate tissue, as well as other changes. “We think maybe there’s a microenvironment inflammation component to the mechanism through which statins are associated with lower risk of lethal prostate cancer,” said Dr. Allott.

The molecular data could identify patient subgroups that could benefit from statins. Dr. Allott said that is the goal, but it will take time. “That’s more obviously translatable to the clinic, but we don’t yet have enough data in this cohort to look at that.”

SOURCE: Allott E et al. AUA 2018, Abstract MP21-01.

SAN FRANCISCO – Long-term use of statins may protect against lethal forms of prostate cancer by altering the inflammatory profile of the tumor microenvironment, according to the results of a new genetic analysis of prostate cancers in men in the Health Professionals Follow Up Study.

A previous analysis from the Health Professionals Follow Up Study published in 2015 showed no difference in the risk of lethal prostate cancer for those who began using statins after diagnosis of their tumors.

Jim Kling/MDedge News

There was no association between lethality and ERG-positive or ERG-negative status. Those who used statins for more than 5 years were less likely to have a PTEN-null tumor (hazard ratio, 0.42; 95% confidence interval, 0.20-0.90) but not more likely to have a PTEN-positive tumor (HR, 1.18; 95% CI, 0.95-1.46).

Compared with never users, long-term statin users also were less likely to have advanced prostate cancer (multivariate analysis, HR, 0.62; 95% CI, 0.45-0.85) as well as lethal prostate cancer (HR, 0.52; 95% CI, 0.35-0.78).

The researchers conducted a gene set enrichment analysis in statin users and found an enrichment of T-cell, B-cell, and PI3K signaling in tumor-adjacent normal prostate tissue, as well as other changes. “We think maybe there’s a microenvironment inflammation component to the mechanism through which statins are associated with lower risk of lethal prostate cancer,” said Dr. Allott.

The molecular data could identify patient subgroups that could benefit from statins. Dr. Allott said that is the goal, but it will take time. “That’s more obviously translatable to the clinic, but we don’t yet have enough data in this cohort to look at that.”

SOURCE: Allott E et al. AUA 2018, Abstract MP21-01.

The Trump administration on June 4 released a Medicaid “scorecard” intended to show how the nation’s largest health program is performing. But the nation’s top Medicaid official didn’t want to draw any conclusions.

“This is about bringing a level of transparency and accountability to the Medicaid program that we have never had before,” said Seema Verma, administrator of the Centers for Medicare & Medicaid Services.

Yet in a meeting with reporters, Ms. Verma refused to discuss the findings in any detail or comment on any individual states that performed poorly or exceptionally.

“I will let you look at the data and make your own conclusions,” she told journalists a few minutes before the report was posted online.

When reporters pressed Ms. Verma to comment on the document, she refused to give an assessment of the Medicaid program, the federal-state health program for low-income residents. She has run Medicaid for the past 15 months.

“The idea here is to give you a sense of where states are on different areas,” she said. “The idea is to be used for best practices,” and it’s “an opportunity for us to identify” and have discussions with states that aren’t performing well.

Medicaid covers about 75 million people, about half of them children.

KHN’s coverage of children’s health care issues is supported in part by the Heising-Simons Foundation. Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.

The Trump administration on June 4 released a Medicaid “scorecard” intended to show how the nation’s largest health program is performing. But the nation’s top Medicaid official didn’t want to draw any conclusions.

“This is about bringing a level of transparency and accountability to the Medicaid program that we have never had before,” said Seema Verma, administrator of the Centers for Medicare & Medicaid Services.

Yet in a meeting with reporters, Ms. Verma refused to discuss the findings in any detail or comment on any individual states that performed poorly or exceptionally.

“I will let you look at the data and make your own conclusions,” she told journalists a few minutes before the report was posted online.

When reporters pressed Ms. Verma to comment on the document, she refused to give an assessment of the Medicaid program, the federal-state health program for low-income residents. She has run Medicaid for the past 15 months.

“The idea here is to give you a sense of where states are on different areas,” she said. “The idea is to be used for best practices,” and it’s “an opportunity for us to identify” and have discussions with states that aren’t performing well.

Medicaid covers about 75 million people, about half of them children.

KHN’s coverage of children’s health care issues is supported in part by the Heising-Simons Foundation. Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.

The Trump administration on June 4 released a Medicaid “scorecard” intended to show how the nation’s largest health program is performing. But the nation’s top Medicaid official didn’t want to draw any conclusions.

“This is about bringing a level of transparency and accountability to the Medicaid program that we have never had before,” said Seema Verma, administrator of the Centers for Medicare & Medicaid Services.

Yet in a meeting with reporters, Ms. Verma refused to discuss the findings in any detail or comment on any individual states that performed poorly or exceptionally.

“I will let you look at the data and make your own conclusions,” she told journalists a few minutes before the report was posted online.

When reporters pressed Ms. Verma to comment on the document, she refused to give an assessment of the Medicaid program, the federal-state health program for low-income residents. She has run Medicaid for the past 15 months.

