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Point/Counterpoint: Is endograft PAA repair durable?
Endovascular repair is durable
Endovascular repair of popliteal artery aneurysms is vastly superior to all other previous techniques of popliteal aneurysm repair. Half of all popliteal artery aneurysms are bilateral, and 40% are associated with abdominal aortic aneurysm; 1%-2% of patients with abdominal aortic aneurysm have a popliteal aneurysm (ANZ J Surg. 2006 Oct;76[10]:912-5). Less than 0.01% of hospitalized patients have popliteal artery aneurysms, and men are 20 times more prone to them than women are.
Traditional treatment involves either bypass with interval ligation or a direct posterior approach with an interposition graft, but surgery is not without its problems. I think of the retired anesthesiologist who came to me with a popliteal artery aneurysm (PAA) that his primary care doctor diagnosed. “I’m not having any damn femoral popliteal bypass operation,” he told me. “Every single one of those patients dies.”
Endograft repair is a technique that is reaching its prime, as a growing number of reports have shown – although none of these studies has large numbers because the volume just isn’t available. One recent paper compared 52 open and 23 endovascular PAA repairs (Ann Vasc Surg. 2016 Jan;30:253-7) and found both had similarly high rates of reintervention – 50% at 4 years. But it is noteworthy that the endovascular results improved with time.
A University of Pittsburgh study of 186 open and endovascular repairs found that patients with acute presentations of embolization or aneurysm thrombosis did better with open surgery. In addition, while open repair had superior patency initially after surgery, midterm secondary patency and amputation rates of open and endovascular repair were similar (J Vasc Surg. 2016 Jan;63[1]:70-6).
A Netherlands study of 72 PAA treated with endografting showed that 84% had primary patency at 1 year, and 74% had assisted primary patency at 3 years (Eur J Vasc Endovasc Surg. 2016 Jul;52[1]:99-104). Among these patients, 13 had late occlusions, 7 were converted to bypass, and 2 required thrombolysis; but none required limb amputation.
A meta-analysis of 540 patients found no statistically significant difference in outcomes between endovascular and open repair for PAA (Eur J Vasc Endovasc Surg. 2015 Sep;50(3):351-9). Another systematic review and meta-analysis of 14 studies and 514 patients also found no difference in pooled primary and secondary patency at 5 years (J Endovasc Ther. 2015 Jun;22[3]:330-7).
There certainly are contradictory studies, such as one by Dr. Alik Farber’s group in Boston that showed open repair is superior to endovascular surgery (J Vasc Surg. 2015 Mar;61[3]:663-9); but retrospective database mining certainly has its limitations. Their retrospective study queried the Vascular Quality Initiative database and found that 95% of patients who had open elective popliteal aneurysm repair were free from major adverse limb events, vs. 80% for endovascular treatments.
The best outcomes of open repair happen with autologous vein, but there is precious little of that around now. Emergency patients would probably do better with open surgery, but in elective repair there is no clear differential data.
So, if that’s the case, I’m going to take the small incision.
Peter Rossi, MD, FACS, is an associate professor of surgery and radiology, and the clinical director of vascular surgery, at the Medical College of Wisconsin, Milwaukee. He is also on staff at Clement J. Zablocki Veterans Affairs Medical Center in Milwaukee. Dr. Rossi had no financial relationships to disclose.
Endovascular repair may not be durable
Debating the durability of elective endovascular repair of popliteal artery aneurysm raises a question: Who determines durability anyway?
Is it the patients who only want the Band-Aid and no incision? I don’t think so. Is it the interventionalist who only does endovascular repairs? I don’t think so. I’m sure it’s not the insurance companies, who only worry about cost containment, either.
So, who should determine durability of endovascular popliteal artery aneurysm (PAA) repair?
So, the question is, do we have such data?
There are multiple reports looking at how well open repair works. It has been done for decades. In 2008, a Veterans Affairs study of 583 open PAA repairs reported low death rates and excellent rates of limb salvage at 2 years, even in high-risk patients (J Vasc Surg. 2008 Oct;48[4]:845-51). Open surgical repair has excellent documented durability, and that is not the question at hand.
Endovascular repair has some presumed advantages. It’s less invasive and involves less postoperative pain and a quicker recovery. But it is not without problems – graft thrombosis and occlusion, endoleaks, distal limb ischemia, and stent fractures among them.
Surgery, to be clear, is not perfect, either. One of my patients who years ago presented with an occluded PAA underwent open bypass repair – but then went on later to have a pseudoaneurysm of the proximal anastomosis. I repaired this with an endograft, and he has done quite well. So, we all do endograft repairs, walk out, chest bump the Gore rep, and send the patient home that day.
Is it durable, though?
Most of the data on endovascular repair are from single-center studies dating back to 2003. There’s only one prospective trial comparing endovascular vs. open repair (J Vasc Surg. 2005 Aug;42[2]:185-93), but it was a single-center trial with a severe power limitation, because it involved only 30 patients. It found endovascular repair was comparable to open surgery. Also, I suspect a great deal of selection bias is involved in studies of endovascular repair.
A number of studies have found endovascular repair is not inferior to surgical repair. For example, a study by Dr. Audra Duncan, at Mayo Clinic, and her colleagues found that primary and secondary patency rates of elective and emergent stenting were excellent – but the study results only extended out to 2 years (J Vasc Surg. 2013 May;57[5]:1299-305). I don’t think we could hang our hat on that.
A Swedish study that compared open and endovascular surgery in 592 patients reported that endovascular repair has “significantly inferior results compared with open repair,” particularly in those who present with acute ischemia (Eur J Vasc Endovasc Surg. 2015 Sep;50[3]:342-50). A close look at the data shows that primary patency rates were 89% for open repair and 67.4% for stent graft.
Referencing the systematic review and meta-analysis that Dr. Rossi cited, the primary patency of endovascular repair was only 69% and the secondary patency rate was 77% at 5 years (J Endovasc Ther. 2015 Jun;22[3]:330-7). As physicians, I submit that we can do better.
A Netherlands study investigated stent fractures, finding that 17% (13 out of 78 cases) had circumferential fractures (J Vasc Surg. 2010 Jun;51[6]:1413-8). This study only included circumferential stent fractures and excluded localized strut fractures. I think these studies show that endovascular repair is not always durable.
I want to remind you that we are vascular surgeons, so it is appropriate for us to embrace surgical bypass and its known durability, especially when the durability of endovascular repair is still not known.
Patrick Muck, MD, is chief of vascular surgery and director of vascular residency and fellowship at Good Samaritan Hospital, Cincinnati. He is also on staff at Bethesda North Hospital, Cincinnati, and is affiliated with TriHealth Heart Institute in southwestern Ohio. Dr. Muck had no financial relationships to disclose.
Endovascular repair is durable
Endovascular repair of popliteal artery aneurysms is vastly superior to all other previous techniques of popliteal aneurysm repair. Half of all popliteal artery aneurysms are bilateral, and 40% are associated with abdominal aortic aneurysm; 1%-2% of patients with abdominal aortic aneurysm have a popliteal aneurysm (ANZ J Surg. 2006 Oct;76[10]:912-5). Less than 0.01% of hospitalized patients have popliteal artery aneurysms, and men are 20 times more prone to them than women are.
Traditional treatment involves either bypass with interval ligation or a direct posterior approach with an interposition graft, but surgery is not without its problems. I think of the retired anesthesiologist who came to me with a popliteal artery aneurysm (PAA) that his primary care doctor diagnosed. “I’m not having any damn femoral popliteal bypass operation,” he told me. “Every single one of those patients dies.”
Endograft repair is a technique that is reaching its prime, as a growing number of reports have shown – although none of these studies has large numbers because the volume just isn’t available. One recent paper compared 52 open and 23 endovascular PAA repairs (Ann Vasc Surg. 2016 Jan;30:253-7) and found both had similarly high rates of reintervention – 50% at 4 years. But it is noteworthy that the endovascular results improved with time.
A University of Pittsburgh study of 186 open and endovascular repairs found that patients with acute presentations of embolization or aneurysm thrombosis did better with open surgery. In addition, while open repair had superior patency initially after surgery, midterm secondary patency and amputation rates of open and endovascular repair were similar (J Vasc Surg. 2016 Jan;63[1]:70-6).
A Netherlands study of 72 PAA treated with endografting showed that 84% had primary patency at 1 year, and 74% had assisted primary patency at 3 years (Eur J Vasc Endovasc Surg. 2016 Jul;52[1]:99-104). Among these patients, 13 had late occlusions, 7 were converted to bypass, and 2 required thrombolysis; but none required limb amputation.
A meta-analysis of 540 patients found no statistically significant difference in outcomes between endovascular and open repair for PAA (Eur J Vasc Endovasc Surg. 2015 Sep;50(3):351-9). Another systematic review and meta-analysis of 14 studies and 514 patients also found no difference in pooled primary and secondary patency at 5 years (J Endovasc Ther. 2015 Jun;22[3]:330-7).
There certainly are contradictory studies, such as one by Dr. Alik Farber’s group in Boston that showed open repair is superior to endovascular surgery (J Vasc Surg. 2015 Mar;61[3]:663-9); but retrospective database mining certainly has its limitations. Their retrospective study queried the Vascular Quality Initiative database and found that 95% of patients who had open elective popliteal aneurysm repair were free from major adverse limb events, vs. 80% for endovascular treatments.
The best outcomes of open repair happen with autologous vein, but there is precious little of that around now. Emergency patients would probably do better with open surgery, but in elective repair there is no clear differential data.
So, if that’s the case, I’m going to take the small incision.
Peter Rossi, MD, FACS, is an associate professor of surgery and radiology, and the clinical director of vascular surgery, at the Medical College of Wisconsin, Milwaukee. He is also on staff at Clement J. Zablocki Veterans Affairs Medical Center in Milwaukee. Dr. Rossi had no financial relationships to disclose.
Endovascular repair may not be durable
Debating the durability of elective endovascular repair of popliteal artery aneurysm raises a question: Who determines durability anyway?
Is it the patients who only want the Band-Aid and no incision? I don’t think so. Is it the interventionalist who only does endovascular repairs? I don’t think so. I’m sure it’s not the insurance companies, who only worry about cost containment, either.
So, who should determine durability of endovascular popliteal artery aneurysm (PAA) repair?
So, the question is, do we have such data?
