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Multidisciplinary care improves surgical outcomes for elderly patients
and were able to leave the hospital after a shorter stay, according to findings from a case-control study of nearly 400 patients.
Data from previous studies suggest that preoperative assessment by geriatric experts can improve outcomes for the elderly, who are more likely than are younger patients to develop preventable postoperative complications, and “this evidence supports the formulation of a different approach to preoperative assessment and postoperative care for this population,” wrote Shelley R. McDonald, DO, of Duke University, Durham, N.C., and colleagues.
The intervention, known as the Perioperative Optimization of Senior Health (POSH), was described as “a quality improvement initiative with prospective data collection.” Patients in a geriatrics clinic within an academic center were selected for the study if they were at high risk for complications linked to elective abdominal surgery. High risk was defined as older than 85 years of age, or older than 65 years of age with conditions including cognitive impairment, recent weight loss, multiple comorbidities, and polypharmacy (JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5513).
The POSH intervention patients received preoperative evaluation from a team including a geriatrician, geriatric resource nurse, social worker, program administrator, and nurse practitioner from the preoperative anesthesia testing clinic. Patients and families were advised on risk management and care optimization involving cognition, comorbidities, medications, mobility, functional status, nutrition, hydration, pain, and advanced care planning.
Patients in the POSH group were on average older, had more comorbidities, and were more likely to be smokers. But despite these disadvantaging characteristics, they still had better outcomes in several important variables than did those in the control group.
The POSH group had significantly shorter hospital stays, compared with controls (4 days vs. 6 days), and significantly lower all-cause readmission rates at both 7 days (2.8% vs. 9.9%) and 30 days (7.8% vs. 18.3%). The significance persisted whether the surgeries were laparoscopic or open.
The overall complication rate was lower in the POSH group, compared with the controls, but fell short of statistical significance (44.8% vs. 58.7%, P = .01). However, rates of specific complications were significantly lower in the POSH group, compared with controls, including postoperative cardiogenic or hypovolemic shock (2.2% vs. 8.4%), bleeding, either during or after surgery (6.1% vs. 15.4%), and postoperative ileus (4.9% vs. 20.3%).
“Delirium was identified in POSH patients at higher rates than in the control group, which is not unexpected because higher postoperative delirium rates are known to be identified with increased screening,” the researchers noted. “Collaborative care allows for increasing the recognition of geriatric syndromes like delirium, more focus on symptom management, and proactively anticipating complications,” they said.
The study results were limited by several factors including a long enrollment period for the POSH patients, and potential changes in surgical protocols, the researchers said. However, the findings support the need for further research and more refined analysis to identify the most beneficial aspects of care, and to support better clinical decision making about the timing of interventions and the type of patient who could benefit, they noted.
The researchers had no financial conflicts to disclose. The John A. Hartford Foundation Center of Excellence National Program Award provided salary and database support.
SOURCE: McDonald S et al. JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5513.
and were able to leave the hospital after a shorter stay, according to findings from a case-control study of nearly 400 patients.
Data from previous studies suggest that preoperative assessment by geriatric experts can improve outcomes for the elderly, who are more likely than are younger patients to develop preventable postoperative complications, and “this evidence supports the formulation of a different approach to preoperative assessment and postoperative care for this population,” wrote Shelley R. McDonald, DO, of Duke University, Durham, N.C., and colleagues.
The intervention, known as the Perioperative Optimization of Senior Health (POSH), was described as “a quality improvement initiative with prospective data collection.” Patients in a geriatrics clinic within an academic center were selected for the study if they were at high risk for complications linked to elective abdominal surgery. High risk was defined as older than 85 years of age, or older than 65 years of age with conditions including cognitive impairment, recent weight loss, multiple comorbidities, and polypharmacy (JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5513).
The POSH intervention patients received preoperative evaluation from a team including a geriatrician, geriatric resource nurse, social worker, program administrator, and nurse practitioner from the preoperative anesthesia testing clinic. Patients and families were advised on risk management and care optimization involving cognition, comorbidities, medications, mobility, functional status, nutrition, hydration, pain, and advanced care planning.
Patients in the POSH group were on average older, had more comorbidities, and were more likely to be smokers. But despite these disadvantaging characteristics, they still had better outcomes in several important variables than did those in the control group.
The POSH group had significantly shorter hospital stays, compared with controls (4 days vs. 6 days), and significantly lower all-cause readmission rates at both 7 days (2.8% vs. 9.9%) and 30 days (7.8% vs. 18.3%). The significance persisted whether the surgeries were laparoscopic or open.
The overall complication rate was lower in the POSH group, compared with the controls, but fell short of statistical significance (44.8% vs. 58.7%, P = .01). However, rates of specific complications were significantly lower in the POSH group, compared with controls, including postoperative cardiogenic or hypovolemic shock (2.2% vs. 8.4%), bleeding, either during or after surgery (6.1% vs. 15.4%), and postoperative ileus (4.9% vs. 20.3%).
“Delirium was identified in POSH patients at higher rates than in the control group, which is not unexpected because higher postoperative delirium rates are known to be identified with increased screening,” the researchers noted. “Collaborative care allows for increasing the recognition of geriatric syndromes like delirium, more focus on symptom management, and proactively anticipating complications,” they said.
The study results were limited by several factors including a long enrollment period for the POSH patients, and potential changes in surgical protocols, the researchers said. However, the findings support the need for further research and more refined analysis to identify the most beneficial aspects of care, and to support better clinical decision making about the timing of interventions and the type of patient who could benefit, they noted.
The researchers had no financial conflicts to disclose. The John A. Hartford Foundation Center of Excellence National Program Award provided salary and database support.
SOURCE: McDonald S et al. JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5513.
and were able to leave the hospital after a shorter stay, according to findings from a case-control study of nearly 400 patients.
Data from previous studies suggest that preoperative assessment by geriatric experts can improve outcomes for the elderly, who are more likely than are younger patients to develop preventable postoperative complications, and “this evidence supports the formulation of a different approach to preoperative assessment and postoperative care for this population,” wrote Shelley R. McDonald, DO, of Duke University, Durham, N.C., and colleagues.
The intervention, known as the Perioperative Optimization of Senior Health (POSH), was described as “a quality improvement initiative with prospective data collection.” Patients in a geriatrics clinic within an academic center were selected for the study if they were at high risk for complications linked to elective abdominal surgery. High risk was defined as older than 85 years of age, or older than 65 years of age with conditions including cognitive impairment, recent weight loss, multiple comorbidities, and polypharmacy (JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5513).
The POSH intervention patients received preoperative evaluation from a team including a geriatrician, geriatric resource nurse, social worker, program administrator, and nurse practitioner from the preoperative anesthesia testing clinic. Patients and families were advised on risk management and care optimization involving cognition, comorbidities, medications, mobility, functional status, nutrition, hydration, pain, and advanced care planning.
Patients in the POSH group were on average older, had more comorbidities, and were more likely to be smokers. But despite these disadvantaging characteristics, they still had better outcomes in several important variables than did those in the control group.
The POSH group had significantly shorter hospital stays, compared with controls (4 days vs. 6 days), and significantly lower all-cause readmission rates at both 7 days (2.8% vs. 9.9%) and 30 days (7.8% vs. 18.3%). The significance persisted whether the surgeries were laparoscopic or open.
The overall complication rate was lower in the POSH group, compared with the controls, but fell short of statistical significance (44.8% vs. 58.7%, P = .01). However, rates of specific complications were significantly lower in the POSH group, compared with controls, including postoperative cardiogenic or hypovolemic shock (2.2% vs. 8.4%), bleeding, either during or after surgery (6.1% vs. 15.4%), and postoperative ileus (4.9% vs. 20.3%).
“Delirium was identified in POSH patients at higher rates than in the control group, which is not unexpected because higher postoperative delirium rates are known to be identified with increased screening,” the researchers noted. “Collaborative care allows for increasing the recognition of geriatric syndromes like delirium, more focus on symptom management, and proactively anticipating complications,” they said.
The study results were limited by several factors including a long enrollment period for the POSH patients, and potential changes in surgical protocols, the researchers said. However, the findings support the need for further research and more refined analysis to identify the most beneficial aspects of care, and to support better clinical decision making about the timing of interventions and the type of patient who could benefit, they noted.
The researchers had no financial conflicts to disclose. The John A. Hartford Foundation Center of Excellence National Program Award provided salary and database support.
SOURCE: McDonald S et al. JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5513.
FROM JAMA SURGERY
Key clinical point: A preoperative surgical intervention improved outcomes and shortened hospital stays for seniors.
Major finding: The POSH group had significantly shorter hospital stays compared with controls (4 days vs. 6 days).
Study details: The data come from a study of 183 surgery patients and 143 controls.
Disclosures: The researchers had no financial conflicts to disclose.
Source: McDonald S JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5513
Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview
Over the past few decades, there has been a dramatic increase in the number of shoulder arthroplasties performed around the world. This increase is the result of an aging and increasingly more active population, better implant technology, and the advent of reverse shoulder arthroplasty (RSA) for rotator cuff arthropathy. Additionally, as the indications for RSA have expanded to include pathologies such as rotator cuff insufficiency, chronic instabilities, trauma, and tumors, the number of arthroplasties will continue to increase. Although the results of most arthroplasties are good and predictable, any glenoid and/or humeral bone deficiencies can have detrimental effects on the clinical outcomes of these procedures. Bone loss becomes more of a problem in revision cases, and, as the number of primary arthroplasties increases, it follows that the number of revision procedures will also increase.
Many of the disease- or procedure-specific processes indicated for shoulder arthroplasty have predictable patterns of bone loss, especially on the glenoid side. Walch and colleagues1 and Bercik and colleagues2 made us aware that many patients with primary osteoarthritis have significant glenoid bone deformity. Similarly, there have been a number of first- and second-generation classification systems for delineating glenoid deformity in rotator cuff tear arthropathy and in revision settings. In revision settings, both glenoid and humeral bone deficiencies can occur as a result of implant removal, iatrogenic fracture, and even infection. Each of these bone loss patterns must be recognized and treated appropriately for the best surgical outcome.
The articles in this month of The American Journal of Orthopedics address the most up-to-date concepts and solutions regarding both humeral and glenoid bone loss in shoulder arthroplasty of all types.
HUMERAL BONE LOSS
Humeral bone loss is typically encountered in proximal humerus fractures, in revision surgery necessitating humeral component removal, and, less commonly, in tumors and infection.
In many displaced proximal humeral fractures indicated for shoulder arthroplasty, the bone is comminuted with displacement of the lesser and greater tuberosities. In these situations, failure of tuberosity healing may result in loss of rotator cuff function with loss of elevation, rotation, and even instability. Humeral shortening can also occur as a result of bone loss and can compromise deltoid function by loss of proper muscle tension, leading to instability, dysfunction, or both. In addition to possible instability, humeral shortening with metaphyseal bone loss can adversely affect long-term fixation of the humeral component, leading to stem loosening or failure. Cuff and colleagues3 showed significantly more rotational micromotion in cases lacking metaphyseal support, leading to aseptic loosening of the humeral stem.
Humeral bone loss can also result from humeral stem component removal in revision shoulder arthroplasty for infection, component failure or loosening, and even periprosthetic fracture resulting from surgery or trauma.
For the surgeon, humeral bone loss can create a complex set of circumstances related to rotator cuff attachment failure, soft-tissue balancing effects, and component fixation issues. Any such issue must be recognized and addressed for best outcomes. Best results can be obtained with preoperative imaging, planning, use of bone graft techniques, proximal humeral allografts, and, more recently, modular and patient-specific implants. All of these issues are discussed comprehensively in the articles this month.
Continue to: GLENOID BONE LOSS
GLENOID BONE LOSS
Proper glenoid component placement with durable fixation is crucial for success in anatomical total shoulder arthroplasty and RSA. Glenoid bone deformity and loss can result from intrinsic deformity characteristics seen in primary osteoarthritis, cuff tear arthropathy, or glenoid component removal in revision situations and infection. These bone deformity complications can be extremely difficult to treat and in some cases lead to catastrophic failure of the index arthroplasty.
We are now aware that one key to success in the face of moderate to severe deformity is proper recognition. Newer imaging techniques, including 2-dimensional (2-D) computed tomography (CT) and 3-dimensional (3-D) modeling and surgical planning software tools, which are outlined in an upcoming article, have given surgeons important new instruments that can help in treating these difficult cases.
Glenoid bone deformity in primary osteoarthritis was well delineated in the 1999 seminal study of CT changes by Walch and colleagues.1 The Walch classification system, which characterized glenoid morphology based on 2-D CT findings, was recently upgraded, based on 3-D imaging technology, to include Walch B3 and D patterns (Figure 1).2 Recognition of certain primary deformities in osteoarthritis has led to increased use of RSA in some cases of Walch B2, B3, and C deformities with substantial glenoid retroversion and/or humeral head subluxation.4
In cases of rotator cuff tear arthropathy, glenoid bone deformities are well described with several classification systems based on degree and dimension of bone insufficiency. The Hamada classification system defines the degree of medial glenoid erosion and superior bone loss, as well as acetabularization of the acromion in 5 grades; 5 Rispoli and colleagues6 defined and graded the degree of medicalization of the glenohumeral joint based on degree of subchondral plate erosion; and Visotsky and colleagues7 based their classification system on wear patterns of bone loss, alignment, and concomitant soft-tissue insufficiencies leading to instability and rotation loss.
In severe glenoid bone deficiency after glenoid component removal, Antuna and colleagues8 described the classic findings related to medial bone loss, anterior and posterior wall failure, and combinations thereof.
Continue to: All these classification systems...
All these classification systems are based on the 2-D appearance of the glenoid and should be considered cautiously. The glenoid is a complex 3-D structure that can be affected by any number of disease processes, trauma, and surgical intervention. Using more modern CT techniques and 3-D imaging, we now know that many deformities previously classified as unidirectional are, instead, complex and multidirectional.
Frankle and colleagues9 developed a classification based more 3-D CT models which has further classified severe glenoid vault deformities in relation to direction and degree of bone loss (Figures 2A-2E). Using this system, they were better able to determine degree and direction of deformity than in previous 2-D evaluations, and they were able to determine the amount of glenoid vault bone available for baseplate fixation. Scalise and colleagues10 further defined the influence of such 3-D planning in total shoulder arthroplasty.
With knowledge of these classification systems and use of contemporary imaging systems, shoulder arthroplasty in cases of severe glenoid deficiency can be more successful. Potentially, we can improve outcomes even more in the more severe cases of bone loss with use of patient-specific planning tools, including the guides and patient-specific implants that are now readily available with many implant systems.11
Preoperative planning tools, bone-grafting techniques, augmented and specialized glenoid and humeral implants, and patient-specific implants are discussed this month to give our readers a comprehensive review of the latest concepts in shoulder arthroplasty in cases of significant bone loss or deformity.
This month of The American Journal of Orthopedics presents the most current and cutting-edge solutions for humeral and glenoid bone deformities and deficiencies in contemporary shoulder arthroplasties.
1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
2. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.
3. Cuff D, Levy JC, Gutiérrez S, Frankle M. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651.
4. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598.
5. Hamada K, Fukuda H, Mikasa M, Kobayashi Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;(254):92-96.
6. Rispoli D, Sperling JW, Athwal GS, Schleck CD, Cofield RH. Humeral head replacement for the treatment of osteoarthritis. J Bone Joint Surg Am. 2006;88(12):2637-2644.
7. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.
8. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.
9. Frankle MA, Teramoto A, Luo ZP, Levy JC, Pupello D. Glenoid morphology in reverse shoulder arthroplasty: classification and surgical implications. J Shoulder Elbow Surg. 2009;18(6):874-885.
10. Scalise JJ, Codsi MJ, Bryan J, Brems JJ, Iannotti JP. The influence of three-dimensional computed tomography images of the shoulder in preoperative planning for total shoulder arthroplasty. J Bone Joint Surg Am. 2008;90(11):2438-2445.
11. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.
Authors’ Disclosure Statement: Dr. David M. Dines reports that he has a financial relationship involving royalties with Zimmer Biomet and Thieme Inc. Dr. Joshua S. Dines reports that he has a financial relationship with Arthrex, and receives royalties from Thieme Inc.
