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Sleep apnea and myocardial preconditioning: A paradigm shift?
The phenomenon of preconditioning reflects complex adaptive responses by living organisms to stimuli such as ischemia, hypoxia, hypothermia, or starvation. Acute ischemic preconditioning, initially described by Murry in 1986 (Circulation. 1986;74[5]:1124), occurs when multiple brief episodes of ischemia followed by reperfusion elicit a protective effect on the heart from a subsequent prolonged period of ischemia, such as a heart attack. This protective effect from ischemic preconditioning can be in the form of a smaller heart attack, lower chance of cardiac arrhythmias, less myocardial cell death, and lower risk of heart muscle failure. The cardioprotective effect of ischemic preconditioning is dependent on the duration and strength of the preconditioning stimulus. If the preconditioning stimulus is too strong or prolonged, detrimental effects on the heart may be observed.
Like ischemic preconditioning, hypoxic preconditioning represents a complex adaptive response that organisms have developed to offset damage inflicted by oxygen deprivation. The concept of hypoxic preconditioning is familiar to humans; for years, athletes have been using hypoxic training (high altitude and other newer technologies) to boost their performance in sporting events. Additionally, there is evidence dating back to before the breakthrough findings of Murry and colleagues who confirm the cardioprotective effects of hypoxia. In 1973, Meerson and colleagues (Am J Cardiol. 1973;31[1]:30) reported that mice exposed to high-altitude hypoxia have reduced mortality and smaller areas of necrotic myocardium after coronary artery occlusion.
Both of the ischemic and hypoxic preconditioning animal experiments mentioned above involve acute exposure to the preconditioning stimuli, resulting in a cardioprotective response for a limited time period. In order to afford a sustained period of cardioprotection, recurrent hypoxic exposure may be necessary. Indeed, recent studies have concentrated on just that; repeated exposure to intermittent hypoxia over a few weeks (Manukhina et al. Exp Biol Med. 2013;238[12]:1413) results in robust cardioprotection after coronary artery occlusion and reperfusion.
Despite the convincing cardioprotective discoveries from ischemic and hypoxic preconditioning, translation into clinical practice as a therapeutic modality is absent. This is partly because human beings are more complex than animals. They have comorbidities and are affected by aging, both of which may alter the milieu for preconditioning stimuli. Furthermore, the therapeutic range for any given preconditioning stimulus is unknown.
Sleep apnea (SA) is exceedingly prevalent in the United States. In SA, an individual stops breathing either completely (apnea) or partially (hypopnea) during sleep resulting in intermittent hypoxia, with arousal from sleep and resumption of breathing leading to reoxygenation. Hence, SA is characterized by intermittent hypoxia followed by reoxygenation. So, one can speculate that SA could exert cardioprotective effects as seen in hypoxic preconditioning and ischemic preconditioning. It is important to note, however, that SA is associated with hypercapnic intermittent hypoxia, whereas most of the investigations on ischemic preconditioning and intermittent hypoxia are with eucapnia or hypocapnia.
The potentially cardioprotective role of SA is supported by a growing body of complementary research that indicates that coronary collateral flow is higher in patients with SA vs. control subjects (Steiner. Chest. 2010;137[3]:516) and that there is an increased mobilization, proliferation, and angiogenic capacity of endothelial progenitor cells from patients with myocardial infarction and SA as compared with cells from controls subjects without SA (Berger. Am J Respir Crit Care Med. 2013;187[1]:90). Some epidemiologic data support a weaker relationship between SA and coronary ischemic events compared with other cardiovascular events (Gottlieb. Circulation. 2010;122[4]:352). Hypoxic preconditioning may explain the relatively decreased pro-thrombotic influence of SA in the coronary vascular bed. Nevertheless, more research is needed to determine if SA is cardioprotective. If, however, cardioprotection from SA is confirmed, it may contribute to a paradigm shift in how SA is considered in relationship to coronary heart disease. Furthermore, future investigations would need to focus on what dose and duration of SA is needed for cardioprotection to occur. Prospective studies may also provide an opportunity for investigating interindividual variability in the susceptibility of the myocardium to the hypoxic preconditioning stimulus from SA.
This article highlights how complex the relationship between hypoxia and myocardial response is. This is further supported by results from a recent clinical trial, AVOID (Air Versus Oxygen In ST-elevation MyocarDial Infarction) (Stub. Circulation. 2015;131[24]:2143). Results from the AVOID trial report that routine oxygen use in normoxic patients hospitalized with a heart attack was not beneficial and, in fact, was harmful. Patients who received oxygen had more myocardial injury than those who did not. Therefore, even though for decades we thought that oxygen therapy helps hospitalized heart attack patients, results from the AVOID trial have initiated a paradigm shift. It remains to be determined whether such a paradigm shift will follow for sleep apnea.
Dr. Shah is with the department of epidemiology and population health, Albert Einstein College of Medicine, N.Y.
The phenomenon of preconditioning reflects complex adaptive responses by living organisms to stimuli such as ischemia, hypoxia, hypothermia, or starvation. Acute ischemic preconditioning, initially described by Murry in 1986 (Circulation. 1986;74[5]:1124), occurs when multiple brief episodes of ischemia followed by reperfusion elicit a protective effect on the heart from a subsequent prolonged period of ischemia, such as a heart attack. This protective effect from ischemic preconditioning can be in the form of a smaller heart attack, lower chance of cardiac arrhythmias, less myocardial cell death, and lower risk of heart muscle failure. The cardioprotective effect of ischemic preconditioning is dependent on the duration and strength of the preconditioning stimulus. If the preconditioning stimulus is too strong or prolonged, detrimental effects on the heart may be observed.
Like ischemic preconditioning, hypoxic preconditioning represents a complex adaptive response that organisms have developed to offset damage inflicted by oxygen deprivation. The concept of hypoxic preconditioning is familiar to humans; for years, athletes have been using hypoxic training (high altitude and other newer technologies) to boost their performance in sporting events. Additionally, there is evidence dating back to before the breakthrough findings of Murry and colleagues who confirm the cardioprotective effects of hypoxia. In 1973, Meerson and colleagues (Am J Cardiol. 1973;31[1]:30) reported that mice exposed to high-altitude hypoxia have reduced mortality and smaller areas of necrotic myocardium after coronary artery occlusion.
Both of the ischemic and hypoxic preconditioning animal experiments mentioned above involve acute exposure to the preconditioning stimuli, resulting in a cardioprotective response for a limited time period. In order to afford a sustained period of cardioprotection, recurrent hypoxic exposure may be necessary. Indeed, recent studies have concentrated on just that; repeated exposure to intermittent hypoxia over a few weeks (Manukhina et al. Exp Biol Med. 2013;238[12]:1413) results in robust cardioprotection after coronary artery occlusion and reperfusion.
Despite the convincing cardioprotective discoveries from ischemic and hypoxic preconditioning, translation into clinical practice as a therapeutic modality is absent. This is partly because human beings are more complex than animals. They have comorbidities and are affected by aging, both of which may alter the milieu for preconditioning stimuli. Furthermore, the therapeutic range for any given preconditioning stimulus is unknown.
Sleep apnea (SA) is exceedingly prevalent in the United States. In SA, an individual stops breathing either completely (apnea) or partially (hypopnea) during sleep resulting in intermittent hypoxia, with arousal from sleep and resumption of breathing leading to reoxygenation. Hence, SA is characterized by intermittent hypoxia followed by reoxygenation. So, one can speculate that SA could exert cardioprotective effects as seen in hypoxic preconditioning and ischemic preconditioning. It is important to note, however, that SA is associated with hypercapnic intermittent hypoxia, whereas most of the investigations on ischemic preconditioning and intermittent hypoxia are with eucapnia or hypocapnia.
The potentially cardioprotective role of SA is supported by a growing body of complementary research that indicates that coronary collateral flow is higher in patients with SA vs. control subjects (Steiner. Chest. 2010;137[3]:516) and that there is an increased mobilization, proliferation, and angiogenic capacity of endothelial progenitor cells from patients with myocardial infarction and SA as compared with cells from controls subjects without SA (Berger. Am J Respir Crit Care Med. 2013;187[1]:90). Some epidemiologic data support a weaker relationship between SA and coronary ischemic events compared with other cardiovascular events (Gottlieb. Circulation. 2010;122[4]:352). Hypoxic preconditioning may explain the relatively decreased pro-thrombotic influence of SA in the coronary vascular bed. Nevertheless, more research is needed to determine if SA is cardioprotective. If, however, cardioprotection from SA is confirmed, it may contribute to a paradigm shift in how SA is considered in relationship to coronary heart disease. Furthermore, future investigations would need to focus on what dose and duration of SA is needed for cardioprotection to occur. Prospective studies may also provide an opportunity for investigating interindividual variability in the susceptibility of the myocardium to the hypoxic preconditioning stimulus from SA.
This article highlights how complex the relationship between hypoxia and myocardial response is. This is further supported by results from a recent clinical trial, AVOID (Air Versus Oxygen In ST-elevation MyocarDial Infarction) (Stub. Circulation. 2015;131[24]:2143). Results from the AVOID trial report that routine oxygen use in normoxic patients hospitalized with a heart attack was not beneficial and, in fact, was harmful. Patients who received oxygen had more myocardial injury than those who did not. Therefore, even though for decades we thought that oxygen therapy helps hospitalized heart attack patients, results from the AVOID trial have initiated a paradigm shift. It remains to be determined whether such a paradigm shift will follow for sleep apnea.
Dr. Shah is with the department of epidemiology and population health, Albert Einstein College of Medicine, N.Y.
The phenomenon of preconditioning reflects complex adaptive responses by living organisms to stimuli such as ischemia, hypoxia, hypothermia, or starvation. Acute ischemic preconditioning, initially described by Murry in 1986 (Circulation. 1986;74[5]:1124), occurs when multiple brief episodes of ischemia followed by reperfusion elicit a protective effect on the heart from a subsequent prolonged period of ischemia, such as a heart attack. This protective effect from ischemic preconditioning can be in the form of a smaller heart attack, lower chance of cardiac arrhythmias, less myocardial cell death, and lower risk of heart muscle failure. The cardioprotective effect of ischemic preconditioning is dependent on the duration and strength of the preconditioning stimulus. If the preconditioning stimulus is too strong or prolonged, detrimental effects on the heart may be observed.
Like ischemic preconditioning, hypoxic preconditioning represents a complex adaptive response that organisms have developed to offset damage inflicted by oxygen deprivation. The concept of hypoxic preconditioning is familiar to humans; for years, athletes have been using hypoxic training (high altitude and other newer technologies) to boost their performance in sporting events. Additionally, there is evidence dating back to before the breakthrough findings of Murry and colleagues who confirm the cardioprotective effects of hypoxia. In 1973, Meerson and colleagues (Am J Cardiol. 1973;31[1]:30) reported that mice exposed to high-altitude hypoxia have reduced mortality and smaller areas of necrotic myocardium after coronary artery occlusion.
Both of the ischemic and hypoxic preconditioning animal experiments mentioned above involve acute exposure to the preconditioning stimuli, resulting in a cardioprotective response for a limited time period. In order to afford a sustained period of cardioprotection, recurrent hypoxic exposure may be necessary. Indeed, recent studies have concentrated on just that; repeated exposure to intermittent hypoxia over a few weeks (Manukhina et al. Exp Biol Med. 2013;238[12]:1413) results in robust cardioprotection after coronary artery occlusion and reperfusion.
Despite the convincing cardioprotective discoveries from ischemic and hypoxic preconditioning, translation into clinical practice as a therapeutic modality is absent. This is partly because human beings are more complex than animals. They have comorbidities and are affected by aging, both of which may alter the milieu for preconditioning stimuli. Furthermore, the therapeutic range for any given preconditioning stimulus is unknown.
Sleep apnea (SA) is exceedingly prevalent in the United States. In SA, an individual stops breathing either completely (apnea) or partially (hypopnea) during sleep resulting in intermittent hypoxia, with arousal from sleep and resumption of breathing leading to reoxygenation. Hence, SA is characterized by intermittent hypoxia followed by reoxygenation. So, one can speculate that SA could exert cardioprotective effects as seen in hypoxic preconditioning and ischemic preconditioning. It is important to note, however, that SA is associated with hypercapnic intermittent hypoxia, whereas most of the investigations on ischemic preconditioning and intermittent hypoxia are with eucapnia or hypocapnia.
The potentially cardioprotective role of SA is supported by a growing body of complementary research that indicates that coronary collateral flow is higher in patients with SA vs. control subjects (Steiner. Chest. 2010;137[3]:516) and that there is an increased mobilization, proliferation, and angiogenic capacity of endothelial progenitor cells from patients with myocardial infarction and SA as compared with cells from controls subjects without SA (Berger. Am J Respir Crit Care Med. 2013;187[1]:90). Some epidemiologic data support a weaker relationship between SA and coronary ischemic events compared with other cardiovascular events (Gottlieb. Circulation. 2010;122[4]:352). Hypoxic preconditioning may explain the relatively decreased pro-thrombotic influence of SA in the coronary vascular bed. Nevertheless, more research is needed to determine if SA is cardioprotective. If, however, cardioprotection from SA is confirmed, it may contribute to a paradigm shift in how SA is considered in relationship to coronary heart disease. Furthermore, future investigations would need to focus on what dose and duration of SA is needed for cardioprotection to occur. Prospective studies may also provide an opportunity for investigating interindividual variability in the susceptibility of the myocardium to the hypoxic preconditioning stimulus from SA.
This article highlights how complex the relationship between hypoxia and myocardial response is. This is further supported by results from a recent clinical trial, AVOID (Air Versus Oxygen In ST-elevation MyocarDial Infarction) (Stub. Circulation. 2015;131[24]:2143). Results from the AVOID trial report that routine oxygen use in normoxic patients hospitalized with a heart attack was not beneficial and, in fact, was harmful. Patients who received oxygen had more myocardial injury than those who did not. Therefore, even though for decades we thought that oxygen therapy helps hospitalized heart attack patients, results from the AVOID trial have initiated a paradigm shift. It remains to be determined whether such a paradigm shift will follow for sleep apnea.
Dr. Shah is with the department of epidemiology and population health, Albert Einstein College of Medicine, N.Y.
Networks
Occupational and Environmental Health
Incident sarcoidosis
The history of sarcoidosis dates back to 1869, when Dr. Jonathan Hutchinson described symmetrical purple skin plaques on the legs and hands of a coal-wharf worker (James and Sharma. Curr Opin Pulm Med. 2002;8[5]:416). However, despite its distant beginning, much remains unknown. It has been hypothesized that environmental factors play a pivotal role in disease onset and course, as is evidenced by the notable exposure in the first historical case.
Research has shown environmental factors, such as wood smoke, tree pollen, insecticides, and mold; as well as occupational exposures, such as flight deck work on aircraft carriers, metalworking, construction, and firefighting, carry increased risk of sarcoidosis (Newman et al. Am J Respir Crit Care Med. 2004;170[12]:1324; Newman and Newman. Curr Opin Allergy Clin Immunol. 2012;12[2]:145). A significantly high annual incidence of sarcoidosis was first demonstrated in FDNY firefighters between 1985 and 1998; 12.9/100,000, as compared with 2.5 to 7.6/100,000 for U.S. white men (Prezant et al. Chest. 1999;116[5]:1183).
Following the attack of the World Trade Center (WTC) on September 11, 2001, a further increase in sarcoidosis incidence was found in FDNY firefighters exposed to WTC “dust” during the collapse and rescue/recovery effort (Izbicki et al. Chest. 2007;131[5]:1414). As of 2015, a total of 75 FDNY firefighters have been identified as having new post-9/11 sarcoidosis.
Since the WTC-exposed FDNY firefighters with new-onset sarcoidosis since September 11, 2001 can be considered to have had a WTC “trigger,” we have a unique opportunity to define the clinical patterns and outcomes of incident sarcoidosis following a distinct exposure. Members of the Occupational and Environmental NetWork Steering Committee are currently investigating this aim and others in a National Institute of Occupational Safety and Health (NIOSH)-granted cohort study. We hypothesize that the patterns of organ involvement, and time course of disease progression or resolution, may significantly differ in this group as compared with the general population. Preliminary results of our study of WTC-exposed FDNY firefighters will be presented at CHEST 2016 in Los Angeles.
Kerry Hena, MD
Physician-in-Training Member
Palliative and End-of-Life Care
Integrated palliative care for mechanical circulatory support
Patients with advanced heart failure (AHF) have well-documented needs for comprehensive supportive care services in the critical care setting. Notable symptom burden, high morbidity and mortality, prognostic uncertainty, and need for care coordination across hospital settings pave the way for palliative care (PC) teams to work symbiotically with advanced heart failure specialists and intensivists. Furthermore, the expanded availability of mechanical circulatory support (MCS) technology extends these clinical and ethical challenges to balancing longevity, quality of life, and resource utilization, most prominently in the ICU.
To date, collaborations between PC, AHF specialists, and critical care have tended to be reactive, not proactive – palliative consultation usually occurs after a medical or surgical crisis (for example, the massive stroke, MCS thrombus, sepsis, and multiorgan failure) or after a prolonged ICU stay without clear improvement in patient function or prognosis. This reactive consult may be misperceived by patient and family as “giving up.”
At our institution, we have worked to develop a model of seamless integration of interdisciplinary palliative care consultation upstream in advanced heart failure patient care that aims to preempt many dilemmas in the ICU around complex medical decision making and end-of-life care. Through development of therapeutic supportive care relationships, preparedness planning, and discussions of goals of care early in treatment pathways involving critical care resources – including MCS evaluation and cardiac transplantation – this model purports to strengthen appropriate critical care delivery for patients with advanced heart failure. This model has evolved to where PC consultation becomes a structured part of the preoperative evaluation of all candidates for left-ventricular assist device as destination therapy (LVAD-DT). The result is a collaborative approach where patients and families see PC as part of the continuum of whole-person AHF care, rather than a negative alternative.
MCS implantation is on the rise. While MCS technology continues to evolve, its recipients remain seriously ill. Normalizing and integrating PC consultation as part of high quality AHF and critical care sends an important message to patients and families: regardless of clinical outcome, relief from suffering matters throughout the trajectory of the illness experience.
Hunter Groninger, MD
Steering Committee Member
Respiratory Care NetWork
Professional relationships in RC
At the 2015 meeting of the American Association for Respiratory Care (AARC) in Tampa, there were more than 20 presentations given by FCCPs! Also, a majority of CHEST’s Respiratory Care NetWork’s steering committee was in attendance at the meeting. To other members of CHEST, that might seem rather unusual. However, many CHEST members have connections with the field of respiratory care. In addition, CHEST as an organization has a professional relationship with the respiratory care field. CHEST has more than 10 official liaisons to respiratory care professional organizations.
Those organizations include: The Commission for Accreditation for Respiratory Care, which credentials all RC educational programs; The National Board for Respiratory Care, which provides the credentialing examinations for all RC practitioners in the United States; The National Association for Medical Direction for Respiratory Care (NAMDRC); the Board of Medical Advisors to the AARC; and the Respiratory Compromise Institute.
The Respiratory Care NetWork has the responsibility of identifying and nominating CHEST members for these liaison positions. These volunteer positions do involve work, yet past and present liaisons have enthusiastically fulfilled their respective roles. As one recently noted, “This work has been some of the most important endeavors of my professional career.”
We are always seeking volunteers for these positions, which vary in time commitment and type of work involved. Please contact the Respiratory Care NetWork (mkosinski@chestnet.org) for further information. These organizations accomplish the type of things that made us all want to get into medicine. Be a part of those important efforts!
Thomas Fuhrman, MD, FCCP
Steering Committee Member
Sleep Medicine
Listening to patient voices: Sleep Apnea Patient-Centered Outcomes Network (MyApnea.org)
The US Department of Transportation’s (DOT) Federal Motor Carrier Safety Administration (FMCSA) and Federal Railroad Administration (FRA) recently called for input for obstructive sleep apnea screening and treatment for transportation workers. The DOT (https://www.transportation.gov) encouraged input from the public regarding this important transportation safety issue. This concept of engaging the public (which includes patients) with sleep disorders is gaining momentum as patients are increasingly partnering with researchers, clinicians, and policy makers to improve the delivery of care and research efforts in sleep medicine.