There are multiple reports looking at how well open repair works. It has been done for decades. In 2008, a Veterans Affairs study of 583 open PAA repairs reported low death rates and excellent rates of limb salvage at 2 years, even in high-risk patients (J Vasc Surg. 2008 Oct;48[4]:845-51). Open surgical repair has excellent documented durability, and that is not the question at hand.
Endovascular repair has some presumed advantages. It’s less invasive and involves less postoperative pain and a quicker recovery. But it is not without problems – graft thrombosis and occlusion, endoleaks, distal limb ischemia, and stent fractures among them.
Surgery, to be clear, is not perfect, either. One of my patients who years ago presented with an occluded PAA underwent open bypass repair – but then went on later to have a pseudoaneurysm of the proximal anastomosis. I repaired this with an endograft, and he has done quite well. So, we all do endograft repairs, walk out, chest bump the Gore rep, and send the patient home that day.
Is it durable, though?
Most of the data on endovascular repair are from single-center studies dating back to 2003. There’s only one prospective trial comparing endovascular vs. open repair (J Vasc Surg. 2005 Aug;42[2]:185-93), but it was a single-center trial with a severe power limitation, because it involved only 30 patients. It found endovascular repair was comparable to open surgery. Also, I suspect a great deal of selection bias is involved in studies of endovascular repair.
A number of studies have found endovascular repair is not inferior to surgical repair. For example, a study by Dr. Audra Duncan, at Mayo Clinic, and her colleagues found that primary and secondary patency rates of elective and emergent stenting were excellent – but the study results only extended out to 2 years (J Vasc Surg. 2013 May;57[5]:1299-305). I don’t think we could hang our hat on that.
A Swedish study that compared open and endovascular surgery in 592 patients reported that endovascular repair has “significantly inferior results compared with open repair,” particularly in those who present with acute ischemia (Eur J Vasc Endovasc Surg. 2015 Sep;50[3]:342-50). A close look at the data shows that primary patency rates were 89% for open repair and 67.4% for stent graft.
Referencing the systematic review and meta-analysis that Dr. Rossi cited, the primary patency of endovascular repair was only 69% and the secondary patency rate was 77% at 5 years (J Endovasc Ther. 2015 Jun;22[3]:330-7). As physicians, I submit that we can do better.
A Netherlands study investigated stent fractures, finding that 17% (13 out of 78 cases) had circumferential fractures (J Vasc Surg. 2010 Jun;51[6]:1413-8). This study only included circumferential stent fractures and excluded localized strut fractures. I think these studies show that endovascular repair is not always durable.
I want to remind you that we are vascular surgeons, so it is appropriate for us to embrace surgical bypass and its known durability, especially when the durability of endovascular repair is still not known.
Patrick Muck, MD, is chief of vascular surgery and director of vascular residency and fellowship at Good Samaritan Hospital, Cincinnati. He is also on staff at Bethesda North Hospital, Cincinnati, and is affiliated with TriHealth Heart Institute in southwestern Ohio. Dr. Muck had no financial relationships to disclose.
Endovascular repair is durable
Endovascular repair of popliteal artery aneurysms is vastly superior to all other previous techniques of popliteal aneurysm repair. Half of all popliteal artery aneurysms are bilateral, and 40% are associated with abdominal aortic aneurysm; 1%-2% of patients with abdominal aortic aneurysm have a popliteal aneurysm (ANZ J Surg. 2006 Oct;76[10]:912-5). Less than 0.01% of hospitalized patients have popliteal artery aneurysms, and men are 20 times more prone to them than women are.
Traditional treatment involves either bypass with interval ligation or a direct posterior approach with an interposition graft, but surgery is not without its problems. I think of the retired anesthesiologist who came to me with a popliteal artery aneurysm (PAA) that his primary care doctor diagnosed. “I’m not having any damn femoral popliteal bypass operation,” he told me. “Every single one of those patients dies.”
Endograft repair is a technique that is reaching its prime, as a growing number of reports have shown – although none of these studies has large numbers because the volume just isn’t available. One recent paper compared 52 open and 23 endovascular PAA repairs (Ann Vasc Surg. 2016 Jan;30:253-7) and found both had similarly high rates of reintervention – 50% at 4 years. But it is noteworthy that the endovascular results improved with time.
A University of Pittsburgh study of 186 open and endovascular repairs found that patients with acute presentations of embolization or aneurysm thrombosis did better with open surgery. In addition, while open repair had superior patency initially after surgery, midterm secondary patency and amputation rates of open and endovascular repair were similar (J Vasc Surg. 2016 Jan;63[1]:70-6).
A Netherlands study of 72 PAA treated with endografting showed that 84% had primary patency at 1 year, and 74% had assisted primary patency at 3 years (Eur J Vasc Endovasc Surg. 2016 Jul;52[1]:99-104). Among these patients, 13 had late occlusions, 7 were converted to bypass, and 2 required thrombolysis; but none required limb amputation.
A meta-analysis of 540 patients found no statistically significant difference in outcomes between endovascular and open repair for PAA (Eur J Vasc Endovasc Surg. 2015 Sep;50(3):351-9). Another systematic review and meta-analysis of 14 studies and 514 patients also found no difference in pooled primary and secondary patency at 5 years (J Endovasc Ther. 2015 Jun;22[3]:330-7).
There certainly are contradictory studies, such as one by Dr. Alik Farber’s group in Boston that showed open repair is superior to endovascular surgery (J Vasc Surg. 2015 Mar;61[3]:663-9); but retrospective database mining certainly has its limitations. Their retrospective study queried the Vascular Quality Initiative database and found that 95% of patients who had open elective popliteal aneurysm repair were free from major adverse limb events, vs. 80% for endovascular treatments.
The best outcomes of open repair happen with autologous vein, but there is precious little of that around now. Emergency patients would probably do better with open surgery, but in elective repair there is no clear differential data.
So, if that’s the case, I’m going to take the small incision.
Peter Rossi, MD, FACS, is an associate professor of surgery and radiology, and the clinical director of vascular surgery, at the Medical College of Wisconsin, Milwaukee. He is also on staff at Clement J. Zablocki Veterans Affairs Medical Center in Milwaukee. Dr. Rossi had no financial relationships to disclose.
Endovascular repair may not be durable
Debating the durability of elective endovascular repair of popliteal artery aneurysm raises a question: Who determines durability anyway?
Is it the patients who only want the Band-Aid and no incision? I don’t think so. Is it the interventionalist who only does endovascular repairs? I don’t think so. I’m sure it’s not the insurance companies, who only worry about cost containment, either.
So, who should determine durability of endovascular popliteal artery aneurysm (PAA) repair?
So, the question is, do we have such data?
There are multiple reports looking at how well open repair works. It has been done for decades. In 2008, a Veterans Affairs study of 583 open PAA repairs reported low death rates and excellent rates of limb salvage at 2 years, even in high-risk patients (J Vasc Surg. 2008 Oct;48[4]:845-51). Open surgical repair has excellent documented durability, and that is not the question at hand.
Endovascular repair has some presumed advantages. It’s less invasive and involves less postoperative pain and a quicker recovery. But it is not without problems – graft thrombosis and occlusion, endoleaks, distal limb ischemia, and stent fractures among them.
Surgery, to be clear, is not perfect, either. One of my patients who years ago presented with an occluded PAA underwent open bypass repair – but then went on later to have a pseudoaneurysm of the proximal anastomosis. I repaired this with an endograft, and he has done quite well. So, we all do endograft repairs, walk out, chest bump the Gore rep, and send the patient home that day.
Is it durable, though?
Most of the data on endovascular repair are from single-center studies dating back to 2003. There’s only one prospective trial comparing endovascular vs. open repair (J Vasc Surg. 2005 Aug;42[2]:185-93), but it was a single-center trial with a severe power limitation, because it involved only 30 patients. It found endovascular repair was comparable to open surgery. Also, I suspect a great deal of selection bias is involved in studies of endovascular repair.
A number of studies have found endovascular repair is not inferior to surgical repair. For example, a study by Dr. Audra Duncan, at Mayo Clinic, and her colleagues found that primary and secondary patency rates of elective and emergent stenting were excellent – but the study results only extended out to 2 years (J Vasc Surg. 2013 May;57[5]:1299-305). I don’t think we could hang our hat on that.
A Swedish study that compared open and endovascular surgery in 592 patients reported that endovascular repair has “significantly inferior results compared with open repair,” particularly in those who present with acute ischemia (Eur J Vasc Endovasc Surg. 2015 Sep;50[3]:342-50). A close look at the data shows that primary patency rates were 89% for open repair and 67.4% for stent graft.
Referencing the systematic review and meta-analysis that Dr. Rossi cited, the primary patency of endovascular repair was only 69% and the secondary patency rate was 77% at 5 years (J Endovasc Ther. 2015 Jun;22[3]:330-7). As physicians, I submit that we can do better.
A Netherlands study investigated stent fractures, finding that 17% (13 out of 78 cases) had circumferential fractures (J Vasc Surg. 2010 Jun;51[6]:1413-8). This study only included circumferential stent fractures and excluded localized strut fractures. I think these studies show that endovascular repair is not always durable.
I want to remind you that we are vascular surgeons, so it is appropriate for us to embrace surgical bypass and its known durability, especially when the durability of endovascular repair is still not known.
Patrick Muck, MD, is chief of vascular surgery and director of vascular residency and fellowship at Good Samaritan Hospital, Cincinnati. He is also on staff at Bethesda North Hospital, Cincinnati, and is affiliated with TriHealth Heart Institute in southwestern Ohio. Dr. Muck had no financial relationships to disclose.
AT MIDWESTERN VASCULAR 2016
The Patellofemoral Compartment: Making Sense of It
Editor’s Note: One of the goals of the new AJO is to offer solutions to common problems we face as orthopedists. With that in mind, this issue tackles the patellofemoral joint and represents a collaboration between our journal and some of the key leaders of the Patellofemoral Study Group. I’m indebted to my friend and mentor, Jack Farr, for organizing this issue and a continuing patellofemoral series. I know this series will provide an invaluable look into the thought process of true orthopedic legends and find a permanent place on your shelf of orthopedic reference materials.