Dr. D.M. Dines is Co-Director, Shoulder Fellowship, and an Attending, Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Professor of Orthopedic Surgery, Weill Cornell Medical College, New York, New York. Dr. J.S. Dines is an Attending Orthopedic Surgeon, Shoulder Fellowship and Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Assistant Professor, Weill Cornell Medical College, New York, New York.
Address correspondence to: David M. Dines, MD, Hospital for Special Surgery, 535 E 70th Street, New York, NY 10021 (tel, 516-482-1037; email, [email protected]).
David M. Dines, MD Joshua S. Dines, MD . Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview. Am J Orthop. January 29, 2018
Authors’ Disclosure Statement: Dr. David M. Dines reports that he has a financial relationship involving royalties with Zimmer Biomet and Thieme Inc. Dr. Joshua S. Dines reports that he has a financial relationship with Arthrex, and receives royalties from Thieme Inc.
Dr. D.M. Dines is Co-Director, Shoulder Fellowship, and an Attending, Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Professor of Orthopedic Surgery, Weill Cornell Medical College, New York, New York. Dr. J.S. Dines is an Attending Orthopedic Surgeon, Shoulder Fellowship and Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Assistant Professor, Weill Cornell Medical College, New York, New York.
Address correspondence to: David M. Dines, MD, Hospital for Special Surgery, 535 E 70th Street, New York, NY 10021 (tel, 516-482-1037; email, [email protected]).
David M. Dines, MD Joshua S. Dines, MD . Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview. Am J Orthop. January 29, 2018
Authors’ Disclosure Statement: Dr. David M. Dines reports that he has a financial relationship involving royalties with Zimmer Biomet and Thieme Inc. Dr. Joshua S. Dines reports that he has a financial relationship with Arthrex, and receives royalties from Thieme Inc.
Dr. D.M. Dines is Co-Director, Shoulder Fellowship, and an Attending, Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Professor of Orthopedic Surgery, Weill Cornell Medical College, New York, New York. Dr. J.S. Dines is an Attending Orthopedic Surgeon, Shoulder Fellowship and Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Assistant Professor, Weill Cornell Medical College, New York, New York.
Address correspondence to: David M. Dines, MD, Hospital for Special Surgery, 535 E 70th Street, New York, NY 10021 (tel, 516-482-1037; email, [email protected]).
David M. Dines, MD Joshua S. Dines, MD . Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview. Am J Orthop. January 29, 2018
Over the past few decades, there has been a dramatic increase in the number of shoulder arthroplasties performed around the world. This increase is the result of an aging and increasingly more active population, better implant technology, and the advent of reverse shoulder arthroplasty (RSA) for rotator cuff arthropathy. Additionally, as the indications for RSA have expanded to include pathologies such as rotator cuff insufficiency, chronic instabilities, trauma, and tumors, the number of arthroplasties will continue to increase. Although the results of most arthroplasties are good and predictable, any glenoid and/or humeral bone deficiencies can have detrimental effects on the clinical outcomes of these procedures. Bone loss becomes more of a problem in revision cases, and, as the number of primary arthroplasties increases, it follows that the number of revision procedures will also increase.
Many of the disease- or procedure-specific processes indicated for shoulder arthroplasty have predictable patterns of bone loss, especially on the glenoid side. Walch and colleagues1 and Bercik and colleagues2 made us aware that many patients with primary osteoarthritis have significant glenoid bone deformity. Similarly, there have been a number of first- and second-generation classification systems for delineating glenoid deformity in rotator cuff tear arthropathy and in revision settings. In revision settings, both glenoid and humeral bone deficiencies can occur as a result of implant removal, iatrogenic fracture, and even infection. Each of these bone loss patterns must be recognized and treated appropriately for the best surgical outcome.
The articles in this month of The American Journal of Orthopedics address the most up-to-date concepts and solutions regarding both humeral and glenoid bone loss in shoulder arthroplasty of all types.
HUMERAL BONE LOSS
Humeral bone loss is typically encountered in proximal humerus fractures, in revision surgery necessitating humeral component removal, and, less commonly, in tumors and infection.
In many displaced proximal humeral fractures indicated for shoulder arthroplasty, the bone is comminuted with displacement of the lesser and greater tuberosities. In these situations, failure of tuberosity healing may result in loss of rotator cuff function with loss of elevation, rotation, and even instability. Humeral shortening can also occur as a result of bone loss and can compromise deltoid function by loss of proper muscle tension, leading to instability, dysfunction, or both. In addition to possible instability, humeral shortening with metaphyseal bone loss can adversely affect long-term fixation of the humeral component, leading to stem loosening or failure. Cuff and colleagues3 showed significantly more rotational micromotion in cases lacking metaphyseal support, leading to aseptic loosening of the humeral stem.
Humeral bone loss can also result from humeral stem component removal in revision shoulder arthroplasty for infection, component failure or loosening, and even periprosthetic fracture resulting from surgery or trauma.
For the surgeon, humeral bone loss can create a complex set of circumstances related to rotator cuff attachment failure, soft-tissue balancing effects, and component fixation issues. Any such issue must be recognized and addressed for best outcomes. Best results can be obtained with preoperative imaging, planning, use of bone graft techniques, proximal humeral allografts, and, more recently, modular and patient-specific implants. All of these issues are discussed comprehensively in the articles this month.
Continue to: GLENOID BONE LOSS
GLENOID BONE LOSS
Proper glenoid component placement with durable fixation is crucial for success in anatomical total shoulder arthroplasty and RSA. Glenoid bone deformity and loss can result from intrinsic deformity characteristics seen in primary osteoarthritis, cuff tear arthropathy, or glenoid component removal in revision situations and infection. These bone deformity complications can be extremely difficult to treat and in some cases lead to catastrophic failure of the index arthroplasty.
We are now aware that one key to success in the face of moderate to severe deformity is proper recognition. Newer imaging techniques, including 2-dimensional (2-D) computed tomography (CT) and 3-dimensional (3-D) modeling and surgical planning software tools, which are outlined in an upcoming article, have given surgeons important new instruments that can help in treating these difficult cases.
Glenoid bone deformity in primary osteoarthritis was well delineated in the 1999 seminal study of CT changes by Walch and colleagues.1 The Walch classification system, which characterized glenoid morphology based on 2-D CT findings, was recently upgraded, based on 3-D imaging technology, to include Walch B3 and D patterns (Figure 1).2 Recognition of certain primary deformities in osteoarthritis has led to increased use of RSA in some cases of Walch B2, B3, and C deformities with substantial glenoid retroversion and/or humeral head subluxation.4
In cases of rotator cuff tear arthropathy, glenoid bone deformities are well described with several classification systems based on degree and dimension of bone insufficiency. The Hamada classification system defines the degree of medial glenoid erosion and superior bone loss, as well as acetabularization of the acromion in 5 grades; 5 Rispoli and colleagues6 defined and graded the degree of medicalization of the glenohumeral joint based on degree of subchondral plate erosion; and Visotsky and colleagues7 based their classification system on wear patterns of bone loss, alignment, and concomitant soft-tissue insufficiencies leading to instability and rotation loss.
In severe glenoid bone deficiency after glenoid component removal, Antuna and colleagues8 described the classic findings related to medial bone loss, anterior and posterior wall failure, and combinations thereof.
Continue to: All these classification systems...
All these classification systems are based on the 2-D appearance of the glenoid and should be considered cautiously. The glenoid is a complex 3-D structure that can be affected by any number of disease processes, trauma, and surgical intervention. Using more modern CT techniques and 3-D imaging, we now know that many deformities previously classified as unidirectional are, instead, complex and multidirectional.
Frankle and colleagues9 developed a classification based more 3-D CT models which has further classified severe glenoid vault deformities in relation to direction and degree of bone loss (Figures 2A-2E). Using this system, they were better able to determine degree and direction of deformity than in previous 2-D evaluations, and they were able to determine the amount of glenoid vault bone available for baseplate fixation. Scalise and colleagues10 further defined the influence of such 3-D planning in total shoulder arthroplasty.
With knowledge of these classification systems and use of contemporary imaging systems, shoulder arthroplasty in cases of severe glenoid deficiency can be more successful. Potentially, we can improve outcomes even more in the more severe cases of bone loss with use of patient-specific planning tools, including the guides and patient-specific implants that are now readily available with many implant systems.11
Preoperative planning tools, bone-grafting techniques, augmented and specialized glenoid and humeral implants, and patient-specific implants are discussed this month to give our readers a comprehensive review of the latest concepts in shoulder arthroplasty in cases of significant bone loss or deformity.
This month of The American Journal of Orthopedics presents the most current and cutting-edge solutions for humeral and glenoid bone deformities and deficiencies in contemporary shoulder arthroplasties.
Over the past few decades, there has been a dramatic increase in the number of shoulder arthroplasties performed around the world. This increase is the result of an aging and increasingly more active population, better implant technology, and the advent of reverse shoulder arthroplasty (RSA) for rotator cuff arthropathy. Additionally, as the indications for RSA have expanded to include pathologies such as rotator cuff insufficiency, chronic instabilities, trauma, and tumors, the number of arthroplasties will continue to increase. Although the results of most arthroplasties are good and predictable, any glenoid and/or humeral bone deficiencies can have detrimental effects on the clinical outcomes of these procedures. Bone loss becomes more of a problem in revision cases, and, as the number of primary arthroplasties increases, it follows that the number of revision procedures will also increase.
Many of the disease- or procedure-specific processes indicated for shoulder arthroplasty have predictable patterns of bone loss, especially on the glenoid side. Walch and colleagues1 and Bercik and colleagues2 made us aware that many patients with primary osteoarthritis have significant glenoid bone deformity. Similarly, there have been a number of first- and second-generation classification systems for delineating glenoid deformity in rotator cuff tear arthropathy and in revision settings. In revision settings, both glenoid and humeral bone deficiencies can occur as a result of implant removal, iatrogenic fracture, and even infection. Each of these bone loss patterns must be recognized and treated appropriately for the best surgical outcome.
The articles in this month of The American Journal of Orthopedics address the most up-to-date concepts and solutions regarding both humeral and glenoid bone loss in shoulder arthroplasty of all types.
HUMERAL BONE LOSS
Humeral bone loss is typically encountered in proximal humerus fractures, in revision surgery necessitating humeral component removal, and, less commonly, in tumors and infection.
In many displaced proximal humeral fractures indicated for shoulder arthroplasty, the bone is comminuted with displacement of the lesser and greater tuberosities. In these situations, failure of tuberosity healing may result in loss of rotator cuff function with loss of elevation, rotation, and even instability. Humeral shortening can also occur as a result of bone loss and can compromise deltoid function by loss of proper muscle tension, leading to instability, dysfunction, or both. In addition to possible instability, humeral shortening with metaphyseal bone loss can adversely affect long-term fixation of the humeral component, leading to stem loosening or failure. Cuff and colleagues3 showed significantly more rotational micromotion in cases lacking metaphyseal support, leading to aseptic loosening of the humeral stem.
Humeral bone loss can also result from humeral stem component removal in revision shoulder arthroplasty for infection, component failure or loosening, and even periprosthetic fracture resulting from surgery or trauma.
For the surgeon, humeral bone loss can create a complex set of circumstances related to rotator cuff attachment failure, soft-tissue balancing effects, and component fixation issues. Any such issue must be recognized and addressed for best outcomes. Best results can be obtained with preoperative imaging, planning, use of bone graft techniques, proximal humeral allografts, and, more recently, modular and patient-specific implants. All of these issues are discussed comprehensively in the articles this month.
Continue to: GLENOID BONE LOSS
GLENOID BONE LOSS
Proper glenoid component placement with durable fixation is crucial for success in anatomical total shoulder arthroplasty and RSA. Glenoid bone deformity and loss can result from intrinsic deformity characteristics seen in primary osteoarthritis, cuff tear arthropathy, or glenoid component removal in revision situations and infection. These bone deformity complications can be extremely difficult to treat and in some cases lead to catastrophic failure of the index arthroplasty.
We are now aware that one key to success in the face of moderate to severe deformity is proper recognition. Newer imaging techniques, including 2-dimensional (2-D) computed tomography (CT) and 3-dimensional (3-D) modeling and surgical planning software tools, which are outlined in an upcoming article, have given surgeons important new instruments that can help in treating these difficult cases.
Glenoid bone deformity in primary osteoarthritis was well delineated in the 1999 seminal study of CT changes by Walch and colleagues.1 The Walch classification system, which characterized glenoid morphology based on 2-D CT findings, was recently upgraded, based on 3-D imaging technology, to include Walch B3 and D patterns (Figure 1).2 Recognition of certain primary deformities in osteoarthritis has led to increased use of RSA in some cases of Walch B2, B3, and C deformities with substantial glenoid retroversion and/or humeral head subluxation.4
In cases of rotator cuff tear arthropathy, glenoid bone deformities are well described with several classification systems based on degree and dimension of bone insufficiency. The Hamada classification system defines the degree of medial glenoid erosion and superior bone loss, as well as acetabularization of the acromion in 5 grades; 5 Rispoli and colleagues6 defined and graded the degree of medicalization of the glenohumeral joint based on degree of subchondral plate erosion; and Visotsky and colleagues7 based their classification system on wear patterns of bone loss, alignment, and concomitant soft-tissue insufficiencies leading to instability and rotation loss.
In severe glenoid bone deficiency after glenoid component removal, Antuna and colleagues8 described the classic findings related to medial bone loss, anterior and posterior wall failure, and combinations thereof.
Continue to: All these classification systems...
All these classification systems are based on the 2-D appearance of the glenoid and should be considered cautiously. The glenoid is a complex 3-D structure that can be affected by any number of disease processes, trauma, and surgical intervention. Using more modern CT techniques and 3-D imaging, we now know that many deformities previously classified as unidirectional are, instead, complex and multidirectional.
Frankle and colleagues9 developed a classification based more 3-D CT models which has further classified severe glenoid vault deformities in relation to direction and degree of bone loss (Figures 2A-2E). Using this system, they were better able to determine degree and direction of deformity than in previous 2-D evaluations, and they were able to determine the amount of glenoid vault bone available for baseplate fixation. Scalise and colleagues10 further defined the influence of such 3-D planning in total shoulder arthroplasty.
With knowledge of these classification systems and use of contemporary imaging systems, shoulder arthroplasty in cases of severe glenoid deficiency can be more successful. Potentially, we can improve outcomes even more in the more severe cases of bone loss with use of patient-specific planning tools, including the guides and patient-specific implants that are now readily available with many implant systems.11
Preoperative planning tools, bone-grafting techniques, augmented and specialized glenoid and humeral implants, and patient-specific implants are discussed this month to give our readers a comprehensive review of the latest concepts in shoulder arthroplasty in cases of significant bone loss or deformity.
This month of The American Journal of Orthopedics presents the most current and cutting-edge solutions for humeral and glenoid bone deformities and deficiencies in contemporary shoulder arthroplasties.
1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
2. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.
3. Cuff D, Levy JC, Gutiérrez S, Frankle M. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651.
4. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598.
5. Hamada K, Fukuda H, Mikasa M, Kobayashi Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;(254):92-96.
6. Rispoli D, Sperling JW, Athwal GS, Schleck CD, Cofield RH. Humeral head replacement for the treatment of osteoarthritis. J Bone Joint Surg Am. 2006;88(12):2637-2644.
7. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.
8. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.
9. Frankle MA, Teramoto A, Luo ZP, Levy JC, Pupello D. Glenoid morphology in reverse shoulder arthroplasty: classification and surgical implications. J Shoulder Elbow Surg. 2009;18(6):874-885.
10. Scalise JJ, Codsi MJ, Bryan J, Brems JJ, Iannotti JP. The influence of three-dimensional computed tomography images of the shoulder in preoperative planning for total shoulder arthroplasty. J Bone Joint Surg Am. 2008;90(11):2438-2445.
11. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.
1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
2. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.
3. Cuff D, Levy JC, Gutiérrez S, Frankle M. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651.
4. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598.