A remarkable example of such an effort is the Sleep Apnea Patient-Centered Outcomes Network (SAPCON; MyApnea.Org) (Redline et al. JCSM. 2016;12[7]:1053). This patient-powered research network was initiated in 2013 to improve the diagnosis and treatment of sleep apnea through the active engagement of patients, families, researchers, and healthcare providers in a virtual community that facilitates patient-centered research. The need for such an initiative reflects the paucity of patient-centric evidence from large populations to inform insurers, public policy makers, medical schools, and clinicians on the best ways to screen, diagnose, and treat patients with sleep apnea.
As of August 2016, over 8,000 individuals across the globe have joined SAPCON. There are approximately 500 unique visitors to the site per day, with over 2,500 posts on over 250 topics, including blogs on a variety of emerging research and public health topics. Among these topics are driving and general transportation safety concerns. Further engagement of patients and key stakeholders through forums and patient-centered networks can promote the “patient voice” in public policy, while linking patient needs for better information with responsive research and policy development.
Neomi Shah, MD, MPH
Steering Committee Member
Occupational and Environmental Health
Incident sarcoidosis
The history of sarcoidosis dates back to 1869, when Dr. Jonathan Hutchinson described symmetrical purple skin plaques on the legs and hands of a coal-wharf worker (James and Sharma. Curr Opin Pulm Med. 2002;8[5]:416). However, despite its distant beginning, much remains unknown. It has been hypothesized that environmental factors play a pivotal role in disease onset and course, as is evidenced by the notable exposure in the first historical case.
Research has shown environmental factors, such as wood smoke, tree pollen, insecticides, and mold; as well as occupational exposures, such as flight deck work on aircraft carriers, metalworking, construction, and firefighting, carry increased risk of sarcoidosis (Newman et al. Am J Respir Crit Care Med. 2004;170[12]:1324; Newman and Newman. Curr Opin Allergy Clin Immunol. 2012;12[2]:145). A significantly high annual incidence of sarcoidosis was first demonstrated in FDNY firefighters between 1985 and 1998; 12.9/100,000, as compared with 2.5 to 7.6/100,000 for U.S. white men (Prezant et al. Chest. 1999;116[5]:1183).
Following the attack of the World Trade Center (WTC) on September 11, 2001, a further increase in sarcoidosis incidence was found in FDNY firefighters exposed to WTC “dust” during the collapse and rescue/recovery effort (Izbicki et al. Chest. 2007;131[5]:1414). As of 2015, a total of 75 FDNY firefighters have been identified as having new post-9/11 sarcoidosis.
Since the WTC-exposed FDNY firefighters with new-onset sarcoidosis since September 11, 2001 can be considered to have had a WTC “trigger,” we have a unique opportunity to define the clinical patterns and outcomes of incident sarcoidosis following a distinct exposure. Members of the Occupational and Environmental NetWork Steering Committee are currently investigating this aim and others in a National Institute of Occupational Safety and Health (NIOSH)-granted cohort study. We hypothesize that the patterns of organ involvement, and time course of disease progression or resolution, may significantly differ in this group as compared with the general population. Preliminary results of our study of WTC-exposed FDNY firefighters will be presented at CHEST 2016 in Los Angeles.
Kerry Hena, MD
Physician-in-Training Member
Palliative and End-of-Life Care
Integrated palliative care for mechanical circulatory support
Patients with advanced heart failure (AHF) have well-documented needs for comprehensive supportive care services in the critical care setting. Notable symptom burden, high morbidity and mortality, prognostic uncertainty, and need for care coordination across hospital settings pave the way for palliative care (PC) teams to work symbiotically with advanced heart failure specialists and intensivists. Furthermore, the expanded availability of mechanical circulatory support (MCS) technology extends these clinical and ethical challenges to balancing longevity, quality of life, and resource utilization, most prominently in the ICU.
To date, collaborations between PC, AHF specialists, and critical care have tended to be reactive, not proactive – palliative consultation usually occurs after a medical or surgical crisis (for example, the massive stroke, MCS thrombus, sepsis, and multiorgan failure) or after a prolonged ICU stay without clear improvement in patient function or prognosis. This reactive consult may be misperceived by patient and family as “giving up.”
At our institution, we have worked to develop a model of seamless integration of interdisciplinary palliative care consultation upstream in advanced heart failure patient care that aims to preempt many dilemmas in the ICU around complex medical decision making and end-of-life care. Through development of therapeutic supportive care relationships, preparedness planning, and discussions of goals of care early in treatment pathways involving critical care resources – including MCS evaluation and cardiac transplantation – this model purports to strengthen appropriate critical care delivery for patients with advanced heart failure. This model has evolved to where PC consultation becomes a structured part of the preoperative evaluation of all candidates for left-ventricular assist device as destination therapy (LVAD-DT). The result is a collaborative approach where patients and families see PC as part of the continuum of whole-person AHF care, rather than a negative alternative.
MCS implantation is on the rise. While MCS technology continues to evolve, its recipients remain seriously ill. Normalizing and integrating PC consultation as part of high quality AHF and critical care sends an important message to patients and families: regardless of clinical outcome, relief from suffering matters throughout the trajectory of the illness experience.
Hunter Groninger, MD
Steering Committee Member
Respiratory Care NetWork
Professional relationships in RC
At the 2015 meeting of the American Association for Respiratory Care (AARC) in Tampa, there were more than 20 presentations given by FCCPs! Also, a majority of CHEST’s Respiratory Care NetWork’s steering committee was in attendance at the meeting. To other members of CHEST, that might seem rather unusual. However, many CHEST members have connections with the field of respiratory care. In addition, CHEST as an organization has a professional relationship with the respiratory care field. CHEST has more than 10 official liaisons to respiratory care professional organizations.
Those organizations include: The Commission for Accreditation for Respiratory Care, which credentials all RC educational programs; The National Board for Respiratory Care, which provides the credentialing examinations for all RC practitioners in the United States; The National Association for Medical Direction for Respiratory Care (NAMDRC); the Board of Medical Advisors to the AARC; and the Respiratory Compromise Institute.
The Respiratory Care NetWork has the responsibility of identifying and nominating CHEST members for these liaison positions. These volunteer positions do involve work, yet past and present liaisons have enthusiastically fulfilled their respective roles. As one recently noted, “This work has been some of the most important endeavors of my professional career.”
We are always seeking volunteers for these positions, which vary in time commitment and type of work involved. Please contact the Respiratory Care NetWork (mkosinski@chestnet.org) for further information. These organizations accomplish the type of things that made us all want to get into medicine. Be a part of those important efforts!
Thomas Fuhrman, MD, FCCP
Steering Committee Member
Sleep Medicine
Listening to patient voices: Sleep Apnea Patient-Centered Outcomes Network (MyApnea.org)
The US Department of Transportation’s (DOT) Federal Motor Carrier Safety Administration (FMCSA) and Federal Railroad Administration (FRA) recently called for input for obstructive sleep apnea screening and treatment for transportation workers. The DOT (https://www.transportation.gov) encouraged input from the public regarding this important transportation safety issue. This concept of engaging the public (which includes patients) with sleep disorders is gaining momentum as patients are increasingly partnering with researchers, clinicians, and policy makers to improve the delivery of care and research efforts in sleep medicine.
A remarkable example of such an effort is the Sleep Apnea Patient-Centered Outcomes Network (SAPCON; MyApnea.Org) (Redline et al. JCSM. 2016;12[7]:1053). This patient-powered research network was initiated in 2013 to improve the diagnosis and treatment of sleep apnea through the active engagement of patients, families, researchers, and healthcare providers in a virtual community that facilitates patient-centered research. The need for such an initiative reflects the paucity of patient-centric evidence from large populations to inform insurers, public policy makers, medical schools, and clinicians on the best ways to screen, diagnose, and treat patients with sleep apnea.
As of August 2016, over 8,000 individuals across the globe have joined SAPCON. There are approximately 500 unique visitors to the site per day, with over 2,500 posts on over 250 topics, including blogs on a variety of emerging research and public health topics. Among these topics are driving and general transportation safety concerns. Further engagement of patients and key stakeholders through forums and patient-centered networks can promote the “patient voice” in public policy, while linking patient needs for better information with responsive research and policy development.
Neomi Shah, MD, MPH
Steering Committee Member
Occupational and Environmental Health
Incident sarcoidosis
The history of sarcoidosis dates back to 1869, when Dr. Jonathan Hutchinson described symmetrical purple skin plaques on the legs and hands of a coal-wharf worker (James and Sharma. Curr Opin Pulm Med. 2002;8[5]:416). However, despite its distant beginning, much remains unknown. It has been hypothesized that environmental factors play a pivotal role in disease onset and course, as is evidenced by the notable exposure in the first historical case.
Research has shown environmental factors, such as wood smoke, tree pollen, insecticides, and mold; as well as occupational exposures, such as flight deck work on aircraft carriers, metalworking, construction, and firefighting, carry increased risk of sarcoidosis (Newman et al. Am J Respir Crit Care Med. 2004;170[12]:1324; Newman and Newman. Curr Opin Allergy Clin Immunol. 2012;12[2]:145). A significantly high annual incidence of sarcoidosis was first demonstrated in FDNY firefighters between 1985 and 1998; 12.9/100,000, as compared with 2.5 to 7.6/100,000 for U.S. white men (Prezant et al. Chest. 1999;116[5]:1183).
Following the attack of the World Trade Center (WTC) on September 11, 2001, a further increase in sarcoidosis incidence was found in FDNY firefighters exposed to WTC “dust” during the collapse and rescue/recovery effort (Izbicki et al. Chest. 2007;131[5]:1414). As of 2015, a total of 75 FDNY firefighters have been identified as having new post-9/11 sarcoidosis.
Since the WTC-exposed FDNY firefighters with new-onset sarcoidosis since September 11, 2001 can be considered to have had a WTC “trigger,” we have a unique opportunity to define the clinical patterns and outcomes of incident sarcoidosis following a distinct exposure. Members of the Occupational and Environmental NetWork Steering Committee are currently investigating this aim and others in a National Institute of Occupational Safety and Health (NIOSH)-granted cohort study. We hypothesize that the patterns of organ involvement, and time course of disease progression or resolution, may significantly differ in this group as compared with the general population. Preliminary results of our study of WTC-exposed FDNY firefighters will be presented at CHEST 2016 in Los Angeles.
Kerry Hena, MD
Physician-in-Training Member
Palliative and End-of-Life Care
Integrated palliative care for mechanical circulatory support
Patients with advanced heart failure (AHF) have well-documented needs for comprehensive supportive care services in the critical care setting. Notable symptom burden, high morbidity and mortality, prognostic uncertainty, and need for care coordination across hospital settings pave the way for palliative care (PC) teams to work symbiotically with advanced heart failure specialists and intensivists. Furthermore, the expanded availability of mechanical circulatory support (MCS) technology extends these clinical and ethical challenges to balancing longevity, quality of life, and resource utilization, most prominently in the ICU.
To date, collaborations between PC, AHF specialists, and critical care have tended to be reactive, not proactive – palliative consultation usually occurs after a medical or surgical crisis (for example, the massive stroke, MCS thrombus, sepsis, and multiorgan failure) or after a prolonged ICU stay without clear improvement in patient function or prognosis. This reactive consult may be misperceived by patient and family as “giving up.”
At our institution, we have worked to develop a model of seamless integration of interdisciplinary palliative care consultation upstream in advanced heart failure patient care that aims to preempt many dilemmas in the ICU around complex medical decision making and end-of-life care. Through development of therapeutic supportive care relationships, preparedness planning, and discussions of goals of care early in treatment pathways involving critical care resources – including MCS evaluation and cardiac transplantation – this model purports to strengthen appropriate critical care delivery for patients with advanced heart failure. This model has evolved to where PC consultation becomes a structured part of the preoperative evaluation of all candidates for left-ventricular assist device as destination therapy (LVAD-DT). The result is a collaborative approach where patients and families see PC as part of the continuum of whole-person AHF care, rather than a negative alternative.
MCS implantation is on the rise. While MCS technology continues to evolve, its recipients remain seriously ill. Normalizing and integrating PC consultation as part of high quality AHF and critical care sends an important message to patients and families: regardless of clinical outcome, relief from suffering matters throughout the trajectory of the illness experience.
Hunter Groninger, MD
Steering Committee Member
Respiratory Care NetWork
Professional relationships in RC
At the 2015 meeting of the American Association for Respiratory Care (AARC) in Tampa, there were more than 20 presentations given by FCCPs! Also, a majority of CHEST’s Respiratory Care NetWork’s steering committee was in attendance at the meeting. To other members of CHEST, that might seem rather unusual. However, many CHEST members have connections with the field of respiratory care. In addition, CHEST as an organization has a professional relationship with the respiratory care field. CHEST has more than 10 official liaisons to respiratory care professional organizations.
Those organizations include: The Commission for Accreditation for Respiratory Care, which credentials all RC educational programs; The National Board for Respiratory Care, which provides the credentialing examinations for all RC practitioners in the United States; The National Association for Medical Direction for Respiratory Care (NAMDRC); the Board of Medical Advisors to the AARC; and the Respiratory Compromise Institute.
The Respiratory Care NetWork has the responsibility of identifying and nominating CHEST members for these liaison positions. These volunteer positions do involve work, yet past and present liaisons have enthusiastically fulfilled their respective roles. As one recently noted, “This work has been some of the most important endeavors of my professional career.”
We are always seeking volunteers for these positions, which vary in time commitment and type of work involved. Please contact the Respiratory Care NetWork (mkosinski@chestnet.org) for further information. These organizations accomplish the type of things that made us all want to get into medicine. Be a part of those important efforts!
Thomas Fuhrman, MD, FCCP
Steering Committee Member
Sleep Medicine
Listening to patient voices: Sleep Apnea Patient-Centered Outcomes Network (MyApnea.org)
The US Department of Transportation’s (DOT) Federal Motor Carrier Safety Administration (FMCSA) and Federal Railroad Administration (FRA) recently called for input for obstructive sleep apnea screening and treatment for transportation workers. The DOT (https://www.transportation.gov) encouraged input from the public regarding this important transportation safety issue. This concept of engaging the public (which includes patients) with sleep disorders is gaining momentum as patients are increasingly partnering with researchers, clinicians, and policy makers to improve the delivery of care and research efforts in sleep medicine.
A remarkable example of such an effort is the Sleep Apnea Patient-Centered Outcomes Network (SAPCON; MyApnea.Org) (Redline et al. JCSM. 2016;12[7]:1053). This patient-powered research network was initiated in 2013 to improve the diagnosis and treatment of sleep apnea through the active engagement of patients, families, researchers, and healthcare providers in a virtual community that facilitates patient-centered research. The need for such an initiative reflects the paucity of patient-centric evidence from large populations to inform insurers, public policy makers, medical schools, and clinicians on the best ways to screen, diagnose, and treat patients with sleep apnea.
As of August 2016, over 8,000 individuals across the globe have joined SAPCON. There are approximately 500 unique visitors to the site per day, with over 2,500 posts on over 250 topics, including blogs on a variety of emerging research and public health topics. Among these topics are driving and general transportation safety concerns. Further engagement of patients and key stakeholders through forums and patient-centered networks can promote the “patient voice” in public policy, while linking patient needs for better information with responsive research and policy development.
Neomi Shah, MD, MPH
Steering Committee Member
Los Angeles Inspires With Arts, Culture
Los Angeles has a flare for the dramatic, and we’re not just talking about Hollywood’s fast-paced, larger-than-life movie industry. When you visit Los Angeles, October 22 – 26, for CHEST 2016, be sure to check out the assortment of arts and culture venues located nearby your home base at CHEST 2016.
Los Angeles has more museums and theaters than any other U.S. city, and we’ll highlight a few local favorites below. For more information on L.A.’s thriving arts and culture scene, check out discoverlosangeles.com.
• The Dorothy Chandler Pavilion – (7-minute drive) – This hall is part of the Los Angeles music center. On October 22 – 23, watch three major U.S. ballet companies share the stage in Celebrate Forsythe. Or, take in The Source, a music-theater production about Chelsea (formerly Bradley) Manning and WikiLeaks.
• The Ahmanson Theatre – (7-minute drive) – This theater is also part of the Los Angeles music center. Be captivated by a 2016 Tony Award–winning play, A View from the Bridge.
• Walt Disney Concert Hall – (6-minute drive) – Home to the Los Angeles Philharmonic Orchestra and the Los Angeles Master Chorale, it is also part of the Los Angeles music center. Listen to the beautiful sounds of Mahler’s Ninth or Hilary Hahn on violin.
• MOCA Grand – (5-minute drive) – The Museum of Contemporary Art has three locations in Los Angeles. The main branch, located on Grand Avenue, is the closest to the convention center. Check out the museum’s main galleries at this location.
• The Getty Center – (30-minute drive) – See spectacular art and architecture at the top of Los Angeles.
Note: all estimated times assume you are starting at the Los Angeles Convention Center.
Los Angeles’ arts and culture scene is sure to inspire you, and CHEST 2016 will move you with the latest clinical information in chest medicine. Join us at CHEST 2016, and you won’t miss a beat with cutting-edge sessions and simulation training designed to update you on the latest patient care strategies. You will be part of an international community of innovative problem solvers. Learn more and register today at chestmeeting.chestnet.org.
Los Angeles has a flare for the dramatic, and we’re not just talking about Hollywood’s fast-paced, larger-than-life movie industry. When you visit Los Angeles, October 22 – 26, for CHEST 2016, be sure to check out the assortment of arts and culture venues located nearby your home base at CHEST 2016.
Los Angeles has more museums and theaters than any other U.S. city, and we’ll highlight a few local favorites below. For more information on L.A.’s thriving arts and culture scene, check out discoverlosangeles.com.
• The Dorothy Chandler Pavilion – (7-minute drive) – This hall is part of the Los Angeles music center. On October 22 – 23, watch three major U.S. ballet companies share the stage in Celebrate Forsythe. Or, take in The Source, a music-theater production about Chelsea (formerly Bradley) Manning and WikiLeaks.
• The Ahmanson Theatre – (7-minute drive) – This theater is also part of the Los Angeles music center. Be captivated by a 2016 Tony Award–winning play, A View from the Bridge.
• Walt Disney Concert Hall – (6-minute drive) – Home to the Los Angeles Philharmonic Orchestra and the Los Angeles Master Chorale, it is also part of the Los Angeles music center. Listen to the beautiful sounds of Mahler’s Ninth or Hilary Hahn on violin.
• MOCA Grand – (5-minute drive) – The Museum of Contemporary Art has three locations in Los Angeles. The main branch, located on Grand Avenue, is the closest to the convention center. Check out the museum’s main galleries at this location.
• The Getty Center – (30-minute drive) – See spectacular art and architecture at the top of Los Angeles.
Note: all estimated times assume you are starting at the Los Angeles Convention Center.
Los Angeles’ arts and culture scene is sure to inspire you, and CHEST 2016 will move you with the latest clinical information in chest medicine. Join us at CHEST 2016, and you won’t miss a beat with cutting-edge sessions and simulation training designed to update you on the latest patient care strategies. You will be part of an international community of innovative problem solvers. Learn more and register today at chestmeeting.chestnet.org.
Los Angeles has a flare for the dramatic, and we’re not just talking about Hollywood’s fast-paced, larger-than-life movie industry. When you visit Los Angeles, October 22 – 26, for CHEST 2016, be sure to check out the assortment of arts and culture venues located nearby your home base at CHEST 2016.
Los Angeles has more museums and theaters than any other U.S. city, and we’ll highlight a few local favorites below. For more information on L.A.’s thriving arts and culture scene, check out discoverlosangeles.com.
• The Dorothy Chandler Pavilion – (7-minute drive) – This hall is part of the Los Angeles music center. On October 22 – 23, watch three major U.S. ballet companies share the stage in Celebrate Forsythe. Or, take in The Source, a music-theater production about Chelsea (formerly Bradley) Manning and WikiLeaks.
• The Ahmanson Theatre – (7-minute drive) – This theater is also part of the Los Angeles music center. Be captivated by a 2016 Tony Award–winning play, A View from the Bridge.
• Walt Disney Concert Hall – (6-minute drive) – Home to the Los Angeles Philharmonic Orchestra and the Los Angeles Master Chorale, it is also part of the Los Angeles music center. Listen to the beautiful sounds of Mahler’s Ninth or Hilary Hahn on violin.
• MOCA Grand – (5-minute drive) – The Museum of Contemporary Art has three locations in Los Angeles. The main branch, located on Grand Avenue, is the closest to the convention center. Check out the museum’s main galleries at this location.
• The Getty Center – (30-minute drive) – See spectacular art and architecture at the top of Los Angeles.
Note: all estimated times assume you are starting at the Los Angeles Convention Center.
