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Should toe amputation be delayed in diabetic patients with osteomyelitis?
Amputation: Resistance is not futile!
What’s in a toe you may ask? Why worry about saving it? Just amputate and move on ...
Not so! I implore you to resist the desire. We vascular surgeons are accustomed to cutting off toes, even feet and legs. But when it comes to diabetic feet please reconsider. Just because there is osteomyelitis, I argue that does not necessitate amputation.
We all agree that ischemic gangrene and black mummified digits are beyond salvage. That’s not what my concern is. My focus is nonhealing ulcers with underlying osteomyelitis. Whether ischemic in etiology or neuropathic (or both), give salvage a try.
Why is this so important? My opponent will try to convince you that it’s not. He’ll try to sell you on how well people walk after amputation and that functional outcomes are great. But think beyond that for a second.
Amputation changes the foot architecture and weight distribution. In a person with neuropathy, this only predisposes them to more ulcers. More ulcers will mean more infection, which will lead to more amputations. This finally culminates in a major amputation.
In one reported study,1 researchers followed more than 200,000 diabetics from 2010 until 2013. While the risk of amputation overall was relatively small (0.36% for major and 0.56% for minor amputations), prior minor amputation increased the risk of major amputation 10-fold and increased the risk of another minor (below-ankle) amputation 20-fold. Of those who had a major amputation, 57% died over the 3 years. This is not insignificant.
This does not also consider the morbidity and impact on lifestyle and quality of life for these patients. Many may not walk. Some will be relegated to nursing homes. Some will suffer from phantom limb pain. Many may never return to work. Even more will have difficulty with their daily lives, not to mention the psychological recovery also required.
The foot seems to be the only place where amputation as first-line therapy for osteomyelitis is accepted. We don’t do a hip disarticulation for ischial pressure sores with osteomyelitis. Calvarial osteomyelitis is also treated with antibiotics. I implore you: Don’t treat toes like vestigial organs.
Granted, there are subsets of patients who would benefit from amputations. A patient with painful Charcot foot may elect to have a below-knee amputation and move on with life. Another who has lost jobs or significant time due to recurrence of osteomyelitis may progress. A patient with severe sepsis and infection into a joint may need amputation.
But what other treatment options are there? I’m glad you inquired.
I primarily treat diabetic feet by treating the soft tissue envelope. Even if a patient presents with midfoot infection or necrotizing soft tissue infection, I treat it like a good old-fashioned abscess or necrotizing fasciitis:
1) Drain pus
2) Resect the dead stuff
3) Supportive care (antibiotics, fluids, aggressive wound care, etc.)
I try to leave the bones intact. When bone is exposed I take biopsies for culture and pathology. Any bone destroyed by the infection is focally debrided. I also take a specimen of the “bone margin” that I’m leaving behind and I send this to pathology looking for residual acute osteomyelitis. These steps are important as they dictate duration and choice of antibiotic therapy. This is in keeping with the consensus recommendations published in 2016.2
Even chronic wounds get a similar approach. If there is granulation, let it granulate and see if it will fill the wound. “Just because osteomyelitis is there, it doesn’t mean that for the toe we won’t care!”
There are exceptions of course. If the soft tissue is severely affected so the phalynx protrudes like something from the movie “Coco,” probably that should be amputated. Repeat offenders also may progress to amputation. But otherwise, hold off and give it a chance.
For the inpatient, aggressive irrigation of the wounds using the Veraflo system promotes granulation, even for short hospital stays of 1 week or less. Any ischemic component is worked up and addressed with percutaneous or open revascularization. We treat with prolonged antibiotics, and in questionable cases err on the side of giving long-term courses. These wounds need to be offloaded for tasks of daily living (going to the bathroom, making a sandwich, etc.) but otherwise we instruct patients to be effectively non–weight-bearing on that limb.
We also refer patients for hyperbaric therapy frequently. Now if you’re done groaning, I assure you this is not phony medicine. There is growing evidence to support not only improved rates of healing, but also significant cost savings and improved quality of life.3
In young patients or those with large defects, we also involve plastic and reconstructive surgery for secondary closure approaches (free flaps, adjacent tissue transfers, local autogenous or prosthetic grafting [Integra, Stravix, Dermacell, etc.] or other advanced techniques). This is particularly important in plantar wounds that will need to bear weight in the future, or in young patients for improved functional and cosmetic outcomes. For smaller wounds, we often use dermal/subdermal graft substitutes ourselves.
Even still, in nonambulatory or chronically debilitated and medically high-risk patients, maybe a different option is palliative wound care with or without antibiotics. A nonoperative approach to allow individuals to live the rest of their remaining days without undergoing a morbid and disfiguring amputation is not unreasonable. Many families are thankful for this option when given it. In the absence of refractory pain or overwhelming sepsis, we just let the wound do what it will do, understanding that someday the plan may change. This allows patients to continue to treat the wound without escalation to surgery or resorting to amputation.
In the end, just like we vascular surgeons tailor our “holistic” approach to the needs and desires of a single particular patient, we should approach wounds with a similar attitude. The presence of osteomyelitis in and of itself should not prompt one to bypass an entire algorithm, go straight to amputation, do not pass “Go” or “collect $200” (although the professional fee for a toe amputation is probably around $200). With a multidisciplinary and multimodal approach, and vested patients, salvage is possible in the majority of cases.
References
1. Diabetologia. 2018 Mar;61(3):626-35.
2. Diabet Foot Ankle. 2016 Jul 12. doi: 10.3402/dfa.v7.30079.
3. Int J Technol Assess Health Care. 2008 Spring;24(2):178-83.
Dr. Issam Koleilat is assistant professor and associate program director, Vascular Surgery Residency and Fellowship, Division of Vascular Surgery, Albert Einstein College of Medicine/Montefiore Medical Center, New York. He had no relevant disclosures.
Amputation: Often the best option
For many years there has been debate about the best management strategy for diabetic foot infection including osteomyelitis. The principles of appropriate antibiotics, surgical debridement, good wound care, and proper offloading will always remain. There are no randomized controlled trials of medical vs. surgical management of diabetic foot ulceration with osteomyelitis.
We now have a number of widely accepted ways to define wounds including Wagner and the SVS-adopted WIFI score. Historical papers are somewhat plagued by heterogeneity in the wounds included. This is even more apparent with any attempted meta-analyses. I think everyone would agree that the superficial toe wound with minimal cellulitis is best managed medically. The issue at hand is the profoundly neuropathic diabetic often with underlying anatomic abnormality and osteomyelitis. My esteemed colleague would suggest that we are too quick to pull a trigger and amputate a toe with underlying osteomyelitis.
I think the initial item for debate is the technique of diagnosis of osteomyelitis. We have multiple ways this is reported. Plain x-ray, bone scan, MRI, and “clinical osteomyelitis” are among the alternative ways osteomyelitis is diagnosed. The reliability of the last is the most variable because clinical osteomyelitis ranges from “probes close to bone” to exposed bone visible protruding from the wound bed. Given the variability of diagnostic techniques, the literature is an amalgam of clinical scenarios and difficult to navigate in a way to affect treatment decisions.
In addition, the medical treatment for osteomyelitis is highly variable. This commonly involves tunneled catheter insertion and 6 weeks to 3 months of IV antibiotics. In some institutions antibiotics are tailored to “wound culture.” Several of our infectious disease specialists prefer bone culture and pathology of bone demonstrating an acute destructive process. Obviously, this often requires surgical debridement to obtain a specimen. Antibiotic duration recommendations may vary from 1 week (if all infected bone is resected) to 90 days if a standalone antibiotic management is selected. Chronic osteomyelitis has a reinfection rate of up to 30%.1
Medical management is not without risk. These risks include recurring infection with resistant organisms, wound deterioration, gastrointestinal complications (Clostridium difficile), catheter-related complications, and acute kidney injury. A recent paper found over 30% of patients treated medically for osteomyelitis developed acute kidney injury. These patients had more frequent hospitalization, recurring ulceration, and infection.2 We have all experienced the patient with multiple hospitalizations and episodic AKI that culminates in ESRD requiring hemodialysis.
If the argument is with good follow-up these patients will ultimately experience preservation of the toe, I would take the stance that in our patient population of diabetics presenting with foot ulcer and osteomyelitis the average hemoglobin A1c is over 9. Although this is not only related to patient compliance, in many instances this is a large piece of the puzzle. It is hard to infer that suddenly with biopsy-proven osteomyelitis the patient will become compliant with medical management of the disease process. Certainly, in some circumstances, this is the case. There are a number of studies with a wide range of findings on HbA1c as it relates to predictive value of wound healing.
There are various studies comparing surgical to medical management for osteomyelitis. Limb salvage is contingent upon location (forefoot, midfoot, hindfoot), the extent of infection, and patient comorbidities. The conclusion of the majority of these studies is that a standalone antibiotic treatment algorithm results in greater limb loss. Patients with peripheral occlusive disease and preadmission antibiotic use have been shown to have decreased wound healing. Minor amputation has been shown to be protective from mortality, risk of major amputation, and unfavorable discharge in patients admitted with a diagnosis of osteomyelitis.3 The major limb amputation rate for antibiotics alone is 20%-30% according to two trials with duration of antibiotics of 3 months.4,5 The available randomized trials tend to exclude patients with severe infection (poorly defined), those with PAD, or those with severe comorbid conditions.
Cost of treatment is even more poorly delineated. Obviously, surgical treatment is not without cost to the health care system. Toe amputation especially when including the metatarsal head shifts pressure points and in the neuropathic patient may lead to recurrent ulceration. The average outpatient cost per patient per ulcer is often over $30,000. The goal of surgical treatment can be defined as trying to maintain the greatest degree of function with the least risk. Removing infected bone (i.e., minor amputation) limits exposure to prolonged antibiotic treatment and hopefully lessens recurring ulceration and hospitalization. This is only one piece of the puzzle, however. A multidisciplinary approach with endocrinology, infectious disease, and orthotics for offloading are keys to decrease future ulceration.
Although I do not advocate for widespread toe carnage as suggested by Dr. Koleilat, I do think liberal application of minor amputation to limit hospital stay, limit antibiotic duration and its inherent risk, and possibly affect readmission is often in the best interest of the patient and the system as a whole. Obviously, based on the variable reports in the literature there cannot be a single approach to these patients and the treatment must be individualized based on extent of infection, compliance of the patient, access to multidisciplinary care, and comorbid conditions.
References
1. World J Diabetes. 2017 Apr 15;8(4):135-42.
2. Diabetes Res Clin Pract. 2018 Jan;135:58-64.
3. Ann Surg. 2005;241(6):885-94.
4. Am J Med. 1987 Oct;83(4):653-60.
5. Am J Med.1989 Jun;86(6 Pt 2):801-8.
Dr. Mark P. Androes is division chief, vascular surgery, Greenville (S.C.) Health System. He had no relevant disclosures.
Amputation: Resistance is not futile!
What’s in a toe you may ask? Why worry about saving it? Just amputate and move on ...
Not so! I implore you to resist the desire. We vascular surgeons are accustomed to cutting off toes, even feet and legs. But when it comes to diabetic feet please reconsider. Just because there is osteomyelitis, I argue that does not necessitate amputation.
We all agree that ischemic gangrene and black mummified digits are beyond salvage. That’s not what my concern is. My focus is nonhealing ulcers with underlying osteomyelitis. Whether ischemic in etiology or neuropathic (or both), give salvage a try.
Why is this so important? My opponent will try to convince you that it’s not. He’ll try to sell you on how well people walk after amputation and that functional outcomes are great. But think beyond that for a second.
Amputation changes the foot architecture and weight distribution. In a person with neuropathy, this only predisposes them to more ulcers. More ulcers will mean more infection, which will lead to more amputations. This finally culminates in a major amputation.
In one reported study,1 researchers followed more than 200,000 diabetics from 2010 until 2013. While the risk of amputation overall was relatively small (0.36% for major and 0.56% for minor amputations), prior minor amputation increased the risk of major amputation 10-fold and increased the risk of another minor (below-ankle) amputation 20-fold. Of those who had a major amputation, 57% died over the 3 years. This is not insignificant.
This does not also consider the morbidity and impact on lifestyle and quality of life for these patients. Many may not walk. Some will be relegated to nursing homes. Some will suffer from phantom limb pain. Many may never return to work. Even more will have difficulty with their daily lives, not to mention the psychological recovery also required.
The foot seems to be the only place where amputation as first-line therapy for osteomyelitis is accepted. We don’t do a hip disarticulation for ischial pressure sores with osteomyelitis. Calvarial osteomyelitis is also treated with antibiotics. I implore you: Don’t treat toes like vestigial organs.
Granted, there are subsets of patients who would benefit from amputations. A patient with painful Charcot foot may elect to have a below-knee amputation and move on with life. Another who has lost jobs or significant time due to recurrence of osteomyelitis may progress. A patient with severe sepsis and infection into a joint may need amputation.
But what other treatment options are there? I’m glad you inquired.
I primarily treat diabetic feet by treating the soft tissue envelope. Even if a patient presents with midfoot infection or necrotizing soft tissue infection, I treat it like a good old-fashioned abscess or necrotizing fasciitis:
1) Drain pus
2) Resect the dead stuff
3) Supportive care (antibiotics, fluids, aggressive wound care, etc.)
I try to leave the bones intact. When bone is exposed I take biopsies for culture and pathology. Any bone destroyed by the infection is focally debrided. I also take a specimen of the “bone margin” that I’m leaving behind and I send this to pathology looking for residual acute osteomyelitis. These steps are important as they dictate duration and choice of antibiotic therapy. This is in keeping with the consensus recommendations published in 2016.2
Even chronic wounds get a similar approach. If there is granulation, let it granulate and see if it will fill the wound. “Just because osteomyelitis is there, it doesn’t mean that for the toe we won’t care!”
There are exceptions of course. If the soft tissue is severely affected so the phalynx protrudes like something from the movie “Coco,” probably that should be amputated. Repeat offenders also may progress to amputation. But otherwise, hold off and give it a chance.
For the inpatient, aggressive irrigation of the wounds using the Veraflo system promotes granulation, even for short hospital stays of 1 week or less. Any ischemic component is worked up and addressed with percutaneous or open revascularization. We treat with prolonged antibiotics, and in questionable cases err on the side of giving long-term courses. These wounds need to be offloaded for tasks of daily living (going to the bathroom, making a sandwich, etc.) but otherwise we instruct patients to be effectively non–weight-bearing on that limb.
We also refer patients for hyperbaric therapy frequently. Now if you’re done groaning, I assure you this is not phony medicine. There is growing evidence to support not only improved rates of healing, but also significant cost savings and improved quality of life.3
In young patients or those with large defects, we also involve plastic and reconstructive surgery for secondary closure approaches (free flaps, adjacent tissue transfers, local autogenous or prosthetic grafting [Integra, Stravix, Dermacell, etc.] or other advanced techniques). This is particularly important in plantar wounds that will need to bear weight in the future, or in young patients for improved functional and cosmetic outcomes. For smaller wounds, we often use dermal/subdermal graft substitutes ourselves.
Even still, in nonambulatory or chronically debilitated and medically high-risk patients, maybe a different option is palliative wound care with or without antibiotics. A nonoperative approach to allow individuals to live the rest of their remaining days without undergoing a morbid and disfiguring amputation is not unreasonable. Many families are thankful for this option when given it. In the absence of refractory pain or overwhelming sepsis, we just let the wound do what it will do, understanding that someday the plan may change. This allows patients to continue to treat the wound without escalation to surgery or resorting to amputation.