5. Hamada K, Fukuda H, Mikasa M, Kobayashi Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;(254):92-96.
6. Rispoli D, Sperling JW, Athwal GS, Schleck CD, Cofield RH. Humeral head replacement for the treatment of osteoarthritis. J Bone Joint Surg Am. 2006;88(12):2637-2644.
7. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.
8. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.
9. Frankle MA, Teramoto A, Luo ZP, Levy JC, Pupello D. Glenoid morphology in reverse shoulder arthroplasty: classification and surgical implications. J Shoulder Elbow Surg. 2009;18(6):874-885.
10. Scalise JJ, Codsi MJ, Bryan J, Brems JJ, Iannotti JP. The influence of three-dimensional computed tomography images of the shoulder in preoperative planning for total shoulder arthroplasty. J Bone Joint Surg Am. 2008;90(11):2438-2445.
11. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.
Society for Vascular Ultrasound, Society for Vascular Surgery and Medstreaming-M2S Introduce New Vascular Ultrasound Registry
The Society for Vascular Ultrasound (SVU), the Society for Vascular Surgery (SVS), and Medstreaming-M2S, announce the development of the Vascular Quality Initiative (VQI) Vascular Ultrasound Registry. This Registry represents an expansion of the SVS VQI which will combine noninvasive (vascular ultrasound) testing data with vascular treatment and outcomes data, making it possible to analyze the relationships between diagnosis and care provided to patients with vascular disease.
The Vascular Ultrasound Registry’s initial efforts will focus on collection and analysis of data associated with the diagnosis and treatment of carotid artery disease. The development of the registry and ongoing research related activities are being led by a VQI Vascular Ultrasound Registry Task Force, chaired by Drs. David Dawson and Gregory Moneta. Groundbreaking in this registry will be the inclusion of actual ultrasound images which will make future machine analysis and learning possible from the collected registry, which currently does not exist.
It is anticipated that the registry will provide the means and an impetus to promote vascular laboratory standardization and thereby improve patient care. “Non-invasive vascular testing has evolved to the point where it is being relied upon heavily to direct patient medical management decisions”, said James Wilkinson, SVU Executive Director. “With the rapid growth and diversification in the number of medical specialties providing testing, there is a lack of standardization in the delivery of testing and the reporting of results. Targeted, yet broad based research will significantly contribute to standardization efforts.”
Fundamental to the VQI Vascular Ultrasound Registry is the ability to link technical data and images to the clinical data collected from the SVS VQI’s existing registries. “The addition of the VQI Vascular Ultrasound Registry, to the existing VQI registries, will further aid the VQI’s mission of improving vascular care by enhancing the data we can make available to our members. We are also pleased that this registry expands the reach of the VQI to include vascular technologists, sonographers and other professionals in the vascular laboratory setting. The VQI has long embraced a team-approach to care with 59% of VQI membership coming from specialties outside of Vascular Surgery, including Cardiology and Radiology,” said Dr. Jens Eldrup-Jorgensen, Medical Director of the SVS Patient Safety Organization.
A key to the success of any registry is providing means for efficient data capture. The VQI Vascular Ultrasound Registry leverages the infrastructure of the preexisting registry with linkages to ultrasound images from the vascular laboratory. “Medstreaming-M2S’s specialty based workflow solutions, along with its clinical data management system for structured data aggregation can be used for uploading of data and images,” noted Wael Elseaidy, Medstreaming-M2S CEO. Initially, only a select number of current VQI sites will participate, but Vascular Ultrasound Registry participation is expected to be broadly available in the next phase of the program, along with an increase in registry content and scope of projects.
“Unique to the VQI Vascular Ultrasound Registry is the inclusion of an imaged based registry component, which will include the actual ultrasound images acquired during patient studies. When combined with powerful analytics and potential for machine learning, we foresee opportunity to normalize ultrasound image data submitted from different sites, develop new benchmarking standards, further explore and promote utilization of all the information embedded in the images, and provide the ultrasound industry with an entirely new platform from which to conduct research and drive product development,” Elseaidy continued.
Ultimately, the Registry will provide opportunity for VQI members to improve quality and conduct additional research regarding vascular ultrasound. “The Registry will provide greater opportunity for members to participate in research, whether through contribution of data pertaining to Society sponsored research projects or their own projects utilizing Registry data, all with the overall objective of quality improvement and better patient care,” Wilkinson concluded.
The Society for Vascular Ultrasound (SVU), the Society for Vascular Surgery (SVS), and Medstreaming-M2S, announce the development of the Vascular Quality Initiative (VQI) Vascular Ultrasound Registry. This Registry represents an expansion of the SVS VQI which will combine noninvasive (vascular ultrasound) testing data with vascular treatment and outcomes data, making it possible to analyze the relationships between diagnosis and care provided to patients with vascular disease.
The Vascular Ultrasound Registry’s initial efforts will focus on collection and analysis of data associated with the diagnosis and treatment of carotid artery disease. The development of the registry and ongoing research related activities are being led by a VQI Vascular Ultrasound Registry Task Force, chaired by Drs. David Dawson and Gregory Moneta. Groundbreaking in this registry will be the inclusion of actual ultrasound images which will make future machine analysis and learning possible from the collected registry, which currently does not exist.
It is anticipated that the registry will provide the means and an impetus to promote vascular laboratory standardization and thereby improve patient care. “Non-invasive vascular testing has evolved to the point where it is being relied upon heavily to direct patient medical management decisions”, said James Wilkinson, SVU Executive Director. “With the rapid growth and diversification in the number of medical specialties providing testing, there is a lack of standardization in the delivery of testing and the reporting of results. Targeted, yet broad based research will significantly contribute to standardization efforts.”
Fundamental to the VQI Vascular Ultrasound Registry is the ability to link technical data and images to the clinical data collected from the SVS VQI’s existing registries. “The addition of the VQI Vascular Ultrasound Registry, to the existing VQI registries, will further aid the VQI’s mission of improving vascular care by enhancing the data we can make available to our members. We are also pleased that this registry expands the reach of the VQI to include vascular technologists, sonographers and other professionals in the vascular laboratory setting. The VQI has long embraced a team-approach to care with 59% of VQI membership coming from specialties outside of Vascular Surgery, including Cardiology and Radiology,” said Dr. Jens Eldrup-Jorgensen, Medical Director of the SVS Patient Safety Organization.
A key to the success of any registry is providing means for efficient data capture. The VQI Vascular Ultrasound Registry leverages the infrastructure of the preexisting registry with linkages to ultrasound images from the vascular laboratory. “Medstreaming-M2S’s specialty based workflow solutions, along with its clinical data management system for structured data aggregation can be used for uploading of data and images,” noted Wael Elseaidy, Medstreaming-M2S CEO. Initially, only a select number of current VQI sites will participate, but Vascular Ultrasound Registry participation is expected to be broadly available in the next phase of the program, along with an increase in registry content and scope of projects.
“Unique to the VQI Vascular Ultrasound Registry is the inclusion of an imaged based registry component, which will include the actual ultrasound images acquired during patient studies. When combined with powerful analytics and potential for machine learning, we foresee opportunity to normalize ultrasound image data submitted from different sites, develop new benchmarking standards, further explore and promote utilization of all the information embedded in the images, and provide the ultrasound industry with an entirely new platform from which to conduct research and drive product development,” Elseaidy continued.
Ultimately, the Registry will provide opportunity for VQI members to improve quality and conduct additional research regarding vascular ultrasound. “The Registry will provide greater opportunity for members to participate in research, whether through contribution of data pertaining to Society sponsored research projects or their own projects utilizing Registry data, all with the overall objective of quality improvement and better patient care,” Wilkinson concluded.
The Society for Vascular Ultrasound (SVU), the Society for Vascular Surgery (SVS), and Medstreaming-M2S, announce the development of the Vascular Quality Initiative (VQI) Vascular Ultrasound Registry. This Registry represents an expansion of the SVS VQI which will combine noninvasive (vascular ultrasound) testing data with vascular treatment and outcomes data, making it possible to analyze the relationships between diagnosis and care provided to patients with vascular disease.
The Vascular Ultrasound Registry’s initial efforts will focus on collection and analysis of data associated with the diagnosis and treatment of carotid artery disease. The development of the registry and ongoing research related activities are being led by a VQI Vascular Ultrasound Registry Task Force, chaired by Drs. David Dawson and Gregory Moneta. Groundbreaking in this registry will be the inclusion of actual ultrasound images which will make future machine analysis and learning possible from the collected registry, which currently does not exist.
It is anticipated that the registry will provide the means and an impetus to promote vascular laboratory standardization and thereby improve patient care. “Non-invasive vascular testing has evolved to the point where it is being relied upon heavily to direct patient medical management decisions”, said James Wilkinson, SVU Executive Director. “With the rapid growth and diversification in the number of medical specialties providing testing, there is a lack of standardization in the delivery of testing and the reporting of results. Targeted, yet broad based research will significantly contribute to standardization efforts.”
Fundamental to the VQI Vascular Ultrasound Registry is the ability to link technical data and images to the clinical data collected from the SVS VQI’s existing registries. “The addition of the VQI Vascular Ultrasound Registry, to the existing VQI registries, will further aid the VQI’s mission of improving vascular care by enhancing the data we can make available to our members. We are also pleased that this registry expands the reach of the VQI to include vascular technologists, sonographers and other professionals in the vascular laboratory setting. The VQI has long embraced a team-approach to care with 59% of VQI membership coming from specialties outside of Vascular Surgery, including Cardiology and Radiology,” said Dr. Jens Eldrup-Jorgensen, Medical Director of the SVS Patient Safety Organization.
A key to the success of any registry is providing means for efficient data capture. The VQI Vascular Ultrasound Registry leverages the infrastructure of the preexisting registry with linkages to ultrasound images from the vascular laboratory. “Medstreaming-M2S’s specialty based workflow solutions, along with its clinical data management system for structured data aggregation can be used for uploading of data and images,” noted Wael Elseaidy, Medstreaming-M2S CEO. Initially, only a select number of current VQI sites will participate, but Vascular Ultrasound Registry participation is expected to be broadly available in the next phase of the program, along with an increase in registry content and scope of projects.
“Unique to the VQI Vascular Ultrasound Registry is the inclusion of an imaged based registry component, which will include the actual ultrasound images acquired during patient studies. When combined with powerful analytics and potential for machine learning, we foresee opportunity to normalize ultrasound image data submitted from different sites, develop new benchmarking standards, further explore and promote utilization of all the information embedded in the images, and provide the ultrasound industry with an entirely new platform from which to conduct research and drive product development,” Elseaidy continued.
Ultimately, the Registry will provide opportunity for VQI members to improve quality and conduct additional research regarding vascular ultrasound. “The Registry will provide greater opportunity for members to participate in research, whether through contribution of data pertaining to Society sponsored research projects or their own projects utilizing Registry data, all with the overall objective of quality improvement and better patient care,” Wilkinson concluded.
First 2018 Membership Application Deadline is March 1
To improve access, efficiency and service to existing and future SVS members, the Society is now reviewing and approving membership applications quarterly, instead of yearly. The first deadline for 2018 is March 1.
Learn more at vsweb.org/JoinSVS and apply today.
To improve access, efficiency and service to existing and future SVS members, the Society is now reviewing and approving membership applications quarterly, instead of yearly. The first deadline for 2018 is March 1.
Learn more at vsweb.org/JoinSVS and apply today.
To improve access, efficiency and service to existing and future SVS members, the Society is now reviewing and approving membership applications quarterly, instead of yearly. The first deadline for 2018 is March 1.
Learn more at vsweb.org/JoinSVS and apply today.
Community-Practice Surgeons! Apply for YOUR Grant
There’s only a month left to apply for the new SVS Foundation grant program for our community practice members and designed at improving community health.
Applications are due March 1 for the new Community Awareness and Prevention Project Grant, intended to help members in community practice environments conduct projects that address wellness and disease prevention and emphasize patient education, public awareness or risk assessment.
Awardees will receive up to $10,000 for an innovative, community-based initiative. Priority will go to projects that will benefit under-served areas or that include community partnerships.
Learn more vsweb.org/CommunityGrants.
The new program complements the Foundation’s expanded mission, which includes not only basic research but also increased public awareness about vascular disease and treatments and efforts to improve patient vascular care.
There’s only a month left to apply for the new SVS Foundation grant program for our community practice members and designed at improving community health.
Applications are due March 1 for the new Community Awareness and Prevention Project Grant, intended to help members in community practice environments conduct projects that address wellness and disease prevention and emphasize patient education, public awareness or risk assessment.
Awardees will receive up to $10,000 for an innovative, community-based initiative. Priority will go to projects that will benefit under-served areas or that include community partnerships.
Learn more vsweb.org/CommunityGrants.
The new program complements the Foundation’s expanded mission, which includes not only basic research but also increased public awareness about vascular disease and treatments and efforts to improve patient vascular care.
There’s only a month left to apply for the new SVS Foundation grant program for our community practice members and designed at improving community health.
Applications are due March 1 for the new Community Awareness and Prevention Project Grant, intended to help members in community practice environments conduct projects that address wellness and disease prevention and emphasize patient education, public awareness or risk assessment.
Awardees will receive up to $10,000 for an innovative, community-based initiative. Priority will go to projects that will benefit under-served areas or that include community partnerships.
Learn more vsweb.org/CommunityGrants.
The new program complements the Foundation’s expanded mission, which includes not only basic research but also increased public awareness about vascular disease and treatments and efforts to improve patient vascular care.
Applications due Feb. 1 for VAM Scholarships, Research Fellowship
SVS members, please encourage medical or pre-med students interested in vascular surgery to apply for scholarships to attend the 2018 Vascular Annual Meeting. Scholarship applications are due by Feb. 1.
The awards are the General Surgery Resident/Medical Student Travel Scholarship and the Diversity Medical Student Travel Scholarship. Recipients become part of the hugely popular scholarship program, designed to let residents and students explore their interest in vascular surgery.
VAM will be held June 20 to 23, 2018, in Boston, with scientific sessions on June 21-23 and exhibits open June 21-22.)
The SVS Foundation seeks applicants for its Student Research Fellowship awards, designed to stimulate laboratory and clinical vascular research by undergraduate college students and medical students attending universities in the United States and Canada. Urge students you know with an interest in research to apply today.
SVS members, please encourage medical or pre-med students interested in vascular surgery to apply for scholarships to attend the 2018 Vascular Annual Meeting. Scholarship applications are due by Feb. 1.
The awards are the General Surgery Resident/Medical Student Travel Scholarship and the Diversity Medical Student Travel Scholarship. Recipients become part of the hugely popular scholarship program, designed to let residents and students explore their interest in vascular surgery.
VAM will be held June 20 to 23, 2018, in Boston, with scientific sessions on June 21-23 and exhibits open June 21-22.)
The SVS Foundation seeks applicants for its Student Research Fellowship awards, designed to stimulate laboratory and clinical vascular research by undergraduate college students and medical students attending universities in the United States and Canada. Urge students you know with an interest in research to apply today.
SVS members, please encourage medical or pre-med students interested in vascular surgery to apply for scholarships to attend the 2018 Vascular Annual Meeting. Scholarship applications are due by Feb. 1.
The awards are the General Surgery Resident/Medical Student Travel Scholarship and the Diversity Medical Student Travel Scholarship. Recipients become part of the hugely popular scholarship program, designed to let residents and students explore their interest in vascular surgery.
VAM will be held June 20 to 23, 2018, in Boston, with scientific sessions on June 21-23 and exhibits open June 21-22.)
The SVS Foundation seeks applicants for its Student Research Fellowship awards, designed to stimulate laboratory and clinical vascular research by undergraduate college students and medical students attending universities in the United States and Canada. Urge students you know with an interest in research to apply today.
Warn patients about the risk of misusing OTC pain meds
Roughly 8 in 10 Americans routinely reach for over-the-counter (OTC) pain pills to relieve headaches, backaches, sore muscles, fevers, or colds, according to a national poll by the American Gastroenterological Association (AGA). Most are unaware that these medications, if used incorrectly, can be just as dangerous as prescription drugs.