Los Angeles’ arts and culture scene is sure to inspire you, and CHEST 2016 will move you with the latest clinical information in chest medicine. Join us at CHEST 2016, and you won’t miss a beat with cutting-edge sessions and simulation training designed to update you on the latest patient care strategies. You will be part of an international community of innovative problem solvers. Learn more and register today at chestmeeting.chestnet.org.
This Month in CHEST: Editor’s Picks
A Novel PF4-Dependent Platelet Activation Assay Identifies Patients Likely to Have
Heparin-Induced Thrombocytopenia/Thrombosis.By Dr. A Padmanabhan et al.
Safety and Tolerability of Alveolar Type II Cell Transplantation in Idiopathic
Pulmonary Fibrosis.By Dr. A. Serrano-Mollar et al.
Hypertension Is Associated With Undiagnosed OSA During Rapid Eye Movement Sleep.By Dr. S. L. Appleton et al.
A Novel PF4-Dependent Platelet Activation Assay Identifies Patients Likely to Have
Heparin-Induced Thrombocytopenia/Thrombosis.By Dr. A Padmanabhan et al.
Safety and Tolerability of Alveolar Type II Cell Transplantation in Idiopathic
Pulmonary Fibrosis.By Dr. A. Serrano-Mollar et al.
Hypertension Is Associated With Undiagnosed OSA During Rapid Eye Movement Sleep.By Dr. S. L. Appleton et al.
A Novel PF4-Dependent Platelet Activation Assay Identifies Patients Likely to Have
Heparin-Induced Thrombocytopenia/Thrombosis.By Dr. A Padmanabhan et al.
Safety and Tolerability of Alveolar Type II Cell Transplantation in Idiopathic
Pulmonary Fibrosis.By Dr. A. Serrano-Mollar et al.
Hypertension Is Associated With Undiagnosed OSA During Rapid Eye Movement Sleep.By Dr. S. L. Appleton et al.
From the CEO
As a 22-year member of the senior staff of the American College of Chest Physicians, I am absolutely thrilled to have the opportunity to serve as its interim EVP/CEO for the current 2016-2017 fiscal year. Over the course of the years, I’ve been fortunate to oversee a number of CHEST’s business units and divisions, including Publications, Marketing, Communications, Membership, International Development, and Information Technology (IT). This background has provided a stable foundation for a smooth transition and ensured that the college continues to move to achieve its strategic plan and operational goals. That plan and those goals ensure that we will fulfill CHEST’s mission and vision: “To champion the prevention, diagnosis, and treatment of chest diseases through education, communication, and research” and to be “the global leader in advancing best patient outcomes through innovative chest medicine education, clinical research, and team-based care,” respectively.
To this end, we are executing well as an organization. Our state-of-the-art Innovation, Simulation, and Training Center at the CHEST Global Headquarters in Glenview, Illinois, continues to provide outstanding hands-on educational events and opportunities, and our Education Calendar has something for just about everyone. Our annual Board Review courses continue to provide excellent content. The CHEST 2016 annual meeting in LA this October will showcase all that CHEST has to offer. And the list goes on.
One of CHEST’s strengths is its spirit of innovation. Whether it’s revamping the highly successful SEEK app into an easily accessible online library, adding more simulation and procedure-based training to our educational offerings, or providing our live courses as captured online “on-demand” programs, we are committed to finding ways to package and deliver meaningful education to our members and community. Our for-profit subsidiary, CHEST Enterprises, is providing professional education to industry through the PREP disease-state immersion program, and developing a data analytics product line that will provide insights into physician behavior. Our charitable foundation, the CHEST Foundation, gives nearly $500,000 in research and community service grants each year, to champion lung health. It has also expanded the number of available patient education resources in partnership with the ALA. And in the past year, we have fully implemented CHEST’s new innovative membership model to welcome more nonphysician health care providers and give them opportunities to engage, learn, and participate. All of these things are incredibly exciting to me, and I’m grateful to be part of them.
But what I’m most excited and grateful for are the people who impact our organization. We have a diverse and passionate membership of physician and nonphysician health care providers who want to provide the best care possible and positively impact outcomes. Our dedicated faculty and volunteers generously give their time to the organization’s work groups and programs so that they can give back to others in the field. Our hard-working leaders take responsibility and ownership of our programs and content. And, our outstanding staff operationalizes the strategic plan and goals of the organization hand-in-hand with those leaders, volunteers, faculty, and members. Together, it all results in the excellent programs you have come to expect from CHEST.
Thank you for participating and supporting this robust, dynamic organization. I am excited for the future for CHEST, and I look forward to seeing you at CHEST 2016 in Los Angeles! If you have thoughts or ideas about how we can enhance our work to be a global leader in chest medicine, connect with me anytime. I invite you to follow and connect with me on Twitter (@RocketSurgery99), or look for me at upcoming CHEST events.
As a 22-year member of the senior staff of the American College of Chest Physicians, I am absolutely thrilled to have the opportunity to serve as its interim EVP/CEO for the current 2016-2017 fiscal year. Over the course of the years, I’ve been fortunate to oversee a number of CHEST’s business units and divisions, including Publications, Marketing, Communications, Membership, International Development, and Information Technology (IT). This background has provided a stable foundation for a smooth transition and ensured that the college continues to move to achieve its strategic plan and operational goals. That plan and those goals ensure that we will fulfill CHEST’s mission and vision: “To champion the prevention, diagnosis, and treatment of chest diseases through education, communication, and research” and to be “the global leader in advancing best patient outcomes through innovative chest medicine education, clinical research, and team-based care,” respectively.
To this end, we are executing well as an organization. Our state-of-the-art Innovation, Simulation, and Training Center at the CHEST Global Headquarters in Glenview, Illinois, continues to provide outstanding hands-on educational events and opportunities, and our Education Calendar has something for just about everyone. Our annual Board Review courses continue to provide excellent content. The CHEST 2016 annual meeting in LA this October will showcase all that CHEST has to offer. And the list goes on.
One of CHEST’s strengths is its spirit of innovation. Whether it’s revamping the highly successful SEEK app into an easily accessible online library, adding more simulation and procedure-based training to our educational offerings, or providing our live courses as captured online “on-demand” programs, we are committed to finding ways to package and deliver meaningful education to our members and community. Our for-profit subsidiary, CHEST Enterprises, is providing professional education to industry through the PREP disease-state immersion program, and developing a data analytics product line that will provide insights into physician behavior. Our charitable foundation, the CHEST Foundation, gives nearly $500,000 in research and community service grants each year, to champion lung health. It has also expanded the number of available patient education resources in partnership with the ALA. And in the past year, we have fully implemented CHEST’s new innovative membership model to welcome more nonphysician health care providers and give them opportunities to engage, learn, and participate. All of these things are incredibly exciting to me, and I’m grateful to be part of them.
But what I’m most excited and grateful for are the people who impact our organization. We have a diverse and passionate membership of physician and nonphysician health care providers who want to provide the best care possible and positively impact outcomes. Our dedicated faculty and volunteers generously give their time to the organization’s work groups and programs so that they can give back to others in the field. Our hard-working leaders take responsibility and ownership of our programs and content. And, our outstanding staff operationalizes the strategic plan and goals of the organization hand-in-hand with those leaders, volunteers, faculty, and members. Together, it all results in the excellent programs you have come to expect from CHEST.
Thank you for participating and supporting this robust, dynamic organization. I am excited for the future for CHEST, and I look forward to seeing you at CHEST 2016 in Los Angeles! If you have thoughts or ideas about how we can enhance our work to be a global leader in chest medicine, connect with me anytime. I invite you to follow and connect with me on Twitter (@RocketSurgery99), or look for me at upcoming CHEST events.
As a 22-year member of the senior staff of the American College of Chest Physicians, I am absolutely thrilled to have the opportunity to serve as its interim EVP/CEO for the current 2016-2017 fiscal year. Over the course of the years, I’ve been fortunate to oversee a number of CHEST’s business units and divisions, including Publications, Marketing, Communications, Membership, International Development, and Information Technology (IT). This background has provided a stable foundation for a smooth transition and ensured that the college continues to move to achieve its strategic plan and operational goals. That plan and those goals ensure that we will fulfill CHEST’s mission and vision: “To champion the prevention, diagnosis, and treatment of chest diseases through education, communication, and research” and to be “the global leader in advancing best patient outcomes through innovative chest medicine education, clinical research, and team-based care,” respectively.
To this end, we are executing well as an organization. Our state-of-the-art Innovation, Simulation, and Training Center at the CHEST Global Headquarters in Glenview, Illinois, continues to provide outstanding hands-on educational events and opportunities, and our Education Calendar has something for just about everyone. Our annual Board Review courses continue to provide excellent content. The CHEST 2016 annual meeting in LA this October will showcase all that CHEST has to offer. And the list goes on.
One of CHEST’s strengths is its spirit of innovation. Whether it’s revamping the highly successful SEEK app into an easily accessible online library, adding more simulation and procedure-based training to our educational offerings, or providing our live courses as captured online “on-demand” programs, we are committed to finding ways to package and deliver meaningful education to our members and community. Our for-profit subsidiary, CHEST Enterprises, is providing professional education to industry through the PREP disease-state immersion program, and developing a data analytics product line that will provide insights into physician behavior. Our charitable foundation, the CHEST Foundation, gives nearly $500,000 in research and community service grants each year, to champion lung health. It has also expanded the number of available patient education resources in partnership with the ALA. And in the past year, we have fully implemented CHEST’s new innovative membership model to welcome more nonphysician health care providers and give them opportunities to engage, learn, and participate. All of these things are incredibly exciting to me, and I’m grateful to be part of them.
But what I’m most excited and grateful for are the people who impact our organization. We have a diverse and passionate membership of physician and nonphysician health care providers who want to provide the best care possible and positively impact outcomes. Our dedicated faculty and volunteers generously give their time to the organization’s work groups and programs so that they can give back to others in the field. Our hard-working leaders take responsibility and ownership of our programs and content. And, our outstanding staff operationalizes the strategic plan and goals of the organization hand-in-hand with those leaders, volunteers, faculty, and members. Together, it all results in the excellent programs you have come to expect from CHEST.
Thank you for participating and supporting this robust, dynamic organization. I am excited for the future for CHEST, and I look forward to seeing you at CHEST 2016 in Los Angeles! If you have thoughts or ideas about how we can enhance our work to be a global leader in chest medicine, connect with me anytime. I invite you to follow and connect with me on Twitter (@RocketSurgery99), or look for me at upcoming CHEST events.
Connect with the CHEST Foundation at CHEST 2016
At this year’s annual meeting, the CHEST Foundation will have several new and exciting events, including three networking happy hours, October 23-25, for women in lung health, international members, and nonphysician providers, and two educational sessions developed by CHEST Foundation leaders and volunteers, Chris Carroll, MD, FCCP, and Muhammad Adrish, MD, FCCP. The new sessions will provide a focus on essential tactics for conducting effective research and a panel discussion featuring past CHEST Foundation grant winners, on how to create a successful community service program. In addition to these events, we will be hosting another “Young Professionals Reception” Monday evening. Be sure to stop by the Donor Lounge to network and mingle with leadership, meet the foundation staff, grab a coffee, and learn how you can engage with the CHEST Foundation. If you arrive early on Saturday, October 22, don’t miss out on our afternoon “Champions for Lung Health Event,” where CHEST Foundation leadership will be giving back to the Los Angeles community by volunteering their time at a COPD screening.
We are also proud to introduce our 2016 CHEST Foundation grantees at this year’s Opening Session on Monday, October 24. This year, we will be awarding nearly a half-million dollars in funding to the next generation of lung health champions. Our grants and programs have made a difference in the lives of our members and their patients through the impactful clinical research and impressive humanitarian projects our grantees have created. Since 1996, we’ve provided over $10 million in funding for clinical research and community service, with a reach that spans from Texas to Tanzania. The foundation is an important go-to resource for young investigators seeking research funding, and the projects we support lead to breakthroughs in the treatment of chest diseases and patient care.
We hope to see you at one of our open invitation activities to learn more about how the CHEST Foundation can support you in your efforts to champion lung health.
At this year’s annual meeting, the CHEST Foundation will have several new and exciting events, including three networking happy hours, October 23-25, for women in lung health, international members, and nonphysician providers, and two educational sessions developed by CHEST Foundation leaders and volunteers, Chris Carroll, MD, FCCP, and Muhammad Adrish, MD, FCCP. The new sessions will provide a focus on essential tactics for conducting effective research and a panel discussion featuring past CHEST Foundation grant winners, on how to create a successful community service program. In addition to these events, we will be hosting another “Young Professionals Reception” Monday evening. Be sure to stop by the Donor Lounge to network and mingle with leadership, meet the foundation staff, grab a coffee, and learn how you can engage with the CHEST Foundation. If you arrive early on Saturday, October 22, don’t miss out on our afternoon “Champions for Lung Health Event,” where CHEST Foundation leadership will be giving back to the Los Angeles community by volunteering their time at a COPD screening.
We are also proud to introduce our 2016 CHEST Foundation grantees at this year’s Opening Session on Monday, October 24. This year, we will be awarding nearly a half-million dollars in funding to the next generation of lung health champions. Our grants and programs have made a difference in the lives of our members and their patients through the impactful clinical research and impressive humanitarian projects our grantees have created. Since 1996, we’ve provided over $10 million in funding for clinical research and community service, with a reach that spans from Texas to Tanzania. The foundation is an important go-to resource for young investigators seeking research funding, and the projects we support lead to breakthroughs in the treatment of chest diseases and patient care.
We hope to see you at one of our open invitation activities to learn more about how the CHEST Foundation can support you in your efforts to champion lung health.
At this year’s annual meeting, the CHEST Foundation will have several new and exciting events, including three networking happy hours, October 23-25, for women in lung health, international members, and nonphysician providers, and two educational sessions developed by CHEST Foundation leaders and volunteers, Chris Carroll, MD, FCCP, and Muhammad Adrish, MD, FCCP. The new sessions will provide a focus on essential tactics for conducting effective research and a panel discussion featuring past CHEST Foundation grant winners, on how to create a successful community service program. In addition to these events, we will be hosting another “Young Professionals Reception” Monday evening. Be sure to stop by the Donor Lounge to network and mingle with leadership, meet the foundation staff, grab a coffee, and learn how you can engage with the CHEST Foundation. If you arrive early on Saturday, October 22, don’t miss out on our afternoon “Champions for Lung Health Event,” where CHEST Foundation leadership will be giving back to the Los Angeles community by volunteering their time at a COPD screening.
We are also proud to introduce our 2016 CHEST Foundation grantees at this year’s Opening Session on Monday, October 24. This year, we will be awarding nearly a half-million dollars in funding to the next generation of lung health champions. Our grants and programs have made a difference in the lives of our members and their patients through the impactful clinical research and impressive humanitarian projects our grantees have created. Since 1996, we’ve provided over $10 million in funding for clinical research and community service, with a reach that spans from Texas to Tanzania. The foundation is an important go-to resource for young investigators seeking research funding, and the projects we support lead to breakthroughs in the treatment of chest diseases and patient care.
We hope to see you at one of our open invitation activities to learn more about how the CHEST Foundation can support you in your efforts to champion lung health.
Early days of IVF marked by competition, innovation
In 1978, when England’s Louise Brown became the world’s first baby born through in vitro fertilization, physicians at academic centers all over the United States scrambled to figure out how they, too, could provide IVF to the thousands of infertile couples for whom nothing else had worked.
Interest in IVF was strong even before British physiologist Robert Edwards and gynecologist Patrick Steptoe announced their success. “We knew that IVF was being developed, that it had been accomplished in animals, and ultimately we knew it was going to succeed in humans,” said reproductive endocrinologist Zev Rosenwaks, MD, of the Weill Cornell Center for Reproductive Medicine in New York.
In the late 1970s, “we were able to help only about two-thirds of couples with infertility, either with tubal surgery, insemination – often with donor sperm – or ovulation induction. A full third could not be helped. We predicted that IVF would allow us to treat virtually everyone,” Dr. Rosenwaks said.
But even after the first IVF birth, information on the revolutionary procedure remained frustratingly scarce.
“Edwards and Steptoe would talk to nobody,” said Richard Marrs, MD, a reproductive endocrinologist and infertility specialist in Los Angeles.
And federal research support for “test-tube babies,” as IVF was known in the media then, was nil thanks to a ban on government-funded human embryo research that persists to this day.
The U.S. physicians who took part in the rush to achieve an IVF birth – most of them young fellows at the time – recall a period of improvisation, collaboration, shoestring budgets, and surprise findings.
“People who just started 10 or even 20 years ago don’t realize what it took for us to learn how to go about doing IVF,” said Dr. Rosenwaks, who in the first years of IVF worked closely with Dr. Howard Jones and Dr. Georgeanna Jones, the first team in the U.S. to announce an IVF baby.
Labs in closets
In the late 1970s, Dr. Marrs, then a fellow at the University of Southern California, was focused on surgical methods to treat infertility – and demand was sky-high. Intrauterine devices used in the 1970s left many women with severe scarring and inflammation of the fallopian tubes.
“I was very surgically oriented,” Dr. Marrs said. “I thought I could fix any disaster in the pelvis that was put in front of me, especially with microsurgery.”
After the news of IVF success in England, Dr. Marrs threw himself into a side project at a nearby cancer center, working on single-cell cultures. “I thought if I could grow tumor cells, I could one day grow embryos,” he said.
A year later, Dr. Marrs set up the first IVF lab at USC – in a storage closet. “I sterilized the place and that was our first IVF lab, literally a closet with an incubator and a microscope.” Its budget was accordingly thin, as the director at the time felt certain that IVF was a dead end. To fund his work, Dr. Marrs asked IVF candidate patients for research donations in lieu of payment.
But before Dr. Marrs attempted to perform his first IVF, two centers in Australia announced their own IVF babies. “I decided I really needed to go see someone who had had a baby,” he said. He used his vacation time to fly to Melbourne, shuttling between two competing clinics that were “four blocks apart and wouldn’t even talk to each other,” he recalled.
Over 6 weeks, “I learned how to stimulate, how to time ovulation. I watched the PhDs in the lab – how they handled the eggs and the sperm, what the conditions were, the incubator settings,” he said.
The first IVF babies in the United States were born only months apart: The first, in December 1981, was at the Jones Institute for Reproductive Medicine in Norfolk, Va., where Dr. Rosenwaks served as the first director.
The second baby born was at USC. After that, “we had 4,000 women on a waiting list, all under age 35,” Dr. Marrs said. The Jones Institute reportedly had 5,000.
As demand soared and more IVF babies arrived, the cloak of secrecy surrounding the procedure started to lift. British, Australian, and U.S. clinicians started getting together regularly. “We would pick a spot in the world, present our data: what we’d done, how many cycles, what we used for stimulation, when we took the eggs out,” Dr. Marrs said. “I don’t know how many hundreds of thousands of miles I flew in the first years of IVF, because it was the only way I could get information. We would literally stay up all night talking.”
Answering safety questions
Alan H. DeCherney, MD, currently an infertility researcher at the National Institutes of Health, started Yale University’s IVF program at around the same time Dr. Marrs and the Joneses were starting theirs. Yale already had a large infertility practice, and only academic centers had the laboratory resources and skilled staff needed to attempt IVF in those years.
In 1983, when Yale announced the birth of its first IVF baby – the fifth in the United States – Dr. DeCherney was starting to think about measuring outcomes, as there was concern over the potential for congenital anomalies related to IVF. “This was such a change in the way conception occurred, people were afraid that all kinds of crazy things would happen,” he said.
One concern was about ovarian stimulation with fertility drugs or gonadotropins. The earliest efforts – including by Dr. Steptoe and Dr. Edwards – used no drugs, instead trying to pinpoint the moment of natural egg release by measuring a woman’s hormone levels constantly, but these proved disappointing. Use of clomiphene citrate and human menopausal gonadotropin allowed for more control over timing, and for multiple mature eggs to be harvested at once.
But there were still many unanswered questions related to these agents’ safety and dosing, both for women and for babies.
When the NIH refused to fund a study of IVF outcomes, Dr. DeCherney and Dr. Marrs collaborated on a registry funded by a gonadotropin maker. “The drug company didn’t want to be associated with some terrible abnormal outcomes,” Dr. DeCherney recalled, though by then, “there were 10, maybe even 20 babies around the world, and they seemed to be fine,” he said.
The first registry results affirmed no changes in the rate of congenital abnormalities. (Larger, more recent studies have shown a small but significant elevation in birth defect risk associated with IVF.) A few years later, ovarian stimulation was adjusted to correspond with ovarian reserve, reducing the risk of ovarian hyperstimulation syndrome.