In the end, just like we vascular surgeons tailor our “holistic” approach to the needs and desires of a single particular patient, we should approach wounds with a similar attitude. The presence of osteomyelitis in and of itself should not prompt one to bypass an entire algorithm, go straight to amputation, do not pass “Go” or “collect $200” (although the professional fee for a toe amputation is probably around $200). With a multidisciplinary and multimodal approach, and vested patients, salvage is possible in the majority of cases.
References
1. Diabetologia. 2018 Mar;61(3):626-35.
2. Diabet Foot Ankle. 2016 Jul 12. doi: 10.3402/dfa.v7.30079.
3. Int J Technol Assess Health Care. 2008 Spring;24(2):178-83.
Dr. Issam Koleilat is assistant professor and associate program director, Vascular Surgery Residency and Fellowship, Division of Vascular Surgery, Albert Einstein College of Medicine/Montefiore Medical Center, New York. He had no relevant disclosures.
Amputation: Often the best option
For many years there has been debate about the best management strategy for diabetic foot infection including osteomyelitis. The principles of appropriate antibiotics, surgical debridement, good wound care, and proper offloading will always remain. There are no randomized controlled trials of medical vs. surgical management of diabetic foot ulceration with osteomyelitis.
We now have a number of widely accepted ways to define wounds including Wagner and the SVS-adopted WIFI score. Historical papers are somewhat plagued by heterogeneity in the wounds included. This is even more apparent with any attempted meta-analyses. I think everyone would agree that the superficial toe wound with minimal cellulitis is best managed medically. The issue at hand is the profoundly neuropathic diabetic often with underlying anatomic abnormality and osteomyelitis. My esteemed colleague would suggest that we are too quick to pull a trigger and amputate a toe with underlying osteomyelitis.
I think the initial item for debate is the technique of diagnosis of osteomyelitis. We have multiple ways this is reported. Plain x-ray, bone scan, MRI, and “clinical osteomyelitis” are among the alternative ways osteomyelitis is diagnosed. The reliability of the last is the most variable because clinical osteomyelitis ranges from “probes close to bone” to exposed bone visible protruding from the wound bed. Given the variability of diagnostic techniques, the literature is an amalgam of clinical scenarios and difficult to navigate in a way to affect treatment decisions.
In addition, the medical treatment for osteomyelitis is highly variable. This commonly involves tunneled catheter insertion and 6 weeks to 3 months of IV antibiotics. In some institutions antibiotics are tailored to “wound culture.” Several of our infectious disease specialists prefer bone culture and pathology of bone demonstrating an acute destructive process. Obviously, this often requires surgical debridement to obtain a specimen. Antibiotic duration recommendations may vary from 1 week (if all infected bone is resected) to 90 days if a standalone antibiotic management is selected. Chronic osteomyelitis has a reinfection rate of up to 30%.1
Medical management is not without risk. These risks include recurring infection with resistant organisms, wound deterioration, gastrointestinal complications (Clostridium difficile), catheter-related complications, and acute kidney injury. A recent paper found over 30% of patients treated medically for osteomyelitis developed acute kidney injury. These patients had more frequent hospitalization, recurring ulceration, and infection.2 We have all experienced the patient with multiple hospitalizations and episodic AKI that culminates in ESRD requiring hemodialysis.
If the argument is with good follow-up these patients will ultimately experience preservation of the toe, I would take the stance that in our patient population of diabetics presenting with foot ulcer and osteomyelitis the average hemoglobin A1c is over 9. Although this is not only related to patient compliance, in many instances this is a large piece of the puzzle. It is hard to infer that suddenly with biopsy-proven osteomyelitis the patient will become compliant with medical management of the disease process. Certainly, in some circumstances, this is the case. There are a number of studies with a wide range of findings on HbA1c as it relates to predictive value of wound healing.
There are various studies comparing surgical to medical management for osteomyelitis. Limb salvage is contingent upon location (forefoot, midfoot, hindfoot), the extent of infection, and patient comorbidities. The conclusion of the majority of these studies is that a standalone antibiotic treatment algorithm results in greater limb loss. Patients with peripheral occlusive disease and preadmission antibiotic use have been shown to have decreased wound healing. Minor amputation has been shown to be protective from mortality, risk of major amputation, and unfavorable discharge in patients admitted with a diagnosis of osteomyelitis.3 The major limb amputation rate for antibiotics alone is 20%-30% according to two trials with duration of antibiotics of 3 months.4,5 The available randomized trials tend to exclude patients with severe infection (poorly defined), those with PAD, or those with severe comorbid conditions.
Cost of treatment is even more poorly delineated. Obviously, surgical treatment is not without cost to the health care system. Toe amputation especially when including the metatarsal head shifts pressure points and in the neuropathic patient may lead to recurrent ulceration. The average outpatient cost per patient per ulcer is often over $30,000. The goal of surgical treatment can be defined as trying to maintain the greatest degree of function with the least risk. Removing infected bone (i.e., minor amputation) limits exposure to prolonged antibiotic treatment and hopefully lessens recurring ulceration and hospitalization. This is only one piece of the puzzle, however. A multidisciplinary approach with endocrinology, infectious disease, and orthotics for offloading are keys to decrease future ulceration.
Although I do not advocate for widespread toe carnage as suggested by Dr. Koleilat, I do think liberal application of minor amputation to limit hospital stay, limit antibiotic duration and its inherent risk, and possibly affect readmission is often in the best interest of the patient and the system as a whole. Obviously, based on the variable reports in the literature there cannot be a single approach to these patients and the treatment must be individualized based on extent of infection, compliance of the patient, access to multidisciplinary care, and comorbid conditions.
References
1. World J Diabetes. 2017 Apr 15;8(4):135-42.
2. Diabetes Res Clin Pract. 2018 Jan;135:58-64.
3. Ann Surg. 2005;241(6):885-94.
4. Am J Med. 1987 Oct;83(4):653-60.
5. Am J Med.1989 Jun;86(6 Pt 2):801-8.
Dr. Mark P. Androes is division chief, vascular surgery, Greenville (S.C.) Health System. He had no relevant disclosures.
Amputation: Resistance is not futile!
What’s in a toe you may ask? Why worry about saving it? Just amputate and move on ...
Not so! I implore you to resist the desire. We vascular surgeons are accustomed to cutting off toes, even feet and legs. But when it comes to diabetic feet please reconsider. Just because there is osteomyelitis, I argue that does not necessitate amputation.
We all agree that ischemic gangrene and black mummified digits are beyond salvage. That’s not what my concern is. My focus is nonhealing ulcers with underlying osteomyelitis. Whether ischemic in etiology or neuropathic (or both), give salvage a try.
Why is this so important? My opponent will try to convince you that it’s not. He’ll try to sell you on how well people walk after amputation and that functional outcomes are great. But think beyond that for a second.
Amputation changes the foot architecture and weight distribution. In a person with neuropathy, this only predisposes them to more ulcers. More ulcers will mean more infection, which will lead to more amputations. This finally culminates in a major amputation.
In one reported study,1 researchers followed more than 200,000 diabetics from 2010 until 2013. While the risk of amputation overall was relatively small (0.36% for major and 0.56% for minor amputations), prior minor amputation increased the risk of major amputation 10-fold and increased the risk of another minor (below-ankle) amputation 20-fold. Of those who had a major amputation, 57% died over the 3 years. This is not insignificant.
This does not also consider the morbidity and impact on lifestyle and quality of life for these patients. Many may not walk. Some will be relegated to nursing homes. Some will suffer from phantom limb pain. Many may never return to work. Even more will have difficulty with their daily lives, not to mention the psychological recovery also required.
The foot seems to be the only place where amputation as first-line therapy for osteomyelitis is accepted. We don’t do a hip disarticulation for ischial pressure sores with osteomyelitis. Calvarial osteomyelitis is also treated with antibiotics. I implore you: Don’t treat toes like vestigial organs.
Granted, there are subsets of patients who would benefit from amputations. A patient with painful Charcot foot may elect to have a below-knee amputation and move on with life. Another who has lost jobs or significant time due to recurrence of osteomyelitis may progress. A patient with severe sepsis and infection into a joint may need amputation.
But what other treatment options are there? I’m glad you inquired.
I primarily treat diabetic feet by treating the soft tissue envelope. Even if a patient presents with midfoot infection or necrotizing soft tissue infection, I treat it like a good old-fashioned abscess or necrotizing fasciitis:
1) Drain pus
2) Resect the dead stuff
3) Supportive care (antibiotics, fluids, aggressive wound care, etc.)
I try to leave the bones intact. When bone is exposed I take biopsies for culture and pathology. Any bone destroyed by the infection is focally debrided. I also take a specimen of the “bone margin” that I’m leaving behind and I send this to pathology looking for residual acute osteomyelitis. These steps are important as they dictate duration and choice of antibiotic therapy. This is in keeping with the consensus recommendations published in 2016.2
Even chronic wounds get a similar approach. If there is granulation, let it granulate and see if it will fill the wound. “Just because osteomyelitis is there, it doesn’t mean that for the toe we won’t care!”
There are exceptions of course. If the soft tissue is severely affected so the phalynx protrudes like something from the movie “Coco,” probably that should be amputated. Repeat offenders also may progress to amputation. But otherwise, hold off and give it a chance.
For the inpatient, aggressive irrigation of the wounds using the Veraflo system promotes granulation, even for short hospital stays of 1 week or less. Any ischemic component is worked up and addressed with percutaneous or open revascularization. We treat with prolonged antibiotics, and in questionable cases err on the side of giving long-term courses. These wounds need to be offloaded for tasks of daily living (going to the bathroom, making a sandwich, etc.) but otherwise we instruct patients to be effectively non–weight-bearing on that limb.
We also refer patients for hyperbaric therapy frequently. Now if you’re done groaning, I assure you this is not phony medicine. There is growing evidence to support not only improved rates of healing, but also significant cost savings and improved quality of life.3
In young patients or those with large defects, we also involve plastic and reconstructive surgery for secondary closure approaches (free flaps, adjacent tissue transfers, local autogenous or prosthetic grafting [Integra, Stravix, Dermacell, etc.] or other advanced techniques). This is particularly important in plantar wounds that will need to bear weight in the future, or in young patients for improved functional and cosmetic outcomes. For smaller wounds, we often use dermal/subdermal graft substitutes ourselves.
Even still, in nonambulatory or chronically debilitated and medically high-risk patients, maybe a different option is palliative wound care with or without antibiotics. A nonoperative approach to allow individuals to live the rest of their remaining days without undergoing a morbid and disfiguring amputation is not unreasonable. Many families are thankful for this option when given it. In the absence of refractory pain or overwhelming sepsis, we just let the wound do what it will do, understanding that someday the plan may change. This allows patients to continue to treat the wound without escalation to surgery or resorting to amputation.
In the end, just like we vascular surgeons tailor our “holistic” approach to the needs and desires of a single particular patient, we should approach wounds with a similar attitude. The presence of osteomyelitis in and of itself should not prompt one to bypass an entire algorithm, go straight to amputation, do not pass “Go” or “collect $200” (although the professional fee for a toe amputation is probably around $200). With a multidisciplinary and multimodal approach, and vested patients, salvage is possible in the majority of cases.
References
1. Diabetologia. 2018 Mar;61(3):626-35.
2. Diabet Foot Ankle. 2016 Jul 12. doi: 10.3402/dfa.v7.30079.
3. Int J Technol Assess Health Care. 2008 Spring;24(2):178-83.
Dr. Issam Koleilat is assistant professor and associate program director, Vascular Surgery Residency and Fellowship, Division of Vascular Surgery, Albert Einstein College of Medicine/Montefiore Medical Center, New York. He had no relevant disclosures.
Amputation: Often the best option
For many years there has been debate about the best management strategy for diabetic foot infection including osteomyelitis. The principles of appropriate antibiotics, surgical debridement, good wound care, and proper offloading will always remain. There are no randomized controlled trials of medical vs. surgical management of diabetic foot ulceration with osteomyelitis.
We now have a number of widely accepted ways to define wounds including Wagner and the SVS-adopted WIFI score. Historical papers are somewhat plagued by heterogeneity in the wounds included. This is even more apparent with any attempted meta-analyses. I think everyone would agree that the superficial toe wound with minimal cellulitis is best managed medically. The issue at hand is the profoundly neuropathic diabetic often with underlying anatomic abnormality and osteomyelitis. My esteemed colleague would suggest that we are too quick to pull a trigger and amputate a toe with underlying osteomyelitis.
I think the initial item for debate is the technique of diagnosis of osteomyelitis. We have multiple ways this is reported. Plain x-ray, bone scan, MRI, and “clinical osteomyelitis” are among the alternative ways osteomyelitis is diagnosed. The reliability of the last is the most variable because clinical osteomyelitis ranges from “probes close to bone” to exposed bone visible protruding from the wound bed. Given the variability of diagnostic techniques, the literature is an amalgam of clinical scenarios and difficult to navigate in a way to affect treatment decisions.
In addition, the medical treatment for osteomyelitis is highly variable. This commonly involves tunneled catheter insertion and 6 weeks to 3 months of IV antibiotics. In some institutions antibiotics are tailored to “wound culture.” Several of our infectious disease specialists prefer bone culture and pathology of bone demonstrating an acute destructive process. Obviously, this often requires surgical debridement to obtain a specimen. Antibiotic duration recommendations may vary from 1 week (if all infected bone is resected) to 90 days if a standalone antibiotic management is selected. Chronic osteomyelitis has a reinfection rate of up to 30%.1
Medical management is not without risk. These risks include recurring infection with resistant organisms, wound deterioration, gastrointestinal complications (Clostridium difficile), catheter-related complications, and acute kidney injury. A recent paper found over 30% of patients treated medically for osteomyelitis developed acute kidney injury. These patients had more frequent hospitalization, recurring ulceration, and infection.2 We have all experienced the patient with multiple hospitalizations and episodic AKI that culminates in ESRD requiring hemodialysis.
If the argument is with good follow-up these patients will ultimately experience preservation of the toe, I would take the stance that in our patient population of diabetics presenting with foot ulcer and osteomyelitis the average hemoglobin A1c is over 9. Although this is not only related to patient compliance, in many instances this is a large piece of the puzzle. It is hard to infer that suddenly with biopsy-proven osteomyelitis the patient will become compliant with medical management of the disease process. Certainly, in some circumstances, this is the case. There are a number of studies with a wide range of findings on HbA1c as it relates to predictive value of wound healing.
There are various studies comparing surgical to medical management for osteomyelitis. Limb salvage is contingent upon location (forefoot, midfoot, hindfoot), the extent of infection, and patient comorbidities. The conclusion of the majority of these studies is that a standalone antibiotic treatment algorithm results in greater limb loss. Patients with peripheral occlusive disease and preadmission antibiotic use have been shown to have decreased wound healing. Minor amputation has been shown to be protective from mortality, risk of major amputation, and unfavorable discharge in patients admitted with a diagnosis of osteomyelitis.3 The major limb amputation rate for antibiotics alone is 20%-30% according to two trials with duration of antibiotics of 3 months.4,5 The available randomized trials tend to exclude patients with severe infection (poorly defined), those with PAD, or those with severe comorbid conditions.
Cost of treatment is even more poorly delineated. Obviously, surgical treatment is not without cost to the health care system. Toe amputation especially when including the metatarsal head shifts pressure points and in the neuropathic patient may lead to recurrent ulceration. The average outpatient cost per patient per ulcer is often over $30,000. The goal of surgical treatment can be defined as trying to maintain the greatest degree of function with the least risk. Removing infected bone (i.e., minor amputation) limits exposure to prolonged antibiotic treatment and hopefully lessens recurring ulceration and hospitalization. This is only one piece of the puzzle, however. A multidisciplinary approach with endocrinology, infectious disease, and orthotics for offloading are keys to decrease future ulceration.