“The idea here is to give you a sense of where states are on different areas,” she said. “The idea is to be used for best practices,” and it’s “an opportunity for us to identify” and have discussions with states that aren’t performing well.

Medicaid covers about 75 million people, about half of them children.

KHN’s coverage of children’s health care issues is supported in part by the Heising-Simons Foundation. Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.

The Food and Drug Administration has approved pegfilgrastim-jmdb as the first biosimilar to pegfilgrastim (Neulasta) to decrease the chance of infection in patients with nonmyeloid cancer who are receiving myelosuppressive chemotherapy and are at risk of febrile neutropenia.

The approval is based on structural and functional characterization, animal study data, human pharmacokinetic and pharmacodynamic data, clinical immunogenicity data, and other clinical safety and effectiveness data that demonstrates pegfilgrastim-jmdb is biosimilar to pegfilgrastim, the FDA said in a statement.

[email protected]

The Food and Drug Administration has approved pegfilgrastim-jmdb as the first biosimilar to pegfilgrastim (Neulasta) to decrease the chance of infection in patients with nonmyeloid cancer who are receiving myelosuppressive chemotherapy and are at risk of febrile neutropenia.

The approval is based on structural and functional characterization, animal study data, human pharmacokinetic and pharmacodynamic data, clinical immunogenicity data, and other clinical safety and effectiveness data that demonstrates pegfilgrastim-jmdb is biosimilar to pegfilgrastim, the FDA said in a statement.

[email protected]

The Food and Drug Administration has approved pegfilgrastim-jmdb as the first biosimilar to pegfilgrastim (Neulasta) to decrease the chance of infection in patients with nonmyeloid cancer who are receiving myelosuppressive chemotherapy and are at risk of febrile neutropenia.

The approval is based on structural and functional characterization, animal study data, human pharmacokinetic and pharmacodynamic data, clinical immunogenicity data, and other clinical safety and effectiveness data that demonstrates pegfilgrastim-jmdb is biosimilar to pegfilgrastim, the FDA said in a statement.

[email protected]

PARIS – Follow-up data from a randomized trial of transcatheter versus surgical aortic valve replacement in low-surgical-risk patients with symptomatic severe aortic stenosis showed sustained superior hemodynamic valve performance and less structural valve deterioration in the transcatheter group through 6 years, Lars Sondergaard, MD, reported at the annual meeting of the European Association of Percutaneous Cardiovascular Interventions.

Moreover, the rate of bioprosthetic valve failure as formally defined in a recent European consensus statement (Eur Heart J. 2017 Dec 1;38[45]:3382-90) was similarly low in the transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR) arms at about 7%, in the randomized study known as NOTION (Nordic Aortic Valve Intervention), added Dr. Sondergaard, professor of cardiology at the University of Copenhagen, who was a coauthor of the consensus statement.

Bruce Jancin/MDedge News

The rate of moderate hemodynamic structural valve deterioration through 6 years of follow-up was 3.6% in the TAVR arm, compared with 23.7% in the SAVR group. The rate of nonstructural valve deterioration was 54.0% with TAVR and 57.8% with SAVR, and there were no cases of moderate or severe aortic regurgitation in either group.

The mean aortic valve gradient in the TAVR group went from 44.9 mm Hg at baseline to 12.2 mm Hg at 3 months and to 14.7 mm Hg at 6 years. In the SAVR group, the figures were 44.9 mm Hg, 8.3 mm Hg, and 9.9 mm Hg, respectively.

The effective orifice area in the TAVR group improved from 0.74 cm² at baseline to 1.37 cm² at 3 months and to 1.16 cm² at 6 years. With SAVR, the effective orifice area was 0.74 cm² at baseline, 1.66 cm² at 3 months, and 1.53 cm² at 6 years.

Through 6 years of follow-up, there were no cases of thrombosis in either study arm, and the rate of endocarditis was just under 6% in each group through 6 years. All-cause mortality through 6 years was 42.5% in the TAVR group, not significantly different from the 37.7% rate in the SAVR arm.

The valve-related death rate was 5.0% in the TAVR arm and similar at 3.7% with SAVR. Reintervention occurred in 2.2% of TAVR patients and in 0.7% of SAVR patients. Severe hemodynamic structural valve deterioration was documented in 0.7% of TAVR patients and 3.0% of SAVR patients. The overall rate of bioprosthetic valve failure – a composite of these three endpoints – was 7.5% with TAVR and similar at 6.7% with SAVR.

Session cochair Alain G. Cribier, MD, a TAVR pioneer who is professor of medicine and director of cardiology at Charles Nicolle Hospital, University of Rouen (France), declared, “This is extremely encouraging.”

However, discussant Corrado Tamburino, MD, was more circumspect.

[email protected]

PARIS – Follow-up data from a randomized trial of transcatheter versus surgical aortic valve replacement in low-surgical-risk patients with symptomatic severe aortic stenosis showed sustained superior hemodynamic valve performance and less structural valve deterioration in the transcatheter group through 6 years, Lars Sondergaard, MD, reported at the annual meeting of the European Association of Percutaneous Cardiovascular Interventions.