But even by the late 1980s, success rates for IVF per attempted cycle were still low overall, leading many critics, even within the profession, to accuse practitioners of misleading couples. Charles E. Miller, MD, an infertility specialist in Chicago, recalled an early investigation by a major newspaper “that looked at all the IVF clinics in Chicago and found the chances of having a baby was under 3%.”
It was true, Dr. Miller acknowledged – “the rates were dismal. But remember that IVF at the time was still considered a procedure of last resort.” Complex diagnostic testing to determine the cause of infertility, surgery, and fertility drugs all came first.
Some important innovations would soon change that and turn IVF into a mainstay of infertility treatment that could help women not only with damaged tubes but also with ovarian failure, low ovarian reserve, or dense pelvic adhesions. Even some types of male factor infertility would find an answer in IVF, by way of intracytoplasmic sperm transfer.
Eggs without surgery
Laparoscopic egg retrieval was the norm in the first decade of IVF. “We went through the belly button, allowing us to directly visualize the ovary and see whether ovulation had already occurred or we had to retrieve it by introducing a needle into the follicle,” Dr. Rosenwaks recalled.
“Some of us were doing 6 or even 10 laparoscopies a day, and it was physically quite challenging,” he said. “There were no video screens in those days. You had to bend over the scope.” And it was worse still for patients, who had to endure multiple surgeries.
Though egg and embryo cryopreservation were already being worked on, it would be years before these techniques were optimized, giving women more chances from a single retrieval of oocytes.
Finding a less invasive means of retrieving eggs was crucial.
Maria Bustillo, MD, an infertility specialist in Miami, recalled being criticized by peers when she and her then-colleagues at the Genetics & IVF Institute in Fairfax, Va., began retrieving eggs via a needle placed in the vagina, using abdominal ultrasound as a guide.
While the technique was far less invasive than laparoscopy, “we were doing it semi-blindly, and were told it was dangerous,” Dr. Bustillo said.
But these freehand ultrasound retrievals paved the way for what would become a revolutionary advance – the vaginal ultrasound probe, which by the end of the 1980s made nonsurgical extraction of eggs the norm.
Dr. Marrs recalled receiving a prototype of a vaginal ultrasound probe, in the mid-1980s, and finding patients unwilling to use it, except one who relented only because she had an empty bladder. Abdominal ultrasonography required a full bladder to work.
“It was as though somebody had removed the cloud cover,” he said. “I couldn’t believe it. I could see everything: her ovaries, tiny follicles, the uterus.”
Later probes were fitted with a needle and aspirator to retrieve eggs. Multiple IVF cycles no longer meant multiple surgeries, and the less-invasive procedure helped in recruiting egg donors, allowing women with ovarian disease or low ovarian reserves, including older women, to receive IVF.
“It didn’t make sense for a volunteer to go through a surgery, especially back in the early ’80s when the results were not all that great,” Dr. Bustillo said.
Improving ‘home brews’
The culture media in which embryos were grown was another strong factor limiting the success rates of early IVF. James Toner, MD, PhD, an IVF specialist in Atlanta, called the early media “home brews.”
“Everyone made them themselves,” said Dr. Toner, who spent 15 years at the Jones Institute. “You had to do a hamster or mouse embryo test on every batch to make sure embryos would grow.” And often they did not.
Poor success rates resulted in the emergence of alternative procedures: GIFT (gamete intrafallopian transfer) and ZIFT (zygote intrafallopian transfer). Both aimed to get embryos back into the patient as soon as possible, with the thought that the natural environment offered a better chance for success.
But advances in culture media allowed more time for embryos to be observed. With longer development, “you could do a better job selecting the ones that had a chance, and de-selecting those with no chance,” Dr. Toner said.
This also meant fewer embryos could be transferred back into patients, lowering the likelihood of multiples. Ultimately, for young women, single-embryo transfer would become the norm. “The problem of multiple pregnancy that we used to have no longer exists for IVF,” Dr. Toner said.
Allowing embryos to reach the blastocyst stage – day 5 or 6 – opened other, previously unthinkable possibilities: placing embryos directly into the uterus, without surgery, and pre-implementation genetic screening for abnormalities.
“As the cell number went up, the idea that you could do a genetic test with minimal impact on the embryo eventually became true,” Dr. Toner said.
A genetic revolution?
While many important IVF innovations were achieved in countries with staunch government support, one of the remarkable things about IVF’s evolution in the United States is that so many occurred with virtually none.
By the mid-1990s, most of the early practitioners had moved from academic settings into private practice, though they continued to publish. “After a while it didn’t help to be in academics. It just sort of slowed you down. Because you weren’t going to get any [government] money anyway, you might as well be in a place that’s a little more nimble,” Dr. Toner said.
At the same time, he said, IVF remains a costly, usually unreimbursed procedure – limiting patients’ willingness to take part in randomized trials. “IVF research is built more on cohort studies.”
Most of the current research focus in IVF is on possibilities for genetic screening. Dr. Miller said that rapid DNA sequencing is allowing specialists to “look at more, pick up more abnormalities. That will continue to improve so that we will be able to see virtually everything.”
But he cautioned there is still much to be done in IVF apart from the genetics – he’s concerned, he said, that the field has moved too far from its surgical origins, and is working with the academic societies to encourage more surgical training.
“We don’t do the same work we did before on fallopian tubes, which is good,” Dr. Miller said, noting that there have been many advances, particularly minimally invasive surgeries in the uterus or ovaries, that have occurred parallel to IVF and can improve success rates. “I think we have a better understanding of what kind of patients require surgical treatments and what kind of surgeries can help enhance fertility, and also what not to do.”
Dr. Bustillo said that “cytogenetics is wonderful, but not everything. You have embryos that are genetically normal and still don’t implant. There’s a lot of work to be done on the interaction between the mother and the embryo.”
Dr. Marrs said that even safety questions related to stimulation have yet to be fully answered. “I’ve always been a big believer that lower is better, but we need to know whether stimulation creates genetic abnormalities and whether less stimulation produces fewer – and we need more data to prove it,” he said. Dr. Marrs is an investigator on a national randomized trial comparing outcomes from IVF with standard-dose and ultra-low dose stimulation.
Access, income, and age
The IVF pioneers agree broadly that access to IVF is nowhere near what it should be in the United States, where only 15 states mandate any insurance coverage for infertility.
“Our limited access to care is a crime,” Dr. Toner said. “People who, through no fault of their own, find themselves infertile are asked to write a check for $15,000 to get pregnant. That’s not fair.”
Dr. DeCherney called access “an ethical issue, because who gets IVF? People with higher incomes. And if IVF allows you to select better embryos – whatever that means – it gives that group another advantage.”
Dr. Toner warned that the push toward genetic testing of embryos, especially in the absence of known hereditary disease, could create new problems for the profession – not unlike in the early days of IVF, when the Jones Institute and other clinics were picketed over the specter of “test tube babies.”
“It’s one thing to say this embryo does not have the right number of chromosomes and couldn’t possibly be a child, so let’s not use it, but what about looking for traits? Sex selection? We have this privileged position in which the government does not really interfere in what we do, but to retain this status we need to stay within the bounds that our society accepts,” Dr. Toner said.
In recent years, IVF uptake has been high among women of advanced reproductive age, which poses its own set of challenges. Outcomes in older women using their own eggs become progressively poorer with age, though donor eggs drastically improve their chances, and egg freezing offers the possibility of preserving quality eggs for later pregnancies.
“We could make this situation better by promoting social freezing, doing more work for women early in their lives to get out their own eggs and store them,” Dr. Miller said. “But again, you still face the issue of access.”
Regardless of what technologies are available or become available in assisted reproduction, doctors and women alike need to be better educated on their options and chances early, with a clearer understanding of what happens as they age, Dr. Bustillo said.
“This is not to pressure them, but just so they understand that when they get to be 42 and are just thinking about reproducing, it’s not a major surprise when I tell them this could be a problem,” she said.
Throughout 2016, Ob.Gyn. News is celebrating its 50th anniversary with exclusive articles looking at the evolution of the specialty, including the history of contraception, changes in gynecologic surgery, and the transformation of the well-woman visit.
In 1978, when England’s Louise Brown became the world’s first baby born through in vitro fertilization, physicians at academic centers all over the United States scrambled to figure out how they, too, could provide IVF to the thousands of infertile couples for whom nothing else had worked.
Interest in IVF was strong even before British physiologist Robert Edwards and gynecologist Patrick Steptoe announced their success. “We knew that IVF was being developed, that it had been accomplished in animals, and ultimately we knew it was going to succeed in humans,” said reproductive endocrinologist Zev Rosenwaks, MD, of the Weill Cornell Center for Reproductive Medicine in New York.
In the late 1970s, “we were able to help only about two-thirds of couples with infertility, either with tubal surgery, insemination – often with donor sperm – or ovulation induction. A full third could not be helped. We predicted that IVF would allow us to treat virtually everyone,” Dr. Rosenwaks said.
But even after the first IVF birth, information on the revolutionary procedure remained frustratingly scarce.
“Edwards and Steptoe would talk to nobody,” said Richard Marrs, MD, a reproductive endocrinologist and infertility specialist in Los Angeles.
And federal research support for “test-tube babies,” as IVF was known in the media then, was nil thanks to a ban on government-funded human embryo research that persists to this day.
The U.S. physicians who took part in the rush to achieve an IVF birth – most of them young fellows at the time – recall a period of improvisation, collaboration, shoestring budgets, and surprise findings.
“People who just started 10 or even 20 years ago don’t realize what it took for us to learn how to go about doing IVF,” said Dr. Rosenwaks, who in the first years of IVF worked closely with Dr. Howard Jones and Dr. Georgeanna Jones, the first team in the U.S. to announce an IVF baby.
Labs in closets
In the late 1970s, Dr. Marrs, then a fellow at the University of Southern California, was focused on surgical methods to treat infertility – and demand was sky-high. Intrauterine devices used in the 1970s left many women with severe scarring and inflammation of the fallopian tubes.
“I was very surgically oriented,” Dr. Marrs said. “I thought I could fix any disaster in the pelvis that was put in front of me, especially with microsurgery.”
After the news of IVF success in England, Dr. Marrs threw himself into a side project at a nearby cancer center, working on single-cell cultures. “I thought if I could grow tumor cells, I could one day grow embryos,” he said.
A year later, Dr. Marrs set up the first IVF lab at USC – in a storage closet. “I sterilized the place and that was our first IVF lab, literally a closet with an incubator and a microscope.” Its budget was accordingly thin, as the director at the time felt certain that IVF was a dead end. To fund his work, Dr. Marrs asked IVF candidate patients for research donations in lieu of payment.
But before Dr. Marrs attempted to perform his first IVF, two centers in Australia announced their own IVF babies. “I decided I really needed to go see someone who had had a baby,” he said. He used his vacation time to fly to Melbourne, shuttling between two competing clinics that were “four blocks apart and wouldn’t even talk to each other,” he recalled.
Over 6 weeks, “I learned how to stimulate, how to time ovulation. I watched the PhDs in the lab – how they handled the eggs and the sperm, what the conditions were, the incubator settings,” he said.
The first IVF babies in the United States were born only months apart: The first, in December 1981, was at the Jones Institute for Reproductive Medicine in Norfolk, Va., where Dr. Rosenwaks served as the first director.
The second baby born was at USC. After that, “we had 4,000 women on a waiting list, all under age 35,” Dr. Marrs said. The Jones Institute reportedly had 5,000.
As demand soared and more IVF babies arrived, the cloak of secrecy surrounding the procedure started to lift. British, Australian, and U.S. clinicians started getting together regularly. “We would pick a spot in the world, present our data: what we’d done, how many cycles, what we used for stimulation, when we took the eggs out,” Dr. Marrs said. “I don’t know how many hundreds of thousands of miles I flew in the first years of IVF, because it was the only way I could get information. We would literally stay up all night talking.”
Answering safety questions
Alan H. DeCherney, MD, currently an infertility researcher at the National Institutes of Health, started Yale University’s IVF program at around the same time Dr. Marrs and the Joneses were starting theirs. Yale already had a large infertility practice, and only academic centers had the laboratory resources and skilled staff needed to attempt IVF in those years.
In 1983, when Yale announced the birth of its first IVF baby – the fifth in the United States – Dr. DeCherney was starting to think about measuring outcomes, as there was concern over the potential for congenital anomalies related to IVF. “This was such a change in the way conception occurred, people were afraid that all kinds of crazy things would happen,” he said.
One concern was about ovarian stimulation with fertility drugs or gonadotropins. The earliest efforts – including by Dr. Steptoe and Dr. Edwards – used no drugs, instead trying to pinpoint the moment of natural egg release by measuring a woman’s hormone levels constantly, but these proved disappointing. Use of clomiphene citrate and human menopausal gonadotropin allowed for more control over timing, and for multiple mature eggs to be harvested at once.
But there were still many unanswered questions related to these agents’ safety and dosing, both for women and for babies.
When the NIH refused to fund a study of IVF outcomes, Dr. DeCherney and Dr. Marrs collaborated on a registry funded by a gonadotropin maker. “The drug company didn’t want to be associated with some terrible abnormal outcomes,” Dr. DeCherney recalled, though by then, “there were 10, maybe even 20 babies around the world, and they seemed to be fine,” he said.
The first registry results affirmed no changes in the rate of congenital abnormalities. (Larger, more recent studies have shown a small but significant elevation in birth defect risk associated with IVF.) A few years later, ovarian stimulation was adjusted to correspond with ovarian reserve, reducing the risk of ovarian hyperstimulation syndrome.
But even by the late 1980s, success rates for IVF per attempted cycle were still low overall, leading many critics, even within the profession, to accuse practitioners of misleading couples. Charles E. Miller, MD, an infertility specialist in Chicago, recalled an early investigation by a major newspaper “that looked at all the IVF clinics in Chicago and found the chances of having a baby was under 3%.”
It was true, Dr. Miller acknowledged – “the rates were dismal. But remember that IVF at the time was still considered a procedure of last resort.” Complex diagnostic testing to determine the cause of infertility, surgery, and fertility drugs all came first.
Some important innovations would soon change that and turn IVF into a mainstay of infertility treatment that could help women not only with damaged tubes but also with ovarian failure, low ovarian reserve, or dense pelvic adhesions. Even some types of male factor infertility would find an answer in IVF, by way of intracytoplasmic sperm transfer.
Eggs without surgery
Laparoscopic egg retrieval was the norm in the first decade of IVF. “We went through the belly button, allowing us to directly visualize the ovary and see whether ovulation had already occurred or we had to retrieve it by introducing a needle into the follicle,” Dr. Rosenwaks recalled.
“Some of us were doing 6 or even 10 laparoscopies a day, and it was physically quite challenging,” he said. “There were no video screens in those days. You had to bend over the scope.” And it was worse still for patients, who had to endure multiple surgeries.
Though egg and embryo cryopreservation were already being worked on, it would be years before these techniques were optimized, giving women more chances from a single retrieval of oocytes.
Finding a less invasive means of retrieving eggs was crucial.
Maria Bustillo, MD, an infertility specialist in Miami, recalled being criticized by peers when she and her then-colleagues at the Genetics & IVF Institute in Fairfax, Va., began retrieving eggs via a needle placed in the vagina, using abdominal ultrasound as a guide.
While the technique was far less invasive than laparoscopy, “we were doing it semi-blindly, and were told it was dangerous,” Dr. Bustillo said.
But these freehand ultrasound retrievals paved the way for what would become a revolutionary advance – the vaginal ultrasound probe, which by the end of the 1980s made nonsurgical extraction of eggs the norm.
Dr. Marrs recalled receiving a prototype of a vaginal ultrasound probe, in the mid-1980s, and finding patients unwilling to use it, except one who relented only because she had an empty bladder. Abdominal ultrasonography required a full bladder to work.
“It was as though somebody had removed the cloud cover,” he said. “I couldn’t believe it. I could see everything: her ovaries, tiny follicles, the uterus.”
Later probes were fitted with a needle and aspirator to retrieve eggs. Multiple IVF cycles no longer meant multiple surgeries, and the less-invasive procedure helped in recruiting egg donors, allowing women with ovarian disease or low ovarian reserves, including older women, to receive IVF.
“It didn’t make sense for a volunteer to go through a surgery, especially back in the early ’80s when the results were not all that great,” Dr. Bustillo said.
Improving ‘home brews’
The culture media in which embryos were grown was another strong factor limiting the success rates of early IVF. James Toner, MD, PhD, an IVF specialist in Atlanta, called the early media “home brews.”
“Everyone made them themselves,” said Dr. Toner, who spent 15 years at the Jones Institute. “You had to do a hamster or mouse embryo test on every batch to make sure embryos would grow.” And often they did not.
Poor success rates resulted in the emergence of alternative procedures: GIFT (gamete intrafallopian transfer) and ZIFT (zygote intrafallopian transfer). Both aimed to get embryos back into the patient as soon as possible, with the thought that the natural environment offered a better chance for success.
But advances in culture media allowed more time for embryos to be observed. With longer development, “you could do a better job selecting the ones that had a chance, and de-selecting those with no chance,” Dr. Toner said.
This also meant fewer embryos could be transferred back into patients, lowering the likelihood of multiples. Ultimately, for young women, single-embryo transfer would become the norm. “The problem of multiple pregnancy that we used to have no longer exists for IVF,” Dr. Toner said.
Allowing embryos to reach the blastocyst stage – day 5 or 6 – opened other, previously unthinkable possibilities: placing embryos directly into the uterus, without surgery, and pre-implementation genetic screening for abnormalities.
“As the cell number went up, the idea that you could do a genetic test with minimal impact on the embryo eventually became true,” Dr. Toner said.
A genetic revolution?
While many important IVF innovations were achieved in countries with staunch government support, one of the remarkable things about IVF’s evolution in the United States is that so many occurred with virtually none.
By the mid-1990s, most of the early practitioners had moved from academic settings into private practice, though they continued to publish. “After a while it didn’t help to be in academics. It just sort of slowed you down. Because you weren’t going to get any [government] money anyway, you might as well be in a place that’s a little more nimble,” Dr. Toner said.
At the same time, he said, IVF remains a costly, usually unreimbursed procedure – limiting patients’ willingness to take part in randomized trials. “IVF research is built more on cohort studies.”
Most of the current research focus in IVF is on possibilities for genetic screening. Dr. Miller said that rapid DNA sequencing is allowing specialists to “look at more, pick up more abnormalities. That will continue to improve so that we will be able to see virtually everything.”
But he cautioned there is still much to be done in IVF apart from the genetics – he’s concerned, he said, that the field has moved too far from its surgical origins, and is working with the academic societies to encourage more surgical training.
“We don’t do the same work we did before on fallopian tubes, which is good,” Dr. Miller said, noting that there have been many advances, particularly minimally invasive surgeries in the uterus or ovaries, that have occurred parallel to IVF and can improve success rates. “I think we have a better understanding of what kind of patients require surgical treatments and what kind of surgeries can help enhance fertility, and also what not to do.”
Dr. Bustillo said that “cytogenetics is wonderful, but not everything. You have embryos that are genetically normal and still don’t implant. There’s a lot of work to be done on the interaction between the mother and the embryo.”
Dr. Marrs said that even safety questions related to stimulation have yet to be fully answered. “I’ve always been a big believer that lower is better, but we need to know whether stimulation creates genetic abnormalities and whether less stimulation produces fewer – and we need more data to prove it,” he said. Dr. Marrs is an investigator on a national randomized trial comparing outcomes from IVF with standard-dose and ultra-low dose stimulation.
Access, income, and age
The IVF pioneers agree broadly that access to IVF is nowhere near what it should be in the United States, where only 15 states mandate any insurance coverage for infertility.
“Our limited access to care is a crime,” Dr. Toner said. “People who, through no fault of their own, find themselves infertile are asked to write a check for $15,000 to get pregnant. That’s not fair.”
Dr. DeCherney called access “an ethical issue, because who gets IVF? People with higher incomes. And if IVF allows you to select better embryos – whatever that means – it gives that group another advantage.”
Dr. Toner warned that the push toward genetic testing of embryos, especially in the absence of known hereditary disease, could create new problems for the profession – not unlike in the early days of IVF, when the Jones Institute and other clinics were picketed over the specter of “test tube babies.”
“It’s one thing to say this embryo does not have the right number of chromosomes and couldn’t possibly be a child, so let’s not use it, but what about looking for traits? Sex selection? We have this privileged position in which the government does not really interfere in what we do, but to retain this status we need to stay within the bounds that our society accepts,” Dr. Toner said.