In my GI practice, I often see cases of accidental OTC pain medicine overdose that have caused stomach bleeding, ulcers, liver damage, and even liver failure. And, I am not alone – the poll found that gastroenterologists see, on average, nearly two patients per week with complications from OTC pain pills.
As the nation’s attention is focused on the opioid crisis, and with good reason, we cannot forget about the risks associated with OTC pain medicines. While it may seem harmless to take more OTC medications than indicated, the body is not capable of absorbing higher doses of pain medicine ingredients at a faster rate.
According to the AGA’s survey, many people are confident they can manage symptoms on their own, without consulting a doctor. Yet, the same poll found that 39% of Americans knowingly took more than the recommended dosage. In most cases, they falsely believed that taking more OTC pain medicine than what was indicated on the label would help them “feel better faster.”
A short time ago, I treated a woman in her 20s who recently had dental surgery. She was taking Lortab, which is a combination of acetaminophen and hydrocodone, an opioid. But when she still felt pain, she took additional OTC acetaminophen to try to find faster relief. When I saw her, her liver tests were abnormal, her acetaminophen level was elevated, and she was feeling very nauseated. In trying to get faster pain relief, she unintentionally overdosed on OTC pain medicine.
To help patients avoid this kind of medication mishap, it’s vital that health care providers initiate conversations at every visit about the dangers of OTC pain medicine overdose. The following tips have helped me advise my patients and educate them on the associated risks:
• Encourage your patients to read and follow all medicine labels, even on OTC drugs – every time they reach for something in the medicine cabinet.
• Talk to your patients about the two main types of oral OTC pain medicines and make sure they know to take only one product at a time containing the same type of active ingredient.
• Ask about all medicines your patients take, including OTC medicines, as they may not know to tell you.
• Patients may not realize that their current health situation, age, and/or medical history can impact their risk for OTC pain medicine overdose. Let them know that products that worked in the past may no longer be the right choice for them now.
If more health care providers emphasized the dangers of incorrect usage of OTC pain medicines, we could easily help patients avoid the dangerous side effects of taking too much.
Dr. Wilcox is professor of medicine in the division of gastroenterology and hepatology at the University of Alabama at Birmingham and a chair of AGA’s Gut Check: Know Your Medicine campaign.
Roughly 8 in 10 Americans routinely reach for over-the-counter (OTC) pain pills to relieve headaches, backaches, sore muscles, fevers, or colds, according to a national poll by the American Gastroenterological Association (AGA). Most are unaware that these medications, if used incorrectly, can be just as dangerous as prescription drugs.
In my GI practice, I often see cases of accidental OTC pain medicine overdose that have caused stomach bleeding, ulcers, liver damage, and even liver failure. And, I am not alone – the poll found that gastroenterologists see, on average, nearly two patients per week with complications from OTC pain pills.
As the nation’s attention is focused on the opioid crisis, and with good reason, we cannot forget about the risks associated with OTC pain medicines. While it may seem harmless to take more OTC medications than indicated, the body is not capable of absorbing higher doses of pain medicine ingredients at a faster rate.
According to the AGA’s survey, many people are confident they can manage symptoms on their own, without consulting a doctor. Yet, the same poll found that 39% of Americans knowingly took more than the recommended dosage. In most cases, they falsely believed that taking more OTC pain medicine than what was indicated on the label would help them “feel better faster.”
A short time ago, I treated a woman in her 20s who recently had dental surgery. She was taking Lortab, which is a combination of acetaminophen and hydrocodone, an opioid. But when she still felt pain, she took additional OTC acetaminophen to try to find faster relief. When I saw her, her liver tests were abnormal, her acetaminophen level was elevated, and she was feeling very nauseated. In trying to get faster pain relief, she unintentionally overdosed on OTC pain medicine.
To help patients avoid this kind of medication mishap, it’s vital that health care providers initiate conversations at every visit about the dangers of OTC pain medicine overdose. The following tips have helped me advise my patients and educate them on the associated risks:
• Encourage your patients to read and follow all medicine labels, even on OTC drugs – every time they reach for something in the medicine cabinet.
• Talk to your patients about the two main types of oral OTC pain medicines and make sure they know to take only one product at a time containing the same type of active ingredient.
• Ask about all medicines your patients take, including OTC medicines, as they may not know to tell you.
• Patients may not realize that their current health situation, age, and/or medical history can impact their risk for OTC pain medicine overdose. Let them know that products that worked in the past may no longer be the right choice for them now.
If more health care providers emphasized the dangers of incorrect usage of OTC pain medicines, we could easily help patients avoid the dangerous side effects of taking too much.
Dr. Wilcox is professor of medicine in the division of gastroenterology and hepatology at the University of Alabama at Birmingham and a chair of AGA’s Gut Check: Know Your Medicine campaign.
Roughly 8 in 10 Americans routinely reach for over-the-counter (OTC) pain pills to relieve headaches, backaches, sore muscles, fevers, or colds, according to a national poll by the American Gastroenterological Association (AGA). Most are unaware that these medications, if used incorrectly, can be just as dangerous as prescription drugs.
In my GI practice, I often see cases of accidental OTC pain medicine overdose that have caused stomach bleeding, ulcers, liver damage, and even liver failure. And, I am not alone – the poll found that gastroenterologists see, on average, nearly two patients per week with complications from OTC pain pills.
As the nation’s attention is focused on the opioid crisis, and with good reason, we cannot forget about the risks associated with OTC pain medicines. While it may seem harmless to take more OTC medications than indicated, the body is not capable of absorbing higher doses of pain medicine ingredients at a faster rate.
According to the AGA’s survey, many people are confident they can manage symptoms on their own, without consulting a doctor. Yet, the same poll found that 39% of Americans knowingly took more than the recommended dosage. In most cases, they falsely believed that taking more OTC pain medicine than what was indicated on the label would help them “feel better faster.”
A short time ago, I treated a woman in her 20s who recently had dental surgery. She was taking Lortab, which is a combination of acetaminophen and hydrocodone, an opioid. But when she still felt pain, she took additional OTC acetaminophen to try to find faster relief. When I saw her, her liver tests were abnormal, her acetaminophen level was elevated, and she was feeling very nauseated. In trying to get faster pain relief, she unintentionally overdosed on OTC pain medicine.
To help patients avoid this kind of medication mishap, it’s vital that health care providers initiate conversations at every visit about the dangers of OTC pain medicine overdose. The following tips have helped me advise my patients and educate them on the associated risks:
• Encourage your patients to read and follow all medicine labels, even on OTC drugs – every time they reach for something in the medicine cabinet.
• Talk to your patients about the two main types of oral OTC pain medicines and make sure they know to take only one product at a time containing the same type of active ingredient.
• Ask about all medicines your patients take, including OTC medicines, as they may not know to tell you.
• Patients may not realize that their current health situation, age, and/or medical history can impact their risk for OTC pain medicine overdose. Let them know that products that worked in the past may no longer be the right choice for them now.
If more health care providers emphasized the dangers of incorrect usage of OTC pain medicines, we could easily help patients avoid the dangerous side effects of taking too much.
Dr. Wilcox is professor of medicine in the division of gastroenterology and hepatology at the University of Alabama at Birmingham and a chair of AGA’s Gut Check: Know Your Medicine campaign.
Support GI Research through the AGA Research Foundation
The way we diagnose and treat patients is thanks to years of research. Decades of research and discoveries by dedicated investigators have revolutionized the care of many digestive disease patients. As the charitable arm of the American Gastroenterological Association (AGA), the AGA Research Foundation contributes to this tradition of discovery.
Federal research funding is at risk. Promising early-stage investigators find it increasingly difficult to secure funding and many leave the field because they are unable to sustain a research career. The foundation provides a key source of funding at a critical juncture in a young investigator’s career.
“As a clinical researcher, funding for investigation is critical in scientific breakthroughs to promote more efficient and robust patient care. My project will provide novel insights into the role of distensibility in the treatment of patients with esophageal eosinophilia, potentially resulting in more efficient treatment selection and disease management.”
By joining others in donating to the AGA Research Foundation, you can help fill the funding gap and protect the next generation of investigators.
Your tax-deductible donation will make a critical difference in retaining talented GI scientists, like Dr. Kristle Lynch, whose research will impact the future care of patients.
Donate on the foundation’s website at www.gastro.org/donateonline or by mail to 4930 Del Ray Avenue, Bethesda, MD 20814.
The way we diagnose and treat patients is thanks to years of research. Decades of research and discoveries by dedicated investigators have revolutionized the care of many digestive disease patients. As the charitable arm of the American Gastroenterological Association (AGA), the AGA Research Foundation contributes to this tradition of discovery.
Federal research funding is at risk. Promising early-stage investigators find it increasingly difficult to secure funding and many leave the field because they are unable to sustain a research career. The foundation provides a key source of funding at a critical juncture in a young investigator’s career.
“As a clinical researcher, funding for investigation is critical in scientific breakthroughs to promote more efficient and robust patient care. My project will provide novel insights into the role of distensibility in the treatment of patients with esophageal eosinophilia, potentially resulting in more efficient treatment selection and disease management.”
By joining others in donating to the AGA Research Foundation, you can help fill the funding gap and protect the next generation of investigators.
Your tax-deductible donation will make a critical difference in retaining talented GI scientists, like Dr. Kristle Lynch, whose research will impact the future care of patients.
Donate on the foundation’s website at www.gastro.org/donateonline or by mail to 4930 Del Ray Avenue, Bethesda, MD 20814.
The way we diagnose and treat patients is thanks to years of research. Decades of research and discoveries by dedicated investigators have revolutionized the care of many digestive disease patients. As the charitable arm of the American Gastroenterological Association (AGA), the AGA Research Foundation contributes to this tradition of discovery.
Federal research funding is at risk. Promising early-stage investigators find it increasingly difficult to secure funding and many leave the field because they are unable to sustain a research career. The foundation provides a key source of funding at a critical juncture in a young investigator’s career.
“As a clinical researcher, funding for investigation is critical in scientific breakthroughs to promote more efficient and robust patient care. My project will provide novel insights into the role of distensibility in the treatment of patients with esophageal eosinophilia, potentially resulting in more efficient treatment selection and disease management.”
By joining others in donating to the AGA Research Foundation, you can help fill the funding gap and protect the next generation of investigators.
Your tax-deductible donation will make a critical difference in retaining talented GI scientists, like Dr. Kristle Lynch, whose research will impact the future care of patients.
Donate on the foundation’s website at www.gastro.org/donateonline or by mail to 4930 Del Ray Avenue, Bethesda, MD 20814.
Pseudo-Pedicle Heterotopic Ossification From Use of Recombinant Human Bone Morphogenetic Protein 2 (rhBMP-2) in Transforaminal Lumbar Interbody Fusion Cages
ABSTRACT
We conducted a study to determine the common characteristics of patients who developed radiculopathy symptoms and corresponding heterotopic ossification (HO) from transforaminal lumbar interbody fusions (TLIF) using recombinant human bone morphogenetic protein 2 (rhBMP-2). HO can arise from a disk space with rhBMP-2 use in TLIF. Formation of bone around nerve roots or the thecal sac can cause a radiculopathy with a consistent pattern of symptoms.
We identified 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years who developed radiculopathy symptoms and corresponding HO from TLIF with rhBMP-2 in the disk space between 2002 and 2015. To document this complication and improve its recognition, we recorded common patterns of symptom development and radiologic findings: specifically, time from implantation of rhBMP-2 to symptom development, consistency with side of TLIF placement, and radiologic findings.
Radicular pain generally developed a mean (SD) of 3.8 (1.0) months after TLIF with rhBMP-2. Development of radiculopathy symptoms corresponded to consistent “pseudo-pedicle”-like HO. In all 38 patients, HO arising from the annulotomy site showed a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. In addition, development of radiculopathy symptoms and corresponding HO appear to be independent of amount of rhBMP-2. HO resulting from TLIF with rhBMP-2 in the disk space is a pain generator and a recognizable complication that can be diagnosed by assessment of symptoms and computed tomography characteristics.
Continue to: Bone morphogenetic proteins...
Bone morphogenetic proteins (BMPs), first isolated by Urist in 19641, are a family of growth factors that stimulate the cascade of bone formation. Recombinant human BMP (rhBMP), specifically rhBMP-2 and rhBMP-7 (also known as osteogenic protein 1 [OP-1]), was developed in the 1990s after the advent of gene splicing. Then, in 2002, the US Food and Drug Administration (FDA) approved use of rhBMP to stimulate fusion in the human spine. Specifically, rhBMP-2 (Medtronic) was approved for use in combination with a specific brand of interbody cage in 1-level anterior lumbar interbody fusion.2 Over the past decade, off-label use of rhBMP-2 to achieve osseous union has increased dramatically, particularly in spinal surgery: transforaminal lumbar interbody fusion (TLIF), posterior lumbar interbody fusion, and posterolateral lumbar fusion.3-9 However, this widespread off-label use for posterior spinal fusion began despite FDA data indicating that specific complications were underreported in the peer-reviewed literature.10,11 Although rhBMP-2 is very effective in increasing osteoblast formation and improving osteogenesis and subsequent bone healing in spinal surgery,12,13 its use in TLIF resulted in significant adverse side effects, including radiculopathy with and without neuroforaminal heterotopic ossification (HO); 14-24 complications in the FDA studies; 14,22,25-27 and osteolysis causing intervertebral cage subsidence, inflammatory radiculitis, genitourinary complications, infections, possible systemic effects, and significant HO complications.10,28-30 Of these, HO complications involved rhBMP leakage through the annulotomy to the disk space that led to HO. Specifically, rhBMP leaked directly out of the disk space and formed a pillar of bone that encased the nerve roots and dura, which led to occlusion of the foramen and symptoms of radiculopathy.10,28-30
Despite this frequent finding of HO in the intervertebral space outside the target fusion area, use of rhBMP-2 with intervertebral cages increased so rapidly that rhBMP-2 was used more often than autologous bone.5,11,17,31 In this study, we reviewed the common characteristics of patients who developed HO and subsequent radiculopathy from TLIF with rhBMP.
METHODS
After this study received Institutional Review Board approval, we retrospectively reviewed cases of radiculopathy symptoms that developed after TLIF with rhBMP between January 2002 and January 2015. During this period, 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years and radiculopathy symptoms arising from TLIF with rhBMP-2 were identified to determine commonalities and defining characteristics that will help facilitate diagnosis.
Inclusion criteria were computed tomography (CT)–documented HO arising from the TLIF annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell with contouring around the thecal sac or nerve roots, as well as recurrence or initial occurrence of radiculopathy with signs and symptoms corresponding to the CT site of aberrant bone growth in terms of laterality and particular nerve root(s) involved. Exclusion criteria were malplacement of interbody cage or pedicle screws, disk herniation, systemic neuropathic disease, and new or unresolved radiculopathy immediately after index surgery.
To improve recognition of this complication, we also documented the amount of BMP used, common patterns of radiculopathy symptom development, and radiologic findings. Type and timing of radiculopathy symptom onset and consistency with side of TLIF placement were documented as well. Radiculopathy symptoms included shooting pain in the legs, incontinence, sexual dysfunction, and severe paralysis. Radiologic findings were specific to bone formation from the disk space (detected with CT).