I’m also pleased to introduce a new feature, our online Lifestyles section. Sometimes, as orthopedists, we spend so much time taking care of others that we forget to look after ourselves and our loved ones. In an effort to make this easier, AJO has collaborated with Inspirato, the premiere luxury destination club. As a member, I’ve enjoyed truly life-changing vacations with my family and now have a way to share that opportunity with our readers. Inspirato is offering a complimentary 6-month Key membership and $250 spending credit to all AJO readers. Simply visit www.inspirato.com/orthopedics to sign up and start booking your vacations like a member. Look for future lifestyle features and special opportunities online in upcoming issues.
—Bryan T. Hanypsiak, MD
The patellofemoral compartment of the knee has been an enigma for many years. Clinicians who enjoy treating patients with knee problems have the choice of either ignoring one-third of the knee or grappling with this unique compartment. In attempting to make sense of this area of the knee, it is necessary to take into account the vast and complex overlay of multiple factors affecting this compartment. These factors span the gamut from psycho-social, to “core to floor” physiologic imbalance, to overuse, to the seemingly more “objective” elements of alignment, stability, morphology, bone, and cartilage.
Fortunately, a small merry band of international experts has made the patellofemoral compartment its “badge of courage” and continues to attempt to make sense of this small mobile sesamoid bone. We have invited a few of these stalwarts to share their experience and wisdom with us in this first of an ongoing patellofemoral series in The American Journal of Orthopedics. I appreciate the honor of assembling the works of these worldly patellofemoral gurus.
How many of us routinely order a “Merchant view”, discuss a “Fulkerson osteotomy”, or tell patients they are out of their Scott Dye “envelope of function” and they need to allow their knee to return to homeostasis through a “core to floor” rehabilitation program? We are lucky to have these living legends offer us insight into their thinking process. I purposely have begun this patellofemoral series with some of my personal mentors to set the tone: think first, understand the problem, design an evidence-based medicine approach and, above all, do no harm. To that point, Dr. Merchant, Dr. Fulkerson, Dr. Dye, and Dr. Post each detail their approach to anterior knee pain, followed by a discussion on nonoperative therapy intervention by Dr. Hiemstra. However, I understand that most readers are surgeons and, therefore I have added two articles to pique your interest: the hot topic of medial patellofemoral ligament (MPFL)—“To repair or not to repair, that is NOT the question.” The question is: “When does repair potentially benefit the patient and when is reconstruction the best approach?” Dr. Duchman and Dr. Bollier address the former, and Dr. Burrus and colleagues discuss optimizing MPFL reconstruction. I hope you enjoy learning from these authors as much as I have while producing this issue.
Am J Orthop. 2017;46(2):64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Editor’s Note: One of the goals of the new AJO is to offer solutions to common problems we face as orthopedists. With that in mind, this issue tackles the patellofemoral joint and represents a collaboration between our journal and some of the key leaders of the Patellofemoral Study Group. I’m indebted to my friend and mentor, Jack Farr, for organizing this issue and a continuing patellofemoral series. I know this series will provide an invaluable look into the thought process of true orthopedic legends and find a permanent place on your shelf of orthopedic reference materials.
I’m also pleased to introduce a new feature, our online Lifestyles section. Sometimes, as orthopedists, we spend so much time taking care of others that we forget to look after ourselves and our loved ones. In an effort to make this easier, AJO has collaborated with Inspirato, the premiere luxury destination club. As a member, I’ve enjoyed truly life-changing vacations with my family and now have a way to share that opportunity with our readers. Inspirato is offering a complimentary 6-month Key membership and $250 spending credit to all AJO readers. Simply visit www.inspirato.com/orthopedics to sign up and start booking your vacations like a member. Look for future lifestyle features and special opportunities online in upcoming issues.
—Bryan T. Hanypsiak, MD
The patellofemoral compartment of the knee has been an enigma for many years. Clinicians who enjoy treating patients with knee problems have the choice of either ignoring one-third of the knee or grappling with this unique compartment. In attempting to make sense of this area of the knee, it is necessary to take into account the vast and complex overlay of multiple factors affecting this compartment. These factors span the gamut from psycho-social, to “core to floor” physiologic imbalance, to overuse, to the seemingly more “objective” elements of alignment, stability, morphology, bone, and cartilage.
Fortunately, a small merry band of international experts has made the patellofemoral compartment its “badge of courage” and continues to attempt to make sense of this small mobile sesamoid bone. We have invited a few of these stalwarts to share their experience and wisdom with us in this first of an ongoing patellofemoral series in The American Journal of Orthopedics. I appreciate the honor of assembling the works of these worldly patellofemoral gurus.
How many of us routinely order a “Merchant view”, discuss a “Fulkerson osteotomy”, or tell patients they are out of their Scott Dye “envelope of function” and they need to allow their knee to return to homeostasis through a “core to floor” rehabilitation program? We are lucky to have these living legends offer us insight into their thinking process. I purposely have begun this patellofemoral series with some of my personal mentors to set the tone: think first, understand the problem, design an evidence-based medicine approach and, above all, do no harm. To that point, Dr. Merchant, Dr. Fulkerson, Dr. Dye, and Dr. Post each detail their approach to anterior knee pain, followed by a discussion on nonoperative therapy intervention by Dr. Hiemstra. However, I understand that most readers are surgeons and, therefore I have added two articles to pique your interest: the hot topic of medial patellofemoral ligament (MPFL)—“To repair or not to repair, that is NOT the question.” The question is: “When does repair potentially benefit the patient and when is reconstruction the best approach?” Dr. Duchman and Dr. Bollier address the former, and Dr. Burrus and colleagues discuss optimizing MPFL reconstruction. I hope you enjoy learning from these authors as much as I have while producing this issue.
Am J Orthop. 2017;46(2):64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Editor’s Note: One of the goals of the new AJO is to offer solutions to common problems we face as orthopedists. With that in mind, this issue tackles the patellofemoral joint and represents a collaboration between our journal and some of the key leaders of the Patellofemoral Study Group. I’m indebted to my friend and mentor, Jack Farr, for organizing this issue and a continuing patellofemoral series. I know this series will provide an invaluable look into the thought process of true orthopedic legends and find a permanent place on your shelf of orthopedic reference materials.
I’m also pleased to introduce a new feature, our online Lifestyles section. Sometimes, as orthopedists, we spend so much time taking care of others that we forget to look after ourselves and our loved ones. In an effort to make this easier, AJO has collaborated with Inspirato, the premiere luxury destination club. As a member, I’ve enjoyed truly life-changing vacations with my family and now have a way to share that opportunity with our readers. Inspirato is offering a complimentary 6-month Key membership and $250 spending credit to all AJO readers. Simply visit www.inspirato.com/orthopedics to sign up and start booking your vacations like a member. Look for future lifestyle features and special opportunities online in upcoming issues.
—Bryan T. Hanypsiak, MD
The patellofemoral compartment of the knee has been an enigma for many years. Clinicians who enjoy treating patients with knee problems have the choice of either ignoring one-third of the knee or grappling with this unique compartment. In attempting to make sense of this area of the knee, it is necessary to take into account the vast and complex overlay of multiple factors affecting this compartment. These factors span the gamut from psycho-social, to “core to floor” physiologic imbalance, to overuse, to the seemingly more “objective” elements of alignment, stability, morphology, bone, and cartilage.
Fortunately, a small merry band of international experts has made the patellofemoral compartment its “badge of courage” and continues to attempt to make sense of this small mobile sesamoid bone. We have invited a few of these stalwarts to share their experience and wisdom with us in this first of an ongoing patellofemoral series in The American Journal of Orthopedics. I appreciate the honor of assembling the works of these worldly patellofemoral gurus.
How many of us routinely order a “Merchant view”, discuss a “Fulkerson osteotomy”, or tell patients they are out of their Scott Dye “envelope of function” and they need to allow their knee to return to homeostasis through a “core to floor” rehabilitation program? We are lucky to have these living legends offer us insight into their thinking process. I purposely have begun this patellofemoral series with some of my personal mentors to set the tone: think first, understand the problem, design an evidence-based medicine approach and, above all, do no harm. To that point, Dr. Merchant, Dr. Fulkerson, Dr. Dye, and Dr. Post each detail their approach to anterior knee pain, followed by a discussion on nonoperative therapy intervention by Dr. Hiemstra. However, I understand that most readers are surgeons and, therefore I have added two articles to pique your interest: the hot topic of medial patellofemoral ligament (MPFL)—“To repair or not to repair, that is NOT the question.” The question is: “When does repair potentially benefit the patient and when is reconstruction the best approach?” Dr. Duchman and Dr. Bollier address the former, and Dr. Burrus and colleagues discuss optimizing MPFL reconstruction. I hope you enjoy learning from these authors as much as I have while producing this issue.
Am J Orthop. 2017;46(2):64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Prazosin and doxazosin for PTSD are underutilized and underdosed
The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).2 Among veterans, the prevalence of PTSD has been reported as:
- 31% among male Vietnam veterans (lifetime)
- 10% among Gulf War veterans
- 14% among Iraq and Afghanistan veterans.3
Why is PTSD overlooked in substance use?
Among individuals with SUD, 10% to 63% have comorbid PTSD.4 A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.5 Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.5 Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.
SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.6 Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.
Targeting mechanisms of action
Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.
Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.7 Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.8 Several studies support the efficacy of prazosin in persons suffering from PTSD.9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)
In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.17 The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.18
Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages8,12,13 might be needed because of the drug’s short half-life.
Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.16 The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.
Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder19-21 and cocaine use disorder.22,23 This “two birds with one stone” approach could become more common in clinical practice.
Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.
1. Zimmerman M, Mattia JI. Is posttraumatic stress disorder underdiagnosed in routine clinical settings? J Nerv Ment Dis. 1999;187(7):420-428.
2. National Comorbidity Survey. 12-month prevalence of DSM-IV/WMH-CIDI disorders by sex and cohort (n=9282). http://www.hcp.med.harvard.edu/ncs/ftpdir/NCS-R_12-month_Prevalence_Estimates.pdf. Published 2005. Accessed February 10, 2017.
3. Gradus JL. Epidemiology of PTSD. http://www.ptsd.va.gov/professional/PTSD-overview/epidemiological-facts-ptsd.asp. Updated February 23, 2016. Accessed February 13, 2017.
4. Debell F, Fear NT, Head M, et al. A systematic review of the comorbidity between PTSD and alcohol misuse. Soc Psychiatry Psychiatr Epidemiol. 2014;49(9):1401-1425.