In recent years, IVF uptake has been high among women of advanced reproductive age, which poses its own set of challenges. Outcomes in older women using their own eggs become progressively poorer with age, though donor eggs drastically improve their chances, and egg freezing offers the possibility of preserving quality eggs for later pregnancies.
“We could make this situation better by promoting social freezing, doing more work for women early in their lives to get out their own eggs and store them,” Dr. Miller said. “But again, you still face the issue of access.”
Regardless of what technologies are available or become available in assisted reproduction, doctors and women alike need to be better educated on their options and chances early, with a clearer understanding of what happens as they age, Dr. Bustillo said.
“This is not to pressure them, but just so they understand that when they get to be 42 and are just thinking about reproducing, it’s not a major surprise when I tell them this could be a problem,” she said.
Throughout 2016, Ob.Gyn. News is celebrating its 50th anniversary with exclusive articles looking at the evolution of the specialty, including the history of contraception, changes in gynecologic surgery, and the transformation of the well-woman visit.
In 1978, when England’s Louise Brown became the world’s first baby born through in vitro fertilization, physicians at academic centers all over the United States scrambled to figure out how they, too, could provide IVF to the thousands of infertile couples for whom nothing else had worked.
Interest in IVF was strong even before British physiologist Robert Edwards and gynecologist Patrick Steptoe announced their success. “We knew that IVF was being developed, that it had been accomplished in animals, and ultimately we knew it was going to succeed in humans,” said reproductive endocrinologist Zev Rosenwaks, MD, of the Weill Cornell Center for Reproductive Medicine in New York.
In the late 1970s, “we were able to help only about two-thirds of couples with infertility, either with tubal surgery, insemination – often with donor sperm – or ovulation induction. A full third could not be helped. We predicted that IVF would allow us to treat virtually everyone,” Dr. Rosenwaks said.
But even after the first IVF birth, information on the revolutionary procedure remained frustratingly scarce.
“Edwards and Steptoe would talk to nobody,” said Richard Marrs, MD, a reproductive endocrinologist and infertility specialist in Los Angeles.
And federal research support for “test-tube babies,” as IVF was known in the media then, was nil thanks to a ban on government-funded human embryo research that persists to this day.
The U.S. physicians who took part in the rush to achieve an IVF birth – most of them young fellows at the time – recall a period of improvisation, collaboration, shoestring budgets, and surprise findings.
“People who just started 10 or even 20 years ago don’t realize what it took for us to learn how to go about doing IVF,” said Dr. Rosenwaks, who in the first years of IVF worked closely with Dr. Howard Jones and Dr. Georgeanna Jones, the first team in the U.S. to announce an IVF baby.
Labs in closets
In the late 1970s, Dr. Marrs, then a fellow at the University of Southern California, was focused on surgical methods to treat infertility – and demand was sky-high. Intrauterine devices used in the 1970s left many women with severe scarring and inflammation of the fallopian tubes.
“I was very surgically oriented,” Dr. Marrs said. “I thought I could fix any disaster in the pelvis that was put in front of me, especially with microsurgery.”
After the news of IVF success in England, Dr. Marrs threw himself into a side project at a nearby cancer center, working on single-cell cultures. “I thought if I could grow tumor cells, I could one day grow embryos,” he said.
A year later, Dr. Marrs set up the first IVF lab at USC – in a storage closet. “I sterilized the place and that was our first IVF lab, literally a closet with an incubator and a microscope.” Its budget was accordingly thin, as the director at the time felt certain that IVF was a dead end. To fund his work, Dr. Marrs asked IVF candidate patients for research donations in lieu of payment.
But before Dr. Marrs attempted to perform his first IVF, two centers in Australia announced their own IVF babies. “I decided I really needed to go see someone who had had a baby,” he said. He used his vacation time to fly to Melbourne, shuttling between two competing clinics that were “four blocks apart and wouldn’t even talk to each other,” he recalled.
Over 6 weeks, “I learned how to stimulate, how to time ovulation. I watched the PhDs in the lab – how they handled the eggs and the sperm, what the conditions were, the incubator settings,” he said.
The first IVF babies in the United States were born only months apart: The first, in December 1981, was at the Jones Institute for Reproductive Medicine in Norfolk, Va., where Dr. Rosenwaks served as the first director.
The second baby born was at USC. After that, “we had 4,000 women on a waiting list, all under age 35,” Dr. Marrs said. The Jones Institute reportedly had 5,000.
As demand soared and more IVF babies arrived, the cloak of secrecy surrounding the procedure started to lift. British, Australian, and U.S. clinicians started getting together regularly. “We would pick a spot in the world, present our data: what we’d done, how many cycles, what we used for stimulation, when we took the eggs out,” Dr. Marrs said. “I don’t know how many hundreds of thousands of miles I flew in the first years of IVF, because it was the only way I could get information. We would literally stay up all night talking.”
Answering safety questions
Alan H. DeCherney, MD, currently an infertility researcher at the National Institutes of Health, started Yale University’s IVF program at around the same time Dr. Marrs and the Joneses were starting theirs. Yale already had a large infertility practice, and only academic centers had the laboratory resources and skilled staff needed to attempt IVF in those years.
In 1983, when Yale announced the birth of its first IVF baby – the fifth in the United States – Dr. DeCherney was starting to think about measuring outcomes, as there was concern over the potential for congenital anomalies related to IVF. “This was such a change in the way conception occurred, people were afraid that all kinds of crazy things would happen,” he said.
One concern was about ovarian stimulation with fertility drugs or gonadotropins. The earliest efforts – including by Dr. Steptoe and Dr. Edwards – used no drugs, instead trying to pinpoint the moment of natural egg release by measuring a woman’s hormone levels constantly, but these proved disappointing. Use of clomiphene citrate and human menopausal gonadotropin allowed for more control over timing, and for multiple mature eggs to be harvested at once.
But there were still many unanswered questions related to these agents’ safety and dosing, both for women and for babies.
When the NIH refused to fund a study of IVF outcomes, Dr. DeCherney and Dr. Marrs collaborated on a registry funded by a gonadotropin maker. “The drug company didn’t want to be associated with some terrible abnormal outcomes,” Dr. DeCherney recalled, though by then, “there were 10, maybe even 20 babies around the world, and they seemed to be fine,” he said.
The first registry results affirmed no changes in the rate of congenital abnormalities. (Larger, more recent studies have shown a small but significant elevation in birth defect risk associated with IVF.) A few years later, ovarian stimulation was adjusted to correspond with ovarian reserve, reducing the risk of ovarian hyperstimulation syndrome.
But even by the late 1980s, success rates for IVF per attempted cycle were still low overall, leading many critics, even within the profession, to accuse practitioners of misleading couples. Charles E. Miller, MD, an infertility specialist in Chicago, recalled an early investigation by a major newspaper “that looked at all the IVF clinics in Chicago and found the chances of having a baby was under 3%.”
It was true, Dr. Miller acknowledged – “the rates were dismal. But remember that IVF at the time was still considered a procedure of last resort.” Complex diagnostic testing to determine the cause of infertility, surgery, and fertility drugs all came first.
Some important innovations would soon change that and turn IVF into a mainstay of infertility treatment that could help women not only with damaged tubes but also with ovarian failure, low ovarian reserve, or dense pelvic adhesions. Even some types of male factor infertility would find an answer in IVF, by way of intracytoplasmic sperm transfer.
Eggs without surgery
Laparoscopic egg retrieval was the norm in the first decade of IVF. “We went through the belly button, allowing us to directly visualize the ovary and see whether ovulation had already occurred or we had to retrieve it by introducing a needle into the follicle,” Dr. Rosenwaks recalled.
“Some of us were doing 6 or even 10 laparoscopies a day, and it was physically quite challenging,” he said. “There were no video screens in those days. You had to bend over the scope.” And it was worse still for patients, who had to endure multiple surgeries.
Though egg and embryo cryopreservation were already being worked on, it would be years before these techniques were optimized, giving women more chances from a single retrieval of oocytes.
Finding a less invasive means of retrieving eggs was crucial.
Maria Bustillo, MD, an infertility specialist in Miami, recalled being criticized by peers when she and her then-colleagues at the Genetics & IVF Institute in Fairfax, Va., began retrieving eggs via a needle placed in the vagina, using abdominal ultrasound as a guide.
While the technique was far less invasive than laparoscopy, “we were doing it semi-blindly, and were told it was dangerous,” Dr. Bustillo said.
But these freehand ultrasound retrievals paved the way for what would become a revolutionary advance – the vaginal ultrasound probe, which by the end of the 1980s made nonsurgical extraction of eggs the norm.
Dr. Marrs recalled receiving a prototype of a vaginal ultrasound probe, in the mid-1980s, and finding patients unwilling to use it, except one who relented only because she had an empty bladder. Abdominal ultrasonography required a full bladder to work.
“It was as though somebody had removed the cloud cover,” he said. “I couldn’t believe it. I could see everything: her ovaries, tiny follicles, the uterus.”
Later probes were fitted with a needle and aspirator to retrieve eggs. Multiple IVF cycles no longer meant multiple surgeries, and the less-invasive procedure helped in recruiting egg donors, allowing women with ovarian disease or low ovarian reserves, including older women, to receive IVF.
“It didn’t make sense for a volunteer to go through a surgery, especially back in the early ’80s when the results were not all that great,” Dr. Bustillo said.
Improving ‘home brews’
The culture media in which embryos were grown was another strong factor limiting the success rates of early IVF. James Toner, MD, PhD, an IVF specialist in Atlanta, called the early media “home brews.”
“Everyone made them themselves,” said Dr. Toner, who spent 15 years at the Jones Institute. “You had to do a hamster or mouse embryo test on every batch to make sure embryos would grow.” And often they did not.
Poor success rates resulted in the emergence of alternative procedures: GIFT (gamete intrafallopian transfer) and ZIFT (zygote intrafallopian transfer). Both aimed to get embryos back into the patient as soon as possible, with the thought that the natural environment offered a better chance for success.
But advances in culture media allowed more time for embryos to be observed. With longer development, “you could do a better job selecting the ones that had a chance, and de-selecting those with no chance,” Dr. Toner said.
This also meant fewer embryos could be transferred back into patients, lowering the likelihood of multiples. Ultimately, for young women, single-embryo transfer would become the norm. “The problem of multiple pregnancy that we used to have no longer exists for IVF,” Dr. Toner said.
Allowing embryos to reach the blastocyst stage – day 5 or 6 – opened other, previously unthinkable possibilities: placing embryos directly into the uterus, without surgery, and pre-implementation genetic screening for abnormalities.
“As the cell number went up, the idea that you could do a genetic test with minimal impact on the embryo eventually became true,” Dr. Toner said.
A genetic revolution?
While many important IVF innovations were achieved in countries with staunch government support, one of the remarkable things about IVF’s evolution in the United States is that so many occurred with virtually none.
By the mid-1990s, most of the early practitioners had moved from academic settings into private practice, though they continued to publish. “After a while it didn’t help to be in academics. It just sort of slowed you down. Because you weren’t going to get any [government] money anyway, you might as well be in a place that’s a little more nimble,” Dr. Toner said.
At the same time, he said, IVF remains a costly, usually unreimbursed procedure – limiting patients’ willingness to take part in randomized trials. “IVF research is built more on cohort studies.”
Most of the current research focus in IVF is on possibilities for genetic screening. Dr. Miller said that rapid DNA sequencing is allowing specialists to “look at more, pick up more abnormalities. That will continue to improve so that we will be able to see virtually everything.”
But he cautioned there is still much to be done in IVF apart from the genetics – he’s concerned, he said, that the field has moved too far from its surgical origins, and is working with the academic societies to encourage more surgical training.
“We don’t do the same work we did before on fallopian tubes, which is good,” Dr. Miller said, noting that there have been many advances, particularly minimally invasive surgeries in the uterus or ovaries, that have occurred parallel to IVF and can improve success rates. “I think we have a better understanding of what kind of patients require surgical treatments and what kind of surgeries can help enhance fertility, and also what not to do.”
Dr. Bustillo said that “cytogenetics is wonderful, but not everything. You have embryos that are genetically normal and still don’t implant. There’s a lot of work to be done on the interaction between the mother and the embryo.”
Dr. Marrs said that even safety questions related to stimulation have yet to be fully answered. “I’ve always been a big believer that lower is better, but we need to know whether stimulation creates genetic abnormalities and whether less stimulation produces fewer – and we need more data to prove it,” he said. Dr. Marrs is an investigator on a national randomized trial comparing outcomes from IVF with standard-dose and ultra-low dose stimulation.
Access, income, and age
The IVF pioneers agree broadly that access to IVF is nowhere near what it should be in the United States, where only 15 states mandate any insurance coverage for infertility.
“Our limited access to care is a crime,” Dr. Toner said. “People who, through no fault of their own, find themselves infertile are asked to write a check for $15,000 to get pregnant. That’s not fair.”
Dr. DeCherney called access “an ethical issue, because who gets IVF? People with higher incomes. And if IVF allows you to select better embryos – whatever that means – it gives that group another advantage.”
Dr. Toner warned that the push toward genetic testing of embryos, especially in the absence of known hereditary disease, could create new problems for the profession – not unlike in the early days of IVF, when the Jones Institute and other clinics were picketed over the specter of “test tube babies.”
“It’s one thing to say this embryo does not have the right number of chromosomes and couldn’t possibly be a child, so let’s not use it, but what about looking for traits? Sex selection? We have this privileged position in which the government does not really interfere in what we do, but to retain this status we need to stay within the bounds that our society accepts,” Dr. Toner said.
In recent years, IVF uptake has been high among women of advanced reproductive age, which poses its own set of challenges. Outcomes in older women using their own eggs become progressively poorer with age, though donor eggs drastically improve their chances, and egg freezing offers the possibility of preserving quality eggs for later pregnancies.
“We could make this situation better by promoting social freezing, doing more work for women early in their lives to get out their own eggs and store them,” Dr. Miller said. “But again, you still face the issue of access.”
Regardless of what technologies are available or become available in assisted reproduction, doctors and women alike need to be better educated on their options and chances early, with a clearer understanding of what happens as they age, Dr. Bustillo said.
“This is not to pressure them, but just so they understand that when they get to be 42 and are just thinking about reproducing, it’s not a major surprise when I tell them this could be a problem,” she said.
Throughout 2016, Ob.Gyn. News is celebrating its 50th anniversary with exclusive articles looking at the evolution of the specialty, including the history of contraception, changes in gynecologic surgery, and the transformation of the well-woman visit.
Expert Recommendations for Optimizing Outcomes in the Management Of Biofilm to Promote Healing of Chronic Wounds in the Veterans Health Administration System
A supplement to Federal Practitioner. This supplement is sponsored by Organogenesis, Inc.
Chronic non-healing wounds are a major problem for patients and wound care practitioners in the VA system. It is self-evident among experienced wound care practitioners that wound infection can delay (or completely prevent) wound healing. Biofilm is a common form of wound contamination that is now recognized to be a major factor in delaying the healing of wounds.
This supplement discusses the awareness of the biology of biofilm, its prevalence, its clinical significance, and optimal treatment approaches that need to be improved. The supplement also reviews the current status of evidence-based management of biofilm with a focus on the optimal use of PuraPly™ Antimicrobial, a native purified collagen matrix containing the antimicrobial polyhexamethylene biguanide (PHMB).
Meeting Participants |
Gregory Shultz, PhD |
Stephen C. Davis |
Jonathan N. Brantley, DPM |
Mark Couture, DPM |
Sean L. Kersh, DPM |
Jake G. Ruff, DPM |
Patrick J. Sanchez, DPM |
Janette Thompson, DPM |
Catherine M. Wittgen, MD |
CLICK HERE TO READ FULL SUPPLEMENT |
A supplement to Federal Practitioner. This supplement is sponsored by Organogenesis, Inc.
Chronic non-healing wounds are a major problem for patients and wound care practitioners in the VA system. It is self-evident among experienced wound care practitioners that wound infection can delay (or completely prevent) wound healing. Biofilm is a common form of wound contamination that is now recognized to be a major factor in delaying the healing of wounds.
This supplement discusses the awareness of the biology of biofilm, its prevalence, its clinical significance, and optimal treatment approaches that need to be improved. The supplement also reviews the current status of evidence-based management of biofilm with a focus on the optimal use of PuraPly™ Antimicrobial, a native purified collagen matrix containing the antimicrobial polyhexamethylene biguanide (PHMB).
Meeting Participants |
Gregory Shultz, PhD |
Stephen C. Davis |
Jonathan N. Brantley, DPM |
Mark Couture, DPM |
Sean L. Kersh, DPM |
Jake G. Ruff, DPM |
Patrick J. Sanchez, DPM |
Janette Thompson, DPM |
Catherine M. Wittgen, MD |
CLICK HERE TO READ FULL SUPPLEMENT |
A supplement to Federal Practitioner. This supplement is sponsored by Organogenesis, Inc.
Chronic non-healing wounds are a major problem for patients and wound care practitioners in the VA system. It is self-evident among experienced wound care practitioners that wound infection can delay (or completely prevent) wound healing. Biofilm is a common form of wound contamination that is now recognized to be a major factor in delaying the healing of wounds.
This supplement discusses the awareness of the biology of biofilm, its prevalence, its clinical significance, and optimal treatment approaches that need to be improved. The supplement also reviews the current status of evidence-based management of biofilm with a focus on the optimal use of PuraPly™ Antimicrobial, a native purified collagen matrix containing the antimicrobial polyhexamethylene biguanide (PHMB).
Meeting Participants |
Gregory Shultz, PhD |
Stephen C. Davis |
Jonathan N. Brantley, DPM |
Mark Couture, DPM |
Sean L. Kersh, DPM |
Jake G. Ruff, DPM |
Patrick J. Sanchez, DPM |
Janette Thompson, DPM |
Catherine M. Wittgen, MD |
CLICK HERE TO READ FULL SUPPLEMENT |
For dermatologists, leadership opportunities abound
NEWPORT BEACH, CALIF. – The way Seemal R. Desai, MD, sees it, becoming a leader in dermatology doesn’t have to involve a huge time commitment.
The effort “can take as little as 5 minutes a week or as much as a few hours a week, depending on your level of interest,” he said at the annual meeting of the Pacific Dermatologic Association. “But I think that we all need to contribute in some way to give back to our specialty, which is constantly under threat from lots of other specialties and other influences.”
He discussed several practical ways to assume a leadership role in the field, such as lecturing to high school, medical school, or even nurse practitioner students; volunteering in the local academic dermatology department or indigent clinic; lobbying local legislative officials; organizing health policy campaigns, or attending events such as the Capitol Hill Skin Cancer Screening and Prevention Health Fair, One Voice Against Cancer (OVAC) Lobby Day, and the American Academy of Dermatology Annual Legislative Conference (held this year in Washington, D.C., Sept. 11-13).
“Your leadership does not have to be in the traditional sense of getting involved in a committee, getting involved on a board, or in your medical society. There are lots of different things we can do to be leaders,” said Dr. Desai, founder and medical director of Plano, Tex.–based Innovative Dermatology.
Resources he highlighted include the AAD’s Leadership Learning Center, which includes videos on topics such as how to talk to legislators, how to review an article for the Journal of the American Academy of Dermatology, and the nuts and bolts of how to run an efficient staff meeting. The site also contains short podcasts on topics such as time management and conflict resolution, and an extensive list of recommended books about leadership, including the New York Times best seller “Quiet: The Power of Introverts in a World That Can’t Stop Talking”(Crown Publishers, 2012), by Susan Cain. “This book highlights some helpful tips on what you can do to make your practice life a lot better in your day-to-day setting,” Dr. Desai said. “That’s really important when we talk about physician burnout.”
He also encouraged dermatologists to become mentors to clinicians entering the field or those in the early stages of their careers. “None of us became leaders without mentors,” said Dr. Desai, who also holds a faculty position in the department of dermatology at the University of Texas Southwestern Medical Center, Dallas. “Being a mentor is a way to advocate for dermatology, because you’re helping someone become a leader, to take our specialty to the next level.” Information about AAD’s mentoring program is available at: www.aad.org/members/leadership-institute/mentoring.
For those inclined to become politically involved, opportunities abound in local, regional, and national dermatology societies, as well as with SkinPAC, the only federal political action committee representing dermatology’s interests, he said. “Advocacy is important to our specialty to make sure that our voices are heard by policymakers at the state and federal level,” Dr. Desai added. “We as dermatologists work hard; we deal with very difficult patients. In fact, studies have shown that we as outpatient physicians are some of the busiest in the entire organized medicine sea. However, people don’t really understand what we as dermatologists do.”