Although I do not advocate for widespread toe carnage as suggested by Dr. Koleilat, I do think liberal application of minor amputation to limit hospital stay, limit antibiotic duration and its inherent risk, and possibly affect readmission is often in the best interest of the patient and the system as a whole. Obviously, based on the variable reports in the literature there cannot be a single approach to these patients and the treatment must be individualized based on extent of infection, compliance of the patient, access to multidisciplinary care, and comorbid conditions.
References
1. World J Diabetes. 2017 Apr 15;8(4):135-42.
2. Diabetes Res Clin Pract. 2018 Jan;135:58-64.
3. Ann Surg. 2005;241(6):885-94.
4. Am J Med. 1987 Oct;83(4):653-60.
5. Am J Med.1989 Jun;86(6 Pt 2):801-8.
Dr. Mark P. Androes is division chief, vascular surgery, Greenville (S.C.) Health System. He had no relevant disclosures.
Point/Counterpoint: Should FEVAR be used for a short neck?
FEVAR is generally the best option
The advent of endovascular aortic aneurysm repair (EVAR) has steadily become the standard of care in the management of infrarenal abdominal aortic aneurysms (AAAs). In fact, it has now surpassed open surgical repair and is the predominant therapeutic modality in managing this disease entity. Clearly, there are specific anatomic and technical factors that may preclude the use of traditional EVAR – most notably, challenging proximal neck anatomy, be it insufficient length or severe angulation.
It is estimated that up to 30%-40% of patients are unsuitable candidates because of these concerns.1 Such patients are thus relegated to traditional open repair with the associated concerns for supravisceral clamping, including dramatic changes in hemodynamics and prolonged ICU and hospital stays.
Open surgical repair of pararenal, juxtarenal, and suprarenal AAAs is tried, tested, and durable. Knott and the group from Mayo Clinic reviewed their repair of 126 consecutive elective juxtarenal AAAs requiring suprarenal aortic clamping noting a 30-day mortality of .8%.2 More recent data from Kabbani and the Henry Ford group involved their 27-year clinical experience suggesting that open repair of complex proximal aortic aneurysms can be performed with clinical outcomes that are similar to those of open infrarenal repair.3 I respectfully accept this traditional – and historic – treatment modality.
However, we vascular surgeons are progressive and resilient in our quest to innovate and modernize – some of us even modified the traditional endografts on the back table. We charged forward despite the initial paucity of data on infrarenal EVAR compared to traditional open repair of aneurysms in the past. Now, a large percentage of infrarenal AAA repairs are performed via EVAR. In fact, our steadfast progression to advanced endovascular techniques has raised the concern that our graduating trainees are no longer proficient, competent, or even capable, in open complex aneurysm repair!
Tsilimparis and colleagues reported the first outcomes comparing open repair and FEVAR.4 They queried the NSQIP database comparing 1,091 patients undergoing open repair with 264 in the FEVAR group. There was an increased risk of morbidity in all combined endpoints including pulmonary and cardiovascular complications as well as length of stay in patients undergoing the open repair group. A larger comprehensive review pooled the results from 8 FEVAR and 12 open repair series. Analysis of the data found the groups to be identical. Open repair, however, was found to have an increased 30-day mortality when compared to FEVAR (relative risk 1.03, 2% increased absolute mortality).5
Gupta and colleagues reported the latest multi-institutional data noting that open repair was associated with higher risk than FEVAR for 30-day mortality, cardiac and pulmonary complications, renal failure requiring dialysis, return to the operating room, and in this age of cost-containment, length of stay (2 days vs. 7 days; P less than .0001).6
A further study by Donas and colleagues evaluated 90 consecutive patients with primary degenerative juxtarenal AAAs to different operative strategies based on morphologic and clinical characteristics – 29 FEVAR, 30 chEVAR, and 31 open repair.7 Early procedure-related and all-cause 30-day mortality was 0% in the endovascular group and 6.4% in the open group.
Although open repair for juxtarenal AAAs is the gold standard, short- and mid-term data on the outcomes for complex endovascular repair are excellent. Data on long-term durability, graft fixation/migration as well as the integrity of the graft and concerns for endoleaks and branch vessel patency, however, are limited. We do not have long-term data because we have not been doing these newer procedures for that long – but the data thus far show great promise.
We need to continue to challenge the status quo, particularly when the current data are satisfactory and the procedure feasible. With our continued appraisal of the data we publish as vascular surgeons, we can then identify if these innovations and techniques will withstand the test of time. After all, we are vascular surgeons (particularly those of us who have trained extensively in open repair) – and if open repair is necessary, then we will be ready.
But, if I can avoid a thoracoabdominal incision for a few percutaneous access sites, then sign me up!
Dr. Mouawad is chief of vascular and endovascular surgery, medical director of the vascular laboratory, and vice-chair of the department of surgery at McLaren Bay Region, Bay City, Mich. He is assistant professor of surgery at Michigan State University and Central Michigan University.
References
1. Perspect Vasc Surg Endovasc Ther. 2009;21:13-8.
2. J Vasc Surg. 2008;47:695-701.
3. J Vasc Surg. 2014;59:1488-94.
4. Ann Vasc Surg. 2013;27(3):267-73.
5. Eur J Vasc Endovasc Surg. 2009;38(1):35-41.
6. J Vasc Surg. 2017 Dec;66(6):1653-8.
7. J Vasc Surg. 2012 Aug;56(2):285-90.
FEVAR may not be the best choice
Over the past 3 decades, EVAR, with its very low periprocedural morbidity and mortality, and satisfactory long-term results, has become the primary treatment modality for the majority of infrarenal AAAs. The success of stent grafts for the repair of AAA relies heavily on satisfactory proximal and distal seal zones. Each commercially available standard EVAR graft has a manufacturer’s instructions for use requiring a proximal landing zone length of between 10 and 15 mm. Patients with less than this required length are considered to have “short necks.” Evaluation of this group of patients has demonstrated that this is not an uncommon finding and that EVAR performed outside the instructions for use has been associated with an increased risk of intraoperative failure, aneurysm expansion, and later complications.1-3
Current treatment options for patients with short necks include open surgical repair (OSR), FEVAR, and EVAR with the chimney graft technique (Ch-EVAR).
Thus, current knowledge acquired from case series, registries, and clinical experience must be used in deciding which therapeutic option to offer patients. Relevant factors influencing this decision include the availability and adaptability of the technique, early outcomes including technical success, morbidity and mortality, and late outcomes including survival, need for reintervention, and other late morbidity. Finally, in an era of value-based medical care, cost also must be considered.
Currently there is only one Food and Drug Administration–approved fenestrated graft. When used in properly selected patients, excellent periprocedural results have been reported approaching those of standard EVAR. However, there are limitations in both the availability and adaptability of FEVAR. These grafts are custom made for each patient, often requiring several weeks of lead time. Adaptability also has its limitations, including access vessels, severe neck angulation, calcification, mural thrombus, and branch vessel size, number, location, and associated arterial disease. Any of these factors may preclude the use of this technology. Open repair, on the other hand, is not limited by graft availability and allows for custom modification for each patient’s specific disease morphology. The essential limitation for open repair is the patient’s physiological ability to withstand the operation.
Several studies attempting to compare the early outcomes of FEVAR versus comparable patients undergoing OSR of similar aneurysms have reported significantly lower 30-day mortality and major morbidity rates for FEVAR.4,5 However, Rao et al., in a recent systematic review and meta-analysis that included data on 2,326 patients from 35 case series reporting on elective repair of juxtarenal aneurysms by either OSR or FEVAR, found perioperative mortality to not be significantly different (4.1% for both). Also, no significant difference was found between the two groups when evaluating postoperative renal insufficiency and need for permanent dialysis. However, OSR did have significantly higher major complication rates (25% vs. 15.7%).6 These findings suggest that both modalities can be performed successfully, but that long term outcomes need to be considered to determine if the increased initial morbidity of OSR is justified by differences in long term results between the two modalities.
Open surgical repair of juxtarenal AAA has been shown to be a durable repair.7 While early and even intermediate results of FEVAR appear to be satisfactory, long-term durability has yet to be determined.4,8 Along with continuing to exclude the aneurysm sac, as with standard EVAR, there is the additional concern regarding the outcome of the organs supplied by the fenestrated/stent-grafted branches with FEVAR. Longer-term follow-up in the same review by Rao et al. showed that significantly more FEVAR patients developed renal failure compared with OSR patients (19.7% vs. 7.7%). FEVAR patients also had a higher rate of reintervention.
And finally, long-term survival was significantly greater in OSR patients compared to FEVAR at 3 and 5 years (80% vs. 74% vs. 73% vs. 55%). These authors concluded that open repair remains the gold standard while FEVAR is a favorable option for high risk patients.6
These new and innovative stent graft devices come at considerable expense. While this aspect of FEVAR has not been extensively studied, Michel et al., in their report from the multicenter prospective Windows registry, attempted to evaluate the economic aspect of FEVAR. They compared a group of patients who underwent FEVAR to patients from a large national hospital discharge database who underwent OSR. No difference in 30-day mortality was noted between these two groups; however, there was a significantly greater cost with FEVAR. The authors concluded that FEVAR did not appear to be justified for patients fit for open surgery with juxtarenal AAA.9
For now, the roles of OSR and FEVAR would appear to be complementary. Current evidence suggests that OSR is the most appropriate intervention for good risk patients with an anticipated longer life expectancy. Patients with appropriate anatomy for FEVAR and who are at higher risk for open repair would benefit from FEVAR. As further experience and outcomes are accumulated, our ability to select the appropriate therapy for individual patients should improve.
Dr. Weaver is an assistant clinical professor for surgery at Wayne State School of Medicine, Detroit, and an attending in the division of vascular surgery, Henry Ford Hospital.
References
1. Ir J Med Sci. 2015;184(1):249-55.
2. Circulation. 2011;123(24):2848-55.
3. J Endovasc Therapy. 2001;8(5):457-64.
4. Eur J Vasc Endovasc Surg. 2009;38(1):35-41.
5. Ann Vasc Surg. 2013;27(3):267-73.
6. J Vasc Surg. 2015;61(1):242-55.
7. J Vasc Surg. 2012;56(1):2-7.
8. J Cardiovasc Surg. 2015;56(3):331-7.
9. Eur J Vasc Endovasc Surg. 2015;50(2):189-96.
FEVAR is generally the best option
The advent of endovascular aortic aneurysm repair (EVAR) has steadily become the standard of care in the management of infrarenal abdominal aortic aneurysms (AAAs). In fact, it has now surpassed open surgical repair and is the predominant therapeutic modality in managing this disease entity. Clearly, there are specific anatomic and technical factors that may preclude the use of traditional EVAR – most notably, challenging proximal neck anatomy, be it insufficient length or severe angulation.
It is estimated that up to 30%-40% of patients are unsuitable candidates because of these concerns.1 Such patients are thus relegated to traditional open repair with the associated concerns for supravisceral clamping, including dramatic changes in hemodynamics and prolonged ICU and hospital stays.
Open surgical repair of pararenal, juxtarenal, and suprarenal AAAs is tried, tested, and durable. Knott and the group from Mayo Clinic reviewed their repair of 126 consecutive elective juxtarenal AAAs requiring suprarenal aortic clamping noting a 30-day mortality of .8%.2 More recent data from Kabbani and the Henry Ford group involved their 27-year clinical experience suggesting that open repair of complex proximal aortic aneurysms can be performed with clinical outcomes that are similar to those of open infrarenal repair.3 I respectfully accept this traditional – and historic – treatment modality.
However, we vascular surgeons are progressive and resilient in our quest to innovate and modernize – some of us even modified the traditional endografts on the back table. We charged forward despite the initial paucity of data on infrarenal EVAR compared to traditional open repair of aneurysms in the past. Now, a large percentage of infrarenal AAA repairs are performed via EVAR. In fact, our steadfast progression to advanced endovascular techniques has raised the concern that our graduating trainees are no longer proficient, competent, or even capable, in open complex aneurysm repair!
Tsilimparis and colleagues reported the first outcomes comparing open repair and FEVAR.4 They queried the NSQIP database comparing 1,091 patients undergoing open repair with 264 in the FEVAR group. There was an increased risk of morbidity in all combined endpoints including pulmonary and cardiovascular complications as well as length of stay in patients undergoing the open repair group. A larger comprehensive review pooled the results from 8 FEVAR and 12 open repair series. Analysis of the data found the groups to be identical. Open repair, however, was found to have an increased 30-day mortality when compared to FEVAR (relative risk 1.03, 2% increased absolute mortality).5
Gupta and colleagues reported the latest multi-institutional data noting that open repair was associated with higher risk than FEVAR for 30-day mortality, cardiac and pulmonary complications, renal failure requiring dialysis, return to the operating room, and in this age of cost-containment, length of stay (2 days vs. 7 days; P less than .0001).6
A further study by Donas and colleagues evaluated 90 consecutive patients with primary degenerative juxtarenal AAAs to different operative strategies based on morphologic and clinical characteristics – 29 FEVAR, 30 chEVAR, and 31 open repair.7 Early procedure-related and all-cause 30-day mortality was 0% in the endovascular group and 6.4% in the open group.
Although open repair for juxtarenal AAAs is the gold standard, short- and mid-term data on the outcomes for complex endovascular repair are excellent. Data on long-term durability, graft fixation/migration as well as the integrity of the graft and concerns for endoleaks and branch vessel patency, however, are limited. We do not have long-term data because we have not been doing these newer procedures for that long – but the data thus far show great promise.
We need to continue to challenge the status quo, particularly when the current data are satisfactory and the procedure feasible. With our continued appraisal of the data we publish as vascular surgeons, we can then identify if these innovations and techniques will withstand the test of time. After all, we are vascular surgeons (particularly those of us who have trained extensively in open repair) – and if open repair is necessary, then we will be ready.
But, if I can avoid a thoracoabdominal incision for a few percutaneous access sites, then sign me up!
Dr. Mouawad is chief of vascular and endovascular surgery, medical director of the vascular laboratory, and vice-chair of the department of surgery at McLaren Bay Region, Bay City, Mich. He is assistant professor of surgery at Michigan State University and Central Michigan University.
References
1. Perspect Vasc Surg Endovasc Ther. 2009;21:13-8.
2. J Vasc Surg. 2008;47:695-701.
3. J Vasc Surg. 2014;59:1488-94.
4. Ann Vasc Surg. 2013;27(3):267-73.
5. Eur J Vasc Endovasc Surg. 2009;38(1):35-41.
6. J Vasc Surg. 2017 Dec;66(6):1653-8.
7. J Vasc Surg. 2012 Aug;56(2):285-90.
FEVAR may not be the best choice
Over the past 3 decades, EVAR, with its very low periprocedural morbidity and mortality, and satisfactory long-term results, has become the primary treatment modality for the majority of infrarenal AAAs. The success of stent grafts for the repair of AAA relies heavily on satisfactory proximal and distal seal zones. Each commercially available standard EVAR graft has a manufacturer’s instructions for use requiring a proximal landing zone length of between 10 and 15 mm. Patients with less than this required length are considered to have “short necks.” Evaluation of this group of patients has demonstrated that this is not an uncommon finding and that EVAR performed outside the instructions for use has been associated with an increased risk of intraoperative failure, aneurysm expansion, and later complications.1-3
Current treatment options for patients with short necks include open surgical repair (OSR), FEVAR, and EVAR with the chimney graft technique (Ch-EVAR).
Thus, current knowledge acquired from case series, registries, and clinical experience must be used in deciding which therapeutic option to offer patients. Relevant factors influencing this decision include the availability and adaptability of the technique, early outcomes including technical success, morbidity and mortality, and late outcomes including survival, need for reintervention, and other late morbidity. Finally, in an era of value-based medical care, cost also must be considered.