5. Vujanovic AA, Bonn-Miller MO, Petry NM. Co-occurring posttraumatic stress and substance use: emerging research on correlates, mechanisms, and treatments-introduction to the special issue. Psychol Addict Behav. 2016;30(7):713-719.
6. Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. 2001;158(8):1184-1190.
7. Raskind MA, Dobie DJ, Kanter ED, et al. The alpha1-adrenergic antagonist prazosin ameliorates combat trauma nightmares in veterans with posttraumatic stress disorder: a report of 4 cases. J Clin Psychiatry. 2000;61(2):129-133.
8. Raskind MA, Peterson K, Williams T, et al. A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. Am J Psychiatry. 2013;170(9):1003-1010.
9. Raskind MA, Peskind ER, Hoff DJ, et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. Biol Psychiatry. 2007;61(8):928-934.
10. Taylor FB, Martin P, Thompson C, et al. Prazosin effects on objective sleep measures and clinical symptoms in civilian trauma posttraumatic stress disorder: a placebo-controlled study. Biol Psychiatry. 2008;63(6):629-632.
11. Raskind MA, Millard SP, Petrie EC, et al. Higher pretreatment blood pressure is associated with greater posttraumatic stress disorder symptom reduction in soldiers treated with prazosin. Biol Psychiatry. 2016;80(10):736-742.
12. Koola MM, Varghese SP, Fawcett JA. High-dose prazosin for the treatment of post-traumatic stress disorder. Ther Adv Psychopharmacol. 2014;4(1):43-47.
13. Vaishnav M, Patel V, Varghese SP, et al. Fludrocortisone in posttraumatic stress disorder: effective for symptoms and prazosin-induced hypotension. Prim Care Companion CNS Disord. 2014;16(6). doi: 10.4088/PCC.14l01676.
14. Rodgman C, Verrico CD, Holst M, et al. Doxazosin XL reduces symptoms of posttraumatic stress disorder in veterans with PTSD: a pilot clinical trial. J Clin Psychiatry. 2016;77(5):e561-e565.
15. Roepke S, Danker-Hopfe H, Repantis D, et al. Doxazosin, an α-1-adrenergic-receptor antagonist, for nightmares in patients with posttraumatic stress disorder and/or borderline personality disorder: a chart review. Pharmacopsychiatry. 2017;50(1):26-31.
16. Smith C, Koola MM. Evidence for using doxazosin in the treatment of posttraumatic stress disorder. Psychiatr Ann. 2016;46(9):553-555.
17. Alexander B, Lund BC, Bernardy NC, et al. Early discontinuation and suboptimal dosing of prazosin: a potential missed opportunity for veterans with posttraumatic stress disorder. J Clin Psychiatry. 2015;76(5):e639-e644.
18. Benedek DM, Friedman MJ, Zatzick D, et al. Guideline watch (March 2009): practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. http://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/acutestressdisorderptsd-watch.pdf. Accessed February 10, 2017.
19. Qazi H, Wijegunaratne H, Savajiyani R, et al. Naltrexone and prazosin combination for posttraumatic stress disorder and alcohol use disorder. Prim Care Companion CNS Disord. 2014;16(4). doi: 10.4088/PCC.14l01638.
20. Simpson TL, Malte CA, Dietel B, et al. A pilot trial of prazosin, an alpha-1 adrenergic antagonist, for comorbid alcohol dependence and posttraumatic stress disorder. Alcohol Clin Exp Res. 2015;39(5):808-817.
21. Kenna GA, Haass-Koffler CL, Zywiak WH, et al. Role of the α1 blocker doxazosin in alcoholism: a proof-of-concept randomized controlled trial. Addict Biol. 2016;21(4):904-914.
22. Shorter D, Lindsay JA, Kosten TR. The alpha-1 adrenergic antagonist doxazosin for treatment of cocaine dependence: a pilot study. Drug Alcohol Depend. 2013;131(1-2):66-70.
23. Newton TF, De La Garza R II, Brown G, et al. Noradrenergic α1 receptor antagonist treatment attenuates positive subjective effects of cocaine in humans: a randomized trial. PLoS One. 2012;7(2):e30854.
The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).2 Among veterans, the prevalence of PTSD has been reported as:
- 31% among male Vietnam veterans (lifetime)
- 10% among Gulf War veterans
- 14% among Iraq and Afghanistan veterans.3
Why is PTSD overlooked in substance use?
Among individuals with SUD, 10% to 63% have comorbid PTSD.4 A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.5 Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.5 Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.
SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.6 Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.
Targeting mechanisms of action
Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.
Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.7 Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.8 Several studies support the efficacy of prazosin in persons suffering from PTSD.9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)
In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.17 The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.18
Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages8,12,13 might be needed because of the drug’s short half-life.
Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.16 The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.
Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder19-21 and cocaine use disorder.22,23 This “two birds with one stone” approach could become more common in clinical practice.
Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.
The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).2 Among veterans, the prevalence of PTSD has been reported as:
- 31% among male Vietnam veterans (lifetime)
- 10% among Gulf War veterans
- 14% among Iraq and Afghanistan veterans.3
Why is PTSD overlooked in substance use?
Among individuals with SUD, 10% to 63% have comorbid PTSD.4 A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.5 Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.5 Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.
SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.6 Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.
Targeting mechanisms of action
Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.
Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.7 Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.8 Several studies support the efficacy of prazosin in persons suffering from PTSD.9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)
In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.17 The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.18
Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages8,12,13 might be needed because of the drug’s short half-life.
Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.16 The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.
Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder19-21 and cocaine use disorder.22,23 This “two birds with one stone” approach could become more common in clinical practice.
Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.
1. Zimmerman M, Mattia JI. Is posttraumatic stress disorder underdiagnosed in routine clinical settings? J Nerv Ment Dis. 1999;187(7):420-428.
2. National Comorbidity Survey. 12-month prevalence of DSM-IV/WMH-CIDI disorders by sex and cohort (n=9282). http://www.hcp.med.harvard.edu/ncs/ftpdir/NCS-R_12-month_Prevalence_Estimates.pdf. Published 2005. Accessed February 10, 2017.
3. Gradus JL. Epidemiology of PTSD. http://www.ptsd.va.gov/professional/PTSD-overview/epidemiological-facts-ptsd.asp. Updated February 23, 2016. Accessed February 13, 2017.
4. Debell F, Fear NT, Head M, et al. A systematic review of the comorbidity between PTSD and alcohol misuse. Soc Psychiatry Psychiatr Epidemiol. 2014;49(9):1401-1425.
5. Vujanovic AA, Bonn-Miller MO, Petry NM. Co-occurring posttraumatic stress and substance use: emerging research on correlates, mechanisms, and treatments-introduction to the special issue. Psychol Addict Behav. 2016;30(7):713-719.
6. Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. 2001;158(8):1184-1190.
7. Raskind MA, Dobie DJ, Kanter ED, et al. The alpha1-adrenergic antagonist prazosin ameliorates combat trauma nightmares in veterans with posttraumatic stress disorder: a report of 4 cases. J Clin Psychiatry. 2000;61(2):129-133.
8. Raskind MA, Peterson K, Williams T, et al. A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. Am J Psychiatry. 2013;170(9):1003-1010.
9. Raskind MA, Peskind ER, Hoff DJ, et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. Biol Psychiatry. 2007;61(8):928-934.
10. Taylor FB, Martin P, Thompson C, et al. Prazosin effects on objective sleep measures and clinical symptoms in civilian trauma posttraumatic stress disorder: a placebo-controlled study. Biol Psychiatry. 2008;63(6):629-632.
11. Raskind MA, Millard SP, Petrie EC, et al. Higher pretreatment blood pressure is associated with greater posttraumatic stress disorder symptom reduction in soldiers treated with prazosin. Biol Psychiatry. 2016;80(10):736-742.
12. Koola MM, Varghese SP, Fawcett JA. High-dose prazosin for the treatment of post-traumatic stress disorder. Ther Adv Psychopharmacol. 2014;4(1):43-47.
13. Vaishnav M, Patel V, Varghese SP, et al. Fludrocortisone in posttraumatic stress disorder: effective for symptoms and prazosin-induced hypotension. Prim Care Companion CNS Disord. 2014;16(6). doi: 10.4088/PCC.14l01676.
14. Rodgman C, Verrico CD, Holst M, et al. Doxazosin XL reduces symptoms of posttraumatic stress disorder in veterans with PTSD: a pilot clinical trial. J Clin Psychiatry. 2016;77(5):e561-e565.
15. Roepke S, Danker-Hopfe H, Repantis D, et al. Doxazosin, an α-1-adrenergic-receptor antagonist, for nightmares in patients with posttraumatic stress disorder and/or borderline personality disorder: a chart review. Pharmacopsychiatry. 2017;50(1):26-31.
16. Smith C, Koola MM. Evidence for using doxazosin in the treatment of posttraumatic stress disorder. Psychiatr Ann. 2016;46(9):553-555.
17. Alexander B, Lund BC, Bernardy NC, et al. Early discontinuation and suboptimal dosing of prazosin: a potential missed opportunity for veterans with posttraumatic stress disorder. J Clin Psychiatry. 2015;76(5):e639-e644.
18. Benedek DM, Friedman MJ, Zatzick D, et al. Guideline watch (March 2009): practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. http://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/acutestressdisorderptsd-watch.pdf. Accessed February 10, 2017.
19. Qazi H, Wijegunaratne H, Savajiyani R, et al. Naltrexone and prazosin combination for posttraumatic stress disorder and alcohol use disorder. Prim Care Companion CNS Disord. 2014;16(4). doi: 10.4088/PCC.14l01638.
20. Simpson TL, Malte CA, Dietel B, et al. A pilot trial of prazosin, an alpha-1 adrenergic antagonist, for comorbid alcohol dependence and posttraumatic stress disorder. Alcohol Clin Exp Res. 2015;39(5):808-817.
21. Kenna GA, Haass-Koffler CL, Zywiak WH, et al. Role of the α1 blocker doxazosin in alcoholism: a proof-of-concept randomized controlled trial. Addict Biol. 2016;21(4):904-914.
22. Shorter D, Lindsay JA, Kosten TR. The alpha-1 adrenergic antagonist doxazosin for treatment of cocaine dependence: a pilot study. Drug Alcohol Depend. 2013;131(1-2):66-70.