Moreover, the rate of bioprosthetic valve failure as formally defined in a recent European consensus statement (Eur Heart J. 2017 Dec 1;38[45]:3382-90) was similarly low in the transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR) arms at about 7%, in the randomized study known as NOTION (Nordic Aortic Valve Intervention), added Dr. Sondergaard, professor of cardiology at the University of Copenhagen, who was a coauthor of the consensus statement.

Bruce Jancin/MDedge News

The rate of moderate hemodynamic structural valve deterioration through 6 years of follow-up was 3.6% in the TAVR arm, compared with 23.7% in the SAVR group. The rate of nonstructural valve deterioration was 54.0% with TAVR and 57.8% with SAVR, and there were no cases of moderate or severe aortic regurgitation in either group.

The mean aortic valve gradient in the TAVR group went from 44.9 mm Hg at baseline to 12.2 mm Hg at 3 months and to 14.7 mm Hg at 6 years. In the SAVR group, the figures were 44.9 mm Hg, 8.3 mm Hg, and 9.9 mm Hg, respectively.

The effective orifice area in the TAVR group improved from 0.74 cm² at baseline to 1.37 cm² at 3 months and to 1.16 cm² at 6 years. With SAVR, the effective orifice area was 0.74 cm² at baseline, 1.66 cm² at 3 months, and 1.53 cm² at 6 years.

Through 6 years of follow-up, there were no cases of thrombosis in either study arm, and the rate of endocarditis was just under 6% in each group through 6 years. All-cause mortality through 6 years was 42.5% in the TAVR group, not significantly different from the 37.7% rate in the SAVR arm.

The valve-related death rate was 5.0% in the TAVR arm and similar at 3.7% with SAVR. Reintervention occurred in 2.2% of TAVR patients and in 0.7% of SAVR patients. Severe hemodynamic structural valve deterioration was documented in 0.7% of TAVR patients and 3.0% of SAVR patients. The overall rate of bioprosthetic valve failure – a composite of these three endpoints – was 7.5% with TAVR and similar at 6.7% with SAVR.

Session cochair Alain G. Cribier, MD, a TAVR pioneer who is professor of medicine and director of cardiology at Charles Nicolle Hospital, University of Rouen (France), declared, “This is extremely encouraging.”

However, discussant Corrado Tamburino, MD, was more circumspect.

[email protected]

PARIS – Follow-up data from a randomized trial of transcatheter versus surgical aortic valve replacement in low-surgical-risk patients with symptomatic severe aortic stenosis showed sustained superior hemodynamic valve performance and less structural valve deterioration in the transcatheter group through 6 years, Lars Sondergaard, MD, reported at the annual meeting of the European Association of Percutaneous Cardiovascular Interventions.

Moreover, the rate of bioprosthetic valve failure as formally defined in a recent European consensus statement (Eur Heart J. 2017 Dec 1;38[45]:3382-90) was similarly low in the transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR) arms at about 7%, in the randomized study known as NOTION (Nordic Aortic Valve Intervention), added Dr. Sondergaard, professor of cardiology at the University of Copenhagen, who was a coauthor of the consensus statement.

Bruce Jancin/MDedge News

The rate of moderate hemodynamic structural valve deterioration through 6 years of follow-up was 3.6% in the TAVR arm, compared with 23.7% in the SAVR group. The rate of nonstructural valve deterioration was 54.0% with TAVR and 57.8% with SAVR, and there were no cases of moderate or severe aortic regurgitation in either group.

The mean aortic valve gradient in the TAVR group went from 44.9 mm Hg at baseline to 12.2 mm Hg at 3 months and to 14.7 mm Hg at 6 years. In the SAVR group, the figures were 44.9 mm Hg, 8.3 mm Hg, and 9.9 mm Hg, respectively.

The effective orifice area in the TAVR group improved from 0.74 cm² at baseline to 1.37 cm² at 3 months and to 1.16 cm² at 6 years. With SAVR, the effective orifice area was 0.74 cm² at baseline, 1.66 cm² at 3 months, and 1.53 cm² at 6 years.

Through 6 years of follow-up, there were no cases of thrombosis in either study arm, and the rate of endocarditis was just under 6% in each group through 6 years. All-cause mortality through 6 years was 42.5% in the TAVR group, not significantly different from the 37.7% rate in the SAVR arm.

The valve-related death rate was 5.0% in the TAVR arm and similar at 3.7% with SAVR. Reintervention occurred in 2.2% of TAVR patients and in 0.7% of SAVR patients. Severe hemodynamic structural valve deterioration was documented in 0.7% of TAVR patients and 3.0% of SAVR patients. The overall rate of bioprosthetic valve failure – a composite of these three endpoints – was 7.5% with TAVR and similar at 6.7% with SAVR.

Session cochair Alain G. Cribier, MD, a TAVR pioneer who is professor of medicine and director of cardiology at Charles Nicolle Hospital, University of Rouen (France), declared, “This is extremely encouraging.”

However, discussant Corrado Tamburino, MD, was more circumspect.

[email protected]