Dr. Desai reported having no relevant financial disclosures.
NEWPORT BEACH, CALIF. – The way Seemal R. Desai, MD, sees it, becoming a leader in dermatology doesn’t have to involve a huge time commitment.
The effort “can take as little as 5 minutes a week or as much as a few hours a week, depending on your level of interest,” he said at the annual meeting of the Pacific Dermatologic Association. “But I think that we all need to contribute in some way to give back to our specialty, which is constantly under threat from lots of other specialties and other influences.”
He discussed several practical ways to assume a leadership role in the field, such as lecturing to high school, medical school, or even nurse practitioner students; volunteering in the local academic dermatology department or indigent clinic; lobbying local legislative officials; organizing health policy campaigns, or attending events such as the Capitol Hill Skin Cancer Screening and Prevention Health Fair, One Voice Against Cancer (OVAC) Lobby Day, and the American Academy of Dermatology Annual Legislative Conference (held this year in Washington, D.C., Sept. 11-13).
“Your leadership does not have to be in the traditional sense of getting involved in a committee, getting involved on a board, or in your medical society. There are lots of different things we can do to be leaders,” said Dr. Desai, founder and medical director of Plano, Tex.–based Innovative Dermatology.
Resources he highlighted include the AAD’s Leadership Learning Center, which includes videos on topics such as how to talk to legislators, how to review an article for the Journal of the American Academy of Dermatology, and the nuts and bolts of how to run an efficient staff meeting. The site also contains short podcasts on topics such as time management and conflict resolution, and an extensive list of recommended books about leadership, including the New York Times best seller “Quiet: The Power of Introverts in a World That Can’t Stop Talking”(Crown Publishers, 2012), by Susan Cain. “This book highlights some helpful tips on what you can do to make your practice life a lot better in your day-to-day setting,” Dr. Desai said. “That’s really important when we talk about physician burnout.”
He also encouraged dermatologists to become mentors to clinicians entering the field or those in the early stages of their careers. “None of us became leaders without mentors,” said Dr. Desai, who also holds a faculty position in the department of dermatology at the University of Texas Southwestern Medical Center, Dallas. “Being a mentor is a way to advocate for dermatology, because you’re helping someone become a leader, to take our specialty to the next level.” Information about AAD’s mentoring program is available at: www.aad.org/members/leadership-institute/mentoring.
For those inclined to become politically involved, opportunities abound in local, regional, and national dermatology societies, as well as with SkinPAC, the only federal political action committee representing dermatology’s interests, he said. “Advocacy is important to our specialty to make sure that our voices are heard by policymakers at the state and federal level,” Dr. Desai added. “We as dermatologists work hard; we deal with very difficult patients. In fact, studies have shown that we as outpatient physicians are some of the busiest in the entire organized medicine sea. However, people don’t really understand what we as dermatologists do.”
Dr. Desai reported having no relevant financial disclosures.
NEWPORT BEACH, CALIF. – The way Seemal R. Desai, MD, sees it, becoming a leader in dermatology doesn’t have to involve a huge time commitment.
The effort “can take as little as 5 minutes a week or as much as a few hours a week, depending on your level of interest,” he said at the annual meeting of the Pacific Dermatologic Association. “But I think that we all need to contribute in some way to give back to our specialty, which is constantly under threat from lots of other specialties and other influences.”
He discussed several practical ways to assume a leadership role in the field, such as lecturing to high school, medical school, or even nurse practitioner students; volunteering in the local academic dermatology department or indigent clinic; lobbying local legislative officials; organizing health policy campaigns, or attending events such as the Capitol Hill Skin Cancer Screening and Prevention Health Fair, One Voice Against Cancer (OVAC) Lobby Day, and the American Academy of Dermatology Annual Legislative Conference (held this year in Washington, D.C., Sept. 11-13).
“Your leadership does not have to be in the traditional sense of getting involved in a committee, getting involved on a board, or in your medical society. There are lots of different things we can do to be leaders,” said Dr. Desai, founder and medical director of Plano, Tex.–based Innovative Dermatology.
Resources he highlighted include the AAD’s Leadership Learning Center, which includes videos on topics such as how to talk to legislators, how to review an article for the Journal of the American Academy of Dermatology, and the nuts and bolts of how to run an efficient staff meeting. The site also contains short podcasts on topics such as time management and conflict resolution, and an extensive list of recommended books about leadership, including the New York Times best seller “Quiet: The Power of Introverts in a World That Can’t Stop Talking”(Crown Publishers, 2012), by Susan Cain. “This book highlights some helpful tips on what you can do to make your practice life a lot better in your day-to-day setting,” Dr. Desai said. “That’s really important when we talk about physician burnout.”
He also encouraged dermatologists to become mentors to clinicians entering the field or those in the early stages of their careers. “None of us became leaders without mentors,” said Dr. Desai, who also holds a faculty position in the department of dermatology at the University of Texas Southwestern Medical Center, Dallas. “Being a mentor is a way to advocate for dermatology, because you’re helping someone become a leader, to take our specialty to the next level.” Information about AAD’s mentoring program is available at: www.aad.org/members/leadership-institute/mentoring.
For those inclined to become politically involved, opportunities abound in local, regional, and national dermatology societies, as well as with SkinPAC, the only federal political action committee representing dermatology’s interests, he said. “Advocacy is important to our specialty to make sure that our voices are heard by policymakers at the state and federal level,” Dr. Desai added. “We as dermatologists work hard; we deal with very difficult patients. In fact, studies have shown that we as outpatient physicians are some of the busiest in the entire organized medicine sea. However, people don’t really understand what we as dermatologists do.”
Dr. Desai reported having no relevant financial disclosures.
EXPERT ANALYSIS AT PDA 2016
High-Grade Articular, Bursal, and Intratendinous Partial-Thickness Rotator Cuff Tears: A Retrospective Study Comparing Functional Outcomes After Completion and Repair
The Ellman1 classification of partial-thickness rotator cuff tears (PTRCTs) is based on tear location or subtype (A, articular; B, bursal; C, intratendinous) and tear depth (grade 1, <3 mm; grade 2, 3-6 mm; grade 3, >6 mm). Ruotolo and colleagues2 reported that the medial-lateral insertion width of the supraspinatus averaged 12.1 mm, and most authors have indicated that tear depth of 6 mm or more represents 50% tendon thickness. Therefore, Ellman grade 3 tears are considered high-grade (>50% thickness).
Advancements in shoulder arthroscopy, imaging modalities, and clinical research have helped refine our understanding of PTRCTs. Classic teaching based on the retrospective study by Weber3 calls for simple débridement of low-grade (<50%) tears and repair of tears thicker than 50%. According to this standard, Ellman grade 1 and 2 tears should be débrided and grade 3 tears repaired. However, Cordasco and colleagues4 provided evidence supporting an algorithm reformation based on tear location. In their study, results of simple débridement were significantly worse for Ellman grade 2B PTRCTs than for 2A tears, suggesting low-grade bursal tears should also be repaired. Although their study supported a change in operative management for grade 2 tears, to our knowledge no one has investigated the need for differing surgical treatments for grade 3 subtypes based on tear location.
Several studies have demonstrated the efficacy of arthroscopic completion and repair for high-grade PTRCTs of the supraspinatus.5-7 Although all these studies addressed articular- and bursal-sided tears, there has been relative silence with respect to the intratendinous subtype. One explanation is that these tears, given their interstitial nature, pose diagnostic challenges. Histologic research has also shown that they can exist in combination with other tears.8 Despite such challenges, these tears are well documented. They were identified in the seminal study by Ellman1 and were the most common PTRCTs encountered in a well-known cadaveric study (N = 249).9,10 More recently, in 2011, a radiologic study using magnetic resonance arthrography found that 33.8% of PTRCTs were intratendinous (N = 68).11 That study also documented the case of a nonoperatively treated intratendinous tear that progressed to a full-thickness tear within about 6 months.11 Given these facts, it was important for the current PTRCT debate to include an intratendinous group when investigating treatment algorithms for grade 3 tears. Although results of the present study may continue reformation of the 50% algorithm, we hypothesized that arthroscopic completion and repair of all grade 3 PTRCTs will be equally effective, regardless of tear location.
Materials and Methods
After obtaining Institutional Review Board approval for this study, we retrospectively reviewed the operative reports of a fellowship-trained shoulder surgeon for the period 2008–2010. Patients who underwent arthroscopic completion and repair of a supraspinatus tendon PTRCT were identified. Preoperative identification of PTRCT was made on the basis of physical examination and magnetic resonance imaging (MRI) findings (Figures 1–3).
Patients with low-grade PTRCTs of the supraspinatus, identified at time of arthroscopy, were excluded, as were patients with tears that extended into other rotator cuff tendons and patients with previous rotator cuff repair, glenohumeral instability, or adhesive capsulitis.
During the initial appointment, each patient completed a standard questionnaire that included standardized subjective scales evaluating pain and function. A fellowship-trained surgeon then took the patient’s history and performed a physical examination. Postoperative clinical outcome was determined at a minimum of 12 months. Clinical outcomes were assessed with 3 validated outcome measures: visual analog scale (VAS) score, American Shoulder and Elbow Surgeons (ASES) score, and Constant score.
Surgical Procedure and Rehabilitation
All procedures were performed with the patient under general anesthesia with or without an interscalene block. The patient was positioned in the upright beach-chair position. Diagnostic arthroscopy was used to assess the rotator cuff and associated pathologic conditions. If impingement was noted, subacromial decompression was performed. An acromioplasty was limited to removal of osteophytic bone. Distal clavicle excision and biceps tenotomy or tenodesis were performed if preoperative evaluation warranted these procedures.
The rotator cuff was assessed from the articular and bursal sides. For articular PTRCTs, a tagging suture was used to identify the lesion from the bursal side. Bursal-sided tears were probed to assess thinning of the tendon and determine tear grade. If preoperative MRI findings suggested an intratendinous tear, a probe was used to confirm thinning of the tendon. An arthroscopic shaver was then carefully used to débride the capsule on either side of the tendon at the location of the suspected tear. The shaver inevitably penetrated the capsule and entered the tear, where any degenerative tissue was further débrided (Figure 4).
After the PTRCT was completed to full thickness, the rotator cuff footprint on the greater tuberosity was débrided to bleeding cortical bone. Depending on tear length, 1 or 2 Bio-Corkscrew absorbable suture anchors (Arthrex) with 2 No. 2 FiberWire sutures (Arthrex) were then placed in the tuberosity 3 to 5 mm lateral to the articular margin. An arthroscopic suture passer was used to move the 2 sutures through the rotator cuff, such that one was placed in the horizontal mattress and the other was placed in a simple fashion deep to the horizontal mattress. The sutures were then tied with a modified Roeder knot.
A standardized postoperative protocol was used for all patients starting within the first week after surgery. Passive range of motion (ROM) was performed for the first 6 weeks after surgery and was advanced to include active ROM from 6 to 8 weeks after surgery. Strengthening was initiated 8 weeks after surgery.
Statistical Analysis
Power analysis demonstrated that a sample size of 20 in each group was adequate for detecting a medium to large effect size with 80% power. Wilcoxon signed rank test was used to compare the preoperative and postoperative scores for each outcome measure, and analysis of variance (ANOVA) was used to compare the amount of improvement for each of the 3 PTRCT subtypes. Paired t test was used to compare preoperative and postoperative ROM values, and unpaired t tests were used to determine the impact of corticosteroid injections and preoperative PT. For statistical analysis, patients were divided into 2 groups (yes, no) regarding injections and 2 groups (yes, no) regarding PT. Last, multiple linear regression analyses were performed for each outcome measure to determine the impact of potential confounders. Covariates included symptom duration, etiology, age, injection, PT, tear location, percentage of tendon torn (medial-lateral), and tear length (anterior-posterior). P < .05 was considered significant.
Results
Patient Sample and Demographics
Sixty-seven patients underwent arthroscopic repair of a PTRCT—22 grade 3A, 23 grade 3B, and 22 grade 3C. In each of the 3 groups, 20 patients returned for end-of-healing evaluation. Thus, the study population consisted of 60 patients (60 shoulders). The 7 patients who did not return for end-of-healing evaluation or who could not be contacted were excluded from the study.
Table 1 summarizes the key patient demographics. Of the 60 patients, 35 were men and 25 were women.
Range of Motion
The sample as a whole exhibited statistically significant improvement in active ROM (Table 2).
Operative Findings
Operative findings included mean tear thickness of 74% for the sample as a whole and mean anterior-to-posterior tear length of 10.7 mm overall. There was very little variance among the articular, bursal, and intratendinous means with respect to percentage of tear thickness (78.3%, 75.0%, and 68.8%, respectively) and anterior-to-posterior tear thickness (11.5 mm, 11.4 mm, and 9.1 mm, respectively). Each of the 6 tears (3 bursal, 2 articular, 1 intratendinous) that were longer than 15 mm required 2 anchors. Fifty-nine repairs (98%) involved subacromial decompression, 38 (63%) involved acromioclavicular resection, 18 (30%) involved débridement of the superior labrum anterior-to-posterior (SLAP), and 12 (20%) involved biceps tenodesis/tenotomy.
Outcome Measures
In the study population as a whole, and in all 3 tear subtypes, postoperative improvement in VAS, ASES, and Constant scores was statistically significant (Table 3).
Multiple linear regression analyses showed that etiology, symptom duration, and steroid injection were the primary predictors of each outcome. After the other variables were adjusted for, injection (vs noninjection) seemed to be associated with more improvement in ASES (P = .0061), VAS (P = .020), and Constant (P = .067) scores. Insidious (vs traumatic) etiology was significantly associated with more improvement in ASES scores (P = .033) and VAS scores (P = .014) but not Constant scores (P = .50). Longer time from symptom onset to surgery was associated with less improvement, though the coefficient was not statistically significant in any of the models at P = .05. The other possible covariates had no significant impact on outcomes.
Complications
There were no intraoperative or postoperative complications, and there were no incidents of recurrent rotator cuff tear or postoperative stiffness.
Discussion
We investigated the effectiveness of arthroscopic completion and repair of Ellman grade 3 PTRCTs by comparing the functional outcomes for each subtype. Although several studies have analyzed results of PTRCT repair, they all either omitted intratendinous tears or were not grade-specific. In a systematic review, Strauss and colleagues13 discussed 4 PTRCT outcome studies4,6,14,15 in which only articular- and bursal-sided tears were addressed. Of these studies, only 1 (Kamath and colleagues6) focused on grade 3 lesions, and the number of bursal tears was insufficient for comparison with the articular tear group. Cordasco and colleagues4 limited their study to grade 1 and 2 tears but did not include intratendinous lesions.
In other research, Itoi and Tabata16 distinguished among the 3 subtypes but did not measure grade. As we did in our study, Deutsch5 focused on grade 3 lesions and used the completion-and-repair method, but he did not include intratendinous tears. Porat and colleagues17 reviewed grade 3 completion-and-repair results but did not compare them by subtype. Last, Uchiyama and colleagues18 reported strong outcomes for intratendinous tears but did not measure grade and used various surgical methods.
These studies have made important contributions to the ongoing PTRCT discussion, but debate about appropriate operative management persists. To limit the influence of external variables and provide the most exhaustive evidence regarding current PTRCT treatment algorithms, we designed the present study to consider outcomes with all 3 Ellman subtypes, only grade 3 lesions of the supraspinatus, only 1 surgical method, and consistent techniques of only 1 fellowship-trained shoulder surgeon.
Results of this chart review confirmed the findings of other grade 3 PTRCT repair studies. For instance, Koh and colleagues15 reported excellent results of 38 grade 3B PTRCTs completed to full thickness and repaired. Specifically, their mean ASES and Constant scores improved 34.1 and 23.7 points, respectively. These results are similar to our ASES and Constant score improvements—38.9 and 24.7 points for the group as a whole and 36 and 25.1 points for the grade 3B cohort. In addition, our ASES scores are nearly identical to the preoperative (46.1) and postoperative (82.1) ASES scores found by Kamath and colleagues.6 Although the mean ASES and VAS score improvements reported by Deutsch5 (51 and 5.7 points, respectively) were slightly better than ours, these results are still comparable and support completion and repair.
Although results of the study by Cordasco and colleagues4 support differing surgical treatments of grade 2 tears based on location, the present findings support the established 50% algorithm for all 3 high-grade PTRCTs. The completion-and-repair method not only produced significant improvements for each PTRCT subtype, but, importantly, there was no significant difference among those outcomes. Unlike previous results for grade 2 tears, the present results confirmed the established algorithm for grade 3 tears.
Our multiple linear regression analyses suggested that etiology, longer duration of symptoms, and steroid injections each had a strong impact on outcomes. The literature on these preoperative factors is often conflicting, and our results continue the trend. For instance, in a study of acute rotator cuff tears, Petersen and Murphy19 studied acute rotator cuff tears and also found tear size had no significant effect on functional outcomes. However, contrary to our findings, they did not find symptom duration to be a significant predictor of results. Also contrary to our findings, Oh and colleagues20 found age and tear size to be significant influences on outcomes for full-thickness tears. The strong correlation of preoperative steroid injection and better outcomes is novel and warrants further investigation.
In this study, we investigated the effectiveness of the completion-and-repair method in treating Ellman grade 3 PTRCTs. Although our findings validate this surgical technique, we acknowledge alternative approaches to high-grade PTRCTs. For instance, the transtendon method, which does not convert PTRCTs to full thickness, has also shown good clinical outcomes.21-23 In fact, the preoperative and postoperative VAS measures used in our study are nearly identical to those used in an Ellman grade 3A transtendon repair study.1 However, we agree with Porat and colleagues17 that the remaining, intact cuff material of PTRCTs is degenerative and may result in poor fixation, increased pain, or retear. In addition, nonoperative treatment typically is attempted before surgery, though little evidence is reported for success specifically in high-grade PTRCTs. One study found that 91% of PTRCT patients were still satisfied 4 years after nonoperative treatment, but it was noted that many of the tears were low-grade.24 To continue an evidence-based discussion on the more effective treatment, we invite advocates of alternative approaches to conduct a similar study on all 3 Ellman grade 3 subtypes.
Study Limitations
Concomitant procedures were not uniform among all patients and therefore may have affected some outcome measurements. Subacromial decompression was nearly universal, as it was performed for surgical visualization in 98% of patients. The additional procedures were also deemed necessary based on the preoperative assessment and arthroscopic findings. Although these procedures may have influenced outcome measurements, similar studies regularly include them as well.5-7,17 Our minimum 12-month follow-up could be considered a restriction, as other studies have cited a 2-year follow-up threshold.5-7 However, Strauss and colleagues13 endorsed a 12-month standard in their systematic review. Last, about 10% (7/67) of our initial patients were lost to follow-up; this percentage, however, is comparable to what has been reported in other PTRCT studies.4-6,14,15,21,22
Conclusion
Our study findings validate use of the current algorithm for Ellman grade 3 PTRCTs of the supraspinatus and advocate their completion and repair, regardless of tear location.
Acknowledgment: The authors thank Lisa Rein, MS, and Sergey Tarima, PhD, of the Division of Biostatistics, Medical College of Wisconsin, for their help in data analysis and manuscript preparation.
Am J Orthop. 2016;45(5):E254-E260. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Ellman H. Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop Relat Res. 1990;(254):64-74.
2. Ruotolo C, Fow JE, Nottage WM. The supraspinatus footprint: an anatomic study of the supraspinatus insertion. Arthroscopy. 2004;20(3):246-249.
3. Weber SC. Arthroscopic debridement and acromioplasty versus mini-open repair in the treatment of significant partial-thickness rotator cuff tears. Arthroscopy. 1999;15(2):126-131.
4. Cordasco FA, Backer M, Craig EV, Klein D, Warren RF. The partial-thickness rotator cuff tear: is acromioplasty without repair sufficient? Am J Sports Med. 2002;30(2):257-260.
5. Deutsch A. Arthroscopic repair of partial-thickness tears of the rotator cuff. J Shoulder Elbow Surg. 2007;16(2):193-201.
6. Kamath G, Galatz LM, Keener JD, Teefey S, Middleton W, Yamaguchi K. Tendon integrity and functional outcome after arthroscopic repair of high-grade partial-thickness supraspinatus tears. J Bone Joint Surg Am. 2009;91(5):1055-1062.