23. Newton TF, De La Garza R II, Brown G, et al. Noradrenergic α1 receptor antagonist treatment attenuates positive subjective effects of cocaine in humans: a randomized trial. PLoS One. 2012;7(2):e30854.
1. Zimmerman M, Mattia JI. Is posttraumatic stress disorder underdiagnosed in routine clinical settings? J Nerv Ment Dis. 1999;187(7):420-428.
2. National Comorbidity Survey. 12-month prevalence of DSM-IV/WMH-CIDI disorders by sex and cohort (n=9282). http://www.hcp.med.harvard.edu/ncs/ftpdir/NCS-R_12-month_Prevalence_Estimates.pdf. Published 2005. Accessed February 10, 2017.
3. Gradus JL. Epidemiology of PTSD. http://www.ptsd.va.gov/professional/PTSD-overview/epidemiological-facts-ptsd.asp. Updated February 23, 2016. Accessed February 13, 2017.
4. Debell F, Fear NT, Head M, et al. A systematic review of the comorbidity between PTSD and alcohol misuse. Soc Psychiatry Psychiatr Epidemiol. 2014;49(9):1401-1425.
5. Vujanovic AA, Bonn-Miller MO, Petry NM. Co-occurring posttraumatic stress and substance use: emerging research on correlates, mechanisms, and treatments-introduction to the special issue. Psychol Addict Behav. 2016;30(7):713-719.
6. Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. 2001;158(8):1184-1190.
7. Raskind MA, Dobie DJ, Kanter ED, et al. The alpha1-adrenergic antagonist prazosin ameliorates combat trauma nightmares in veterans with posttraumatic stress disorder: a report of 4 cases. J Clin Psychiatry. 2000;61(2):129-133.
8. Raskind MA, Peterson K, Williams T, et al. A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. Am J Psychiatry. 2013;170(9):1003-1010.
9. Raskind MA, Peskind ER, Hoff DJ, et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. Biol Psychiatry. 2007;61(8):928-934.
10. Taylor FB, Martin P, Thompson C, et al. Prazosin effects on objective sleep measures and clinical symptoms in civilian trauma posttraumatic stress disorder: a placebo-controlled study. Biol Psychiatry. 2008;63(6):629-632.
11. Raskind MA, Millard SP, Petrie EC, et al. Higher pretreatment blood pressure is associated with greater posttraumatic stress disorder symptom reduction in soldiers treated with prazosin. Biol Psychiatry. 2016;80(10):736-742.
12. Koola MM, Varghese SP, Fawcett JA. High-dose prazosin for the treatment of post-traumatic stress disorder. Ther Adv Psychopharmacol. 2014;4(1):43-47.
13. Vaishnav M, Patel V, Varghese SP, et al. Fludrocortisone in posttraumatic stress disorder: effective for symptoms and prazosin-induced hypotension. Prim Care Companion CNS Disord. 2014;16(6). doi: 10.4088/PCC.14l01676.
14. Rodgman C, Verrico CD, Holst M, et al. Doxazosin XL reduces symptoms of posttraumatic stress disorder in veterans with PTSD: a pilot clinical trial. J Clin Psychiatry. 2016;77(5):e561-e565.
15. Roepke S, Danker-Hopfe H, Repantis D, et al. Doxazosin, an α-1-adrenergic-receptor antagonist, for nightmares in patients with posttraumatic stress disorder and/or borderline personality disorder: a chart review. Pharmacopsychiatry. 2017;50(1):26-31.
16. Smith C, Koola MM. Evidence for using doxazosin in the treatment of posttraumatic stress disorder. Psychiatr Ann. 2016;46(9):553-555.
17. Alexander B, Lund BC, Bernardy NC, et al. Early discontinuation and suboptimal dosing of prazosin: a potential missed opportunity for veterans with posttraumatic stress disorder. J Clin Psychiatry. 2015;76(5):e639-e644.
18. Benedek DM, Friedman MJ, Zatzick D, et al. Guideline watch (March 2009): practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. http://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/acutestressdisorderptsd-watch.pdf. Accessed February 10, 2017.
19. Qazi H, Wijegunaratne H, Savajiyani R, et al. Naltrexone and prazosin combination for posttraumatic stress disorder and alcohol use disorder. Prim Care Companion CNS Disord. 2014;16(4). doi: 10.4088/PCC.14l01638.
20. Simpson TL, Malte CA, Dietel B, et al. A pilot trial of prazosin, an alpha-1 adrenergic antagonist, for comorbid alcohol dependence and posttraumatic stress disorder. Alcohol Clin Exp Res. 2015;39(5):808-817.
21. Kenna GA, Haass-Koffler CL, Zywiak WH, et al. Role of the α1 blocker doxazosin in alcoholism: a proof-of-concept randomized controlled trial. Addict Biol. 2016;21(4):904-914.
22. Shorter D, Lindsay JA, Kosten TR. The alpha-1 adrenergic antagonist doxazosin for treatment of cocaine dependence: a pilot study. Drug Alcohol Depend. 2013;131(1-2):66-70.
23. Newton TF, De La Garza R II, Brown G, et al. Noradrenergic α1 receptor antagonist treatment attenuates positive subjective effects of cocaine in humans: a randomized trial. PLoS One. 2012;7(2):e30854.
The elements of pain care that the guidelines don’t address
You are probably one of the million+ physicians who received a letter from the Surgeon General urging us to use opioids judiciously,1 and you are likely familiar with the 2016 CDC Guideline for Prescribing Opioids for Chronic Pain.2 (See JFP’s “Opioids for chronic pain: The CDC’s 12 recommendations,” 2016;65:906-909.) Most of these recommendations are common-sense practices, such as reducing doses, using alternative medications and treatments, monitoring prescribing through state databases, conducting random drug tests, consulting pain and addiction specialists, and establishing clear treatment goals.
But the guidelines only go so far. They don’t address the empathy, perseverance, and insight needed to stick with these patients and oversee their care. And they don’t directly address the patients who are already taking opioids for chronic pain when they arrive at our offices. Despite nearly 40 years of practicing family medicine, I can count on one hand the number of patients for whom I initiated opioid medication. Yet I have managed many patients with chronic pain who were already on hefty doses of narcotics when they became my patients. Rather than refuse to care for them, we should seek to understand their story, continuously try other medications and therapies, repeatedly attempt to reduce dosages, and frequently check substance databases.
Following the guidelines is no guarantee that our prescribing practices won’t be called into question. I have seen excellent family physicians censured by state licensing boards unjustifiably. One colleague was accused by a patient of “getting him addicted,” only after the physician refused to continue prescribing narcotics. Based on this single complaint, the physician had his license temporarily revoked with no due process whatsoever. He got his license back after an appeals process that took several months, cost many dollars, and inflicted significant emotional trauma. No wonder some of us just say “No” to caring for patients with chronic pain.
Perseverance and motivation. I remind myself that good, well-intentioned, and careful primary care physicians are NOT the cause of this epidemic. I encourage you to stick with these patients (lest they turn to the streets to obtain heroin laced with fentanyl), and look for sources of motivation. You may be motivated, as I was, by a physician’s story in JAMA about his 49-year-old younger sister, a vibrant, accomplished, caring woman whose chronic pain led to her death in a jail cell after she became combative in the ED.3 Had she been treated as a patient with a chronic illness, rather than a criminal with a character flaw, I suspect she would be alive today.
1. Turn the Tide: the Surgeon General’s call to end the opioid crisis. Available at: http://turnthetiderx.org/#. Accessed February 15, 2017.
2. Dowell D, Haegerich TM, Chou R. CDC guideline for prescribing opioids for chronic pain—United States, 2016. MMWR Recomm Rep. 2016;65:1-49. Available at: https://www.cdc.gov/mmwr/volumes/65/rr/rr6501e1.htm. Accessed February 15, 2017.
3. Weeks WB. Hailey. JAMA. 2016;316:1975-1976.
Editor-in-Chief
Editor-in-Chief
Editor-in-Chief
You are probably one of the million+ physicians who received a letter from the Surgeon General urging us to use opioids judiciously,1 and you are likely familiar with the 2016 CDC Guideline for Prescribing Opioids for Chronic Pain.2 (See JFP’s “Opioids for chronic pain: The CDC’s 12 recommendations,” 2016;65:906-909.) Most of these recommendations are common-sense practices, such as reducing doses, using alternative medications and treatments, monitoring prescribing through state databases, conducting random drug tests, consulting pain and addiction specialists, and establishing clear treatment goals.
But the guidelines only go so far. They don’t address the empathy, perseverance, and insight needed to stick with these patients and oversee their care. And they don’t directly address the patients who are already taking opioids for chronic pain when they arrive at our offices. Despite nearly 40 years of practicing family medicine, I can count on one hand the number of patients for whom I initiated opioid medication. Yet I have managed many patients with chronic pain who were already on hefty doses of narcotics when they became my patients. Rather than refuse to care for them, we should seek to understand their story, continuously try other medications and therapies, repeatedly attempt to reduce dosages, and frequently check substance databases.
Following the guidelines is no guarantee that our prescribing practices won’t be called into question. I have seen excellent family physicians censured by state licensing boards unjustifiably. One colleague was accused by a patient of “getting him addicted,” only after the physician refused to continue prescribing narcotics. Based on this single complaint, the physician had his license temporarily revoked with no due process whatsoever. He got his license back after an appeals process that took several months, cost many dollars, and inflicted significant emotional trauma. No wonder some of us just say “No” to caring for patients with chronic pain.
Perseverance and motivation. I remind myself that good, well-intentioned, and careful primary care physicians are NOT the cause of this epidemic. I encourage you to stick with these patients (lest they turn to the streets to obtain heroin laced with fentanyl), and look for sources of motivation. You may be motivated, as I was, by a physician’s story in JAMA about his 49-year-old younger sister, a vibrant, accomplished, caring woman whose chronic pain led to her death in a jail cell after she became combative in the ED.3 Had she been treated as a patient with a chronic illness, rather than a criminal with a character flaw, I suspect she would be alive today.
You are probably one of the million+ physicians who received a letter from the Surgeon General urging us to use opioids judiciously,1 and you are likely familiar with the 2016 CDC Guideline for Prescribing Opioids for Chronic Pain.2 (See JFP’s “Opioids for chronic pain: The CDC’s 12 recommendations,” 2016;65:906-909.) Most of these recommendations are common-sense practices, such as reducing doses, using alternative medications and treatments, monitoring prescribing through state databases, conducting random drug tests, consulting pain and addiction specialists, and establishing clear treatment goals.