Continue to: RESULTS
RESULTS
All 38 selected patients had radiculopathy symptoms from HO out of the intervertebral space. The Table lists the patients’ overall characteristics. The left side had the most radiculopathy symptoms (31/38 patients), followed by the right side (5/38) and both sides (2/38). Radiculopathy symptoms began a mean (SD) of 3.8 (1.0) months (range, 2-6 months) after index surgery. The 38 patients had 4 characteristics in common:
Table. Transforaminal Lumbar Interbody Fusion With Recombinant Human Bone Morphogenetic Protein 2: Onset Time for Radiculopathy Symptoms, Surgery Level, Side of Pseudo-Pedicle Bone Formation, and Subsequent Complications
| Pt | Sympton Onset, mo | Surgery Level(s) | Side(s) | Complication(s) |
| 1 | 3 | L3-L5 (2) | Both | Radiculopathy, pseudo-pedicle, urine |
| 2 | 3 | L4-L5 (2) | R | Radiculopathy, pseudo-pedicle |
| 3 | 4 | L5-S1 (1) | R | Radiculopathy, pseudo-pedicle |
| 4 | 5 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 5 | 4 | L4-S1 (2) | L | Radiculopathy, pseudo-pedicle, subsidence |
| 6 | 5 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 7 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 8 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 9 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 10 | 2 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 11 | 2 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, subsidence, neurologic |
| 12 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 13 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, neurologic |
| 14 | 2 | L2-L3 (1) | R | Radiculopathy, pseudo-pedicle |
| 15 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 16 | 3 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 17 | 3 | L2-L3, L4-L5 (2) | L | Radiculopathy, pseudo-pedicle |
| 18 | 3 | L4-L5, L2-L3 (1) | L | Radiculopathy, pseudo-pedicle, nonunion |
| 19 | 4 | L4-L5 (1) | R | Radiculopathy, pseudo-pedicle |
| 20 | 5 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 21 | 5 | L5-S1 (1) | R | Radiculopathy, pseudo-pedicle |
| 22 | 3 | L3-L4, L5-S1 (2) | Both | Radiculopathy, pseudo-pedicle |
| 23 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 24 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 25 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 26 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, urine, bowel |
| 27 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 28 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 29 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 30 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 31 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 32 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 33 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 34 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 35 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 36 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 37 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 38 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
1. Bone growing out of the annulotomy site for TLIF cage placement was present and in continuity with the disk space in 33 (87%) of the 38 cases. In the other 5 cases (13%), HO was present around the neural tissue, but not necessarily in continuity with the disk space. This bone appeared ectopic and not osteophytic and facet-related, as it formed a shell around either the nerve root or the thecal sac, contouring to the structure.
2. The common, novel finding on CT was a “pseudo-pedicle” (Figures 1A, 1B), which appeared as ectopic growth from the disk space—a solid piece of bone in the same direction as the anatomical pedicle. Confusing similarity to the anatomical pedicle is present on axial cuts and during surgery. The pseudo-pedicle varied in thickness and extent out of the disk space, but was always presented as a bar of bone arising from the annulotomy site. After arising from the disk space, the HO could disperse in any direction, further calcifying neural structures or the facet joints above or below. There was no apparent distinguishable repeating pattern, given the variable nature of arthritic facet changes, scoliotic deformities, size of annulotomies, amount of rhBMP used, and placement in cage and disk space or only in cage.
3. In 36 (95%) of the 38 cases, the initial interpretation of HO on magnetic resonance imaging (MRI) was of tissue other than bone, such as fibrous tissue, granulation tissue, recurrent disk herniation, or postoperative changes. However, this tissue was later determined to be bone from HO complications, which we confirmed with CT in all 38 cases. It is important to note that HO on MRI (Figures 2A, 2B) was initially interpreted by a radiologist as fibrous tissue, but same-level CT of the same case (Figures 3A, 3B) showed clear HO.
4. The radiculopathy symptoms caused by HO were independent of the amount of rhBMP-2 used in TLIF. Of the 38 patients, 19 had 1 rhBMP-2 sponge placed in the cage, 12 had a small kit sponge (1.05 mg), 5 had 1 sponge placed in the cage and 1 sponge placed directly in the disk space before cage placement (no notation of precise size or amount of rhBMP-2), and 2 had 1 sponge placed in the cage (no notation of rhBMP-2 amount). The data showed that HO can occur with even a small amount of rhBMP-2.
Continue to: Bone formation with rhBMP-2...
Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.
DISCUSSION
We identified 38 patients with a recognizable and consistent pattern of complications of off-label use of rhBMP-2 in TLIF performed at our institution between 2002 and 2015. This pattern included consistent radiculopathy symptoms with corresponding HO at the annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell around the thecal sac or nerve roots, as well as showing a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. Our finding differs from other findings of similar complication characteristics, but with much larger variations without consistency within the patient population.19,20,22,24 Specifically, previous studies found an association between off-label rhBMP-2 use in the posterior spine and radiculopathy with and without neuroforaminal HO. However, our study found consistent radiculopathy symptoms with pseudo-pedicle-like HO complications in all its 38 patients a mean (SD) of 3.8 (1.0) months after surgery.
In this study, consistent radiculopathy symptoms with pseudo-pedicle-like HO complications were independent of the amount of rhBMP-2 used, as some complications occurred with use of small pack rhBMP-2 with TLIF. It is well understood that high doses of rhBMP-2 may be required to improve fusion rates, but to our knowledge an optimal dosing strategy for TLIF has not been reported, particularly with respect to potential complications.8,20,31-33 For anterior lumbar interbody fusion surgery, the FDA-approved use of rhBMP-2 appears to have a significantly decreased risk of neuroforaminal HO complications. This may be attributable to the protective presence of the intact posterior annulus and longitudinal ligament for this procedure.20,33 For TLIF, it has been suggested that rhBMP-2 should be placed only along the anterior annulus with a posterior strut and morselized bone allograft barricade,33 and that fibrin glue should be used to limit BMP diffusion through the annulotomy site31 to prevent this complication.
Our study results suggest that radiculopathy symptoms with pseudo-pedicle-like HO complications appear to be caused by leakage of rhBMP-2 from the disk space through the annulotomy site. This was often initially interpreted incorrectly on MRI in the first year after surgery as being fibrous or granulation tissue, or even postoperative changes that the heterotopic tissue was bone was obvious only on CT. Even then the tissue may be incorrectly identified, as the encasing nerve roots in bone are similar to the scar tissue having no compressive effect. HO may compress, but it also has an inflammatory component that the scars lack. Additionally, the HO from the disk space, caused by leakage of the BMP placed in or around the fusion cage, can create a pseudo-pedicle of varying size and extent. This was present in all 38 of our cases.
This retrospective case series had its limitations. Its clinical and radiographic findings were not blinded. Confounding variables cannot be isolated for causal relationships, if any, to the complication in a case series such as this.
Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.
1. Urist MR. Bone: formation by autoinduction. Science. 1965;150(3698):893-899.
2. Burkus JK, Gornet MF, Schuler TC, Kleeman TJ, Zdeblick TA. Six-year outcomes of anterior lumbar interbody arthrodesis with use of interbody fusion cages and recombinant human bone morphogenetic protein-2. J Bone Joint Surg Am. 2009;91(5):1181-1189.
3. Boden SD, Kang J, Sandhu H, Heller JG. Use of recombinant human bone morphogenetic protein-2 to achieve posterolateral lumbar spine fusion in humans: a prospective, randomized clinical pilot trial: 2002 Volvo award in clinical studies. Spine. 2002;27(23):2662-2673.
4. Boden SD, Zdeblick TA, Sandhu HS, Heim SE. The use of rhBMP-2 in interbody fusion cages. Definitive evidence of osteoinduction in humans: a preliminary report. Spine. 2000;25(3):376-381.
5. Haid RW Jr, Branch CL Jr, Alexander JT, Burkus JK. Posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. Spine J. 2004;4(5):527-538.
6. Meisel HJ, Schnöring M, Hohaus C, et al. Posterior lumbar interbody fusion using rhBMP-2. Eur Spine J. 2008;17(12):1735-1744.
7. Mummaneni PV, Pan J, Haid RW, Rodts GE. Contribution of recombinant human bone morphogenetic protein-2 to the rapid creation of interbody fusion when used in transforaminal lumbar interbody fusion: a preliminary report. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine. 2004;1(1):19-23.
8. Shimer AL, Oner FC, Vaccaro AR. Spinal reconstruction and bone morphogenetic proteins: open questions. Injury. 2009;40(suppl 3):S32-S38.
9. Slosar PJ, Josey R, Reynolds J. Accelerating lumbar fusions by combining rhBMP-2 with allograft bone: a prospective analysis of interbody fusion rates and clinical outcomes. Spine J. 2007;7(3):301-307.
10. Knox JB, Dai JM 3rd, Orchowski J. Osteolysis in transforaminal lumbar interbody fusion with bone morphogenetic protein-2. Spine. 2011;36(8):672-676.
11. Owens K, Glassman SD, Howard JM, Djurasovic M, Witten JL, Carreon LY. Perioperative complications with rhBMP-2 in transforaminal lumbar interbody fusion. Eur Spine J. 2011;20(4):612-617.
12. Mindea SA, Shih P, Song JK. Recombinant human bone morphogenetic protein-2-induced radiculitis in elective minimally invasive transforaminal lumbar interbody fusions: a series review. Spine. 2009;34(14):1480-1484.
13. Yoon ST, Park JS, Kim KS, et al. ISSLS prize winner: LMP-1 upregulates intervertebral disc cell production of proteoglycans and BMPs in vitro and in vivo. Spine. 2004;29(23):2603-2611.
14. Cahill KS, Chi JH, Day A, Claus EB. Prevalence, complications, and hospital charges associated with use of bone-morphogenetic proteins in spinal fusion procedures. JAMA. 2009;302(1):58-66.
15. Carragee EJ, Hurwitz EL, Weiner BK. A critical review of recombinant human bone morphogenetic protein-2 trials in spinal surgery: emerging safety concerns and lessons learned. Spine J. 2011;11(6):471-491.
16. Chen NF, Smith ZA, Stiner E, Armin S, Sheikh H, Khoo LT. Symptomatic ectopic bone formation after off-label use of recombinant human bone morphogenetic protein-2 in transforaminal lumbar interbody fusion. J Neurosurg Spine. 2010;12(1):40-46.
17. Joseph V, Rampersaud YR. Heterotopic bone formation with the use of rhBMP2 in posterior minimal access interbody fusion: a CT analysis. Spine. 2007;32(25):2885-2890.
18. McClellan JW, Mulconrey DS, Forbes RJ, Fullmer N. Vertebral bone resorption after transforaminal lumbar interbody fusion with bone morphogenetic protein (rhBMP-2). J Spinal Disord Tech. 2006;19(7):483-486.
19. Mroz TE, Wang JC, Hashimoto R, Norvell DC. Complications related to osteobiologics use in spine surgery: a systematic review. Spine. 2010;35(9 suppl):S86-S104.
20. Muchow RD, Hsu WK, Anderson PA. Histopathologic inflammatory response induced by recombinant bone morphogenetic protein-2 causing radiculopathy after transforaminal lumbar interbody fusion. Spine J. 2010;10(9):e1-e6.
21. Ong KL, Villarraga ML, Lau E, Carreon LY, Kurtz SM, Glassman SD. Off-label use of bone morphogenetic proteins in the United States using administrative data. Spine. 2010;35(19):1794-1800.
22. Rihn JA, Patel R, Makda J, et al. Complications associated with single-level transforaminal lumbar interbody fusion. Spine J. 2009;9(8):623-629.
23. Vaidya R, Sethi A, Bartol S, Jacobson M, Coe C, Craig JG. Complications in the use of rhBMP-2 in PEEK cages for interbody spinal fusions. J Spinal Disord Tech. 2008;21(8):557-562.
24. Wong DA, Kumar A, Jatana S, Ghiselli G, Wong K. Neurologic impairment from ectopic bone in the lumbar canal: a potential complication of off-label PLIF/TLIF use of bone morphogenetic protein-2 (BMP-2). Spine J. 2008;8(6):1011-1018.
25. Delawi D, Dhert WJ, Rillardon L, et al. A prospective, randomized, controlled, multicenter study of osteogenic protein-1 in instrumented posterolateral fusions: report on safety and feasibility. Spine. 2010;35(12):1185-1191.
26. Vaccaro AR, Patel T, Fischgrund J, et al. A pilot study evaluating the safety and efficacy of OP-1 putty (rhBMP-7) as a replacement for iliac crest autograft in posterolateral lumbar arthrodesis for degenerative spondylolisthesis. Spine. 2004;29(17):1885-1892.
27. Vaidya R, Weir R, Sethi A, Meisterling S, Hakeos W, Wybo CD. Interbody fusion with allograft and rhBMP-2 leads to consistent fusion but early subsidence. J Bone Joint Surg Br. 2007;89(3):342-345.
28. Glassman SD, Howard J, Dimar J, Sweet A, Wilson G, Carreon L. Complications with recombinant human bone morphogenic protein-2 in posterolateral spine fusion: a consecutive series of 1037 cases. Spine. 2011;36(22):1849-1854.
29. Helgeson MD, Lehman RA Jr, Patzkowski JC, Dmitriev AE, Rosner MK, Mack AW. Adjacent vertebral body osteolysis with bone morphogenetic protein use in transforaminal lumbar interbody fusion. Spine J. 2011;11(6):507-510.
30. Hoffmann MF, Jones CB, Sietsema DL. Adjuncts in posterior lumbar spine fusion: comparison of complications and efficacy. Arch Orthop Trauma Surg. 2012;132(8):1105-1110.
31. Villavicencio AT, Burneikiene S, Nelson EL, Bulsara KR, Favors M, Thramann J. Safety of transforaminal lumbar interbody fusion and intervertebral recombinant human bone morphogenetic protein-2. J Neurosurg Spine. 2005;3(6):436-443.
32. Patel VV, Zhao L, Wong P, et al. Controlling bone morphogenetic protein diffusion and bone morphogenetic protein-stimulated bone growth using fibrin glue. Spine. 2006;31(11):1201-1206.
33. Zhang H, Sucato DJ, Welch RD. Recombinant human bone morphogenic protein-2-enhanced anterior spine fusion without bone encroachment into the spinal canal: a histomorphometric study in a thoracoscopically instrumented porcine model. Spine. 2005;30(5):512-518.
ABSTRACT
We conducted a study to determine the common characteristics of patients who developed radiculopathy symptoms and corresponding heterotopic ossification (HO) from transforaminal lumbar interbody fusions (TLIF) using recombinant human bone morphogenetic protein 2 (rhBMP-2). HO can arise from a disk space with rhBMP-2 use in TLIF. Formation of bone around nerve roots or the thecal sac can cause a radiculopathy with a consistent pattern of symptoms.
We identified 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years who developed radiculopathy symptoms and corresponding HO from TLIF with rhBMP-2 in the disk space between 2002 and 2015. To document this complication and improve its recognition, we recorded common patterns of symptom development and radiologic findings: specifically, time from implantation of rhBMP-2 to symptom development, consistency with side of TLIF placement, and radiologic findings.
Radicular pain generally developed a mean (SD) of 3.8 (1.0) months after TLIF with rhBMP-2. Development of radiculopathy symptoms corresponded to consistent “pseudo-pedicle”-like HO. In all 38 patients, HO arising from the annulotomy site showed a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. In addition, development of radiculopathy symptoms and corresponding HO appear to be independent of amount of rhBMP-2. HO resulting from TLIF with rhBMP-2 in the disk space is a pain generator and a recognizable complication that can be diagnosed by assessment of symptoms and computed tomography characteristics.
Continue to: Bone morphogenetic proteins...
Bone morphogenetic proteins (BMPs), first isolated by Urist in 19641, are a family of growth factors that stimulate the cascade of bone formation. Recombinant human BMP (rhBMP), specifically rhBMP-2 and rhBMP-7 (also known as osteogenic protein 1 [OP-1]), was developed in the 1990s after the advent of gene splicing. Then, in 2002, the US Food and Drug Administration (FDA) approved use of rhBMP to stimulate fusion in the human spine. Specifically, rhBMP-2 (Medtronic) was approved for use in combination with a specific brand of interbody cage in 1-level anterior lumbar interbody fusion.2 Over the past decade, off-label use of rhBMP-2 to achieve osseous union has increased dramatically, particularly in spinal surgery: transforaminal lumbar interbody fusion (TLIF), posterior lumbar interbody fusion, and posterolateral lumbar fusion.3-9 However, this widespread off-label use for posterior spinal fusion began despite FDA data indicating that specific complications were underreported in the peer-reviewed literature.10,11 Although rhBMP-2 is very effective in increasing osteoblast formation and improving osteogenesis and subsequent bone healing in spinal surgery,12,13 its use in TLIF resulted in significant adverse side effects, including radiculopathy with and without neuroforaminal heterotopic ossification (HO); 14-24 complications in the FDA studies; 14,22,25-27 and osteolysis causing intervertebral cage subsidence, inflammatory radiculitis, genitourinary complications, infections, possible systemic effects, and significant HO complications.10,28-30 Of these, HO complications involved rhBMP leakage through the annulotomy to the disk space that led to HO. Specifically, rhBMP leaked directly out of the disk space and formed a pillar of bone that encased the nerve roots and dura, which led to occlusion of the foramen and symptoms of radiculopathy.10,28-30
Despite this frequent finding of HO in the intervertebral space outside the target fusion area, use of rhBMP-2 with intervertebral cages increased so rapidly that rhBMP-2 was used more often than autologous bone.5,11,17,31 In this study, we reviewed the common characteristics of patients who developed HO and subsequent radiculopathy from TLIF with rhBMP.