7. Park JY, Yoo MJ, Kim MH. Comparison of surgical outcome between bursal and articular partial thickness rotator cuff tears. Orthopedics. 2003;26(4):387-390.
8. Fukuda H, Hamada K, Nakajima T, Tomonaga A. Pathology and pathogenesis of the intratendinous tearing of the rotator cuff viewed from en bloc histologic sections. Clin Orthop Relat Res. 1994;(304):60-67.
9. Fukuda H, Mikasa M, Yamanaka K. Incomplete thickness rotator cuff tears diagnosed by subacromial bursography. Clin Orthop Relat Res. 1987;(223):51-58.
10. Yamanaka K, Fukuda H, Hamada K, Mikasa M. Incomplete thickness tears of the rotator cuff [abstract]. Orthop Surg Traumatol (Toyko). 1983;26:713.
11. Schaeffeler C, Mueller D, Kirchhoff C, Wolf P, Rummeny EJ, Woertler K. Tears at the rotator cuff footprint: prevalence and imaging characteristics in 305 MR arthrograms of the shoulder. Eur Radiol. 2011;21(7):1477-1484.
12. Nakagawa S, Yoneda M, Mizuno N, Hayashida K, Mae T, Take Y. Throwing shoulder injury involving the anterior rotator cuff: concealed tears not as uncommon as previously thought. Arthroscopy. 2006;22(12):1298-1303.
13. Strauss EJ, Salata MJ, Kercher J, et al. Multimedia article. The arthroscopic management of partial-thickness rotator cuff tears: a systematic review of the literature. Arthroscopy. 2011;27(4):568-580.
14. Kartus J, Kartus C, Rostgard-Christensen L, Sernert N, Read J, Perko M. Long-term clinical and ultrasound evaluation after arthroscopic acromioplasty in patients with partial rotator cuff tears. Arthroscopy. 2006;22(1):44-49.
15. Koh KH, Shon MS, Lim TK, Yoo JC. Clinical and magnetic resonance imaging results of arthroscopic full-layer repair of bursal-side partial-thickness rotator cuff tears. Am J Sports Med. 2011;39(8):1660-1667.
16. Itoi E, Tabata S. Incomplete rotator cuff tears. Results of operative treatment. Clin Orthop Relat Res. 1992;(284):128-135.
17. Porat S, Nottage WM, Fouse MN. Repair of partial thickness rotator cuff tears: a retrospective review with minimum two-year follow-up. J Shoulder Elbow Surg. 2008;17(5):729-731.
18. Uchiyama Y, Hamada K, Khruekarnchana P, et al. Surgical treatment of confirmed intratendinous rotator cuff tears: retrospective analysis after an average of eight years of follow-up. J Shoulder Elbow Surg. 2010;19(6):837-846.
19. Petersen SA, Murphy TP. The timing of rotator cuff repair for the restoration of function. J Shoulder Elbow Surg. 2011;20(1):62-68.
20. Oh JH, Kim SH, Ji HM, Jo KH, Bin SW, Gong HS. Prognostic factors affecting anatomic outcome of rotator cuff repair and correlation with functional outcome. Arthroscopy. 2009;25(1):30-39.
21. Castagna A, Delle Rose G, Conti M, Snyder SJ, Borroni M, Garofalo R. Predictive factors of subtle residual shoulder symptoms after transtendinous arthroscopic cuff repair: a clinical study. Am J Sports Med. 2009;37(1):103-108.
22. Castricini R, Panfoli N, Nittoli R, Spurio S, Pirani O. Transtendon arthroscopic repair of partial-thickness, articular surface tears of the supraspinatus: results at 2 years. Chir Organi Mov. 2009;93(suppl 1):S49-S54.
23. Spencer EE Jr. Partial-thickness articular surface rotator cuff tears: an all-inside repair technique. Clin Orthop Relat Res. 2010;468(6):1514-1520.
24. Denkers M, Pletsch K, Boorman R, Hollinshead R, Lo IKY. Partial thickness rotator cuff tears: observe or operative. In: Proceedings of the American Academy of Orthopaedic Surgeons Annual Meeting; February 2012; San Francisco, CA.
The Ellman1 classification of partial-thickness rotator cuff tears (PTRCTs) is based on tear location or subtype (A, articular; B, bursal; C, intratendinous) and tear depth (grade 1, <3 mm; grade 2, 3-6 mm; grade 3, >6 mm). Ruotolo and colleagues2 reported that the medial-lateral insertion width of the supraspinatus averaged 12.1 mm, and most authors have indicated that tear depth of 6 mm or more represents 50% tendon thickness. Therefore, Ellman grade 3 tears are considered high-grade (>50% thickness).
Advancements in shoulder arthroscopy, imaging modalities, and clinical research have helped refine our understanding of PTRCTs. Classic teaching based on the retrospective study by Weber3 calls for simple débridement of low-grade (<50%) tears and repair of tears thicker than 50%. According to this standard, Ellman grade 1 and 2 tears should be débrided and grade 3 tears repaired. However, Cordasco and colleagues4 provided evidence supporting an algorithm reformation based on tear location. In their study, results of simple débridement were significantly worse for Ellman grade 2B PTRCTs than for 2A tears, suggesting low-grade bursal tears should also be repaired. Although their study supported a change in operative management for grade 2 tears, to our knowledge no one has investigated the need for differing surgical treatments for grade 3 subtypes based on tear location.
Several studies have demonstrated the efficacy of arthroscopic completion and repair for high-grade PTRCTs of the supraspinatus.5-7 Although all these studies addressed articular- and bursal-sided tears, there has been relative silence with respect to the intratendinous subtype. One explanation is that these tears, given their interstitial nature, pose diagnostic challenges. Histologic research has also shown that they can exist in combination with other tears.8 Despite such challenges, these tears are well documented. They were identified in the seminal study by Ellman1 and were the most common PTRCTs encountered in a well-known cadaveric study (N = 249).9,10 More recently, in 2011, a radiologic study using magnetic resonance arthrography found that 33.8% of PTRCTs were intratendinous (N = 68).11 That study also documented the case of a nonoperatively treated intratendinous tear that progressed to a full-thickness tear within about 6 months.11 Given these facts, it was important for the current PTRCT debate to include an intratendinous group when investigating treatment algorithms for grade 3 tears. Although results of the present study may continue reformation of the 50% algorithm, we hypothesized that arthroscopic completion and repair of all grade 3 PTRCTs will be equally effective, regardless of tear location.
Materials and Methods
After obtaining Institutional Review Board approval for this study, we retrospectively reviewed the operative reports of a fellowship-trained shoulder surgeon for the period 2008–2010. Patients who underwent arthroscopic completion and repair of a supraspinatus tendon PTRCT were identified. Preoperative identification of PTRCT was made on the basis of physical examination and magnetic resonance imaging (MRI) findings (Figures 1–3).
Patients with low-grade PTRCTs of the supraspinatus, identified at time of arthroscopy, were excluded, as were patients with tears that extended into other rotator cuff tendons and patients with previous rotator cuff repair, glenohumeral instability, or adhesive capsulitis.
During the initial appointment, each patient completed a standard questionnaire that included standardized subjective scales evaluating pain and function. A fellowship-trained surgeon then took the patient’s history and performed a physical examination. Postoperative clinical outcome was determined at a minimum of 12 months. Clinical outcomes were assessed with 3 validated outcome measures: visual analog scale (VAS) score, American Shoulder and Elbow Surgeons (ASES) score, and Constant score.
Surgical Procedure and Rehabilitation
All procedures were performed with the patient under general anesthesia with or without an interscalene block. The patient was positioned in the upright beach-chair position. Diagnostic arthroscopy was used to assess the rotator cuff and associated pathologic conditions. If impingement was noted, subacromial decompression was performed. An acromioplasty was limited to removal of osteophytic bone. Distal clavicle excision and biceps tenotomy or tenodesis were performed if preoperative evaluation warranted these procedures.
The rotator cuff was assessed from the articular and bursal sides. For articular PTRCTs, a tagging suture was used to identify the lesion from the bursal side. Bursal-sided tears were probed to assess thinning of the tendon and determine tear grade. If preoperative MRI findings suggested an intratendinous tear, a probe was used to confirm thinning of the tendon. An arthroscopic shaver was then carefully used to débride the capsule on either side of the tendon at the location of the suspected tear. The shaver inevitably penetrated the capsule and entered the tear, where any degenerative tissue was further débrided (Figure 4).
After the PTRCT was completed to full thickness, the rotator cuff footprint on the greater tuberosity was débrided to bleeding cortical bone. Depending on tear length, 1 or 2 Bio-Corkscrew absorbable suture anchors (Arthrex) with 2 No. 2 FiberWire sutures (Arthrex) were then placed in the tuberosity 3 to 5 mm lateral to the articular margin. An arthroscopic suture passer was used to move the 2 sutures through the rotator cuff, such that one was placed in the horizontal mattress and the other was placed in a simple fashion deep to the horizontal mattress. The sutures were then tied with a modified Roeder knot.
A standardized postoperative protocol was used for all patients starting within the first week after surgery. Passive range of motion (ROM) was performed for the first 6 weeks after surgery and was advanced to include active ROM from 6 to 8 weeks after surgery. Strengthening was initiated 8 weeks after surgery.
Statistical Analysis
Power analysis demonstrated that a sample size of 20 in each group was adequate for detecting a medium to large effect size with 80% power. Wilcoxon signed rank test was used to compare the preoperative and postoperative scores for each outcome measure, and analysis of variance (ANOVA) was used to compare the amount of improvement for each of the 3 PTRCT subtypes. Paired t test was used to compare preoperative and postoperative ROM values, and unpaired t tests were used to determine the impact of corticosteroid injections and preoperative PT. For statistical analysis, patients were divided into 2 groups (yes, no) regarding injections and 2 groups (yes, no) regarding PT. Last, multiple linear regression analyses were performed for each outcome measure to determine the impact of potential confounders. Covariates included symptom duration, etiology, age, injection, PT, tear location, percentage of tendon torn (medial-lateral), and tear length (anterior-posterior). P < .05 was considered significant.
Results
Patient Sample and Demographics
Sixty-seven patients underwent arthroscopic repair of a PTRCT—22 grade 3A, 23 grade 3B, and 22 grade 3C. In each of the 3 groups, 20 patients returned for end-of-healing evaluation. Thus, the study population consisted of 60 patients (60 shoulders). The 7 patients who did not return for end-of-healing evaluation or who could not be contacted were excluded from the study.
Table 1 summarizes the key patient demographics. Of the 60 patients, 35 were men and 25 were women.
Range of Motion
The sample as a whole exhibited statistically significant improvement in active ROM (Table 2).
Operative Findings
Operative findings included mean tear thickness of 74% for the sample as a whole and mean anterior-to-posterior tear length of 10.7 mm overall. There was very little variance among the articular, bursal, and intratendinous means with respect to percentage of tear thickness (78.3%, 75.0%, and 68.8%, respectively) and anterior-to-posterior tear thickness (11.5 mm, 11.4 mm, and 9.1 mm, respectively). Each of the 6 tears (3 bursal, 2 articular, 1 intratendinous) that were longer than 15 mm required 2 anchors. Fifty-nine repairs (98%) involved subacromial decompression, 38 (63%) involved acromioclavicular resection, 18 (30%) involved débridement of the superior labrum anterior-to-posterior (SLAP), and 12 (20%) involved biceps tenodesis/tenotomy.
Outcome Measures
In the study population as a whole, and in all 3 tear subtypes, postoperative improvement in VAS, ASES, and Constant scores was statistically significant (Table 3).
Multiple linear regression analyses showed that etiology, symptom duration, and steroid injection were the primary predictors of each outcome. After the other variables were adjusted for, injection (vs noninjection) seemed to be associated with more improvement in ASES (P = .0061), VAS (P = .020), and Constant (P = .067) scores. Insidious (vs traumatic) etiology was significantly associated with more improvement in ASES scores (P = .033) and VAS scores (P = .014) but not Constant scores (P = .50). Longer time from symptom onset to surgery was associated with less improvement, though the coefficient was not statistically significant in any of the models at P = .05. The other possible covariates had no significant impact on outcomes.
Complications
There were no intraoperative or postoperative complications, and there were no incidents of recurrent rotator cuff tear or postoperative stiffness.
Discussion
We investigated the effectiveness of arthroscopic completion and repair of Ellman grade 3 PTRCTs by comparing the functional outcomes for each subtype. Although several studies have analyzed results of PTRCT repair, they all either omitted intratendinous tears or were not grade-specific. In a systematic review, Strauss and colleagues13 discussed 4 PTRCT outcome studies4,6,14,15 in which only articular- and bursal-sided tears were addressed. Of these studies, only 1 (Kamath and colleagues6) focused on grade 3 lesions, and the number of bursal tears was insufficient for comparison with the articular tear group. Cordasco and colleagues4 limited their study to grade 1 and 2 tears but did not include intratendinous lesions.
In other research, Itoi and Tabata16 distinguished among the 3 subtypes but did not measure grade. As we did in our study, Deutsch5 focused on grade 3 lesions and used the completion-and-repair method, but he did not include intratendinous tears. Porat and colleagues17 reviewed grade 3 completion-and-repair results but did not compare them by subtype. Last, Uchiyama and colleagues18 reported strong outcomes for intratendinous tears but did not measure grade and used various surgical methods.
These studies have made important contributions to the ongoing PTRCT discussion, but debate about appropriate operative management persists. To limit the influence of external variables and provide the most exhaustive evidence regarding current PTRCT treatment algorithms, we designed the present study to consider outcomes with all 3 Ellman subtypes, only grade 3 lesions of the supraspinatus, only 1 surgical method, and consistent techniques of only 1 fellowship-trained shoulder surgeon.
Results of this chart review confirmed the findings of other grade 3 PTRCT repair studies. For instance, Koh and colleagues15 reported excellent results of 38 grade 3B PTRCTs completed to full thickness and repaired. Specifically, their mean ASES and Constant scores improved 34.1 and 23.7 points, respectively. These results are similar to our ASES and Constant score improvements—38.9 and 24.7 points for the group as a whole and 36 and 25.1 points for the grade 3B cohort. In addition, our ASES scores are nearly identical to the preoperative (46.1) and postoperative (82.1) ASES scores found by Kamath and colleagues.6 Although the mean ASES and VAS score improvements reported by Deutsch5 (51 and 5.7 points, respectively) were slightly better than ours, these results are still comparable and support completion and repair.
Although results of the study by Cordasco and colleagues4 support differing surgical treatments of grade 2 tears based on location, the present findings support the established 50% algorithm for all 3 high-grade PTRCTs. The completion-and-repair method not only produced significant improvements for each PTRCT subtype, but, importantly, there was no significant difference among those outcomes. Unlike previous results for grade 2 tears, the present results confirmed the established algorithm for grade 3 tears.
Our multiple linear regression analyses suggested that etiology, longer duration of symptoms, and steroid injections each had a strong impact on outcomes. The literature on these preoperative factors is often conflicting, and our results continue the trend. For instance, in a study of acute rotator cuff tears, Petersen and Murphy19 studied acute rotator cuff tears and also found tear size had no significant effect on functional outcomes. However, contrary to our findings, they did not find symptom duration to be a significant predictor of results. Also contrary to our findings, Oh and colleagues20 found age and tear size to be significant influences on outcomes for full-thickness tears. The strong correlation of preoperative steroid injection and better outcomes is novel and warrants further investigation.
In this study, we investigated the effectiveness of the completion-and-repair method in treating Ellman grade 3 PTRCTs. Although our findings validate this surgical technique, we acknowledge alternative approaches to high-grade PTRCTs. For instance, the transtendon method, which does not convert PTRCTs to full thickness, has also shown good clinical outcomes.21-23 In fact, the preoperative and postoperative VAS measures used in our study are nearly identical to those used in an Ellman grade 3A transtendon repair study.1 However, we agree with Porat and colleagues17 that the remaining, intact cuff material of PTRCTs is degenerative and may result in poor fixation, increased pain, or retear. In addition, nonoperative treatment typically is attempted before surgery, though little evidence is reported for success specifically in high-grade PTRCTs. One study found that 91% of PTRCT patients were still satisfied 4 years after nonoperative treatment, but it was noted that many of the tears were low-grade.24 To continue an evidence-based discussion on the more effective treatment, we invite advocates of alternative approaches to conduct a similar study on all 3 Ellman grade 3 subtypes.
Study Limitations
Concomitant procedures were not uniform among all patients and therefore may have affected some outcome measurements. Subacromial decompression was nearly universal, as it was performed for surgical visualization in 98% of patients. The additional procedures were also deemed necessary based on the preoperative assessment and arthroscopic findings. Although these procedures may have influenced outcome measurements, similar studies regularly include them as well.5-7,17 Our minimum 12-month follow-up could be considered a restriction, as other studies have cited a 2-year follow-up threshold.5-7 However, Strauss and colleagues13 endorsed a 12-month standard in their systematic review. Last, about 10% (7/67) of our initial patients were lost to follow-up; this percentage, however, is comparable to what has been reported in other PTRCT studies.4-6,14,15,21,22
Conclusion
Our study findings validate use of the current algorithm for Ellman grade 3 PTRCTs of the supraspinatus and advocate their completion and repair, regardless of tear location.
Acknowledgment: The authors thank Lisa Rein, MS, and Sergey Tarima, PhD, of the Division of Biostatistics, Medical College of Wisconsin, for their help in data analysis and manuscript preparation.
Am J Orthop. 2016;45(5):E254-E260. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
The Ellman1 classification of partial-thickness rotator cuff tears (PTRCTs) is based on tear location or subtype (A, articular; B, bursal; C, intratendinous) and tear depth (grade 1, <3 mm; grade 2, 3-6 mm; grade 3, >6 mm). Ruotolo and colleagues2 reported that the medial-lateral insertion width of the supraspinatus averaged 12.1 mm, and most authors have indicated that tear depth of 6 mm or more represents 50% tendon thickness. Therefore, Ellman grade 3 tears are considered high-grade (>50% thickness).
Advancements in shoulder arthroscopy, imaging modalities, and clinical research have helped refine our understanding of PTRCTs. Classic teaching based on the retrospective study by Weber3 calls for simple débridement of low-grade (<50%) tears and repair of tears thicker than 50%. According to this standard, Ellman grade 1 and 2 tears should be débrided and grade 3 tears repaired. However, Cordasco and colleagues4 provided evidence supporting an algorithm reformation based on tear location. In their study, results of simple débridement were significantly worse for Ellman grade 2B PTRCTs than for 2A tears, suggesting low-grade bursal tears should also be repaired. Although their study supported a change in operative management for grade 2 tears, to our knowledge no one has investigated the need for differing surgical treatments for grade 3 subtypes based on tear location.
Several studies have demonstrated the efficacy of arthroscopic completion and repair for high-grade PTRCTs of the supraspinatus.5-7 Although all these studies addressed articular- and bursal-sided tears, there has been relative silence with respect to the intratendinous subtype. One explanation is that these tears, given their interstitial nature, pose diagnostic challenges. Histologic research has also shown that they can exist in combination with other tears.8 Despite such challenges, these tears are well documented. They were identified in the seminal study by Ellman1 and were the most common PTRCTs encountered in a well-known cadaveric study (N = 249).9,10 More recently, in 2011, a radiologic study using magnetic resonance arthrography found that 33.8% of PTRCTs were intratendinous (N = 68).11 That study also documented the case of a nonoperatively treated intratendinous tear that progressed to a full-thickness tear within about 6 months.11 Given these facts, it was important for the current PTRCT debate to include an intratendinous group when investigating treatment algorithms for grade 3 tears. Although results of the present study may continue reformation of the 50% algorithm, we hypothesized that arthroscopic completion and repair of all grade 3 PTRCTs will be equally effective, regardless of tear location.
Materials and Methods
After obtaining Institutional Review Board approval for this study, we retrospectively reviewed the operative reports of a fellowship-trained shoulder surgeon for the period 2008–2010. Patients who underwent arthroscopic completion and repair of a supraspinatus tendon PTRCT were identified. Preoperative identification of PTRCT was made on the basis of physical examination and magnetic resonance imaging (MRI) findings (Figures 1–3).
Patients with low-grade PTRCTs of the supraspinatus, identified at time of arthroscopy, were excluded, as were patients with tears that extended into other rotator cuff tendons and patients with previous rotator cuff repair, glenohumeral instability, or adhesive capsulitis.