But the guidelines only go so far. They don’t address the empathy, perseverance, and insight needed to stick with these patients and oversee their care. And they don’t directly address the patients who are already taking opioids for chronic pain when they arrive at our offices. Despite nearly 40 years of practicing family medicine, I can count on one hand the number of patients for whom I initiated opioid medication. Yet I have managed many patients with chronic pain who were already on hefty doses of narcotics when they became my patients. Rather than refuse to care for them, we should seek to understand their story, continuously try other medications and therapies, repeatedly attempt to reduce dosages, and frequently check substance databases.
Following the guidelines is no guarantee that our prescribing practices won’t be called into question. I have seen excellent family physicians censured by state licensing boards unjustifiably. One colleague was accused by a patient of “getting him addicted,” only after the physician refused to continue prescribing narcotics. Based on this single complaint, the physician had his license temporarily revoked with no due process whatsoever. He got his license back after an appeals process that took several months, cost many dollars, and inflicted significant emotional trauma. No wonder some of us just say “No” to caring for patients with chronic pain.
Perseverance and motivation. I remind myself that good, well-intentioned, and careful primary care physicians are NOT the cause of this epidemic. I encourage you to stick with these patients (lest they turn to the streets to obtain heroin laced with fentanyl), and look for sources of motivation. You may be motivated, as I was, by a physician’s story in JAMA about his 49-year-old younger sister, a vibrant, accomplished, caring woman whose chronic pain led to her death in a jail cell after she became combative in the ED.3 Had she been treated as a patient with a chronic illness, rather than a criminal with a character flaw, I suspect she would be alive today.
1. Turn the Tide: the Surgeon General’s call to end the opioid crisis. Available at: http://turnthetiderx.org/#. Accessed February 15, 2017.
2. Dowell D, Haegerich TM, Chou R. CDC guideline for prescribing opioids for chronic pain—United States, 2016. MMWR Recomm Rep. 2016;65:1-49. Available at: https://www.cdc.gov/mmwr/volumes/65/rr/rr6501e1.htm. Accessed February 15, 2017.
3. Weeks WB. Hailey. JAMA. 2016;316:1975-1976.
1. Turn the Tide: the Surgeon General’s call to end the opioid crisis. Available at: http://turnthetiderx.org/#. Accessed February 15, 2017.
2. Dowell D, Haegerich TM, Chou R. CDC guideline for prescribing opioids for chronic pain—United States, 2016. MMWR Recomm Rep. 2016;65:1-49. Available at: https://www.cdc.gov/mmwr/volumes/65/rr/rr6501e1.htm. Accessed February 15, 2017.
3. Weeks WB. Hailey. JAMA. 2016;316:1975-1976.
Readers weigh in on opioid epidemic
I read Dr. Unger’s guest editorial, “Staring down the opioid epidemic” (J Fam Pract. 2017;66:8) and thought that he made some good points, but as an internist for 38 years and a detox addiction specialist for the past 7 years, I have seen too much “pendulum swinging” with regard to opioids.
The state of Pennsylvania is enforcing opioid prescription laws so intensely that I now see underprescribing of needed medications by physicians and dentists. For example, I recently had dental surgery and wasn’t prescribed a narcotic. I suffered for 24 hours with ineffective nonsteroidal anti-inflammatory drugs. And a relative of mine experienced excessive pain following gynecologic cancer surgery because the surgeon wouldn’t prescribe opioids for fear of reprisal.
I would like to see someone conduct a nationwide survey of primary care physicians regarding their views on narcotics for pain so that I can better understand my colleagues’ perspectives on this issue.
Don Sesso, DO, FCCP
Gwynedd Valley, PA
In his guest editorial, Dr. Unger urged family physicians to treat patients who are addicted to opioids with buprenorphine. It’s a shame that so few of us do so.
Patients who are addicted to opioids are no more difficult to treat than patients with diabetes, yet we, as family physicians, often fail to fulfill our basic duty to respond to their illness. Using buprenorphine to help a patient who is addicted to opioids achieve sobriety is highly effective. And treating these patients is amazingly satisfying, as you’ll never have more grateful patients than these.
I began integrating buprenorphine treatment into my family practice 10 years ago. It has made me much more effective in treating my patients who are addicted to alcohol, and it has provided me with a great deal of personal satisfaction in the latter part of my career.
I challenge all family physicians to step up and do their duty to help combat the opioid epidemic.
David A. Moore, MD
Salt Lake City, Utah
I read Dr. Unger’s guest editorial, “Staring down the opioid epidemic” (J Fam Pract. 2017;66:8) and thought that he made some good points, but as an internist for 38 years and a detox addiction specialist for the past 7 years, I have seen too much “pendulum swinging” with regard to opioids.
The state of Pennsylvania is enforcing opioid prescription laws so intensely that I now see underprescribing of needed medications by physicians and dentists. For example, I recently had dental surgery and wasn’t prescribed a narcotic. I suffered for 24 hours with ineffective nonsteroidal anti-inflammatory drugs. And a relative of mine experienced excessive pain following gynecologic cancer surgery because the surgeon wouldn’t prescribe opioids for fear of reprisal.
I would like to see someone conduct a nationwide survey of primary care physicians regarding their views on narcotics for pain so that I can better understand my colleagues’ perspectives on this issue.
Don Sesso, DO, FCCP
Gwynedd Valley, PA
In his guest editorial, Dr. Unger urged family physicians to treat patients who are addicted to opioids with buprenorphine. It’s a shame that so few of us do so.
Patients who are addicted to opioids are no more difficult to treat than patients with diabetes, yet we, as family physicians, often fail to fulfill our basic duty to respond to their illness. Using buprenorphine to help a patient who is addicted to opioids achieve sobriety is highly effective. And treating these patients is amazingly satisfying, as you’ll never have more grateful patients than these.
I began integrating buprenorphine treatment into my family practice 10 years ago. It has made me much more effective in treating my patients who are addicted to alcohol, and it has provided me with a great deal of personal satisfaction in the latter part of my career.
I challenge all family physicians to step up and do their duty to help combat the opioid epidemic.
David A. Moore, MD
Salt Lake City, Utah
I read Dr. Unger’s guest editorial, “Staring down the opioid epidemic” (J Fam Pract. 2017;66:8) and thought that he made some good points, but as an internist for 38 years and a detox addiction specialist for the past 7 years, I have seen too much “pendulum swinging” with regard to opioids.
The state of Pennsylvania is enforcing opioid prescription laws so intensely that I now see underprescribing of needed medications by physicians and dentists. For example, I recently had dental surgery and wasn’t prescribed a narcotic. I suffered for 24 hours with ineffective nonsteroidal anti-inflammatory drugs. And a relative of mine experienced excessive pain following gynecologic cancer surgery because the surgeon wouldn’t prescribe opioids for fear of reprisal.
I would like to see someone conduct a nationwide survey of primary care physicians regarding their views on narcotics for pain so that I can better understand my colleagues’ perspectives on this issue.
Don Sesso, DO, FCCP
Gwynedd Valley, PA
In his guest editorial, Dr. Unger urged family physicians to treat patients who are addicted to opioids with buprenorphine. It’s a shame that so few of us do so.
Patients who are addicted to opioids are no more difficult to treat than patients with diabetes, yet we, as family physicians, often fail to fulfill our basic duty to respond to their illness. Using buprenorphine to help a patient who is addicted to opioids achieve sobriety is highly effective. And treating these patients is amazingly satisfying, as you’ll never have more grateful patients than these.
I began integrating buprenorphine treatment into my family practice 10 years ago. It has made me much more effective in treating my patients who are addicted to alcohol, and it has provided me with a great deal of personal satisfaction in the latter part of my career.
I challenge all family physicians to step up and do their duty to help combat the opioid epidemic.
David A. Moore, MD
Salt Lake City, Utah
An overlooked Rx for nasal obstruction relief
In the article, “Improving your approach to nasal obstruction” (J Fam Pract. 2016;65:889-893,898-899), I noticed that ipratropium nasal spray was not mentioned in Table 2, which listed commonly used medications for nasal obstruction.
We frequently recommend ipratropium nasal spray in our office, as it is an effective, non-addictive nasal decongestant. It is available in 2 strengths, .03% and .06%, and we usually prescribe 2 sprays in each nostril, 2 to 3 times a day, as needed.
We have found this to be very effective for short-term use. Its value, of course, is that it acts rapidly and there is no limit on how long it may be used.
Walter D. Leventhal, MD
Summerville, SC
In the article, “Improving your approach to nasal obstruction” (J Fam Pract. 2016;65:889-893,898-899), I noticed that ipratropium nasal spray was not mentioned in Table 2, which listed commonly used medications for nasal obstruction.
We frequently recommend ipratropium nasal spray in our office, as it is an effective, non-addictive nasal decongestant. It is available in 2 strengths, .03% and .06%, and we usually prescribe 2 sprays in each nostril, 2 to 3 times a day, as needed.
We have found this to be very effective for short-term use. Its value, of course, is that it acts rapidly and there is no limit on how long it may be used.
Walter D. Leventhal, MD
Summerville, SC
In the article, “Improving your approach to nasal obstruction” (J Fam Pract. 2016;65:889-893,898-899), I noticed that ipratropium nasal spray was not mentioned in Table 2, which listed commonly used medications for nasal obstruction.
We frequently recommend ipratropium nasal spray in our office, as it is an effective, non-addictive nasal decongestant. It is available in 2 strengths, .03% and .06%, and we usually prescribe 2 sprays in each nostril, 2 to 3 times a day, as needed.
We have found this to be very effective for short-term use. Its value, of course, is that it acts rapidly and there is no limit on how long it may be used.
Walter D. Leventhal, MD
Summerville, SC
Medical marijuana: Irresponsible medical care?
As we know, the active ingredient of marijuana, delta-9 tetrahydrocannabinol (THC), has been available by prescription since 1985.1 The Food and Drug Administration (FDA) has allowed a pill form to be prescribed for wasting related to acquired immunodeficiency syndrome and for patients with terminal cancer.
And while the FDA can extend use of the pills to other conditions when scientific, evidence-based studies prove that they are effective, it has not done so. The reason? The evidence is lacking.