Currently there is only one Food and Drug Administration–approved fenestrated graft. When used in properly selected patients, excellent periprocedural results have been reported approaching those of standard EVAR. However, there are limitations in both the availability and adaptability of FEVAR. These grafts are custom made for each patient, often requiring several weeks of lead time. Adaptability also has its limitations, including access vessels, severe neck angulation, calcification, mural thrombus, and branch vessel size, number, location, and associated arterial disease. Any of these factors may preclude the use of this technology. Open repair, on the other hand, is not limited by graft availability and allows for custom modification for each patient’s specific disease morphology. The essential limitation for open repair is the patient’s physiological ability to withstand the operation.
Several studies attempting to compare the early outcomes of FEVAR versus comparable patients undergoing OSR of similar aneurysms have reported significantly lower 30-day mortality and major morbidity rates for FEVAR.4,5 However, Rao et al., in a recent systematic review and meta-analysis that included data on 2,326 patients from 35 case series reporting on elective repair of juxtarenal aneurysms by either OSR or FEVAR, found perioperative mortality to not be significantly different (4.1% for both). Also, no significant difference was found between the two groups when evaluating postoperative renal insufficiency and need for permanent dialysis. However, OSR did have significantly higher major complication rates (25% vs. 15.7%).6 These findings suggest that both modalities can be performed successfully, but that long term outcomes need to be considered to determine if the increased initial morbidity of OSR is justified by differences in long term results between the two modalities.
Open surgical repair of juxtarenal AAA has been shown to be a durable repair.7 While early and even intermediate results of FEVAR appear to be satisfactory, long-term durability has yet to be determined.4,8 Along with continuing to exclude the aneurysm sac, as with standard EVAR, there is the additional concern regarding the outcome of the organs supplied by the fenestrated/stent-grafted branches with FEVAR. Longer-term follow-up in the same review by Rao et al. showed that significantly more FEVAR patients developed renal failure compared with OSR patients (19.7% vs. 7.7%). FEVAR patients also had a higher rate of reintervention.
And finally, long-term survival was significantly greater in OSR patients compared to FEVAR at 3 and 5 years (80% vs. 74% vs. 73% vs. 55%). These authors concluded that open repair remains the gold standard while FEVAR is a favorable option for high risk patients.6
These new and innovative stent graft devices come at considerable expense. While this aspect of FEVAR has not been extensively studied, Michel et al., in their report from the multicenter prospective Windows registry, attempted to evaluate the economic aspect of FEVAR. They compared a group of patients who underwent FEVAR to patients from a large national hospital discharge database who underwent OSR. No difference in 30-day mortality was noted between these two groups; however, there was a significantly greater cost with FEVAR. The authors concluded that FEVAR did not appear to be justified for patients fit for open surgery with juxtarenal AAA.9
For now, the roles of OSR and FEVAR would appear to be complementary. Current evidence suggests that OSR is the most appropriate intervention for good risk patients with an anticipated longer life expectancy. Patients with appropriate anatomy for FEVAR and who are at higher risk for open repair would benefit from FEVAR. As further experience and outcomes are accumulated, our ability to select the appropriate therapy for individual patients should improve.
Dr. Weaver is an assistant clinical professor for surgery at Wayne State School of Medicine, Detroit, and an attending in the division of vascular surgery, Henry Ford Hospital.
References
1. Ir J Med Sci. 2015;184(1):249-55.
2. Circulation. 2011;123(24):2848-55.
3. J Endovasc Therapy. 2001;8(5):457-64.
4. Eur J Vasc Endovasc Surg. 2009;38(1):35-41.
5. Ann Vasc Surg. 2013;27(3):267-73.
6. J Vasc Surg. 2015;61(1):242-55.
7. J Vasc Surg. 2012;56(1):2-7.
8. J Cardiovasc Surg. 2015;56(3):331-7.
9. Eur J Vasc Endovasc Surg. 2015;50(2):189-96.
FEVAR is generally the best option
The advent of endovascular aortic aneurysm repair (EVAR) has steadily become the standard of care in the management of infrarenal abdominal aortic aneurysms (AAAs). In fact, it has now surpassed open surgical repair and is the predominant therapeutic modality in managing this disease entity. Clearly, there are specific anatomic and technical factors that may preclude the use of traditional EVAR – most notably, challenging proximal neck anatomy, be it insufficient length or severe angulation.
It is estimated that up to 30%-40% of patients are unsuitable candidates because of these concerns.1 Such patients are thus relegated to traditional open repair with the associated concerns for supravisceral clamping, including dramatic changes in hemodynamics and prolonged ICU and hospital stays.
Open surgical repair of pararenal, juxtarenal, and suprarenal AAAs is tried, tested, and durable. Knott and the group from Mayo Clinic reviewed their repair of 126 consecutive elective juxtarenal AAAs requiring suprarenal aortic clamping noting a 30-day mortality of .8%.2 More recent data from Kabbani and the Henry Ford group involved their 27-year clinical experience suggesting that open repair of complex proximal aortic aneurysms can be performed with clinical outcomes that are similar to those of open infrarenal repair.3 I respectfully accept this traditional – and historic – treatment modality.
However, we vascular surgeons are progressive and resilient in our quest to innovate and modernize – some of us even modified the traditional endografts on the back table. We charged forward despite the initial paucity of data on infrarenal EVAR compared to traditional open repair of aneurysms in the past. Now, a large percentage of infrarenal AAA repairs are performed via EVAR. In fact, our steadfast progression to advanced endovascular techniques has raised the concern that our graduating trainees are no longer proficient, competent, or even capable, in open complex aneurysm repair!
Tsilimparis and colleagues reported the first outcomes comparing open repair and FEVAR.4 They queried the NSQIP database comparing 1,091 patients undergoing open repair with 264 in the FEVAR group. There was an increased risk of morbidity in all combined endpoints including pulmonary and cardiovascular complications as well as length of stay in patients undergoing the open repair group. A larger comprehensive review pooled the results from 8 FEVAR and 12 open repair series. Analysis of the data found the groups to be identical. Open repair, however, was found to have an increased 30-day mortality when compared to FEVAR (relative risk 1.03, 2% increased absolute mortality).5
Gupta and colleagues reported the latest multi-institutional data noting that open repair was associated with higher risk than FEVAR for 30-day mortality, cardiac and pulmonary complications, renal failure requiring dialysis, return to the operating room, and in this age of cost-containment, length of stay (2 days vs. 7 days; P less than .0001).6
A further study by Donas and colleagues evaluated 90 consecutive patients with primary degenerative juxtarenal AAAs to different operative strategies based on morphologic and clinical characteristics – 29 FEVAR, 30 chEVAR, and 31 open repair.7 Early procedure-related and all-cause 30-day mortality was 0% in the endovascular group and 6.4% in the open group.
Although open repair for juxtarenal AAAs is the gold standard, short- and mid-term data on the outcomes for complex endovascular repair are excellent. Data on long-term durability, graft fixation/migration as well as the integrity of the graft and concerns for endoleaks and branch vessel patency, however, are limited. We do not have long-term data because we have not been doing these newer procedures for that long – but the data thus far show great promise.
We need to continue to challenge the status quo, particularly when the current data are satisfactory and the procedure feasible. With our continued appraisal of the data we publish as vascular surgeons, we can then identify if these innovations and techniques will withstand the test of time. After all, we are vascular surgeons (particularly those of us who have trained extensively in open repair) – and if open repair is necessary, then we will be ready.
But, if I can avoid a thoracoabdominal incision for a few percutaneous access sites, then sign me up!
Dr. Mouawad is chief of vascular and endovascular surgery, medical director of the vascular laboratory, and vice-chair of the department of surgery at McLaren Bay Region, Bay City, Mich. He is assistant professor of surgery at Michigan State University and Central Michigan University.
References
1. Perspect Vasc Surg Endovasc Ther. 2009;21:13-8.
2. J Vasc Surg. 2008;47:695-701.
3. J Vasc Surg. 2014;59:1488-94.
4. Ann Vasc Surg. 2013;27(3):267-73.
5. Eur J Vasc Endovasc Surg. 2009;38(1):35-41.
6. J Vasc Surg. 2017 Dec;66(6):1653-8.
7. J Vasc Surg. 2012 Aug;56(2):285-90.
FEVAR may not be the best choice
Over the past 3 decades, EVAR, with its very low periprocedural morbidity and mortality, and satisfactory long-term results, has become the primary treatment modality for the majority of infrarenal AAAs. The success of stent grafts for the repair of AAA relies heavily on satisfactory proximal and distal seal zones. Each commercially available standard EVAR graft has a manufacturer’s instructions for use requiring a proximal landing zone length of between 10 and 15 mm. Patients with less than this required length are considered to have “short necks.” Evaluation of this group of patients has demonstrated that this is not an uncommon finding and that EVAR performed outside the instructions for use has been associated with an increased risk of intraoperative failure, aneurysm expansion, and later complications.1-3
Current treatment options for patients with short necks include open surgical repair (OSR), FEVAR, and EVAR with the chimney graft technique (Ch-EVAR).
Thus, current knowledge acquired from case series, registries, and clinical experience must be used in deciding which therapeutic option to offer patients. Relevant factors influencing this decision include the availability and adaptability of the technique, early outcomes including technical success, morbidity and mortality, and late outcomes including survival, need for reintervention, and other late morbidity. Finally, in an era of value-based medical care, cost also must be considered.
Currently there is only one Food and Drug Administration–approved fenestrated graft. When used in properly selected patients, excellent periprocedural results have been reported approaching those of standard EVAR. However, there are limitations in both the availability and adaptability of FEVAR. These grafts are custom made for each patient, often requiring several weeks of lead time. Adaptability also has its limitations, including access vessels, severe neck angulation, calcification, mural thrombus, and branch vessel size, number, location, and associated arterial disease. Any of these factors may preclude the use of this technology. Open repair, on the other hand, is not limited by graft availability and allows for custom modification for each patient’s specific disease morphology. The essential limitation for open repair is the patient’s physiological ability to withstand the operation.
Several studies attempting to compare the early outcomes of FEVAR versus comparable patients undergoing OSR of similar aneurysms have reported significantly lower 30-day mortality and major morbidity rates for FEVAR.4,5 However, Rao et al., in a recent systematic review and meta-analysis that included data on 2,326 patients from 35 case series reporting on elective repair of juxtarenal aneurysms by either OSR or FEVAR, found perioperative mortality to not be significantly different (4.1% for both). Also, no significant difference was found between the two groups when evaluating postoperative renal insufficiency and need for permanent dialysis. However, OSR did have significantly higher major complication rates (25% vs. 15.7%).6 These findings suggest that both modalities can be performed successfully, but that long term outcomes need to be considered to determine if the increased initial morbidity of OSR is justified by differences in long term results between the two modalities.
Open surgical repair of juxtarenal AAA has been shown to be a durable repair.7 While early and even intermediate results of FEVAR appear to be satisfactory, long-term durability has yet to be determined.4,8 Along with continuing to exclude the aneurysm sac, as with standard EVAR, there is the additional concern regarding the outcome of the organs supplied by the fenestrated/stent-grafted branches with FEVAR. Longer-term follow-up in the same review by Rao et al. showed that significantly more FEVAR patients developed renal failure compared with OSR patients (19.7% vs. 7.7%). FEVAR patients also had a higher rate of reintervention.
And finally, long-term survival was significantly greater in OSR patients compared to FEVAR at 3 and 5 years (80% vs. 74% vs. 73% vs. 55%). These authors concluded that open repair remains the gold standard while FEVAR is a favorable option for high risk patients.6
These new and innovative stent graft devices come at considerable expense. While this aspect of FEVAR has not been extensively studied, Michel et al., in their report from the multicenter prospective Windows registry, attempted to evaluate the economic aspect of FEVAR. They compared a group of patients who underwent FEVAR to patients from a large national hospital discharge database who underwent OSR. No difference in 30-day mortality was noted between these two groups; however, there was a significantly greater cost with FEVAR. The authors concluded that FEVAR did not appear to be justified for patients fit for open surgery with juxtarenal AAA.9
For now, the roles of OSR and FEVAR would appear to be complementary. Current evidence suggests that OSR is the most appropriate intervention for good risk patients with an anticipated longer life expectancy. Patients with appropriate anatomy for FEVAR and who are at higher risk for open repair would benefit from FEVAR. As further experience and outcomes are accumulated, our ability to select the appropriate therapy for individual patients should improve.
Dr. Weaver is an assistant clinical professor for surgery at Wayne State School of Medicine, Detroit, and an attending in the division of vascular surgery, Henry Ford Hospital.
References
1. Ir J Med Sci. 2015;184(1):249-55.
2. Circulation. 2011;123(24):2848-55.
3. J Endovasc Therapy. 2001;8(5):457-64.
4. Eur J Vasc Endovasc Surg. 2009;38(1):35-41.
5. Ann Vasc Surg. 2013;27(3):267-73.
6. J Vasc Surg. 2015;61(1):242-55.
7. J Vasc Surg. 2012;56(1):2-7.
8. J Cardiovasc Surg. 2015;56(3):331-7.
9. Eur J Vasc Endovasc Surg. 2015;50(2):189-96.
Should carotid body tumors be embolized preoperatively?
Preop embolization is safe and effective
To embolize or not to embolize ... that is the question when it comes to the management of carotid body tumors. Carotid body tumors (CBTs) are rare benign neoplasms that are almost always nonfunctional and account for up to 80% of all head and neck paragangliomas. Radiographic characteristics include tumor location at the carotid bifurcation, splaying apart the internal and external carotid arteries. Surgical resection is the mainstay of definitive treatment and is preferably performed at diagnosis. CBTs are categorized based upon their involvement with surrounding structures: Shamblin I tumors are small, without encasement of the carotid arteries; Shamblin II tumors partially encase the vessels; and Shamblin III tumors completely encase the vessels. When it comes to operative complications, advanced Shamblin stage is associated with a higher rate of cranial nerve injury when the tumor is resected.1
Pertinent to the technical aspects of surgical resection, CBTs are characteristically encased with an elaborate network of friable vessels which may contribute to significant intraoperative bleeding, especially with resection of larger tumors. The blood supply to CBTs typically originates from the branches of the external carotid artery. These branches may be sacrificed with minimal consequence using preoperative embolization. This common practice is felt by many to facilitate safe resection while minimizing intraoperative blood loss. Although the reduction of blood loss has not been observed universally, there is enough evidence of this in the literature to support the use of selective preoperative embolization. Several embolic agents have been described in this setting, including polyvinyl alcohol particles (150-1000 microns), polymerized glue (n-butyl cyanoacrylate), and more recently, ethylene-vinyl alcohol copolymer (Onyx, ev3, Irvine, Calif.). Risks of complications related to CBT embolization in experienced hands are quite low with no adverse events reported in a number of reports describing the technique.2,3
Although embolization is argued to decrease blood loss, its impact on rates of neurologic complications is admittedly insignificant. One might question the added cost of the embolization procedure in the current atmosphere of focus on cost-containment, but this may be defrayed by lower rates of postoperative hematoma and operative times. Although blood loss has been shown to be decreased in a number of reports, translating this to decreased need for transfusion has unfortunately yet to be demonstrated. Until large-volume prospective randomized studies of the outcomes associated with preoperative embolization of CBTs are available, its use should be considered mainly when risks of blood loss are significant in advanced stage tumors and only if the associated complication risks associated with its use can be kept to acceptably low rates. As with other adjunctive procedures whose merit has not yet been convincingly sorted out in the available data, personal experience and preference often play a role in the decision making process we all face. For those who have experienced the added challenge of the meticulous dissection of the CBT in the face of a bloodied field, having such tools as embolization at our fingertips is a reassuring adjunct to be considered.