During the initial appointment, each patient completed a standard questionnaire that included standardized subjective scales evaluating pain and function. A fellowship-trained surgeon then took the patient’s history and performed a physical examination. Postoperative clinical outcome was determined at a minimum of 12 months. Clinical outcomes were assessed with 3 validated outcome measures: visual analog scale (VAS) score, American Shoulder and Elbow Surgeons (ASES) score, and Constant score.
Surgical Procedure and Rehabilitation
All procedures were performed with the patient under general anesthesia with or without an interscalene block. The patient was positioned in the upright beach-chair position. Diagnostic arthroscopy was used to assess the rotator cuff and associated pathologic conditions. If impingement was noted, subacromial decompression was performed. An acromioplasty was limited to removal of osteophytic bone. Distal clavicle excision and biceps tenotomy or tenodesis were performed if preoperative evaluation warranted these procedures.
The rotator cuff was assessed from the articular and bursal sides. For articular PTRCTs, a tagging suture was used to identify the lesion from the bursal side. Bursal-sided tears were probed to assess thinning of the tendon and determine tear grade. If preoperative MRI findings suggested an intratendinous tear, a probe was used to confirm thinning of the tendon. An arthroscopic shaver was then carefully used to débride the capsule on either side of the tendon at the location of the suspected tear. The shaver inevitably penetrated the capsule and entered the tear, where any degenerative tissue was further débrided (Figure 4).
After the PTRCT was completed to full thickness, the rotator cuff footprint on the greater tuberosity was débrided to bleeding cortical bone. Depending on tear length, 1 or 2 Bio-Corkscrew absorbable suture anchors (Arthrex) with 2 No. 2 FiberWire sutures (Arthrex) were then placed in the tuberosity 3 to 5 mm lateral to the articular margin. An arthroscopic suture passer was used to move the 2 sutures through the rotator cuff, such that one was placed in the horizontal mattress and the other was placed in a simple fashion deep to the horizontal mattress. The sutures were then tied with a modified Roeder knot.
A standardized postoperative protocol was used for all patients starting within the first week after surgery. Passive range of motion (ROM) was performed for the first 6 weeks after surgery and was advanced to include active ROM from 6 to 8 weeks after surgery. Strengthening was initiated 8 weeks after surgery.
Statistical Analysis
Power analysis demonstrated that a sample size of 20 in each group was adequate for detecting a medium to large effect size with 80% power. Wilcoxon signed rank test was used to compare the preoperative and postoperative scores for each outcome measure, and analysis of variance (ANOVA) was used to compare the amount of improvement for each of the 3 PTRCT subtypes. Paired t test was used to compare preoperative and postoperative ROM values, and unpaired t tests were used to determine the impact of corticosteroid injections and preoperative PT. For statistical analysis, patients were divided into 2 groups (yes, no) regarding injections and 2 groups (yes, no) regarding PT. Last, multiple linear regression analyses were performed for each outcome measure to determine the impact of potential confounders. Covariates included symptom duration, etiology, age, injection, PT, tear location, percentage of tendon torn (medial-lateral), and tear length (anterior-posterior). P < .05 was considered significant.
Results
Patient Sample and Demographics
Sixty-seven patients underwent arthroscopic repair of a PTRCT—22 grade 3A, 23 grade 3B, and 22 grade 3C. In each of the 3 groups, 20 patients returned for end-of-healing evaluation. Thus, the study population consisted of 60 patients (60 shoulders). The 7 patients who did not return for end-of-healing evaluation or who could not be contacted were excluded from the study.
Table 1 summarizes the key patient demographics. Of the 60 patients, 35 were men and 25 were women.
Range of Motion
The sample as a whole exhibited statistically significant improvement in active ROM (Table 2).
Operative Findings
Operative findings included mean tear thickness of 74% for the sample as a whole and mean anterior-to-posterior tear length of 10.7 mm overall. There was very little variance among the articular, bursal, and intratendinous means with respect to percentage of tear thickness (78.3%, 75.0%, and 68.8%, respectively) and anterior-to-posterior tear thickness (11.5 mm, 11.4 mm, and 9.1 mm, respectively). Each of the 6 tears (3 bursal, 2 articular, 1 intratendinous) that were longer than 15 mm required 2 anchors. Fifty-nine repairs (98%) involved subacromial decompression, 38 (63%) involved acromioclavicular resection, 18 (30%) involved débridement of the superior labrum anterior-to-posterior (SLAP), and 12 (20%) involved biceps tenodesis/tenotomy.
Outcome Measures
In the study population as a whole, and in all 3 tear subtypes, postoperative improvement in VAS, ASES, and Constant scores was statistically significant (Table 3).
Multiple linear regression analyses showed that etiology, symptom duration, and steroid injection were the primary predictors of each outcome. After the other variables were adjusted for, injection (vs noninjection) seemed to be associated with more improvement in ASES (P = .0061), VAS (P = .020), and Constant (P = .067) scores. Insidious (vs traumatic) etiology was significantly associated with more improvement in ASES scores (P = .033) and VAS scores (P = .014) but not Constant scores (P = .50). Longer time from symptom onset to surgery was associated with less improvement, though the coefficient was not statistically significant in any of the models at P = .05. The other possible covariates had no significant impact on outcomes.
Complications
There were no intraoperative or postoperative complications, and there were no incidents of recurrent rotator cuff tear or postoperative stiffness.
Discussion
We investigated the effectiveness of arthroscopic completion and repair of Ellman grade 3 PTRCTs by comparing the functional outcomes for each subtype. Although several studies have analyzed results of PTRCT repair, they all either omitted intratendinous tears or were not grade-specific. In a systematic review, Strauss and colleagues13 discussed 4 PTRCT outcome studies4,6,14,15 in which only articular- and bursal-sided tears were addressed. Of these studies, only 1 (Kamath and colleagues6) focused on grade 3 lesions, and the number of bursal tears was insufficient for comparison with the articular tear group. Cordasco and colleagues4 limited their study to grade 1 and 2 tears but did not include intratendinous lesions.
In other research, Itoi and Tabata16 distinguished among the 3 subtypes but did not measure grade. As we did in our study, Deutsch5 focused on grade 3 lesions and used the completion-and-repair method, but he did not include intratendinous tears. Porat and colleagues17 reviewed grade 3 completion-and-repair results but did not compare them by subtype. Last, Uchiyama and colleagues18 reported strong outcomes for intratendinous tears but did not measure grade and used various surgical methods.
These studies have made important contributions to the ongoing PTRCT discussion, but debate about appropriate operative management persists. To limit the influence of external variables and provide the most exhaustive evidence regarding current PTRCT treatment algorithms, we designed the present study to consider outcomes with all 3 Ellman subtypes, only grade 3 lesions of the supraspinatus, only 1 surgical method, and consistent techniques of only 1 fellowship-trained shoulder surgeon.
Results of this chart review confirmed the findings of other grade 3 PTRCT repair studies. For instance, Koh and colleagues15 reported excellent results of 38 grade 3B PTRCTs completed to full thickness and repaired. Specifically, their mean ASES and Constant scores improved 34.1 and 23.7 points, respectively. These results are similar to our ASES and Constant score improvements—38.9 and 24.7 points for the group as a whole and 36 and 25.1 points for the grade 3B cohort. In addition, our ASES scores are nearly identical to the preoperative (46.1) and postoperative (82.1) ASES scores found by Kamath and colleagues.6 Although the mean ASES and VAS score improvements reported by Deutsch5 (51 and 5.7 points, respectively) were slightly better than ours, these results are still comparable and support completion and repair.
Although results of the study by Cordasco and colleagues4 support differing surgical treatments of grade 2 tears based on location, the present findings support the established 50% algorithm for all 3 high-grade PTRCTs. The completion-and-repair method not only produced significant improvements for each PTRCT subtype, but, importantly, there was no significant difference among those outcomes. Unlike previous results for grade 2 tears, the present results confirmed the established algorithm for grade 3 tears.
Our multiple linear regression analyses suggested that etiology, longer duration of symptoms, and steroid injections each had a strong impact on outcomes. The literature on these preoperative factors is often conflicting, and our results continue the trend. For instance, in a study of acute rotator cuff tears, Petersen and Murphy19 studied acute rotator cuff tears and also found tear size had no significant effect on functional outcomes. However, contrary to our findings, they did not find symptom duration to be a significant predictor of results. Also contrary to our findings, Oh and colleagues20 found age and tear size to be significant influences on outcomes for full-thickness tears. The strong correlation of preoperative steroid injection and better outcomes is novel and warrants further investigation.
In this study, we investigated the effectiveness of the completion-and-repair method in treating Ellman grade 3 PTRCTs. Although our findings validate this surgical technique, we acknowledge alternative approaches to high-grade PTRCTs. For instance, the transtendon method, which does not convert PTRCTs to full thickness, has also shown good clinical outcomes.21-23 In fact, the preoperative and postoperative VAS measures used in our study are nearly identical to those used in an Ellman grade 3A transtendon repair study.1 However, we agree with Porat and colleagues17 that the remaining, intact cuff material of PTRCTs is degenerative and may result in poor fixation, increased pain, or retear. In addition, nonoperative treatment typically is attempted before surgery, though little evidence is reported for success specifically in high-grade PTRCTs. One study found that 91% of PTRCT patients were still satisfied 4 years after nonoperative treatment, but it was noted that many of the tears were low-grade.24 To continue an evidence-based discussion on the more effective treatment, we invite advocates of alternative approaches to conduct a similar study on all 3 Ellman grade 3 subtypes.
Study Limitations
Concomitant procedures were not uniform among all patients and therefore may have affected some outcome measurements. Subacromial decompression was nearly universal, as it was performed for surgical visualization in 98% of patients. The additional procedures were also deemed necessary based on the preoperative assessment and arthroscopic findings. Although these procedures may have influenced outcome measurements, similar studies regularly include them as well.5-7,17 Our minimum 12-month follow-up could be considered a restriction, as other studies have cited a 2-year follow-up threshold.5-7 However, Strauss and colleagues13 endorsed a 12-month standard in their systematic review. Last, about 10% (7/67) of our initial patients were lost to follow-up; this percentage, however, is comparable to what has been reported in other PTRCT studies.4-6,14,15,21,22
Conclusion
Our study findings validate use of the current algorithm for Ellman grade 3 PTRCTs of the supraspinatus and advocate their completion and repair, regardless of tear location.
Acknowledgment: The authors thank Lisa Rein, MS, and Sergey Tarima, PhD, of the Division of Biostatistics, Medical College of Wisconsin, for their help in data analysis and manuscript preparation.
Am J Orthop. 2016;45(5):E254-E260. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Ellman H. Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop Relat Res. 1990;(254):64-74.
2. Ruotolo C, Fow JE, Nottage WM. The supraspinatus footprint: an anatomic study of the supraspinatus insertion. Arthroscopy. 2004;20(3):246-249.
3. Weber SC. Arthroscopic debridement and acromioplasty versus mini-open repair in the treatment of significant partial-thickness rotator cuff tears. Arthroscopy. 1999;15(2):126-131.
4. Cordasco FA, Backer M, Craig EV, Klein D, Warren RF. The partial-thickness rotator cuff tear: is acromioplasty without repair sufficient? Am J Sports Med. 2002;30(2):257-260.
5. Deutsch A. Arthroscopic repair of partial-thickness tears of the rotator cuff. J Shoulder Elbow Surg. 2007;16(2):193-201.
6. Kamath G, Galatz LM, Keener JD, Teefey S, Middleton W, Yamaguchi K. Tendon integrity and functional outcome after arthroscopic repair of high-grade partial-thickness supraspinatus tears. J Bone Joint Surg Am. 2009;91(5):1055-1062.
7. Park JY, Yoo MJ, Kim MH. Comparison of surgical outcome between bursal and articular partial thickness rotator cuff tears. Orthopedics. 2003;26(4):387-390.
8. Fukuda H, Hamada K, Nakajima T, Tomonaga A. Pathology and pathogenesis of the intratendinous tearing of the rotator cuff viewed from en bloc histologic sections. Clin Orthop Relat Res. 1994;(304):60-67.
9. Fukuda H, Mikasa M, Yamanaka K. Incomplete thickness rotator cuff tears diagnosed by subacromial bursography. Clin Orthop Relat Res. 1987;(223):51-58.
10. Yamanaka K, Fukuda H, Hamada K, Mikasa M. Incomplete thickness tears of the rotator cuff [abstract]. Orthop Surg Traumatol (Toyko). 1983;26:713.
11. Schaeffeler C, Mueller D, Kirchhoff C, Wolf P, Rummeny EJ, Woertler K. Tears at the rotator cuff footprint: prevalence and imaging characteristics in 305 MR arthrograms of the shoulder. Eur Radiol. 2011;21(7):1477-1484.
12. Nakagawa S, Yoneda M, Mizuno N, Hayashida K, Mae T, Take Y. Throwing shoulder injury involving the anterior rotator cuff: concealed tears not as uncommon as previously thought. Arthroscopy. 2006;22(12):1298-1303.
13. Strauss EJ, Salata MJ, Kercher J, et al. Multimedia article. The arthroscopic management of partial-thickness rotator cuff tears: a systematic review of the literature. Arthroscopy. 2011;27(4):568-580.
14. Kartus J, Kartus C, Rostgard-Christensen L, Sernert N, Read J, Perko M. Long-term clinical and ultrasound evaluation after arthroscopic acromioplasty in patients with partial rotator cuff tears. Arthroscopy. 2006;22(1):44-49.
15. Koh KH, Shon MS, Lim TK, Yoo JC. Clinical and magnetic resonance imaging results of arthroscopic full-layer repair of bursal-side partial-thickness rotator cuff tears. Am J Sports Med. 2011;39(8):1660-1667.
16. Itoi E, Tabata S. Incomplete rotator cuff tears. Results of operative treatment. Clin Orthop Relat Res. 1992;(284):128-135.
17. Porat S, Nottage WM, Fouse MN. Repair of partial thickness rotator cuff tears: a retrospective review with minimum two-year follow-up. J Shoulder Elbow Surg. 2008;17(5):729-731.
18. Uchiyama Y, Hamada K, Khruekarnchana P, et al. Surgical treatment of confirmed intratendinous rotator cuff tears: retrospective analysis after an average of eight years of follow-up. J Shoulder Elbow Surg. 2010;19(6):837-846.
19. Petersen SA, Murphy TP. The timing of rotator cuff repair for the restoration of function. J Shoulder Elbow Surg. 2011;20(1):62-68.
20. Oh JH, Kim SH, Ji HM, Jo KH, Bin SW, Gong HS. Prognostic factors affecting anatomic outcome of rotator cuff repair and correlation with functional outcome. Arthroscopy. 2009;25(1):30-39.
21. Castagna A, Delle Rose G, Conti M, Snyder SJ, Borroni M, Garofalo R. Predictive factors of subtle residual shoulder symptoms after transtendinous arthroscopic cuff repair: a clinical study. Am J Sports Med. 2009;37(1):103-108.
22. Castricini R, Panfoli N, Nittoli R, Spurio S, Pirani O. Transtendon arthroscopic repair of partial-thickness, articular surface tears of the supraspinatus: results at 2 years. Chir Organi Mov. 2009;93(suppl 1):S49-S54.
23. Spencer EE Jr. Partial-thickness articular surface rotator cuff tears: an all-inside repair technique. Clin Orthop Relat Res. 2010;468(6):1514-1520.
24. Denkers M, Pletsch K, Boorman R, Hollinshead R, Lo IKY. Partial thickness rotator cuff tears: observe or operative. In: Proceedings of the American Academy of Orthopaedic Surgeons Annual Meeting; February 2012; San Francisco, CA.
1. Ellman H. Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop Relat Res. 1990;(254):64-74.
2. Ruotolo C, Fow JE, Nottage WM. The supraspinatus footprint: an anatomic study of the supraspinatus insertion. Arthroscopy. 2004;20(3):246-249.
3. Weber SC. Arthroscopic debridement and acromioplasty versus mini-open repair in the treatment of significant partial-thickness rotator cuff tears. Arthroscopy. 1999;15(2):126-131.
4. Cordasco FA, Backer M, Craig EV, Klein D, Warren RF. The partial-thickness rotator cuff tear: is acromioplasty without repair sufficient? Am J Sports Med. 2002;30(2):257-260.
5. Deutsch A. Arthroscopic repair of partial-thickness tears of the rotator cuff. J Shoulder Elbow Surg. 2007;16(2):193-201.
6. Kamath G, Galatz LM, Keener JD, Teefey S, Middleton W, Yamaguchi K. Tendon integrity and functional outcome after arthroscopic repair of high-grade partial-thickness supraspinatus tears. J Bone Joint Surg Am. 2009;91(5):1055-1062.
7. Park JY, Yoo MJ, Kim MH. Comparison of surgical outcome between bursal and articular partial thickness rotator cuff tears. Orthopedics. 2003;26(4):387-390.
8. Fukuda H, Hamada K, Nakajima T, Tomonaga A. Pathology and pathogenesis of the intratendinous tearing of the rotator cuff viewed from en bloc histologic sections. Clin Orthop Relat Res. 1994;(304):60-67.
9. Fukuda H, Mikasa M, Yamanaka K. Incomplete thickness rotator cuff tears diagnosed by subacromial bursography. Clin Orthop Relat Res. 1987;(223):51-58.
10. Yamanaka K, Fukuda H, Hamada K, Mikasa M. Incomplete thickness tears of the rotator cuff [abstract]. Orthop Surg Traumatol (Toyko). 1983;26:713.
11. Schaeffeler C, Mueller D, Kirchhoff C, Wolf P, Rummeny EJ, Woertler K. Tears at the rotator cuff footprint: prevalence and imaging characteristics in 305 MR arthrograms of the shoulder. Eur Radiol. 2011;21(7):1477-1484.
12. Nakagawa S, Yoneda M, Mizuno N, Hayashida K, Mae T, Take Y. Throwing shoulder injury involving the anterior rotator cuff: concealed tears not as uncommon as previously thought. Arthroscopy. 2006;22(12):1298-1303.
13. Strauss EJ, Salata MJ, Kercher J, et al. Multimedia article. The arthroscopic management of partial-thickness rotator cuff tears: a systematic review of the literature. Arthroscopy. 2011;27(4):568-580.
14. Kartus J, Kartus C, Rostgard-Christensen L, Sernert N, Read J, Perko M. Long-term clinical and ultrasound evaluation after arthroscopic acromioplasty in patients with partial rotator cuff tears. Arthroscopy. 2006;22(1):44-49.
15. Koh KH, Shon MS, Lim TK, Yoo JC. Clinical and magnetic resonance imaging results of arthroscopic full-layer repair of bursal-side partial-thickness rotator cuff tears. Am J Sports Med. 2011;39(8):1660-1667.
16. Itoi E, Tabata S. Incomplete rotator cuff tears. Results of operative treatment. Clin Orthop Relat Res. 1992;(284):128-135.
17. Porat S, Nottage WM, Fouse MN. Repair of partial thickness rotator cuff tears: a retrospective review with minimum two-year follow-up. J Shoulder Elbow Surg. 2008;17(5):729-731.
18. Uchiyama Y, Hamada K, Khruekarnchana P, et al. Surgical treatment of confirmed intratendinous rotator cuff tears: retrospective analysis after an average of eight years of follow-up. J Shoulder Elbow Surg. 2010;19(6):837-846.
19. Petersen SA, Murphy TP. The timing of rotator cuff repair for the restoration of function. J Shoulder Elbow Surg. 2011;20(1):62-68.
20. Oh JH, Kim SH, Ji HM, Jo KH, Bin SW, Gong HS. Prognostic factors affecting anatomic outcome of rotator cuff repair and correlation with functional outcome. Arthroscopy. 2009;25(1):30-39.
21. Castagna A, Delle Rose G, Conti M, Snyder SJ, Borroni M, Garofalo R. Predictive factors of subtle residual shoulder symptoms after transtendinous arthroscopic cuff repair: a clinical study. Am J Sports Med. 2009;37(1):103-108.
22. Castricini R, Panfoli N, Nittoli R, Spurio S, Pirani O. Transtendon arthroscopic repair of partial-thickness, articular surface tears of the supraspinatus: results at 2 years. Chir Organi Mov. 2009;93(suppl 1):S49-S54.
23. Spencer EE Jr. Partial-thickness articular surface rotator cuff tears: an all-inside repair technique. Clin Orthop Relat Res. 2010;468(6):1514-1520.
24. Denkers M, Pletsch K, Boorman R, Hollinshead R, Lo IKY. Partial thickness rotator cuff tears: observe or operative. In: Proceedings of the American Academy of Orthopaedic Surgeons Annual Meeting; February 2012; San Francisco, CA.