According to The Medical Letter on Drugs and Therapeutics (August 1, 2016), no adequate studies of cannabis (botanical marijuana) are available for such indications as cancer pain, multiple sclerosis, epilepsy, and neuropathic pain.1 Thus, I feel that there isn’t a need for “medical marijuana clinics,” which sell a product that isn’t regulated, is of unknown quality and strength, and may be dangerous or ineffective.
Illness should continue to be treated by health professionals employing scientific evidence. This is responsible policy. It is not appropriate or medically justified for family physicians to refer patients to medical marijuana clinics; instead, they should inform their patients that medical treatment must be based on scientific evidence.
Nayvin Gordon, MD
Oakland, Calif
1. Cannabis and cannabinoids. Med Lett Drugs Ther. 2016;58:97-98.
As we know, the active ingredient of marijuana, delta-9 tetrahydrocannabinol (THC), has been available by prescription since 1985.1 The Food and Drug Administration (FDA) has allowed a pill form to be prescribed for wasting related to acquired immunodeficiency syndrome and for patients with terminal cancer.
And while the FDA can extend use of the pills to other conditions when scientific, evidence-based studies prove that they are effective, it has not done so. The reason? The evidence is lacking.
According to The Medical Letter on Drugs and Therapeutics (August 1, 2016), no adequate studies of cannabis (botanical marijuana) are available for such indications as cancer pain, multiple sclerosis, epilepsy, and neuropathic pain.1 Thus, I feel that there isn’t a need for “medical marijuana clinics,” which sell a product that isn’t regulated, is of unknown quality and strength, and may be dangerous or ineffective.
Illness should continue to be treated by health professionals employing scientific evidence. This is responsible policy. It is not appropriate or medically justified for family physicians to refer patients to medical marijuana clinics; instead, they should inform their patients that medical treatment must be based on scientific evidence.
Nayvin Gordon, MD
Oakland, Calif
As we know, the active ingredient of marijuana, delta-9 tetrahydrocannabinol (THC), has been available by prescription since 1985.1 The Food and Drug Administration (FDA) has allowed a pill form to be prescribed for wasting related to acquired immunodeficiency syndrome and for patients with terminal cancer.
And while the FDA can extend use of the pills to other conditions when scientific, evidence-based studies prove that they are effective, it has not done so. The reason? The evidence is lacking.
According to The Medical Letter on Drugs and Therapeutics (August 1, 2016), no adequate studies of cannabis (botanical marijuana) are available for such indications as cancer pain, multiple sclerosis, epilepsy, and neuropathic pain.1 Thus, I feel that there isn’t a need for “medical marijuana clinics,” which sell a product that isn’t regulated, is of unknown quality and strength, and may be dangerous or ineffective.
Illness should continue to be treated by health professionals employing scientific evidence. This is responsible policy. It is not appropriate or medically justified for family physicians to refer patients to medical marijuana clinics; instead, they should inform their patients that medical treatment must be based on scientific evidence.
Nayvin Gordon, MD
Oakland, Calif
1. Cannabis and cannabinoids. Med Lett Drugs Ther. 2016;58:97-98.
1. Cannabis and cannabinoids. Med Lett Drugs Ther. 2016;58:97-98.
Dysmenorrhea and ginger
Up to 90% of reproductive women around the world describe experiencing painful menstrual periods (dysmenorrhea) at some point. Younger women struggle more than older women. Dysmenorrhea can lead to absenteeism and presenteeism to the tune of about $2 billion annually.
The next step was to find an alternate treatment method. Ginger root is used throughout the world as a seasoning, spice, and medicine. Ginger has been shown to inhibit COX-2 and has been studied for its potential role in reducing pain and inflammation. As a result, ginger may have a role in the treatment of dysmenorrhea.
James W. Daily, PhD, conducted a systematic review of the literature on the efficacy of ginger for treating primary dysmenorrhea (Pain Med. 2015 Dec;16[12]:2243-55).
It included all randomized trials investigating the effect of ginger powder on younger women. Included studies evaluated ginger efficacy on individuals aged 13-30 years. Most included studies excluded women with irregular menstrual cycles and individuals using hormonal medications, oral or intrauterine contraceptives, or a pregnancy history. Dosing was 750-2,000 mg ginger powder capsules per day for the first 3 days of the menstrual cycle.
Four studies were included in the meta-analysis, which suggested that ginger powder given during the first 3-4 days of the menstrual cycle was associated with significant reduction in the pain visual analog scale (risk ratio, –1.85; 95% confidence interval: –2.87 to –0.84; P = .0003).
I am not a consistent proponent of alternative therapies but mostly because it is difficult for me to keep up on the evidence for these treatment options. In this case, my bias is that individuals in this age group are much more willing to engage with alternative therapies and offering them may build trust.
For these patients, offering ginger powder may engage patients in self-help and help them appreciate you as a clinician willing to embrace alternative therapies. The hard part is recommending a brand that you know and trust, complicated by the lack of oversight and quality control for over-the-counter, nontraditional therapies.
Dr. Ebbert is a professor of medicine and general internist at the Mayo Clinic in Rochester, Minn. and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article.
Up to 90% of reproductive women around the world describe experiencing painful menstrual periods (dysmenorrhea) at some point. Younger women struggle more than older women. Dysmenorrhea can lead to absenteeism and presenteeism to the tune of about $2 billion annually.
The next step was to find an alternate treatment method. Ginger root is used throughout the world as a seasoning, spice, and medicine. Ginger has been shown to inhibit COX-2 and has been studied for its potential role in reducing pain and inflammation. As a result, ginger may have a role in the treatment of dysmenorrhea.
James W. Daily, PhD, conducted a systematic review of the literature on the efficacy of ginger for treating primary dysmenorrhea (Pain Med. 2015 Dec;16[12]:2243-55).
It included all randomized trials investigating the effect of ginger powder on younger women. Included studies evaluated ginger efficacy on individuals aged 13-30 years. Most included studies excluded women with irregular menstrual cycles and individuals using hormonal medications, oral or intrauterine contraceptives, or a pregnancy history. Dosing was 750-2,000 mg ginger powder capsules per day for the first 3 days of the menstrual cycle.
Four studies were included in the meta-analysis, which suggested that ginger powder given during the first 3-4 days of the menstrual cycle was associated with significant reduction in the pain visual analog scale (risk ratio, –1.85; 95% confidence interval: –2.87 to –0.84; P = .0003).
I am not a consistent proponent of alternative therapies but mostly because it is difficult for me to keep up on the evidence for these treatment options. In this case, my bias is that individuals in this age group are much more willing to engage with alternative therapies and offering them may build trust.
For these patients, offering ginger powder may engage patients in self-help and help them appreciate you as a clinician willing to embrace alternative therapies. The hard part is recommending a brand that you know and trust, complicated by the lack of oversight and quality control for over-the-counter, nontraditional therapies.
Dr. Ebbert is a professor of medicine and general internist at the Mayo Clinic in Rochester, Minn. and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article.
Up to 90% of reproductive women around the world describe experiencing painful menstrual periods (dysmenorrhea) at some point. Younger women struggle more than older women. Dysmenorrhea can lead to absenteeism and presenteeism to the tune of about $2 billion annually.
The next step was to find an alternate treatment method. Ginger root is used throughout the world as a seasoning, spice, and medicine. Ginger has been shown to inhibit COX-2 and has been studied for its potential role in reducing pain and inflammation. As a result, ginger may have a role in the treatment of dysmenorrhea.
James W. Daily, PhD, conducted a systematic review of the literature on the efficacy of ginger for treating primary dysmenorrhea (Pain Med. 2015 Dec;16[12]:2243-55).
It included all randomized trials investigating the effect of ginger powder on younger women. Included studies evaluated ginger efficacy on individuals aged 13-30 years. Most included studies excluded women with irregular menstrual cycles and individuals using hormonal medications, oral or intrauterine contraceptives, or a pregnancy history. Dosing was 750-2,000 mg ginger powder capsules per day for the first 3 days of the menstrual cycle.
Four studies were included in the meta-analysis, which suggested that ginger powder given during the first 3-4 days of the menstrual cycle was associated with significant reduction in the pain visual analog scale (risk ratio, –1.85; 95% confidence interval: –2.87 to –0.84; P = .0003).
I am not a consistent proponent of alternative therapies but mostly because it is difficult for me to keep up on the evidence for these treatment options. In this case, my bias is that individuals in this age group are much more willing to engage with alternative therapies and offering them may build trust.
For these patients, offering ginger powder may engage patients in self-help and help them appreciate you as a clinician willing to embrace alternative therapies. The hard part is recommending a brand that you know and trust, complicated by the lack of oversight and quality control for over-the-counter, nontraditional therapies.
Dr. Ebbert is a professor of medicine and general internist at the Mayo Clinic in Rochester, Minn. and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article.
Palliative care ‘in my hands’
A randomized controlled multicenter study published by Carson et al. in JAMA concluded that, for patients with “chronic critical illness” (defined as requiring 7 days of mechanical ventilation), palliative care team-led informational and emotional support meetings did not reduce anxiety or depression for families and may have increased posttraumatic stress disorder symptoms (2016:316[1]:51-62. doi: 10.1001/jama.2016.8474).
This report may surprise surgeons, as well as practitioners in other specialties, as the disconnect between palliative care and critical care services has been previously perceived as an education and access issue, not an outcome problem.
Carson and colleagues point out that fidelity to some components of the meeting “templates” was low, suggesting that there was some flexibility baked into the study design. However, as Russ and Kaufman aptly described, patients and families vary greatly in their appetite for explicit information about prognosis (Cult Med Psychiatry 2005;29[1]:103-23). Conversely, the hypothesis that direct communication about prognosis will be welcomed by families is a core element of the Carson study. The manuscript supplement reports that discussion of the patient’s condition and prognosis took place in 100% of initial meetings. If the same variability in family receptiveness to this information exists in this population as was described by Russ and Kaufman, it is not hard to see why some families experienced negative consequences because of these discussions.
Furthermore, the authors of the Carson study point out that it was not intended to replicate the components of specialist palliative care (JAMA. 2016;316[15]:1598-9).