References
1. J Vasc Surg. 2013;57:64-8S.
2. J Vasc Interv Neurol. 2008;1(2):37-41.
3. Am J Neuroradiol. 2009;30:1594-97.
4. J Vasc Surg. 2012;56:979-89.
5. Vasc Endovasc Surg. 2009;43:457-61.
Too many downsides
As vascular surgeons, we are frequently confronting situations where the “best” approach to a problem is far from established. The evidence to make a clinical decision may simply not exist, and we need to choose a course of therapy based more on personal preference than science. Such is the case with preoperative embolization for the resection of carotid body tumors (CBT).
It has been over 35 years since the technique for preoperative embolization of CBT was described, the aim being reduction in blood loss, decreased operative time, and improved visualization for safer tumor resection. This is based on the fact that most of the arterial supply to these tumors arises from external carotid branches (particularly the ascending pharyngeal), and these that can be safely sacrificed. Although this technique is certainly now a standard part of treatment for many vascular surgeons, the evidence of benefit is certainly not overwhelming, and like all interventions, nothing comes without risks.
So what are the downsides of preoperative embolization? The cost of the procedure itself is not insignificant, in some cases doubling the expense of the intervention. And there can also be organizational issues with coordinating the time in the endovascular suite versus the operating room. In my experience, we have taken patients directly from embolization for the CBT resection, and there are frequently delays and transport issues. Although advocates may claim decreased operative time as a benefit of embolization, this is attained at an overall increase in anesthetic time for the combined procedures. If a day or two separates the procedures, some patients do report the pain or fevers that can accompany any tumor embolization.
While the above may be nuisances, there are serious adverse effects from preoperative embolization as well. A review of 11 studies of preoperative embolization for CBT found a 2.5% rate of complications, including temporary aphasia, vocal cord paralysis, and arterial dissection. Stroke with permanent deficit has also been reported secondary to CBT embolization. Access site hematoma has also been reported as with any catheter-based intervention.
With regards to “selective” preoperative embolization, the literature again offers a mixed bag. Many advocates of embolization rely upon the Shamblin classification for selecting candidates, reserving embolization for Shamblin II and III tumors. However, the extent of carotid involvement is sometimes a surgical diagnosis. Although size of tumor generally correlates with Shamblin class, even smaller tumors can demonstrate arterial wall involvement. Abu-Ghanem provides a succinct review of the uncertainty regarding size, Shamblin class, and the impact these have on cranial nerve injury.2 The bottom line is that there is no data-based algorithm for deciding whom to select for preoperative embolization.
In the absence of compelling data for the use of preoperative embolization, this technique is difficult to recommend. There are undoubtedly cases with giant CBTs where a surgeon will want to take advantage of any preoperative adjuvant therapy that is available. However, for the vast majority of CBTs, the important principles are to stay in the correct plane, identify and protect the nerves at risk, and control the tumor blood supply in a systematic fashion. In the absence of a forthcoming randomized prospective study to evaluate preoperative embolization for CBT resection, I will rely on the wisdom of my mentor, Dr. Wesley Moore. He never utilized preoperative embolization for these cases. At least not that he will admit to me.
References
1. Surgery. 1980;87:459-464.
2. Head Neck. 2016;38:E2386-E2394.
3. J Vasc Surg. 2015;61:1081-91.
4. Otolaryngol Head Neck Surg. 2015;153:942-950.
Preop embolization is safe and effective
To embolize or not to embolize ... that is the question when it comes to the management of carotid body tumors. Carotid body tumors (CBTs) are rare benign neoplasms that are almost always nonfunctional and account for up to 80% of all head and neck paragangliomas. Radiographic characteristics include tumor location at the carotid bifurcation, splaying apart the internal and external carotid arteries. Surgical resection is the mainstay of definitive treatment and is preferably performed at diagnosis. CBTs are categorized based upon their involvement with surrounding structures: Shamblin I tumors are small, without encasement of the carotid arteries; Shamblin II tumors partially encase the vessels; and Shamblin III tumors completely encase the vessels. When it comes to operative complications, advanced Shamblin stage is associated with a higher rate of cranial nerve injury when the tumor is resected.1
Pertinent to the technical aspects of surgical resection, CBTs are characteristically encased with an elaborate network of friable vessels which may contribute to significant intraoperative bleeding, especially with resection of larger tumors. The blood supply to CBTs typically originates from the branches of the external carotid artery. These branches may be sacrificed with minimal consequence using preoperative embolization. This common practice is felt by many to facilitate safe resection while minimizing intraoperative blood loss. Although the reduction of blood loss has not been observed universally, there is enough evidence of this in the literature to support the use of selective preoperative embolization. Several embolic agents have been described in this setting, including polyvinyl alcohol particles (150-1000 microns), polymerized glue (n-butyl cyanoacrylate), and more recently, ethylene-vinyl alcohol copolymer (Onyx, ev3, Irvine, Calif.). Risks of complications related to CBT embolization in experienced hands are quite low with no adverse events reported in a number of reports describing the technique.2,3
Although embolization is argued to decrease blood loss, its impact on rates of neurologic complications is admittedly insignificant. One might question the added cost of the embolization procedure in the current atmosphere of focus on cost-containment, but this may be defrayed by lower rates of postoperative hematoma and operative times. Although blood loss has been shown to be decreased in a number of reports, translating this to decreased need for transfusion has unfortunately yet to be demonstrated. Until large-volume prospective randomized studies of the outcomes associated with preoperative embolization of CBTs are available, its use should be considered mainly when risks of blood loss are significant in advanced stage tumors and only if the associated complication risks associated with its use can be kept to acceptably low rates. As with other adjunctive procedures whose merit has not yet been convincingly sorted out in the available data, personal experience and preference often play a role in the decision making process we all face. For those who have experienced the added challenge of the meticulous dissection of the CBT in the face of a bloodied field, having such tools as embolization at our fingertips is a reassuring adjunct to be considered.
References
1. J Vasc Surg. 2013;57:64-8S.
2. J Vasc Interv Neurol. 2008;1(2):37-41.
3. Am J Neuroradiol. 2009;30:1594-97.
4. J Vasc Surg. 2012;56:979-89.
5. Vasc Endovasc Surg. 2009;43:457-61.
Too many downsides
As vascular surgeons, we are frequently confronting situations where the “best” approach to a problem is far from established. The evidence to make a clinical decision may simply not exist, and we need to choose a course of therapy based more on personal preference than science. Such is the case with preoperative embolization for the resection of carotid body tumors (CBT).
It has been over 35 years since the technique for preoperative embolization of CBT was described, the aim being reduction in blood loss, decreased operative time, and improved visualization for safer tumor resection. This is based on the fact that most of the arterial supply to these tumors arises from external carotid branches (particularly the ascending pharyngeal), and these that can be safely sacrificed. Although this technique is certainly now a standard part of treatment for many vascular surgeons, the evidence of benefit is certainly not overwhelming, and like all interventions, nothing comes without risks.
So what are the downsides of preoperative embolization? The cost of the procedure itself is not insignificant, in some cases doubling the expense of the intervention. And there can also be organizational issues with coordinating the time in the endovascular suite versus the operating room. In my experience, we have taken patients directly from embolization for the CBT resection, and there are frequently delays and transport issues. Although advocates may claim decreased operative time as a benefit of embolization, this is attained at an overall increase in anesthetic time for the combined procedures. If a day or two separates the procedures, some patients do report the pain or fevers that can accompany any tumor embolization.
While the above may be nuisances, there are serious adverse effects from preoperative embolization as well. A review of 11 studies of preoperative embolization for CBT found a 2.5% rate of complications, including temporary aphasia, vocal cord paralysis, and arterial dissection. Stroke with permanent deficit has also been reported secondary to CBT embolization. Access site hematoma has also been reported as with any catheter-based intervention.
With regards to “selective” preoperative embolization, the literature again offers a mixed bag. Many advocates of embolization rely upon the Shamblin classification for selecting candidates, reserving embolization for Shamblin II and III tumors. However, the extent of carotid involvement is sometimes a surgical diagnosis. Although size of tumor generally correlates with Shamblin class, even smaller tumors can demonstrate arterial wall involvement. Abu-Ghanem provides a succinct review of the uncertainty regarding size, Shamblin class, and the impact these have on cranial nerve injury.2 The bottom line is that there is no data-based algorithm for deciding whom to select for preoperative embolization.
In the absence of compelling data for the use of preoperative embolization, this technique is difficult to recommend. There are undoubtedly cases with giant CBTs where a surgeon will want to take advantage of any preoperative adjuvant therapy that is available. However, for the vast majority of CBTs, the important principles are to stay in the correct plane, identify and protect the nerves at risk, and control the tumor blood supply in a systematic fashion. In the absence of a forthcoming randomized prospective study to evaluate preoperative embolization for CBT resection, I will rely on the wisdom of my mentor, Dr. Wesley Moore. He never utilized preoperative embolization for these cases. At least not that he will admit to me.
References
1. Surgery. 1980;87:459-464.
2. Head Neck. 2016;38:E2386-E2394.
3. J Vasc Surg. 2015;61:1081-91.
4. Otolaryngol Head Neck Surg. 2015;153:942-950.
Preop embolization is safe and effective
To embolize or not to embolize ... that is the question when it comes to the management of carotid body tumors. Carotid body tumors (CBTs) are rare benign neoplasms that are almost always nonfunctional and account for up to 80% of all head and neck paragangliomas. Radiographic characteristics include tumor location at the carotid bifurcation, splaying apart the internal and external carotid arteries. Surgical resection is the mainstay of definitive treatment and is preferably performed at diagnosis. CBTs are categorized based upon their involvement with surrounding structures: Shamblin I tumors are small, without encasement of the carotid arteries; Shamblin II tumors partially encase the vessels; and Shamblin III tumors completely encase the vessels. When it comes to operative complications, advanced Shamblin stage is associated with a higher rate of cranial nerve injury when the tumor is resected.1
Pertinent to the technical aspects of surgical resection, CBTs are characteristically encased with an elaborate network of friable vessels which may contribute to significant intraoperative bleeding, especially with resection of larger tumors. The blood supply to CBTs typically originates from the branches of the external carotid artery. These branches may be sacrificed with minimal consequence using preoperative embolization. This common practice is felt by many to facilitate safe resection while minimizing intraoperative blood loss. Although the reduction of blood loss has not been observed universally, there is enough evidence of this in the literature to support the use of selective preoperative embolization. Several embolic agents have been described in this setting, including polyvinyl alcohol particles (150-1000 microns), polymerized glue (n-butyl cyanoacrylate), and more recently, ethylene-vinyl alcohol copolymer (Onyx, ev3, Irvine, Calif.). Risks of complications related to CBT embolization in experienced hands are quite low with no adverse events reported in a number of reports describing the technique.2,3
Although embolization is argued to decrease blood loss, its impact on rates of neurologic complications is admittedly insignificant. One might question the added cost of the embolization procedure in the current atmosphere of focus on cost-containment, but this may be defrayed by lower rates of postoperative hematoma and operative times. Although blood loss has been shown to be decreased in a number of reports, translating this to decreased need for transfusion has unfortunately yet to be demonstrated. Until large-volume prospective randomized studies of the outcomes associated with preoperative embolization of CBTs are available, its use should be considered mainly when risks of blood loss are significant in advanced stage tumors and only if the associated complication risks associated with its use can be kept to acceptably low rates. As with other adjunctive procedures whose merit has not yet been convincingly sorted out in the available data, personal experience and preference often play a role in the decision making process we all face. For those who have experienced the added challenge of the meticulous dissection of the CBT in the face of a bloodied field, having such tools as embolization at our fingertips is a reassuring adjunct to be considered.
References
1. J Vasc Surg. 2013;57:64-8S.
2. J Vasc Interv Neurol. 2008;1(2):37-41.
3. Am J Neuroradiol. 2009;30:1594-97.
4. J Vasc Surg. 2012;56:979-89.
5. Vasc Endovasc Surg. 2009;43:457-61.
Too many downsides
As vascular surgeons, we are frequently confronting situations where the “best” approach to a problem is far from established. The evidence to make a clinical decision may simply not exist, and we need to choose a course of therapy based more on personal preference than science. Such is the case with preoperative embolization for the resection of carotid body tumors (CBT).
It has been over 35 years since the technique for preoperative embolization of CBT was described, the aim being reduction in blood loss, decreased operative time, and improved visualization for safer tumor resection. This is based on the fact that most of the arterial supply to these tumors arises from external carotid branches (particularly the ascending pharyngeal), and these that can be safely sacrificed. Although this technique is certainly now a standard part of treatment for many vascular surgeons, the evidence of benefit is certainly not overwhelming, and like all interventions, nothing comes without risks.
So what are the downsides of preoperative embolization? The cost of the procedure itself is not insignificant, in some cases doubling the expense of the intervention. And there can also be organizational issues with coordinating the time in the endovascular suite versus the operating room. In my experience, we have taken patients directly from embolization for the CBT resection, and there are frequently delays and transport issues. Although advocates may claim decreased operative time as a benefit of embolization, this is attained at an overall increase in anesthetic time for the combined procedures. If a day or two separates the procedures, some patients do report the pain or fevers that can accompany any tumor embolization.
While the above may be nuisances, there are serious adverse effects from preoperative embolization as well. A review of 11 studies of preoperative embolization for CBT found a 2.5% rate of complications, including temporary aphasia, vocal cord paralysis, and arterial dissection. Stroke with permanent deficit has also been reported secondary to CBT embolization. Access site hematoma has also been reported as with any catheter-based intervention.
With regards to “selective” preoperative embolization, the literature again offers a mixed bag. Many advocates of embolization rely upon the Shamblin classification for selecting candidates, reserving embolization for Shamblin II and III tumors. However, the extent of carotid involvement is sometimes a surgical diagnosis. Although size of tumor generally correlates with Shamblin class, even smaller tumors can demonstrate arterial wall involvement. Abu-Ghanem provides a succinct review of the uncertainty regarding size, Shamblin class, and the impact these have on cranial nerve injury.2 The bottom line is that there is no data-based algorithm for deciding whom to select for preoperative embolization.
In the absence of compelling data for the use of preoperative embolization, this technique is difficult to recommend. There are undoubtedly cases with giant CBTs where a surgeon will want to take advantage of any preoperative adjuvant therapy that is available. However, for the vast majority of CBTs, the important principles are to stay in the correct plane, identify and protect the nerves at risk, and control the tumor blood supply in a systematic fashion. In the absence of a forthcoming randomized prospective study to evaluate preoperative embolization for CBT resection, I will rely on the wisdom of my mentor, Dr. Wesley Moore. He never utilized preoperative embolization for these cases. At least not that he will admit to me.
References
1. Surgery. 1980;87:459-464.
2. Head Neck. 2016;38:E2386-E2394.
3. J Vasc Surg. 2015;61:1081-91.
4. Otolaryngol Head Neck Surg. 2015;153:942-950.
Open vs. endo repair for ruptured AAA
Open repair should be offered to all patients with rAAA
With the advent of endovascular repair of abdominal aortic aneurysms (EVAR), the treatment of elective AAAs was revolutionized. Since ruptured abdominal aortic aneurysms (rAAAs) carry a higher morbidity and mortality than elective AAA repair the use of EVAR has been advocated for these patients.1 Dr. Aziz contends that EVAR should be utilized in all patients presenting with a rAAA. It is my contention that endovascular repair cannot replace open aneurysm repair in all situations. The best treatment option should be offered taking patient and institutional considerations into account. Forcing a given procedure and trying to “make it work” is not best for the patient.