METHODS
After this study received Institutional Review Board approval, we retrospectively reviewed cases of radiculopathy symptoms that developed after TLIF with rhBMP between January 2002 and January 2015. During this period, 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years and radiculopathy symptoms arising from TLIF with rhBMP-2 were identified to determine commonalities and defining characteristics that will help facilitate diagnosis.
Inclusion criteria were computed tomography (CT)–documented HO arising from the TLIF annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell with contouring around the thecal sac or nerve roots, as well as recurrence or initial occurrence of radiculopathy with signs and symptoms corresponding to the CT site of aberrant bone growth in terms of laterality and particular nerve root(s) involved. Exclusion criteria were malplacement of interbody cage or pedicle screws, disk herniation, systemic neuropathic disease, and new or unresolved radiculopathy immediately after index surgery.
To improve recognition of this complication, we also documented the amount of BMP used, common patterns of radiculopathy symptom development, and radiologic findings. Type and timing of radiculopathy symptom onset and consistency with side of TLIF placement were documented as well. Radiculopathy symptoms included shooting pain in the legs, incontinence, sexual dysfunction, and severe paralysis. Radiologic findings were specific to bone formation from the disk space (detected with CT).
Continue to: RESULTS
RESULTS
All 38 selected patients had radiculopathy symptoms from HO out of the intervertebral space. The Table lists the patients’ overall characteristics. The left side had the most radiculopathy symptoms (31/38 patients), followed by the right side (5/38) and both sides (2/38). Radiculopathy symptoms began a mean (SD) of 3.8 (1.0) months (range, 2-6 months) after index surgery. The 38 patients had 4 characteristics in common:
Table. Transforaminal Lumbar Interbody Fusion With Recombinant Human Bone Morphogenetic Protein 2: Onset Time for Radiculopathy Symptoms, Surgery Level, Side of Pseudo-Pedicle Bone Formation, and Subsequent Complications
| Pt | Sympton Onset, mo | Surgery Level(s) | Side(s) | Complication(s) |
| 1 | 3 | L3-L5 (2) | Both | Radiculopathy, pseudo-pedicle, urine |
| 2 | 3 | L4-L5 (2) | R | Radiculopathy, pseudo-pedicle |
| 3 | 4 | L5-S1 (1) | R | Radiculopathy, pseudo-pedicle |
| 4 | 5 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 5 | 4 | L4-S1 (2) | L | Radiculopathy, pseudo-pedicle, subsidence |
| 6 | 5 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 7 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 8 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 9 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 10 | 2 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 11 | 2 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, subsidence, neurologic |
| 12 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 13 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, neurologic |
| 14 | 2 | L2-L3 (1) | R | Radiculopathy, pseudo-pedicle |
| 15 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 16 | 3 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 17 | 3 | L2-L3, L4-L5 (2) | L | Radiculopathy, pseudo-pedicle |
| 18 | 3 | L4-L5, L2-L3 (1) | L | Radiculopathy, pseudo-pedicle, nonunion |
| 19 | 4 | L4-L5 (1) | R | Radiculopathy, pseudo-pedicle |
| 20 | 5 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 21 | 5 | L5-S1 (1) | R | Radiculopathy, pseudo-pedicle |
| 22 | 3 | L3-L4, L5-S1 (2) | Both | Radiculopathy, pseudo-pedicle |
| 23 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 24 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 25 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 26 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, urine, bowel |
| 27 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 28 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 29 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 30 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 31 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 32 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 33 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 34 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 35 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 36 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 37 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 38 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
1. Bone growing out of the annulotomy site for TLIF cage placement was present and in continuity with the disk space in 33 (87%) of the 38 cases. In the other 5 cases (13%), HO was present around the neural tissue, but not necessarily in continuity with the disk space. This bone appeared ectopic and not osteophytic and facet-related, as it formed a shell around either the nerve root or the thecal sac, contouring to the structure.
2. The common, novel finding on CT was a “pseudo-pedicle” (Figures 1A, 1B), which appeared as ectopic growth from the disk space—a solid piece of bone in the same direction as the anatomical pedicle. Confusing similarity to the anatomical pedicle is present on axial cuts and during surgery. The pseudo-pedicle varied in thickness and extent out of the disk space, but was always presented as a bar of bone arising from the annulotomy site. After arising from the disk space, the HO could disperse in any direction, further calcifying neural structures or the facet joints above or below. There was no apparent distinguishable repeating pattern, given the variable nature of arthritic facet changes, scoliotic deformities, size of annulotomies, amount of rhBMP used, and placement in cage and disk space or only in cage.
3. In 36 (95%) of the 38 cases, the initial interpretation of HO on magnetic resonance imaging (MRI) was of tissue other than bone, such as fibrous tissue, granulation tissue, recurrent disk herniation, or postoperative changes. However, this tissue was later determined to be bone from HO complications, which we confirmed with CT in all 38 cases. It is important to note that HO on MRI (Figures 2A, 2B) was initially interpreted by a radiologist as fibrous tissue, but same-level CT of the same case (Figures 3A, 3B) showed clear HO.
4. The radiculopathy symptoms caused by HO were independent of the amount of rhBMP-2 used in TLIF. Of the 38 patients, 19 had 1 rhBMP-2 sponge placed in the cage, 12 had a small kit sponge (1.05 mg), 5 had 1 sponge placed in the cage and 1 sponge placed directly in the disk space before cage placement (no notation of precise size or amount of rhBMP-2), and 2 had 1 sponge placed in the cage (no notation of rhBMP-2 amount). The data showed that HO can occur with even a small amount of rhBMP-2.
Continue to: Bone formation with rhBMP-2...
Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.
DISCUSSION
We identified 38 patients with a recognizable and consistent pattern of complications of off-label use of rhBMP-2 in TLIF performed at our institution between 2002 and 2015. This pattern included consistent radiculopathy symptoms with corresponding HO at the annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell around the thecal sac or nerve roots, as well as showing a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. Our finding differs from other findings of similar complication characteristics, but with much larger variations without consistency within the patient population.19,20,22,24 Specifically, previous studies found an association between off-label rhBMP-2 use in the posterior spine and radiculopathy with and without neuroforaminal HO. However, our study found consistent radiculopathy symptoms with pseudo-pedicle-like HO complications in all its 38 patients a mean (SD) of 3.8 (1.0) months after surgery.
In this study, consistent radiculopathy symptoms with pseudo-pedicle-like HO complications were independent of the amount of rhBMP-2 used, as some complications occurred with use of small pack rhBMP-2 with TLIF. It is well understood that high doses of rhBMP-2 may be required to improve fusion rates, but to our knowledge an optimal dosing strategy for TLIF has not been reported, particularly with respect to potential complications.8,20,31-33 For anterior lumbar interbody fusion surgery, the FDA-approved use of rhBMP-2 appears to have a significantly decreased risk of neuroforaminal HO complications. This may be attributable to the protective presence of the intact posterior annulus and longitudinal ligament for this procedure.20,33 For TLIF, it has been suggested that rhBMP-2 should be placed only along the anterior annulus with a posterior strut and morselized bone allograft barricade,33 and that fibrin glue should be used to limit BMP diffusion through the annulotomy site31 to prevent this complication.
Our study results suggest that radiculopathy symptoms with pseudo-pedicle-like HO complications appear to be caused by leakage of rhBMP-2 from the disk space through the annulotomy site. This was often initially interpreted incorrectly on MRI in the first year after surgery as being fibrous or granulation tissue, or even postoperative changes that the heterotopic tissue was bone was obvious only on CT. Even then the tissue may be incorrectly identified, as the encasing nerve roots in bone are similar to the scar tissue having no compressive effect. HO may compress, but it also has an inflammatory component that the scars lack. Additionally, the HO from the disk space, caused by leakage of the BMP placed in or around the fusion cage, can create a pseudo-pedicle of varying size and extent. This was present in all 38 of our cases.
This retrospective case series had its limitations. Its clinical and radiographic findings were not blinded. Confounding variables cannot be isolated for causal relationships, if any, to the complication in a case series such as this.
Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.
ABSTRACT
We conducted a study to determine the common characteristics of patients who developed radiculopathy symptoms and corresponding heterotopic ossification (HO) from transforaminal lumbar interbody fusions (TLIF) using recombinant human bone morphogenetic protein 2 (rhBMP-2). HO can arise from a disk space with rhBMP-2 use in TLIF. Formation of bone around nerve roots or the thecal sac can cause a radiculopathy with a consistent pattern of symptoms.
We identified 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years who developed radiculopathy symptoms and corresponding HO from TLIF with rhBMP-2 in the disk space between 2002 and 2015. To document this complication and improve its recognition, we recorded common patterns of symptom development and radiologic findings: specifically, time from implantation of rhBMP-2 to symptom development, consistency with side of TLIF placement, and radiologic findings.
Radicular pain generally developed a mean (SD) of 3.8 (1.0) months after TLIF with rhBMP-2. Development of radiculopathy symptoms corresponded to consistent “pseudo-pedicle”-like HO. In all 38 patients, HO arising from the annulotomy site showed a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. In addition, development of radiculopathy symptoms and corresponding HO appear to be independent of amount of rhBMP-2. HO resulting from TLIF with rhBMP-2 in the disk space is a pain generator and a recognizable complication that can be diagnosed by assessment of symptoms and computed tomography characteristics.
Continue to: Bone morphogenetic proteins...
Bone morphogenetic proteins (BMPs), first isolated by Urist in 19641, are a family of growth factors that stimulate the cascade of bone formation. Recombinant human BMP (rhBMP), specifically rhBMP-2 and rhBMP-7 (also known as osteogenic protein 1 [OP-1]), was developed in the 1990s after the advent of gene splicing. Then, in 2002, the US Food and Drug Administration (FDA) approved use of rhBMP to stimulate fusion in the human spine. Specifically, rhBMP-2 (Medtronic) was approved for use in combination with a specific brand of interbody cage in 1-level anterior lumbar interbody fusion.2 Over the past decade, off-label use of rhBMP-2 to achieve osseous union has increased dramatically, particularly in spinal surgery: transforaminal lumbar interbody fusion (TLIF), posterior lumbar interbody fusion, and posterolateral lumbar fusion.3-9 However, this widespread off-label use for posterior spinal fusion began despite FDA data indicating that specific complications were underreported in the peer-reviewed literature.10,11 Although rhBMP-2 is very effective in increasing osteoblast formation and improving osteogenesis and subsequent bone healing in spinal surgery,12,13 its use in TLIF resulted in significant adverse side effects, including radiculopathy with and without neuroforaminal heterotopic ossification (HO); 14-24 complications in the FDA studies; 14,22,25-27 and osteolysis causing intervertebral cage subsidence, inflammatory radiculitis, genitourinary complications, infections, possible systemic effects, and significant HO complications.10,28-30 Of these, HO complications involved rhBMP leakage through the annulotomy to the disk space that led to HO. Specifically, rhBMP leaked directly out of the disk space and formed a pillar of bone that encased the nerve roots and dura, which led to occlusion of the foramen and symptoms of radiculopathy.10,28-30
Despite this frequent finding of HO in the intervertebral space outside the target fusion area, use of rhBMP-2 with intervertebral cages increased so rapidly that rhBMP-2 was used more often than autologous bone.5,11,17,31 In this study, we reviewed the common characteristics of patients who developed HO and subsequent radiculopathy from TLIF with rhBMP.
METHODS
After this study received Institutional Review Board approval, we retrospectively reviewed cases of radiculopathy symptoms that developed after TLIF with rhBMP between January 2002 and January 2015. During this period, 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years and radiculopathy symptoms arising from TLIF with rhBMP-2 were identified to determine commonalities and defining characteristics that will help facilitate diagnosis.
Inclusion criteria were computed tomography (CT)–documented HO arising from the TLIF annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell with contouring around the thecal sac or nerve roots, as well as recurrence or initial occurrence of radiculopathy with signs and symptoms corresponding to the CT site of aberrant bone growth in terms of laterality and particular nerve root(s) involved. Exclusion criteria were malplacement of interbody cage or pedicle screws, disk herniation, systemic neuropathic disease, and new or unresolved radiculopathy immediately after index surgery.
To improve recognition of this complication, we also documented the amount of BMP used, common patterns of radiculopathy symptom development, and radiologic findings. Type and timing of radiculopathy symptom onset and consistency with side of TLIF placement were documented as well. Radiculopathy symptoms included shooting pain in the legs, incontinence, sexual dysfunction, and severe paralysis. Radiologic findings were specific to bone formation from the disk space (detected with CT).
Continue to: RESULTS
RESULTS
All 38 selected patients had radiculopathy symptoms from HO out of the intervertebral space. The Table lists the patients’ overall characteristics. The left side had the most radiculopathy symptoms (31/38 patients), followed by the right side (5/38) and both sides (2/38). Radiculopathy symptoms began a mean (SD) of 3.8 (1.0) months (range, 2-6 months) after index surgery. The 38 patients had 4 characteristics in common:
Table. Transforaminal Lumbar Interbody Fusion With Recombinant Human Bone Morphogenetic Protein 2: Onset Time for Radiculopathy Symptoms, Surgery Level, Side of Pseudo-Pedicle Bone Formation, and Subsequent Complications
| Pt | Sympton Onset, mo | Surgery Level(s) | Side(s) | Complication(s) |
| 1 | 3 | L3-L5 (2) | Both | Radiculopathy, pseudo-pedicle, urine |
| 2 | 3 | L4-L5 (2) | R | Radiculopathy, pseudo-pedicle |
| 3 | 4 | L5-S1 (1) | R | Radiculopathy, pseudo-pedicle |
| 4 | 5 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 5 | 4 | L4-S1 (2) | L | Radiculopathy, pseudo-pedicle, subsidence |
| 6 | 5 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 7 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 8 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 9 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 10 | 2 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 11 | 2 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, subsidence, neurologic |
| 12 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 13 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, neurologic |
| 14 | 2 | L2-L3 (1) | R | Radiculopathy, pseudo-pedicle |
| 15 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 16 | 3 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 17 | 3 | L2-L3, L4-L5 (2) | L | Radiculopathy, pseudo-pedicle |
| 18 | 3 | L4-L5, L2-L3 (1) | L | Radiculopathy, pseudo-pedicle, nonunion |
| 19 | 4 | L4-L5 (1) | R | Radiculopathy, pseudo-pedicle |
| 20 | 5 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 21 | 5 | L5-S1 (1) | R | Radiculopathy, pseudo-pedicle |
| 22 | 3 | L3-L4, L5-S1 (2) | Both | Radiculopathy, pseudo-pedicle |
| 23 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 24 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 25 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 26 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle, urine, bowel |
| 27 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 28 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 29 | 6 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 30 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 31 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 32 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 33 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 34 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 35 | 4 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 36 | 3 | L5-S1 (1) | L | Radiculopathy, pseudo-pedicle |
| 37 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
| 38 | 4 | L4-L5 (1) | L | Radiculopathy, pseudo-pedicle |
1. Bone growing out of the annulotomy site for TLIF cage placement was present and in continuity with the disk space in 33 (87%) of the 38 cases. In the other 5 cases (13%), HO was present around the neural tissue, but not necessarily in continuity with the disk space. This bone appeared ectopic and not osteophytic and facet-related, as it formed a shell around either the nerve root or the thecal sac, contouring to the structure.