Essential elements of specialist palliative care include symptom management, a multidisciplinary approach, and fairly close contact in the acute care setting. These features were lacking in the study protocol. Experienced providers of palliative care will often use symptom assessment and symptom management optimization as a conduit for building rapport and to avoid focusing on prognosis until trust has been established. A period of delay before broaching challenging subjects also allows the palliative care team to develop an understanding of the patient’s or surrogates’ preferences regarding the amount and type of information communicated. Palliative care providers benefit from the deepening of relationships with patients and families over time, as much as or possibly more so than providers of other specialties.
The necessity of the multidisciplinary approach to successful palliative care outcomes cannot be overstated. In many programs, patients seen for specialist palliative care consultation are seen by a physician or advanced practitioner, a chaplain, and a social worker within 24-48 hours of initial referral, and these providers have key roles in addressing the sequelae of anxiety, depression, and stress that were the key outcomes in the JAMA study. In the study, the “support and information team” included a palliative care physician and an advanced practice nurse but not a chaplain or social worker, despite the significance of existential/spiritual and social consequences of ventilator withdrawal or progression to tracheostomy for long-term vent support.
Palliative care providers consider the family meeting to be the “procedure” of their field, a belief that may seem incongruous with a surgical understanding of the nature of procedures but is informative as a framework for understanding the results of the Carson study. Just as surgical procedures carry risk of complications or adverse outcomes, family meetings have risk for worsening instead of improving the coping of families and surrogates. And, as surgical technique can be connected to complications, the family meeting technique applied by Carson et al. may be related to its results. Although there was formalized communication between the ICU team and the palliative care team regarding the patient’s condition, prognosis, and treatment plan, there was not a representative from the critical care team present during the majority of the support and information team led family meetings. This represents a marked deviation from common practice at our institution and many others. Our usual practice is to have a member of the ICU team present for discussions focused on patient prognosis, in order to make sure that there is alignment between the messages of the ICU and palliative care teams and also to prevent the crippling of palliative support that occurs when it becomes the sole repository of unwelcome news.
Because the relief of suffering is a core value of surgery and palliative care, there are countless ways these disciplines can inform one another. The outcome of the Carson study is a cautionary tale about the fallibility of the integration of surgical and palliative care teams, both of which would acknowledge the importance of the multidisciplinary approach, relationships developed over time, and symptom management. As surgeons intuitively understand from their operative experience, the “procedure” (the family meeting) has the potential for both risk and benefit, the outcome of which may be determined “in my hands.”
Dr. Rivet is a colon and rectal surgeon with training and board certification in hospice and palliative medicine. She is an assistant professor, departments of surgery and internal medicine, Virginia Commonwealth University, Richmond. She has no disclosures.
A randomized controlled multicenter study published by Carson et al. in JAMA concluded that, for patients with “chronic critical illness” (defined as requiring 7 days of mechanical ventilation), palliative care team-led informational and emotional support meetings did not reduce anxiety or depression for families and may have increased posttraumatic stress disorder symptoms (2016:316[1]:51-62. doi: 10.1001/jama.2016.8474).
This report may surprise surgeons, as well as practitioners in other specialties, as the disconnect between palliative care and critical care services has been previously perceived as an education and access issue, not an outcome problem.
Carson and colleagues point out that fidelity to some components of the meeting “templates” was low, suggesting that there was some flexibility baked into the study design. However, as Russ and Kaufman aptly described, patients and families vary greatly in their appetite for explicit information about prognosis (Cult Med Psychiatry 2005;29[1]:103-23). Conversely, the hypothesis that direct communication about prognosis will be welcomed by families is a core element of the Carson study. The manuscript supplement reports that discussion of the patient’s condition and prognosis took place in 100% of initial meetings. If the same variability in family receptiveness to this information exists in this population as was described by Russ and Kaufman, it is not hard to see why some families experienced negative consequences because of these discussions.
Furthermore, the authors of the Carson study point out that it was not intended to replicate the components of specialist palliative care (JAMA. 2016;316[15]:1598-9).
Essential elements of specialist palliative care include symptom management, a multidisciplinary approach, and fairly close contact in the acute care setting. These features were lacking in the study protocol. Experienced providers of palliative care will often use symptom assessment and symptom management optimization as a conduit for building rapport and to avoid focusing on prognosis until trust has been established. A period of delay before broaching challenging subjects also allows the palliative care team to develop an understanding of the patient’s or surrogates’ preferences regarding the amount and type of information communicated. Palliative care providers benefit from the deepening of relationships with patients and families over time, as much as or possibly more so than providers of other specialties.
The necessity of the multidisciplinary approach to successful palliative care outcomes cannot be overstated. In many programs, patients seen for specialist palliative care consultation are seen by a physician or advanced practitioner, a chaplain, and a social worker within 24-48 hours of initial referral, and these providers have key roles in addressing the sequelae of anxiety, depression, and stress that were the key outcomes in the JAMA study. In the study, the “support and information team” included a palliative care physician and an advanced practice nurse but not a chaplain or social worker, despite the significance of existential/spiritual and social consequences of ventilator withdrawal or progression to tracheostomy for long-term vent support.
Palliative care providers consider the family meeting to be the “procedure” of their field, a belief that may seem incongruous with a surgical understanding of the nature of procedures but is informative as a framework for understanding the results of the Carson study. Just as surgical procedures carry risk of complications or adverse outcomes, family meetings have risk for worsening instead of improving the coping of families and surrogates. And, as surgical technique can be connected to complications, the family meeting technique applied by Carson et al. may be related to its results. Although there was formalized communication between the ICU team and the palliative care team regarding the patient’s condition, prognosis, and treatment plan, there was not a representative from the critical care team present during the majority of the support and information team led family meetings. This represents a marked deviation from common practice at our institution and many others. Our usual practice is to have a member of the ICU team present for discussions focused on patient prognosis, in order to make sure that there is alignment between the messages of the ICU and palliative care teams and also to prevent the crippling of palliative support that occurs when it becomes the sole repository of unwelcome news.
Because the relief of suffering is a core value of surgery and palliative care, there are countless ways these disciplines can inform one another. The outcome of the Carson study is a cautionary tale about the fallibility of the integration of surgical and palliative care teams, both of which would acknowledge the importance of the multidisciplinary approach, relationships developed over time, and symptom management. As surgeons intuitively understand from their operative experience, the “procedure” (the family meeting) has the potential for both risk and benefit, the outcome of which may be determined “in my hands.”
Dr. Rivet is a colon and rectal surgeon with training and board certification in hospice and palliative medicine. She is an assistant professor, departments of surgery and internal medicine, Virginia Commonwealth University, Richmond. She has no disclosures.
A randomized controlled multicenter study published by Carson et al. in JAMA concluded that, for patients with “chronic critical illness” (defined as requiring 7 days of mechanical ventilation), palliative care team-led informational and emotional support meetings did not reduce anxiety or depression for families and may have increased posttraumatic stress disorder symptoms (2016:316[1]:51-62. doi: 10.1001/jama.2016.8474).
This report may surprise surgeons, as well as practitioners in other specialties, as the disconnect between palliative care and critical care services has been previously perceived as an education and access issue, not an outcome problem.
Carson and colleagues point out that fidelity to some components of the meeting “templates” was low, suggesting that there was some flexibility baked into the study design. However, as Russ and Kaufman aptly described, patients and families vary greatly in their appetite for explicit information about prognosis (Cult Med Psychiatry 2005;29[1]:103-23). Conversely, the hypothesis that direct communication about prognosis will be welcomed by families is a core element of the Carson study. The manuscript supplement reports that discussion of the patient’s condition and prognosis took place in 100% of initial meetings. If the same variability in family receptiveness to this information exists in this population as was described by Russ and Kaufman, it is not hard to see why some families experienced negative consequences because of these discussions.
Furthermore, the authors of the Carson study point out that it was not intended to replicate the components of specialist palliative care (JAMA. 2016;316[15]:1598-9).
Essential elements of specialist palliative care include symptom management, a multidisciplinary approach, and fairly close contact in the acute care setting. These features were lacking in the study protocol. Experienced providers of palliative care will often use symptom assessment and symptom management optimization as a conduit for building rapport and to avoid focusing on prognosis until trust has been established. A period of delay before broaching challenging subjects also allows the palliative care team to develop an understanding of the patient’s or surrogates’ preferences regarding the amount and type of information communicated. Palliative care providers benefit from the deepening of relationships with patients and families over time, as much as or possibly more so than providers of other specialties.
The necessity of the multidisciplinary approach to successful palliative care outcomes cannot be overstated. In many programs, patients seen for specialist palliative care consultation are seen by a physician or advanced practitioner, a chaplain, and a social worker within 24-48 hours of initial referral, and these providers have key roles in addressing the sequelae of anxiety, depression, and stress that were the key outcomes in the JAMA study. In the study, the “support and information team” included a palliative care physician and an advanced practice nurse but not a chaplain or social worker, despite the significance of existential/spiritual and social consequences of ventilator withdrawal or progression to tracheostomy for long-term vent support.
Palliative care providers consider the family meeting to be the “procedure” of their field, a belief that may seem incongruous with a surgical understanding of the nature of procedures but is informative as a framework for understanding the results of the Carson study. Just as surgical procedures carry risk of complications or adverse outcomes, family meetings have risk for worsening instead of improving the coping of families and surrogates. And, as surgical technique can be connected to complications, the family meeting technique applied by Carson et al. may be related to its results. Although there was formalized communication between the ICU team and the palliative care team regarding the patient’s condition, prognosis, and treatment plan, there was not a representative from the critical care team present during the majority of the support and information team led family meetings. This represents a marked deviation from common practice at our institution and many others. Our usual practice is to have a member of the ICU team present for discussions focused on patient prognosis, in order to make sure that there is alignment between the messages of the ICU and palliative care teams and also to prevent the crippling of palliative support that occurs when it becomes the sole repository of unwelcome news.
Because the relief of suffering is a core value of surgery and palliative care, there are countless ways these disciplines can inform one another. The outcome of the Carson study is a cautionary tale about the fallibility of the integration of surgical and palliative care teams, both of which would acknowledge the importance of the multidisciplinary approach, relationships developed over time, and symptom management. As surgeons intuitively understand from their operative experience, the “procedure” (the family meeting) has the potential for both risk and benefit, the outcome of which may be determined “in my hands.”
Dr. Rivet is a colon and rectal surgeon with training and board certification in hospice and palliative medicine. She is an assistant professor, departments of surgery and internal medicine, Virginia Commonwealth University, Richmond. She has no disclosures.