In a systematic literature review of patients presenting with rAAAs, selection bias regarding treatment choice (EVAR vs. open repair) was found consistently.2 In an effort to show that EVAR is superior to open repair for rAAA, Hinchliffe et al. published a randomized trial that showed no difference in 30-day mortality (53%) in each treatment group.3 The AJAX trial randomized 116 patients and did not show benefit for EVAR with respect to 30-day morbidity or mortality.4 The ECAR trial randomized 107 patients and also failed to show a difference in mortality between EVAR and open techniques for rAAA.5
Determining suitability for EVAR includes assessing diameter of the neck of the aneurysm, angulation, size of iliac arteries, presence of atherosclerotic occlusive disease, presence of accessory renal arteries, and presence of concurrent aneurysms of the iliac arteries.7,8 In the IMPROVE trial, patients were randomized depending on anatomic suitability for EVAR.9 Anatomy was determined by imaging in those patients stable enough to undergo preoperative computed tomography angiogram (CTA). Therefore, given anatomic differences, patients presenting with rAAA were not randomized without significant treatment bias.
A true pararenal or paravisceral rupture certainly elevates the complexity of the case. Open repair can deal with this difficult challenge by adapting additional established techniques to the situation. Although some authors have advocated EVAR for rAAA using snorkels and chimneys, these techniques may not be appropriate in the treatment of rAAA in most institutions.10 These procedures take longer, require considerable experience and resources and are therefore not appropriate in unstable patients. No randomized control trial exists at this time to address superiority of EVAR to open repair in patients with complex anatomy.
Patients presenting with rAAA that have had prior endovascular intervention also pose complex anatomic and technical challenges.11 These patients can present with hemodynamic instability and rupture but now are complicated by having device failure. Salvage using endovascular means may not be possible. The risk of re-intervention with endovascular repair for rAAA is much higher than with open repair.12
Emergency vascular surgery is best approached with protocols and systems in place no matter what approach is chosen.13 Skilled staff in the emergency department and in the operating room must be available without delay especially for rAAA, as time is of the essence. Skilled surgeons, skilled operating room staff, knowledgeable anesthesia staff are necessary to quickly move a patient from the emergency department to the operating room for definitive treatment. Other ancillary services, such as blood banks and laboratories are necessary to assist in the care for the patient intraoperatively. In endovascular surgery, trained technologists, fluoroscopy, a full armamentarium of interventional equipment (wires, balloons, stents, etc.), and a full stock of stent grafts and associated ancillary equipment are mandatory. Many hospitals may not have the variety of stent grafts available for emergency use. Regionalization of care has been suggested to improve outcomes in the treatment of rAAAs.14 In a study by Warner et al., mortality was decreased by 20% at the tertiary center compared to the smaller community hospitals in both EVAR and open repairs for rAAA. Zettervall et al. published data that showed that significant regional variation exists in perioperative outcomes and length of stay, and mortality in repair for rAAA approached with open or endovascular means.15 Low volume centers have worse outcomes, and teaching hospitals may have better outcomes treating AAA.16
EVAR is also reported to be associated with a 27-36% higher cost of care than open surgery for rAAA.17 Many institutions may not have the means to provide the resources needed to support such a program.
There is no question that EVAR has greatly impacted the treatment of aortic aneurysms. However, not every aneurysm is appropriate for endovascular repair at this time. For the many reasons cited, we cannot permit open repair to become an extinct skill. Vascular training programs must include open repair of rAAA just as it should for other vascular conditions.
I would agree with Dr. Aziz that we do not yet have a prospective, randomized study and Level 1 evidence to support either view and given the complexity and urgency associated with these patients, such a study may not be forthcoming. Till then, patients with a RAAA should have ‘all of the above’ approach including open surgery depending on the institutional experience and resources and urgency of the situation.
References
1. J Vasc Surg 2016; 2:297-305
2. J Vasc Surg 2009; 49:1077-1080.
3. Eur J Vasc Endovasc Surg 2006; 32:506-513
4. Ann Surg 2013. Aug 258 (2) 248-56
5. J Vasc Surg 2010; 51:267-70
6. Ann Vasc Surg 2017; 38:59-63
7. J Vasc Surg 2009: 50:243-50
8. J Endovasc Ther 2016; 23: 919-927
9. BJM 2014; 101:216-224
10. Radiographics 2015; 35:593-615.
11. Ann Vasc Surg 2013; 27:844-50
12. J Vasc Surg 2017; 65:52-57
13. Semin Vasc Surg 2016; 29:35-40
14. J Vasc Surg 2014; 59:1512-7
15. Ann Surg 2017; 264:538-43
16. J Vasc Surg 2016; 22 pii W0741-5214 (16) 31247-2
17. J Vasc Surg 2008; 47:1165-70
Dr. Ozsvatrh is a professor of surgery at Albany Medical College, Albany, N.Y., and a vascular attending, at Albany Medical Center Hospital, Albany, and chief, department of surgery, Samaritan Hospital, Troy, N.Y.
EVAR should be offered to all patients with rAAA
Since the inception of EVAR two decades ago, it has largely replaced open abdominal aortic aneurysm repair as the operation of choice for elective treatment of abdominal aortic aneurysms. Shorter duration of operation, avoiding general anesthesia and aortic cross clamping, ability to obtain balloon control of aorta, fast recovery time and reduced hospital length of hospital stay are among the most commonly cited reasons for this change in paradigm for treatment of abdominal aortic aneurysms. Since vascular surgeons have adopted the widespread use of EVAR, the total number of aneurysm related deaths has significantly reduced.1 While EVAR has become the most commonly used operation to treat AAAs electively, it’s utility to treat ruptured AAAs has been questioned. Recent analysis of nationwide trends for the operations for the diagnosis of ruptured AAA show that almost half of the patients with ruptured AAA are still treated with open surgical repair.2
Opponents of REVAR (EVAR for rAAA) cite comparable outcomes of open surgery and REVAR in randomized controlled trials, requirement of a specific REVAR protocol, increased cost and lack of resources and more importantly, lack of level I evidence to support it’s use in all cases of rAAA.
It is no surprise that REVAR is associated with significantly lower perioperative mortality (24%) as compared to open repair of ruptured AAA (44%).3 Mortality after open repair of ruptured AAA can vary anywhere from 30-70%.4,5 Improved mortality rates after REVAR are not only limited to stable patients, but also extend to those patients with ruptured AAA who are considered hemodynamically unstable at the time of initial presentation.6
The survival advantage among REVAR patients is not only evident in short term (30-days), but it also extends up to 5 years after the operation.3 Patients undergoing REVAR are less likely to require intra-operative blood transfusions, as compared to patients who undergo open repair of rAAA.7 Development of acute renal failure after surgical treatment of rAAAs is associated with significant mortality and REVAR has been associated with significantly lower incidence of acute renal failure as compared to open repair of ruptured AAA.2
Due to inherent issues of patient instability, emergent presentation and inequality among hospital resources and patient volumes, it is difficult to design a flawless, randomized controlled trial to compare REVAR with open surgical repair. The results from published randomized controlled trials on this topic should be interpreted with caution. The Nottingham trial from the United Kingdom8 showed similar mortality (53%) between REVAR and open surgical operation, however, out of the 203 patients enrolled in the trial, 70% were not randomized and REVAR was offered to only 15 patients. Likewise, the AJAX Trial from Netherlands9 showed that there was no significant difference in mortality between the two treatment groups (42% with REVAR and 47% with open repair), however almost 80% of enrolled patients were not randomized and there was a disagreement between the interpreters about CTA diagnosis of rAAA. In addition, the conversion rates from REVAR to open repair were unexpectedly high (14%), pointing to the surgeons’ inexperience.
Similarly, the IMPROVE trial from United Kingdom10 suffered from poor rates of randomization (50% of enrolled patients) and poor methodology (obtaining CTA after randomization, and making requirement of CTA optional for patients allocated to open surgery group). The trial showed equivalent mortality rates between the two surgical groups (35% with REVAR and 37% with open repair).
Due to flawed methodology and poor rates of randomization, results of these trials do not provide us with level I evidence, which is required to make any scientific recommendations about the treatment of choice for the treatment of rAAAs. Hence, the large body of evidence, obtained from retrospective studies should be used while comparing the outcomes of operations for ruptured AAAs. So far, all retrospective analyses, comparing REVAR with open repair in national registries, such as National Inpatient Sample (NIS) database11,12 American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database7 and Medicare database13 have clearly shown that the outcomes of REVAR are better than open surgical repair of ruptured AAA. Likewise, multi-center observational studies14,15 have demonstrated superiority of REVAR over open surgical repair.
To summarize, REVAR is a safe procedure, can be performed under local anesthetic, has shorter operative time and is associated with improved outcomes as compared to open surgery. REVAR should be the treatment of choice for all patients who meet the anatomic criteria for endovascular repair. With increasing experience of vascular surgeons with the endovascular technology, it is foreseeable that REVAR will soon become the treatment of choice for ruptured abdominal aortic aneurysms.
References
1. J Vasc Surg 2009;49:543-50; discussion 50-1.
2. Ann Vasc Surg 2016;35:147-55.
3. J Vasc Surg 2013;57:368-75.
4. J Vasc Surg 2001;34:41-6.
5. J Vasc Surg 1991;13:240-5; discussion 5-7.
6. J Vasc Surg 2014;60:1439-45.
7. J Vasc Surg 2010;51:305-9 e1.
8. Eur J Vasc Endovasc Surg 2006;32:506-13; discussion 14-5.
9. Ann Surg 2013;258:248-56.
10. BMJ 2014;348:f7661.
11. J Vasc Surg 2009;49:817-26.
12. J Vasc Surg 2008;47:1165-70; discussion 70-1.
13. J Vasc Surg 2014;59:575-82.
14. Ann Surg 2012;256:688-95; discussion 95-6.
15. Ann Surg 2009;250:818-24.
Dr. Aziz is in the division of vascular surgery, Penn State Heart and Vascular Institute, Pennsylvania State University College of Medicine, Hershey, Penn.
Open repair should be offered to all patients with rAAA
With the advent of endovascular repair of abdominal aortic aneurysms (EVAR), the treatment of elective AAAs was revolutionized. Since ruptured abdominal aortic aneurysms (rAAAs) carry a higher morbidity and mortality than elective AAA repair the use of EVAR has been advocated for these patients.1 Dr. Aziz contends that EVAR should be utilized in all patients presenting with a rAAA. It is my contention that endovascular repair cannot replace open aneurysm repair in all situations. The best treatment option should be offered taking patient and institutional considerations into account. Forcing a given procedure and trying to “make it work” is not best for the patient.
In a systematic literature review of patients presenting with rAAAs, selection bias regarding treatment choice (EVAR vs. open repair) was found consistently.2 In an effort to show that EVAR is superior to open repair for rAAA, Hinchliffe et al. published a randomized trial that showed no difference in 30-day mortality (53%) in each treatment group.3 The AJAX trial randomized 116 patients and did not show benefit for EVAR with respect to 30-day morbidity or mortality.4 The ECAR trial randomized 107 patients and also failed to show a difference in mortality between EVAR and open techniques for rAAA.5
Determining suitability for EVAR includes assessing diameter of the neck of the aneurysm, angulation, size of iliac arteries, presence of atherosclerotic occlusive disease, presence of accessory renal arteries, and presence of concurrent aneurysms of the iliac arteries.7,8 In the IMPROVE trial, patients were randomized depending on anatomic suitability for EVAR.9 Anatomy was determined by imaging in those patients stable enough to undergo preoperative computed tomography angiogram (CTA). Therefore, given anatomic differences, patients presenting with rAAA were not randomized without significant treatment bias.
A true pararenal or paravisceral rupture certainly elevates the complexity of the case. Open repair can deal with this difficult challenge by adapting additional established techniques to the situation. Although some authors have advocated EVAR for rAAA using snorkels and chimneys, these techniques may not be appropriate in the treatment of rAAA in most institutions.10 These procedures take longer, require considerable experience and resources and are therefore not appropriate in unstable patients. No randomized control trial exists at this time to address superiority of EVAR to open repair in patients with complex anatomy.
Patients presenting with rAAA that have had prior endovascular intervention also pose complex anatomic and technical challenges.11 These patients can present with hemodynamic instability and rupture but now are complicated by having device failure. Salvage using endovascular means may not be possible. The risk of re-intervention with endovascular repair for rAAA is much higher than with open repair.12
Emergency vascular surgery is best approached with protocols and systems in place no matter what approach is chosen.13 Skilled staff in the emergency department and in the operating room must be available without delay especially for rAAA, as time is of the essence. Skilled surgeons, skilled operating room staff, knowledgeable anesthesia staff are necessary to quickly move a patient from the emergency department to the operating room for definitive treatment. Other ancillary services, such as blood banks and laboratories are necessary to assist in the care for the patient intraoperatively. In endovascular surgery, trained technologists, fluoroscopy, a full armamentarium of interventional equipment (wires, balloons, stents, etc.), and a full stock of stent grafts and associated ancillary equipment are mandatory. Many hospitals may not have the variety of stent grafts available for emergency use. Regionalization of care has been suggested to improve outcomes in the treatment of rAAAs.14 In a study by Warner et al., mortality was decreased by 20% at the tertiary center compared to the smaller community hospitals in both EVAR and open repairs for rAAA. Zettervall et al. published data that showed that significant regional variation exists in perioperative outcomes and length of stay, and mortality in repair for rAAA approached with open or endovascular means.15 Low volume centers have worse outcomes, and teaching hospitals may have better outcomes treating AAA.16
EVAR is also reported to be associated with a 27-36% higher cost of care than open surgery for rAAA.17 Many institutions may not have the means to provide the resources needed to support such a program.
There is no question that EVAR has greatly impacted the treatment of aortic aneurysms. However, not every aneurysm is appropriate for endovascular repair at this time. For the many reasons cited, we cannot permit open repair to become an extinct skill. Vascular training programs must include open repair of rAAA just as it should for other vascular conditions.
I would agree with Dr. Aziz that we do not yet have a prospective, randomized study and Level 1 evidence to support either view and given the complexity and urgency associated with these patients, such a study may not be forthcoming. Till then, patients with a RAAA should have ‘all of the above’ approach including open surgery depending on the institutional experience and resources and urgency of the situation.
References
1. J Vasc Surg 2016; 2:297-305
2. J Vasc Surg 2009; 49:1077-1080.
3. Eur J Vasc Endovasc Surg 2006; 32:506-513
4. Ann Surg 2013. Aug 258 (2) 248-56
5. J Vasc Surg 2010; 51:267-70
6. Ann Vasc Surg 2017; 38:59-63
7. J Vasc Surg 2009: 50:243-50
8. J Endovasc Ther 2016; 23: 919-927
9. BJM 2014; 101:216-224
10. Radiographics 2015; 35:593-615.
11. Ann Vasc Surg 2013; 27:844-50
12. J Vasc Surg 2017; 65:52-57
13. Semin Vasc Surg 2016; 29:35-40
14. J Vasc Surg 2014; 59:1512-7
15. Ann Surg 2017; 264:538-43
16. J Vasc Surg 2016; 22 pii W0741-5214 (16) 31247-2
17. J Vasc Surg 2008; 47:1165-70
Dr. Ozsvatrh is a professor of surgery at Albany Medical College, Albany, N.Y., and a vascular attending, at Albany Medical Center Hospital, Albany, and chief, department of surgery, Samaritan Hospital, Troy, N.Y.