2. The common, novel finding on CT was a “pseudo-pedicle” (Figures 1A, 1B), which appeared as ectopic growth from the disk space—a solid piece of bone in the same direction as the anatomical pedicle. Confusing similarity to the anatomical pedicle is present on axial cuts and during surgery. The pseudo-pedicle varied in thickness and extent out of the disk space, but was always presented as a bar of bone arising from the annulotomy site. After arising from the disk space, the HO could disperse in any direction, further calcifying neural structures or the facet joints above or below. There was no apparent distinguishable repeating pattern, given the variable nature of arthritic facet changes, scoliotic deformities, size of annulotomies, amount of rhBMP used, and placement in cage and disk space or only in cage.
3. In 36 (95%) of the 38 cases, the initial interpretation of HO on magnetic resonance imaging (MRI) was of tissue other than bone, such as fibrous tissue, granulation tissue, recurrent disk herniation, or postoperative changes. However, this tissue was later determined to be bone from HO complications, which we confirmed with CT in all 38 cases. It is important to note that HO on MRI (Figures 2A, 2B) was initially interpreted by a radiologist as fibrous tissue, but same-level CT of the same case (Figures 3A, 3B) showed clear HO.
4. The radiculopathy symptoms caused by HO were independent of the amount of rhBMP-2 used in TLIF. Of the 38 patients, 19 had 1 rhBMP-2 sponge placed in the cage, 12 had a small kit sponge (1.05 mg), 5 had 1 sponge placed in the cage and 1 sponge placed directly in the disk space before cage placement (no notation of precise size or amount of rhBMP-2), and 2 had 1 sponge placed in the cage (no notation of rhBMP-2 amount). The data showed that HO can occur with even a small amount of rhBMP-2.
Continue to: Bone formation with rhBMP-2...
Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.
DISCUSSION
We identified 38 patients with a recognizable and consistent pattern of complications of off-label use of rhBMP-2 in TLIF performed at our institution between 2002 and 2015. This pattern included consistent radiculopathy symptoms with corresponding HO at the annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell around the thecal sac or nerve roots, as well as showing a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. Our finding differs from other findings of similar complication characteristics, but with much larger variations without consistency within the patient population.19,20,22,24 Specifically, previous studies found an association between off-label rhBMP-2 use in the posterior spine and radiculopathy with and without neuroforaminal HO. However, our study found consistent radiculopathy symptoms with pseudo-pedicle-like HO complications in all its 38 patients a mean (SD) of 3.8 (1.0) months after surgery.
In this study, consistent radiculopathy symptoms with pseudo-pedicle-like HO complications were independent of the amount of rhBMP-2 used, as some complications occurred with use of small pack rhBMP-2 with TLIF. It is well understood that high doses of rhBMP-2 may be required to improve fusion rates, but to our knowledge an optimal dosing strategy for TLIF has not been reported, particularly with respect to potential complications.8,20,31-33 For anterior lumbar interbody fusion surgery, the FDA-approved use of rhBMP-2 appears to have a significantly decreased risk of neuroforaminal HO complications. This may be attributable to the protective presence of the intact posterior annulus and longitudinal ligament for this procedure.20,33 For TLIF, it has been suggested that rhBMP-2 should be placed only along the anterior annulus with a posterior strut and morselized bone allograft barricade,33 and that fibrin glue should be used to limit BMP diffusion through the annulotomy site31 to prevent this complication.
Our study results suggest that radiculopathy symptoms with pseudo-pedicle-like HO complications appear to be caused by leakage of rhBMP-2 from the disk space through the annulotomy site. This was often initially interpreted incorrectly on MRI in the first year after surgery as being fibrous or granulation tissue, or even postoperative changes that the heterotopic tissue was bone was obvious only on CT. Even then the tissue may be incorrectly identified, as the encasing nerve roots in bone are similar to the scar tissue having no compressive effect. HO may compress, but it also has an inflammatory component that the scars lack. Additionally, the HO from the disk space, caused by leakage of the BMP placed in or around the fusion cage, can create a pseudo-pedicle of varying size and extent. This was present in all 38 of our cases.
This retrospective case series had its limitations. Its clinical and radiographic findings were not blinded. Confounding variables cannot be isolated for causal relationships, if any, to the complication in a case series such as this.
Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.
1. Urist MR. Bone: formation by autoinduction. Science. 1965;150(3698):893-899.
2. Burkus JK, Gornet MF, Schuler TC, Kleeman TJ, Zdeblick TA. Six-year outcomes of anterior lumbar interbody arthrodesis with use of interbody fusion cages and recombinant human bone morphogenetic protein-2. J Bone Joint Surg Am. 2009;91(5):1181-1189.
3. Boden SD, Kang J, Sandhu H, Heller JG. Use of recombinant human bone morphogenetic protein-2 to achieve posterolateral lumbar spine fusion in humans: a prospective, randomized clinical pilot trial: 2002 Volvo award in clinical studies. Spine. 2002;27(23):2662-2673.
4. Boden SD, Zdeblick TA, Sandhu HS, Heim SE. The use of rhBMP-2 in interbody fusion cages. Definitive evidence of osteoinduction in humans: a preliminary report. Spine. 2000;25(3):376-381.
5. Haid RW Jr, Branch CL Jr, Alexander JT, Burkus JK. Posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. Spine J. 2004;4(5):527-538.
6. Meisel HJ, Schnöring M, Hohaus C, et al. Posterior lumbar interbody fusion using rhBMP-2. Eur Spine J. 2008;17(12):1735-1744.
7. Mummaneni PV, Pan J, Haid RW, Rodts GE. Contribution of recombinant human bone morphogenetic protein-2 to the rapid creation of interbody fusion when used in transforaminal lumbar interbody fusion: a preliminary report. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine. 2004;1(1):19-23.
8. Shimer AL, Oner FC, Vaccaro AR. Spinal reconstruction and bone morphogenetic proteins: open questions. Injury. 2009;40(suppl 3):S32-S38.
9. Slosar PJ, Josey R, Reynolds J. Accelerating lumbar fusions by combining rhBMP-2 with allograft bone: a prospective analysis of interbody fusion rates and clinical outcomes. Spine J. 2007;7(3):301-307.
10. Knox JB, Dai JM 3rd, Orchowski J. Osteolysis in transforaminal lumbar interbody fusion with bone morphogenetic protein-2. Spine. 2011;36(8):672-676.
11. Owens K, Glassman SD, Howard JM, Djurasovic M, Witten JL, Carreon LY. Perioperative complications with rhBMP-2 in transforaminal lumbar interbody fusion. Eur Spine J. 2011;20(4):612-617.
12. Mindea SA, Shih P, Song JK. Recombinant human bone morphogenetic protein-2-induced radiculitis in elective minimally invasive transforaminal lumbar interbody fusions: a series review. Spine. 2009;34(14):1480-1484.
13. Yoon ST, Park JS, Kim KS, et al. ISSLS prize winner: LMP-1 upregulates intervertebral disc cell production of proteoglycans and BMPs in vitro and in vivo. Spine. 2004;29(23):2603-2611.
14. Cahill KS, Chi JH, Day A, Claus EB. Prevalence, complications, and hospital charges associated with use of bone-morphogenetic proteins in spinal fusion procedures. JAMA. 2009;302(1):58-66.
15. Carragee EJ, Hurwitz EL, Weiner BK. A critical review of recombinant human bone morphogenetic protein-2 trials in spinal surgery: emerging safety concerns and lessons learned. Spine J. 2011;11(6):471-491.
16. Chen NF, Smith ZA, Stiner E, Armin S, Sheikh H, Khoo LT. Symptomatic ectopic bone formation after off-label use of recombinant human bone morphogenetic protein-2 in transforaminal lumbar interbody fusion. J Neurosurg Spine. 2010;12(1):40-46.
17. Joseph V, Rampersaud YR. Heterotopic bone formation with the use of rhBMP2 in posterior minimal access interbody fusion: a CT analysis. Spine. 2007;32(25):2885-2890.
18. McClellan JW, Mulconrey DS, Forbes RJ, Fullmer N. Vertebral bone resorption after transforaminal lumbar interbody fusion with bone morphogenetic protein (rhBMP-2). J Spinal Disord Tech. 2006;19(7):483-486.
19. Mroz TE, Wang JC, Hashimoto R, Norvell DC. Complications related to osteobiologics use in spine surgery: a systematic review. Spine. 2010;35(9 suppl):S86-S104.
20. Muchow RD, Hsu WK, Anderson PA. Histopathologic inflammatory response induced by recombinant bone morphogenetic protein-2 causing radiculopathy after transforaminal lumbar interbody fusion. Spine J. 2010;10(9):e1-e6.
21. Ong KL, Villarraga ML, Lau E, Carreon LY, Kurtz SM, Glassman SD. Off-label use of bone morphogenetic proteins in the United States using administrative data. Spine. 2010;35(19):1794-1800.
22. Rihn JA, Patel R, Makda J, et al. Complications associated with single-level transforaminal lumbar interbody fusion. Spine J. 2009;9(8):623-629.
23. Vaidya R, Sethi A, Bartol S, Jacobson M, Coe C, Craig JG. Complications in the use of rhBMP-2 in PEEK cages for interbody spinal fusions. J Spinal Disord Tech. 2008;21(8):557-562.
24. Wong DA, Kumar A, Jatana S, Ghiselli G, Wong K. Neurologic impairment from ectopic bone in the lumbar canal: a potential complication of off-label PLIF/TLIF use of bone morphogenetic protein-2 (BMP-2). Spine J. 2008;8(6):1011-1018.
25. Delawi D, Dhert WJ, Rillardon L, et al. A prospective, randomized, controlled, multicenter study of osteogenic protein-1 in instrumented posterolateral fusions: report on safety and feasibility. Spine. 2010;35(12):1185-1191.
26. Vaccaro AR, Patel T, Fischgrund J, et al. A pilot study evaluating the safety and efficacy of OP-1 putty (rhBMP-7) as a replacement for iliac crest autograft in posterolateral lumbar arthrodesis for degenerative spondylolisthesis. Spine. 2004;29(17):1885-1892.
27. Vaidya R, Weir R, Sethi A, Meisterling S, Hakeos W, Wybo CD. Interbody fusion with allograft and rhBMP-2 leads to consistent fusion but early subsidence. J Bone Joint Surg Br. 2007;89(3):342-345.
28. Glassman SD, Howard J, Dimar J, Sweet A, Wilson G, Carreon L. Complications with recombinant human bone morphogenic protein-2 in posterolateral spine fusion: a consecutive series of 1037 cases. Spine. 2011;36(22):1849-1854.
29. Helgeson MD, Lehman RA Jr, Patzkowski JC, Dmitriev AE, Rosner MK, Mack AW. Adjacent vertebral body osteolysis with bone morphogenetic protein use in transforaminal lumbar interbody fusion. Spine J. 2011;11(6):507-510.
30. Hoffmann MF, Jones CB, Sietsema DL. Adjuncts in posterior lumbar spine fusion: comparison of complications and efficacy. Arch Orthop Trauma Surg. 2012;132(8):1105-1110.
31. Villavicencio AT, Burneikiene S, Nelson EL, Bulsara KR, Favors M, Thramann J. Safety of transforaminal lumbar interbody fusion and intervertebral recombinant human bone morphogenetic protein-2. J Neurosurg Spine. 2005;3(6):436-443.
32. Patel VV, Zhao L, Wong P, et al. Controlling bone morphogenetic protein diffusion and bone morphogenetic protein-stimulated bone growth using fibrin glue. Spine. 2006;31(11):1201-1206.
33. Zhang H, Sucato DJ, Welch RD. Recombinant human bone morphogenic protein-2-enhanced anterior spine fusion without bone encroachment into the spinal canal: a histomorphometric study in a thoracoscopically instrumented porcine model. Spine. 2005;30(5):512-518.
1. Urist MR. Bone: formation by autoinduction. Science. 1965;150(3698):893-899.
2. Burkus JK, Gornet MF, Schuler TC, Kleeman TJ, Zdeblick TA. Six-year outcomes of anterior lumbar interbody arthrodesis with use of interbody fusion cages and recombinant human bone morphogenetic protein-2. J Bone Joint Surg Am. 2009;91(5):1181-1189.
3. Boden SD, Kang J, Sandhu H, Heller JG. Use of recombinant human bone morphogenetic protein-2 to achieve posterolateral lumbar spine fusion in humans: a prospective, randomized clinical pilot trial: 2002 Volvo award in clinical studies. Spine. 2002;27(23):2662-2673.
4. Boden SD, Zdeblick TA, Sandhu HS, Heim SE. The use of rhBMP-2 in interbody fusion cages. Definitive evidence of osteoinduction in humans: a preliminary report. Spine. 2000;25(3):376-381.
5. Haid RW Jr, Branch CL Jr, Alexander JT, Burkus JK. Posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. Spine J. 2004;4(5):527-538.
6. Meisel HJ, Schnöring M, Hohaus C, et al. Posterior lumbar interbody fusion using rhBMP-2. Eur Spine J. 2008;17(12):1735-1744.
7. Mummaneni PV, Pan J, Haid RW, Rodts GE. Contribution of recombinant human bone morphogenetic protein-2 to the rapid creation of interbody fusion when used in transforaminal lumbar interbody fusion: a preliminary report. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine. 2004;1(1):19-23.
8. Shimer AL, Oner FC, Vaccaro AR. Spinal reconstruction and bone morphogenetic proteins: open questions. Injury. 2009;40(suppl 3):S32-S38.
9. Slosar PJ, Josey R, Reynolds J. Accelerating lumbar fusions by combining rhBMP-2 with allograft bone: a prospective analysis of interbody fusion rates and clinical outcomes. Spine J. 2007;7(3):301-307.
10. Knox JB, Dai JM 3rd, Orchowski J. Osteolysis in transforaminal lumbar interbody fusion with bone morphogenetic protein-2. Spine. 2011;36(8):672-676.
11. Owens K, Glassman SD, Howard JM, Djurasovic M, Witten JL, Carreon LY. Perioperative complications with rhBMP-2 in transforaminal lumbar interbody fusion. Eur Spine J. 2011;20(4):612-617.
12. Mindea SA, Shih P, Song JK. Recombinant human bone morphogenetic protein-2-induced radiculitis in elective minimally invasive transforaminal lumbar interbody fusions: a series review. Spine. 2009;34(14):1480-1484.
13. Yoon ST, Park JS, Kim KS, et al. ISSLS prize winner: LMP-1 upregulates intervertebral disc cell production of proteoglycans and BMPs in vitro and in vivo. Spine. 2004;29(23):2603-2611.
14. Cahill KS, Chi JH, Day A, Claus EB. Prevalence, complications, and hospital charges associated with use of bone-morphogenetic proteins in spinal fusion procedures. JAMA. 2009;302(1):58-66.
15. Carragee EJ, Hurwitz EL, Weiner BK. A critical review of recombinant human bone morphogenetic protein-2 trials in spinal surgery: emerging safety concerns and lessons learned. Spine J. 2011;11(6):471-491.
16. Chen NF, Smith ZA, Stiner E, Armin S, Sheikh H, Khoo LT. Symptomatic ectopic bone formation after off-label use of recombinant human bone morphogenetic protein-2 in transforaminal lumbar interbody fusion. J Neurosurg Spine. 2010;12(1):40-46.
17. Joseph V, Rampersaud YR. Heterotopic bone formation with the use of rhBMP2 in posterior minimal access interbody fusion: a CT analysis. Spine. 2007;32(25):2885-2890.
18. McClellan JW, Mulconrey DS, Forbes RJ, Fullmer N. Vertebral bone resorption after transforaminal lumbar interbody fusion with bone morphogenetic protein (rhBMP-2). J Spinal Disord Tech. 2006;19(7):483-486.
19. Mroz TE, Wang JC, Hashimoto R, Norvell DC. Complications related to osteobiologics use in spine surgery: a systematic review. Spine. 2010;35(9 suppl):S86-S104.
20. Muchow RD, Hsu WK, Anderson PA. Histopathologic inflammatory response induced by recombinant bone morphogenetic protein-2 causing radiculopathy after transforaminal lumbar interbody fusion. Spine J. 2010;10(9):e1-e6.