EVAR should be offered to all patients with rAAA
Since the inception of EVAR two decades ago, it has largely replaced open abdominal aortic aneurysm repair as the operation of choice for elective treatment of abdominal aortic aneurysms. Shorter duration of operation, avoiding general anesthesia and aortic cross clamping, ability to obtain balloon control of aorta, fast recovery time and reduced hospital length of hospital stay are among the most commonly cited reasons for this change in paradigm for treatment of abdominal aortic aneurysms. Since vascular surgeons have adopted the widespread use of EVAR, the total number of aneurysm related deaths has significantly reduced.1 While EVAR has become the most commonly used operation to treat AAAs electively, it’s utility to treat ruptured AAAs has been questioned. Recent analysis of nationwide trends for the operations for the diagnosis of ruptured AAA show that almost half of the patients with ruptured AAA are still treated with open surgical repair.2
Opponents of REVAR (EVAR for rAAA) cite comparable outcomes of open surgery and REVAR in randomized controlled trials, requirement of a specific REVAR protocol, increased cost and lack of resources and more importantly, lack of level I evidence to support it’s use in all cases of rAAA.
It is no surprise that REVAR is associated with significantly lower perioperative mortality (24%) as compared to open repair of ruptured AAA (44%).3 Mortality after open repair of ruptured AAA can vary anywhere from 30-70%.4,5 Improved mortality rates after REVAR are not only limited to stable patients, but also extend to those patients with ruptured AAA who are considered hemodynamically unstable at the time of initial presentation.6
The survival advantage among REVAR patients is not only evident in short term (30-days), but it also extends up to 5 years after the operation.3 Patients undergoing REVAR are less likely to require intra-operative blood transfusions, as compared to patients who undergo open repair of rAAA.7 Development of acute renal failure after surgical treatment of rAAAs is associated with significant mortality and REVAR has been associated with significantly lower incidence of acute renal failure as compared to open repair of ruptured AAA.2
Due to inherent issues of patient instability, emergent presentation and inequality among hospital resources and patient volumes, it is difficult to design a flawless, randomized controlled trial to compare REVAR with open surgical repair. The results from published randomized controlled trials on this topic should be interpreted with caution. The Nottingham trial from the United Kingdom8 showed similar mortality (53%) between REVAR and open surgical operation, however, out of the 203 patients enrolled in the trial, 70% were not randomized and REVAR was offered to only 15 patients. Likewise, the AJAX Trial from Netherlands9 showed that there was no significant difference in mortality between the two treatment groups (42% with REVAR and 47% with open repair), however almost 80% of enrolled patients were not randomized and there was a disagreement between the interpreters about CTA diagnosis of rAAA. In addition, the conversion rates from REVAR to open repair were unexpectedly high (14%), pointing to the surgeons’ inexperience.
Similarly, the IMPROVE trial from United Kingdom10 suffered from poor rates of randomization (50% of enrolled patients) and poor methodology (obtaining CTA after randomization, and making requirement of CTA optional for patients allocated to open surgery group). The trial showed equivalent mortality rates between the two surgical groups (35% with REVAR and 37% with open repair).
Due to flawed methodology and poor rates of randomization, results of these trials do not provide us with level I evidence, which is required to make any scientific recommendations about the treatment of choice for the treatment of rAAAs. Hence, the large body of evidence, obtained from retrospective studies should be used while comparing the outcomes of operations for ruptured AAAs. So far, all retrospective analyses, comparing REVAR with open repair in national registries, such as National Inpatient Sample (NIS) database11,12 American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database7 and Medicare database13 have clearly shown that the outcomes of REVAR are better than open surgical repair of ruptured AAA. Likewise, multi-center observational studies14,15 have demonstrated superiority of REVAR over open surgical repair.
To summarize, REVAR is a safe procedure, can be performed under local anesthetic, has shorter operative time and is associated with improved outcomes as compared to open surgery. REVAR should be the treatment of choice for all patients who meet the anatomic criteria for endovascular repair. With increasing experience of vascular surgeons with the endovascular technology, it is foreseeable that REVAR will soon become the treatment of choice for ruptured abdominal aortic aneurysms.
References
1. J Vasc Surg 2009;49:543-50; discussion 50-1.
2. Ann Vasc Surg 2016;35:147-55.
3. J Vasc Surg 2013;57:368-75.
4. J Vasc Surg 2001;34:41-6.
5. J Vasc Surg 1991;13:240-5; discussion 5-7.
6. J Vasc Surg 2014;60:1439-45.
7. J Vasc Surg 2010;51:305-9 e1.
8. Eur J Vasc Endovasc Surg 2006;32:506-13; discussion 14-5.
9. Ann Surg 2013;258:248-56.
10. BMJ 2014;348:f7661.
11. J Vasc Surg 2009;49:817-26.
12. J Vasc Surg 2008;47:1165-70; discussion 70-1.
13. J Vasc Surg 2014;59:575-82.
14. Ann Surg 2012;256:688-95; discussion 95-6.
15. Ann Surg 2009;250:818-24.
Dr. Aziz is in the division of vascular surgery, Penn State Heart and Vascular Institute, Pennsylvania State University College of Medicine, Hershey, Penn.
Open repair should be offered to all patients with rAAA
With the advent of endovascular repair of abdominal aortic aneurysms (EVAR), the treatment of elective AAAs was revolutionized. Since ruptured abdominal aortic aneurysms (rAAAs) carry a higher morbidity and mortality than elective AAA repair the use of EVAR has been advocated for these patients.1 Dr. Aziz contends that EVAR should be utilized in all patients presenting with a rAAA. It is my contention that endovascular repair cannot replace open aneurysm repair in all situations. The best treatment option should be offered taking patient and institutional considerations into account. Forcing a given procedure and trying to “make it work” is not best for the patient.
In a systematic literature review of patients presenting with rAAAs, selection bias regarding treatment choice (EVAR vs. open repair) was found consistently.2 In an effort to show that EVAR is superior to open repair for rAAA, Hinchliffe et al. published a randomized trial that showed no difference in 30-day mortality (53%) in each treatment group.3 The AJAX trial randomized 116 patients and did not show benefit for EVAR with respect to 30-day morbidity or mortality.4 The ECAR trial randomized 107 patients and also failed to show a difference in mortality between EVAR and open techniques for rAAA.5
Determining suitability for EVAR includes assessing diameter of the neck of the aneurysm, angulation, size of iliac arteries, presence of atherosclerotic occlusive disease, presence of accessory renal arteries, and presence of concurrent aneurysms of the iliac arteries.7,8 In the IMPROVE trial, patients were randomized depending on anatomic suitability for EVAR.9 Anatomy was determined by imaging in those patients stable enough to undergo preoperative computed tomography angiogram (CTA). Therefore, given anatomic differences, patients presenting with rAAA were not randomized without significant treatment bias.
A true pararenal or paravisceral rupture certainly elevates the complexity of the case. Open repair can deal with this difficult challenge by adapting additional established techniques to the situation. Although some authors have advocated EVAR for rAAA using snorkels and chimneys, these techniques may not be appropriate in the treatment of rAAA in most institutions.10 These procedures take longer, require considerable experience and resources and are therefore not appropriate in unstable patients. No randomized control trial exists at this time to address superiority of EVAR to open repair in patients with complex anatomy.
Patients presenting with rAAA that have had prior endovascular intervention also pose complex anatomic and technical challenges.11 These patients can present with hemodynamic instability and rupture but now are complicated by having device failure. Salvage using endovascular means may not be possible. The risk of re-intervention with endovascular repair for rAAA is much higher than with open repair.12
Emergency vascular surgery is best approached with protocols and systems in place no matter what approach is chosen.13 Skilled staff in the emergency department and in the operating room must be available without delay especially for rAAA, as time is of the essence. Skilled surgeons, skilled operating room staff, knowledgeable anesthesia staff are necessary to quickly move a patient from the emergency department to the operating room for definitive treatment. Other ancillary services, such as blood banks and laboratories are necessary to assist in the care for the patient intraoperatively. In endovascular surgery, trained technologists, fluoroscopy, a full armamentarium of interventional equipment (wires, balloons, stents, etc.), and a full stock of stent grafts and associated ancillary equipment are mandatory. Many hospitals may not have the variety of stent grafts available for emergency use. Regionalization of care has been suggested to improve outcomes in the treatment of rAAAs.14 In a study by Warner et al., mortality was decreased by 20% at the tertiary center compared to the smaller community hospitals in both EVAR and open repairs for rAAA. Zettervall et al. published data that showed that significant regional variation exists in perioperative outcomes and length of stay, and mortality in repair for rAAA approached with open or endovascular means.15 Low volume centers have worse outcomes, and teaching hospitals may have better outcomes treating AAA.16
EVAR is also reported to be associated with a 27-36% higher cost of care than open surgery for rAAA.17 Many institutions may not have the means to provide the resources needed to support such a program.
There is no question that EVAR has greatly impacted the treatment of aortic aneurysms. However, not every aneurysm is appropriate for endovascular repair at this time. For the many reasons cited, we cannot permit open repair to become an extinct skill. Vascular training programs must include open repair of rAAA just as it should for other vascular conditions.
I would agree with Dr. Aziz that we do not yet have a prospective, randomized study and Level 1 evidence to support either view and given the complexity and urgency associated with these patients, such a study may not be forthcoming. Till then, patients with a RAAA should have ‘all of the above’ approach including open surgery depending on the institutional experience and resources and urgency of the situation.
References
1. J Vasc Surg 2016; 2:297-305
2. J Vasc Surg 2009; 49:1077-1080.
3. Eur J Vasc Endovasc Surg 2006; 32:506-513
4. Ann Surg 2013. Aug 258 (2) 248-56
5. J Vasc Surg 2010; 51:267-70
6. Ann Vasc Surg 2017; 38:59-63
7. J Vasc Surg 2009: 50:243-50
8. J Endovasc Ther 2016; 23: 919-927
9. BJM 2014; 101:216-224
10. Radiographics 2015; 35:593-615.
11. Ann Vasc Surg 2013; 27:844-50
12. J Vasc Surg 2017; 65:52-57
13. Semin Vasc Surg 2016; 29:35-40
14. J Vasc Surg 2014; 59:1512-7
15. Ann Surg 2017; 264:538-43
16. J Vasc Surg 2016; 22 pii W0741-5214 (16) 31247-2
17. J Vasc Surg 2008; 47:1165-70
Dr. Ozsvatrh is a professor of surgery at Albany Medical College, Albany, N.Y., and a vascular attending, at Albany Medical Center Hospital, Albany, and chief, department of surgery, Samaritan Hospital, Troy, N.Y.
EVAR should be offered to all patients with rAAA
Since the inception of EVAR two decades ago, it has largely replaced open abdominal aortic aneurysm repair as the operation of choice for elective treatment of abdominal aortic aneurysms. Shorter duration of operation, avoiding general anesthesia and aortic cross clamping, ability to obtain balloon control of aorta, fast recovery time and reduced hospital length of hospital stay are among the most commonly cited reasons for this change in paradigm for treatment of abdominal aortic aneurysms. Since vascular surgeons have adopted the widespread use of EVAR, the total number of aneurysm related deaths has significantly reduced.1 While EVAR has become the most commonly used operation to treat AAAs electively, it’s utility to treat ruptured AAAs has been questioned. Recent analysis of nationwide trends for the operations for the diagnosis of ruptured AAA show that almost half of the patients with ruptured AAA are still treated with open surgical repair.2
Opponents of REVAR (EVAR for rAAA) cite comparable outcomes of open surgery and REVAR in randomized controlled trials, requirement of a specific REVAR protocol, increased cost and lack of resources and more importantly, lack of level I evidence to support it’s use in all cases of rAAA.
It is no surprise that REVAR is associated with significantly lower perioperative mortality (24%) as compared to open repair of ruptured AAA (44%).3 Mortality after open repair of ruptured AAA can vary anywhere from 30-70%.4,5 Improved mortality rates after REVAR are not only limited to stable patients, but also extend to those patients with ruptured AAA who are considered hemodynamically unstable at the time of initial presentation.6
The survival advantage among REVAR patients is not only evident in short term (30-days), but it also extends up to 5 years after the operation.3 Patients undergoing REVAR are less likely to require intra-operative blood transfusions, as compared to patients who undergo open repair of rAAA.7 Development of acute renal failure after surgical treatment of rAAAs is associated with significant mortality and REVAR has been associated with significantly lower incidence of acute renal failure as compared to open repair of ruptured AAA.2
Due to inherent issues of patient instability, emergent presentation and inequality among hospital resources and patient volumes, it is difficult to design a flawless, randomized controlled trial to compare REVAR with open surgical repair. The results from published randomized controlled trials on this topic should be interpreted with caution. The Nottingham trial from the United Kingdom8 showed similar mortality (53%) between REVAR and open surgical operation, however, out of the 203 patients enrolled in the trial, 70% were not randomized and REVAR was offered to only 15 patients. Likewise, the AJAX Trial from Netherlands9 showed that there was no significant difference in mortality between the two treatment groups (42% with REVAR and 47% with open repair), however almost 80% of enrolled patients were not randomized and there was a disagreement between the interpreters about CTA diagnosis of rAAA. In addition, the conversion rates from REVAR to open repair were unexpectedly high (14%), pointing to the surgeons’ inexperience.
Similarly, the IMPROVE trial from United Kingdom10 suffered from poor rates of randomization (50% of enrolled patients) and poor methodology (obtaining CTA after randomization, and making requirement of CTA optional for patients allocated to open surgery group). The trial showed equivalent mortality rates between the two surgical groups (35% with REVAR and 37% with open repair).
Due to flawed methodology and poor rates of randomization, results of these trials do not provide us with level I evidence, which is required to make any scientific recommendations about the treatment of choice for the treatment of rAAAs. Hence, the large body of evidence, obtained from retrospective studies should be used while comparing the outcomes of operations for ruptured AAAs. So far, all retrospective analyses, comparing REVAR with open repair in national registries, such as National Inpatient Sample (NIS) database11,12 American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database7 and Medicare database13 have clearly shown that the outcomes of REVAR are better than open surgical repair of ruptured AAA. Likewise, multi-center observational studies14,15 have demonstrated superiority of REVAR over open surgical repair.
To summarize, REVAR is a safe procedure, can be performed under local anesthetic, has shorter operative time and is associated with improved outcomes as compared to open surgery. REVAR should be the treatment of choice for all patients who meet the anatomic criteria for endovascular repair. With increasing experience of vascular surgeons with the endovascular technology, it is foreseeable that REVAR will soon become the treatment of choice for ruptured abdominal aortic aneurysms.
References
1. J Vasc Surg 2009;49:543-50; discussion 50-1.
2. Ann Vasc Surg 2016;35:147-55.
3. J Vasc Surg 2013;57:368-75.
4. J Vasc Surg 2001;34:41-6.
5. J Vasc Surg 1991;13:240-5; discussion 5-7.
6. J Vasc Surg 2014;60:1439-45.
7. J Vasc Surg 2010;51:305-9 e1.
8. Eur J Vasc Endovasc Surg 2006;32:506-13; discussion 14-5.
9. Ann Surg 2013;258:248-56.
10. BMJ 2014;348:f7661.
11. J Vasc Surg 2009;49:817-26.
12. J Vasc Surg 2008;47:1165-70; discussion 70-1.
13. J Vasc Surg 2014;59:575-82.
14. Ann Surg 2012;256:688-95; discussion 95-6.
15. Ann Surg 2009;250:818-24.
Dr. Aziz is in the division of vascular surgery, Penn State Heart and Vascular Institute, Pennsylvania State University College of Medicine, Hershey, Penn.
Points/Counterpoint: Should surgeons operate on functional tricuspid regurgitation?