21. Ong KL, Villarraga ML, Lau E, Carreon LY, Kurtz SM, Glassman SD. Off-label use of bone morphogenetic proteins in the United States using administrative data. Spine. 2010;35(19):1794-1800.
22. Rihn JA, Patel R, Makda J, et al. Complications associated with single-level transforaminal lumbar interbody fusion. Spine J. 2009;9(8):623-629.
23. Vaidya R, Sethi A, Bartol S, Jacobson M, Coe C, Craig JG. Complications in the use of rhBMP-2 in PEEK cages for interbody spinal fusions. J Spinal Disord Tech. 2008;21(8):557-562.
24. Wong DA, Kumar A, Jatana S, Ghiselli G, Wong K. Neurologic impairment from ectopic bone in the lumbar canal: a potential complication of off-label PLIF/TLIF use of bone morphogenetic protein-2 (BMP-2). Spine J. 2008;8(6):1011-1018.
25. Delawi D, Dhert WJ, Rillardon L, et al. A prospective, randomized, controlled, multicenter study of osteogenic protein-1 in instrumented posterolateral fusions: report on safety and feasibility. Spine. 2010;35(12):1185-1191.
26. Vaccaro AR, Patel T, Fischgrund J, et al. A pilot study evaluating the safety and efficacy of OP-1 putty (rhBMP-7) as a replacement for iliac crest autograft in posterolateral lumbar arthrodesis for degenerative spondylolisthesis. Spine. 2004;29(17):1885-1892.
27. Vaidya R, Weir R, Sethi A, Meisterling S, Hakeos W, Wybo CD. Interbody fusion with allograft and rhBMP-2 leads to consistent fusion but early subsidence. J Bone Joint Surg Br. 2007;89(3):342-345.
28. Glassman SD, Howard J, Dimar J, Sweet A, Wilson G, Carreon L. Complications with recombinant human bone morphogenic protein-2 in posterolateral spine fusion: a consecutive series of 1037 cases. Spine. 2011;36(22):1849-1854.
29. Helgeson MD, Lehman RA Jr, Patzkowski JC, Dmitriev AE, Rosner MK, Mack AW. Adjacent vertebral body osteolysis with bone morphogenetic protein use in transforaminal lumbar interbody fusion. Spine J. 2011;11(6):507-510.
30. Hoffmann MF, Jones CB, Sietsema DL. Adjuncts in posterior lumbar spine fusion: comparison of complications and efficacy. Arch Orthop Trauma Surg. 2012;132(8):1105-1110.
31. Villavicencio AT, Burneikiene S, Nelson EL, Bulsara KR, Favors M, Thramann J. Safety of transforaminal lumbar interbody fusion and intervertebral recombinant human bone morphogenetic protein-2. J Neurosurg Spine. 2005;3(6):436-443.
32. Patel VV, Zhao L, Wong P, et al. Controlling bone morphogenetic protein diffusion and bone morphogenetic protein-stimulated bone growth using fibrin glue. Spine. 2006;31(11):1201-1206.
33. Zhang H, Sucato DJ, Welch RD. Recombinant human bone morphogenic protein-2-enhanced anterior spine fusion without bone encroachment into the spinal canal: a histomorphometric study in a thoracoscopically instrumented porcine model. Spine. 2005;30(5):512-518.
TAKE-HOME POINTS
- Use of rhBMP-2 in TLIF cages can result in HO out of the cage into the spinal canal.
- HO from rhBMP-2 in TLIF cages can result in a radiculopathy from compression or inflammatory reaction.
- HO out of the cage into the spinal canal resulting from use of rhBMP-2 in TLIF cages can be adequately diagnosed only with CT.
- HO can appear as a pedicle or pseudo-pedicle.
- Consider potential HO when using rhBMP-2 in TLIF cages.
Tough patient cases from 2017
AGA’s member-only online networking platform, the AGA Community, was the hub for clinical case scenarios in 2017. About 100 deidentified patient cases were submitted to the forum, generating over 475 private and public responses from your peers.
Here is a summary of the three cases that sparked the most discussion among AGA members. You can view all discussions in the forum at community.gastro.org/discussions.
#3 “Esophageal hyperkeratosis” (February 2017)
Patient scenario: Patient was having dysphagia. EGD showed circumferential thickening of esophageal lining in the lower half of the esophagus causing partial obstruction; lumen diameter was 7 mm (scope was able to pass with mild resistance). Human papillomavirus (HPV) stain was negative. Multiple biopsies were negative for malignancy, so the practice did not recommend esophagectomy and believed the symptoms were consistent with hyperkeratosis of esophagus. Endoscopic cryotherapy was being considered.
Question: Has anyone come across a case like this?
#2 Thickened stomach (May 2017)
Patient scenario: A 74-year-old male presented early satiety, anemia, and dyspepsia. EGD showed diffuse moderate erythema of the stomach sparing the antrum, and two small superficial duodenal ulcers. Biopsies showed mild chronic inflammation, duodenitis, and negative for H. pylori. The patient was started on a proton pump inhibitor (PPI).
One month later, patient reported early satiety, a 40-pound weight loss over last few months, nausea and vomiting, with minimal improvement while using the PPI. A CT scan of the abdomen and pelvis showed diffuse thickening of the stomach, but was otherwise unremarkable.
One month after that, a repeated EGD showed moderate erythema with enlarged gastric folds, cobblestone of mucosa, again all sparing the antrum. The colonoscopy results were unremarkable. Gastric biopsies showed mild chronic inflammation. Endoscopic ultrasound showed a thickened gastric wall to 14 mm (normal 5 mm) and fine needle aspiration showed normal gastric foveolar epithelium. The patient received a PEG-J tube to maintain nutrition, and then had a laparoscopic assisted full thickness gastric biopsy, which showed benign hypertrophic gastric smooth muscle tissue.
Serum protein electrophoresis and urine protein electrophoresis test results were normal, with total IgG and IgA normal, total IgM low at 31 (normal 60-265), albumin low, other proteins normal, and immunofixation negative. Prealbumin was low at 5 (normal 15-45). Albumin initially normal and over a couple of days low at 2.6 (normal 3.4-5.0). Total protein initially normal and over a couple of days was low at 6.3 (normal 6.8-8.8). Gastrin level was insignificant on the PPI, in the 400s. Zollinger Ellison gastrin not impressive, and the patient is HIV negative.
Question: With a negative biopsy and other test results, Menetrier’s, malignancy, sarcoidosis, eosinophilic gastroenteritis, and amyloidosis can be ruled out. What could the diagnosis be?
#1 IBD and prior hep B (July 2017)
Patient scenario: A 53-year-old male diagnosed with ulcerative colitis (UC) at outside hospital after presenting with abdominal pain, perforation of sigmoid colon. He underwent total colectomy with ileostomy, which showed he has remnant rectum, and the path of colon showed UC with sigmoid stricture. There is no malignancy or dysplasia, and the terminal ileum included in the resection was normal. He had complicated post-op course with enterocutaneous fistula.
He underwent takedown of ileostomy, small bowel resection and ileostomy revision. Path showed segmental small bowel showing viable mucosa with acute serositis and serial adhesions. Ileal mucosa was normal. Rectum has inflammation, and he has symptoms of mucus, urgency, and blood. He had rectal burning and did not tolerate CANASA® suppository. He did not seem to improve with hydrocortisone suppository either.
In trying to decipher next treatment step, hepatitis panel was done, which showed positive hepatitis B core antibody (IgM). Hepatitis B viral load was undetectable. Hepatitis B surface antibody test (HBsAb) quantitative was 6 (not quite the range for immunity of greater than 10). Hepatitis B “e” antigen (HBeAg) negative and hepatitis B “e” antibody (HBeAb) positive. This patient’s hep B core total was positive and hep B surface antigen was negative.
Question: How would you treat this patient? Would you use Imuran?
Share your difficult patient case for the GI community to help you solve at community.gastro.org/quickpost.
AGA’s member-only online networking platform, the AGA Community, was the hub for clinical case scenarios in 2017. About 100 deidentified patient cases were submitted to the forum, generating over 475 private and public responses from your peers.
Here is a summary of the three cases that sparked the most discussion among AGA members. You can view all discussions in the forum at community.gastro.org/discussions.
#3 “Esophageal hyperkeratosis” (February 2017)
Patient scenario: Patient was having dysphagia. EGD showed circumferential thickening of esophageal lining in the lower half of the esophagus causing partial obstruction; lumen diameter was 7 mm (scope was able to pass with mild resistance). Human papillomavirus (HPV) stain was negative. Multiple biopsies were negative for malignancy, so the practice did not recommend esophagectomy and believed the symptoms were consistent with hyperkeratosis of esophagus. Endoscopic cryotherapy was being considered.
Question: Has anyone come across a case like this?
#2 Thickened stomach (May 2017)
Patient scenario: A 74-year-old male presented early satiety, anemia, and dyspepsia. EGD showed diffuse moderate erythema of the stomach sparing the antrum, and two small superficial duodenal ulcers. Biopsies showed mild chronic inflammation, duodenitis, and negative for H. pylori. The patient was started on a proton pump inhibitor (PPI).
One month later, patient reported early satiety, a 40-pound weight loss over last few months, nausea and vomiting, with minimal improvement while using the PPI. A CT scan of the abdomen and pelvis showed diffuse thickening of the stomach, but was otherwise unremarkable.
One month after that, a repeated EGD showed moderate erythema with enlarged gastric folds, cobblestone of mucosa, again all sparing the antrum. The colonoscopy results were unremarkable. Gastric biopsies showed mild chronic inflammation. Endoscopic ultrasound showed a thickened gastric wall to 14 mm (normal 5 mm) and fine needle aspiration showed normal gastric foveolar epithelium. The patient received a PEG-J tube to maintain nutrition, and then had a laparoscopic assisted full thickness gastric biopsy, which showed benign hypertrophic gastric smooth muscle tissue.
Serum protein electrophoresis and urine protein electrophoresis test results were normal, with total IgG and IgA normal, total IgM low at 31 (normal 60-265), albumin low, other proteins normal, and immunofixation negative. Prealbumin was low at 5 (normal 15-45). Albumin initially normal and over a couple of days low at 2.6 (normal 3.4-5.0). Total protein initially normal and over a couple of days was low at 6.3 (normal 6.8-8.8). Gastrin level was insignificant on the PPI, in the 400s. Zollinger Ellison gastrin not impressive, and the patient is HIV negative.
Question: With a negative biopsy and other test results, Menetrier’s, malignancy, sarcoidosis, eosinophilic gastroenteritis, and amyloidosis can be ruled out. What could the diagnosis be?
#1 IBD and prior hep B (July 2017)
Patient scenario: A 53-year-old male diagnosed with ulcerative colitis (UC) at outside hospital after presenting with abdominal pain, perforation of sigmoid colon. He underwent total colectomy with ileostomy, which showed he has remnant rectum, and the path of colon showed UC with sigmoid stricture. There is no malignancy or dysplasia, and the terminal ileum included in the resection was normal. He had complicated post-op course with enterocutaneous fistula.
He underwent takedown of ileostomy, small bowel resection and ileostomy revision. Path showed segmental small bowel showing viable mucosa with acute serositis and serial adhesions. Ileal mucosa was normal. Rectum has inflammation, and he has symptoms of mucus, urgency, and blood. He had rectal burning and did not tolerate CANASA® suppository. He did not seem to improve with hydrocortisone suppository either.
In trying to decipher next treatment step, hepatitis panel was done, which showed positive hepatitis B core antibody (IgM). Hepatitis B viral load was undetectable. Hepatitis B surface antibody test (HBsAb) quantitative was 6 (not quite the range for immunity of greater than 10). Hepatitis B “e” antigen (HBeAg) negative and hepatitis B “e” antibody (HBeAb) positive. This patient’s hep B core total was positive and hep B surface antigen was negative.
Question: How would you treat this patient? Would you use Imuran?
Share your difficult patient case for the GI community to help you solve at community.gastro.org/quickpost.
AGA’s member-only online networking platform, the AGA Community, was the hub for clinical case scenarios in 2017. About 100 deidentified patient cases were submitted to the forum, generating over 475 private and public responses from your peers.
Here is a summary of the three cases that sparked the most discussion among AGA members. You can view all discussions in the forum at community.gastro.org/discussions.
#3 “Esophageal hyperkeratosis” (February 2017)
Patient scenario: Patient was having dysphagia. EGD showed circumferential thickening of esophageal lining in the lower half of the esophagus causing partial obstruction; lumen diameter was 7 mm (scope was able to pass with mild resistance). Human papillomavirus (HPV) stain was negative. Multiple biopsies were negative for malignancy, so the practice did not recommend esophagectomy and believed the symptoms were consistent with hyperkeratosis of esophagus. Endoscopic cryotherapy was being considered.
Question: Has anyone come across a case like this?
#2 Thickened stomach (May 2017)
Patient scenario: A 74-year-old male presented early satiety, anemia, and dyspepsia. EGD showed diffuse moderate erythema of the stomach sparing the antrum, and two small superficial duodenal ulcers. Biopsies showed mild chronic inflammation, duodenitis, and negative for H. pylori. The patient was started on a proton pump inhibitor (PPI).
One month later, patient reported early satiety, a 40-pound weight loss over last few months, nausea and vomiting, with minimal improvement while using the PPI. A CT scan of the abdomen and pelvis showed diffuse thickening of the stomach, but was otherwise unremarkable.
One month after that, a repeated EGD showed moderate erythema with enlarged gastric folds, cobblestone of mucosa, again all sparing the antrum. The colonoscopy results were unremarkable. Gastric biopsies showed mild chronic inflammation. Endoscopic ultrasound showed a thickened gastric wall to 14 mm (normal 5 mm) and fine needle aspiration showed normal gastric foveolar epithelium. The patient received a PEG-J tube to maintain nutrition, and then had a laparoscopic assisted full thickness gastric biopsy, which showed benign hypertrophic gastric smooth muscle tissue.
Serum protein electrophoresis and urine protein electrophoresis test results were normal, with total IgG and IgA normal, total IgM low at 31 (normal 60-265), albumin low, other proteins normal, and immunofixation negative. Prealbumin was low at 5 (normal 15-45). Albumin initially normal and over a couple of days low at 2.6 (normal 3.4-5.0). Total protein initially normal and over a couple of days was low at 6.3 (normal 6.8-8.8). Gastrin level was insignificant on the PPI, in the 400s. Zollinger Ellison gastrin not impressive, and the patient is HIV negative.
Question: With a negative biopsy and other test results, Menetrier’s, malignancy, sarcoidosis, eosinophilic gastroenteritis, and amyloidosis can be ruled out. What could the diagnosis be?
#1 IBD and prior hep B (July 2017)
Patient scenario: A 53-year-old male diagnosed with ulcerative colitis (UC) at outside hospital after presenting with abdominal pain, perforation of sigmoid colon. He underwent total colectomy with ileostomy, which showed he has remnant rectum, and the path of colon showed UC with sigmoid stricture. There is no malignancy or dysplasia, and the terminal ileum included in the resection was normal. He had complicated post-op course with enterocutaneous fistula.
He underwent takedown of ileostomy, small bowel resection and ileostomy revision. Path showed segmental small bowel showing viable mucosa with acute serositis and serial adhesions. Ileal mucosa was normal. Rectum has inflammation, and he has symptoms of mucus, urgency, and blood. He had rectal burning and did not tolerate CANASA® suppository. He did not seem to improve with hydrocortisone suppository either.
In trying to decipher next treatment step, hepatitis panel was done, which showed positive hepatitis B core antibody (IgM). Hepatitis B viral load was undetectable. Hepatitis B surface antibody test (HBsAb) quantitative was 6 (not quite the range for immunity of greater than 10). Hepatitis B “e” antigen (HBeAg) negative and hepatitis B “e” antibody (HBeAb) positive. This patient’s hep B core total was positive and hep B surface antigen was negative.
Question: How would you treat this patient? Would you use Imuran?
Share your difficult patient case for the GI community to help you solve at community.gastro.org/quickpost.