Yes, functional TR is worth repairing (David H. Adams, MD)
Functional tricuspid regurgitation is a common finding in patients undergoing degenerative mitral valve repair. Severe tricuspid regurgitation is unusual, and clearly there is little debate on the merits of concomitant tricuspid repair for these patients. Moderate tricuspid regurgitation is identified preoperatively in around 15% of patients undergoing degenerative mitral repair (J Thorac Cardiovasc Surg. 2011;142:608-13), and concomitant tricuspid repair in these patients is certainly supported by both the American and European guidelines (J Am Coll Cardiol. 2017. doi: 10.1016/j.jacc.2017.03.011; Eur Heart J. 2012;33:2451-96).
What experience and evidence has led us to a more aggressive approach? One of the most important influences on our early adoption of tricuspid repair at the time of mitral surgery was linked to observations that tricuspid regurgitation (TR) sometimes progressed after isolated mitral valve repair (MVR), with some patients developing moderate or worse insufficiency. Certainly, the impact of significant tricuspid regurgitation on the quality and length of patients’ lives and the challenges of reoperation for isolated tricuspid regurgitation are well known to all surgeons.
Consequently, the importance of treating significant annular dilatation, even without significant tricuspid regurgitation, is supported by the guidelines. Our own experience with an aggressive approach to functional tricuspid regurgitation (FTR) at the time of mitral surgery put an exclamation point on this (J Am Coll Cardiol. 2015;65:1931-8). We found that concomitant tricuspid repair in patients who were worse off before surgery with more TR and higher rates of atrial fibrillation and right-sided dysfunction, actually did better during 5 years of follow-up than the isolated mitral repair patients who started with completely normal tricuspid valve anatomy and ventricular function.
Benign neglect is always an option (J Thorac Cardiovasc Surg. 2017;154:125-6), but we agree with Roberto Dion, MD – despite our friends’ opinions in Toronto and Rochester – we would much prefer to have minimal TR and a normal sized tricuspid valve after MVR. Ask yourself: would you rather have no TR and a normal sized tricuspid valve after you undergo a mitral operation, or a very dilated annulus and perhaps moderate FTR? I am pretty sure I know the answer, but if you are not sure, read our paper.
Dr. Adams is cardiac surgeon-in-chief, Mount Sinai Health System, and Marie-Josée and Henry R. Kravis Professor and Chairman, department of cardiovascular surgery, Icahn School of Medicine at Mount Sinai and The Mount Sinai Hospital, and president-elect of the American Association for Thoracic Surgery. He disclosed he is the national co-principal investigator for the Medtronic NeoChord trial, and receives royalties from Medtronic and Edwards Lifesciences. The Icahn School of Medicine at Mount Sinai receives royalty payments from Edwards Lifesciences and Medtronic for intellectual property related to Dr. Adams’ involvement in the development of 2 mitral valve repair rings and 1 tricuspid valve repair ring.
No, a patient with FTR does not necessarily need repair (Tirone David, MD)
In our clinic, a patient who undergoes MVR and has FTR generally goes home without an annuloplasty. We now have 12 years or more of follow-up in these patients, and they do not develop TR if their MVR is competent. We have reported that preoperative TR in patients who had MVR is associated with mitral valve disease and often improves after the operation (J Thorac Cardiovasc Surg. 2017;154:110-22). New postoperative TR is uncommon.
Ninety percent of my mitral valve repair patients today have no symptoms. Of those patients, a small proportion have moderate TR.
Dr. David is a professor of surgery at Toronto General Hospital. He reported no financial relationships.
Yes, but repair of FTR requires caution (Gilles Dreyfus, MD)
The controversy surrounding the legitimacy of concomitant tricuspid annuloplasty for functional TR during MVR begs for a clinical trial, but before we can conduct a clinical trial, we must define the primary and secondary endpoints. We’ve seen recent prospective, randomized trials that have reported faulty conclusions because the primary endpoints were wrong.
We need a strong debate to agree on those endpoints. Mortality as an endpoint will probably take a very long time to arrive at.
We’re mixing up many different factors. We’re mixing up TR grading, and we know that grading is unreliable. We have all seen patients with full-fledged TR, and after we put them on Lasix (furosemide, Sanofi), 3 days later they have mild TR. So the same patient with no treatment becomes let’s say a “Dreyfus indication,” and then suddenly in 3 days the patient doesn’t need surgery. At any further stage of his life this patient can experience severe TR again; tricuspid annuloplasty will prevent that from happening.
Moderate TR according to the common definition does not exist. If you look at the reports in echocardiography and if you ask any cardiologist, everything between no TR and severe TR is considered moderate. We have proposed a new staging system for evaluating FTR that uses three factors: TR severity; annular dilatation; and extent of tethering, or mode of leaflet coaptation (J Am Coll Cardiol. 2015;65:2331-6).
Dr. Dreyfus is director of the medical and surgical team at the Cardiothoracic Centre of Monaco in Monte Carlo and professor of cardiothoracic surgery at Paris V University and the Imperial College of London. He disclosed receiving speaker fees from Edwards Lifesciences, LivaNova, and Medtronic.
No, few FTR patients at risk after MVR (Hartzell Schaff, MD)
Echocardiography can provide a great deal of information about when concomitant repair for TR is indicated during MVR. We’ve found that if the patient has no right-sided signs, has normal right atrial pressure, and has mild or mild/moderate TR at the time of repair to the journey mitral valve, the chance of him returning for a tricuspid valve procedure is near zero.
A few patients do return after MVR. They develop atrial fibrillation and may need a pacemaker, but we see very few patients return for tricuspid surgery.
It’s fair to say we cannot demonstrate any benefit of correcting functional mitral regurgitation. Why would we think there’s a benefit of correcting FTR? We can say we’re going to look at grade of TR down the road, or we could look at some other endpoint, but think about it this way: If we cannot prove that correcting functional mitral regurgitation is helpful, why is correcting FTR going to help?
Dr. Schaff is a cardiothoracic surgeon at Mayo Clinic Foundation, Rochester, Minn. He reported no financial relationships.
Yes, functional TR is worth repairing (David H. Adams, MD)
Functional tricuspid regurgitation is a common finding in patients undergoing degenerative mitral valve repair. Severe tricuspid regurgitation is unusual, and clearly there is little debate on the merits of concomitant tricuspid repair for these patients. Moderate tricuspid regurgitation is identified preoperatively in around 15% of patients undergoing degenerative mitral repair (J Thorac Cardiovasc Surg. 2011;142:608-13), and concomitant tricuspid repair in these patients is certainly supported by both the American and European guidelines (J Am Coll Cardiol. 2017. doi: 10.1016/j.jacc.2017.03.011; Eur Heart J. 2012;33:2451-96).
What experience and evidence has led us to a more aggressive approach? One of the most important influences on our early adoption of tricuspid repair at the time of mitral surgery was linked to observations that tricuspid regurgitation (TR) sometimes progressed after isolated mitral valve repair (MVR), with some patients developing moderate or worse insufficiency. Certainly, the impact of significant tricuspid regurgitation on the quality and length of patients’ lives and the challenges of reoperation for isolated tricuspid regurgitation are well known to all surgeons.
Consequently, the importance of treating significant annular dilatation, even without significant tricuspid regurgitation, is supported by the guidelines. Our own experience with an aggressive approach to functional tricuspid regurgitation (FTR) at the time of mitral surgery put an exclamation point on this (J Am Coll Cardiol. 2015;65:1931-8). We found that concomitant tricuspid repair in patients who were worse off before surgery with more TR and higher rates of atrial fibrillation and right-sided dysfunction, actually did better during 5 years of follow-up than the isolated mitral repair patients who started with completely normal tricuspid valve anatomy and ventricular function.
Benign neglect is always an option (J Thorac Cardiovasc Surg. 2017;154:125-6), but we agree with Roberto Dion, MD – despite our friends’ opinions in Toronto and Rochester – we would much prefer to have minimal TR and a normal sized tricuspid valve after MVR. Ask yourself: would you rather have no TR and a normal sized tricuspid valve after you undergo a mitral operation, or a very dilated annulus and perhaps moderate FTR? I am pretty sure I know the answer, but if you are not sure, read our paper.
Dr. Adams is cardiac surgeon-in-chief, Mount Sinai Health System, and Marie-Josée and Henry R. Kravis Professor and Chairman, department of cardiovascular surgery, Icahn School of Medicine at Mount Sinai and The Mount Sinai Hospital, and president-elect of the American Association for Thoracic Surgery. He disclosed he is the national co-principal investigator for the Medtronic NeoChord trial, and receives royalties from Medtronic and Edwards Lifesciences. The Icahn School of Medicine at Mount Sinai receives royalty payments from Edwards Lifesciences and Medtronic for intellectual property related to Dr. Adams’ involvement in the development of 2 mitral valve repair rings and 1 tricuspid valve repair ring.
No, a patient with FTR does not necessarily need repair (Tirone David, MD)
In our clinic, a patient who undergoes MVR and has FTR generally goes home without an annuloplasty. We now have 12 years or more of follow-up in these patients, and they do not develop TR if their MVR is competent. We have reported that preoperative TR in patients who had MVR is associated with mitral valve disease and often improves after the operation (J Thorac Cardiovasc Surg. 2017;154:110-22). New postoperative TR is uncommon.
Ninety percent of my mitral valve repair patients today have no symptoms. Of those patients, a small proportion have moderate TR.
Dr. David is a professor of surgery at Toronto General Hospital. He reported no financial relationships.
Yes, but repair of FTR requires caution (Gilles Dreyfus, MD)
The controversy surrounding the legitimacy of concomitant tricuspid annuloplasty for functional TR during MVR begs for a clinical trial, but before we can conduct a clinical trial, we must define the primary and secondary endpoints. We’ve seen recent prospective, randomized trials that have reported faulty conclusions because the primary endpoints were wrong.
We need a strong debate to agree on those endpoints. Mortality as an endpoint will probably take a very long time to arrive at.
We’re mixing up many different factors. We’re mixing up TR grading, and we know that grading is unreliable. We have all seen patients with full-fledged TR, and after we put them on Lasix (furosemide, Sanofi), 3 days later they have mild TR. So the same patient with no treatment becomes let’s say a “Dreyfus indication,” and then suddenly in 3 days the patient doesn’t need surgery. At any further stage of his life this patient can experience severe TR again; tricuspid annuloplasty will prevent that from happening.
Moderate TR according to the common definition does not exist. If you look at the reports in echocardiography and if you ask any cardiologist, everything between no TR and severe TR is considered moderate. We have proposed a new staging system for evaluating FTR that uses three factors: TR severity; annular dilatation; and extent of tethering, or mode of leaflet coaptation (J Am Coll Cardiol. 2015;65:2331-6).
Dr. Dreyfus is director of the medical and surgical team at the Cardiothoracic Centre of Monaco in Monte Carlo and professor of cardiothoracic surgery at Paris V University and the Imperial College of London. He disclosed receiving speaker fees from Edwards Lifesciences, LivaNova, and Medtronic.
No, few FTR patients at risk after MVR (Hartzell Schaff, MD)
Echocardiography can provide a great deal of information about when concomitant repair for TR is indicated during MVR. We’ve found that if the patient has no right-sided signs, has normal right atrial pressure, and has mild or mild/moderate TR at the time of repair to the journey mitral valve, the chance of him returning for a tricuspid valve procedure is near zero.
A few patients do return after MVR. They develop atrial fibrillation and may need a pacemaker, but we see very few patients return for tricuspid surgery.
It’s fair to say we cannot demonstrate any benefit of correcting functional mitral regurgitation. Why would we think there’s a benefit of correcting FTR? We can say we’re going to look at grade of TR down the road, or we could look at some other endpoint, but think about it this way: If we cannot prove that correcting functional mitral regurgitation is helpful, why is correcting FTR going to help?
Dr. Schaff is a cardiothoracic surgeon at Mayo Clinic Foundation, Rochester, Minn. He reported no financial relationships.
Yes, functional TR is worth repairing (David H. Adams, MD)
Functional tricuspid regurgitation is a common finding in patients undergoing degenerative mitral valve repair. Severe tricuspid regurgitation is unusual, and clearly there is little debate on the merits of concomitant tricuspid repair for these patients. Moderate tricuspid regurgitation is identified preoperatively in around 15% of patients undergoing degenerative mitral repair (J Thorac Cardiovasc Surg. 2011;142:608-13), and concomitant tricuspid repair in these patients is certainly supported by both the American and European guidelines (J Am Coll Cardiol. 2017. doi: 10.1016/j.jacc.2017.03.011; Eur Heart J. 2012;33:2451-96).
What experience and evidence has led us to a more aggressive approach? One of the most important influences on our early adoption of tricuspid repair at the time of mitral surgery was linked to observations that tricuspid regurgitation (TR) sometimes progressed after isolated mitral valve repair (MVR), with some patients developing moderate or worse insufficiency. Certainly, the impact of significant tricuspid regurgitation on the quality and length of patients’ lives and the challenges of reoperation for isolated tricuspid regurgitation are well known to all surgeons.
Consequently, the importance of treating significant annular dilatation, even without significant tricuspid regurgitation, is supported by the guidelines. Our own experience with an aggressive approach to functional tricuspid regurgitation (FTR) at the time of mitral surgery put an exclamation point on this (J Am Coll Cardiol. 2015;65:1931-8). We found that concomitant tricuspid repair in patients who were worse off before surgery with more TR and higher rates of atrial fibrillation and right-sided dysfunction, actually did better during 5 years of follow-up than the isolated mitral repair patients who started with completely normal tricuspid valve anatomy and ventricular function.
Benign neglect is always an option (J Thorac Cardiovasc Surg. 2017;154:125-6), but we agree with Roberto Dion, MD – despite our friends’ opinions in Toronto and Rochester – we would much prefer to have minimal TR and a normal sized tricuspid valve after MVR. Ask yourself: would you rather have no TR and a normal sized tricuspid valve after you undergo a mitral operation, or a very dilated annulus and perhaps moderate FTR? I am pretty sure I know the answer, but if you are not sure, read our paper.
Dr. Adams is cardiac surgeon-in-chief, Mount Sinai Health System, and Marie-Josée and Henry R. Kravis Professor and Chairman, department of cardiovascular surgery, Icahn School of Medicine at Mount Sinai and The Mount Sinai Hospital, and president-elect of the American Association for Thoracic Surgery. He disclosed he is the national co-principal investigator for the Medtronic NeoChord trial, and receives royalties from Medtronic and Edwards Lifesciences. The Icahn School of Medicine at Mount Sinai receives royalty payments from Edwards Lifesciences and Medtronic for intellectual property related to Dr. Adams’ involvement in the development of 2 mitral valve repair rings and 1 tricuspid valve repair ring.
No, a patient with FTR does not necessarily need repair (Tirone David, MD)
In our clinic, a patient who undergoes MVR and has FTR generally goes home without an annuloplasty. We now have 12 years or more of follow-up in these patients, and they do not develop TR if their MVR is competent. We have reported that preoperative TR in patients who had MVR is associated with mitral valve disease and often improves after the operation (J Thorac Cardiovasc Surg. 2017;154:110-22). New postoperative TR is uncommon.
Ninety percent of my mitral valve repair patients today have no symptoms. Of those patients, a small proportion have moderate TR.
Dr. David is a professor of surgery at Toronto General Hospital. He reported no financial relationships.
Yes, but repair of FTR requires caution (Gilles Dreyfus, MD)
The controversy surrounding the legitimacy of concomitant tricuspid annuloplasty for functional TR during MVR begs for a clinical trial, but before we can conduct a clinical trial, we must define the primary and secondary endpoints. We’ve seen recent prospective, randomized trials that have reported faulty conclusions because the primary endpoints were wrong.
We need a strong debate to agree on those endpoints. Mortality as an endpoint will probably take a very long time to arrive at.
We’re mixing up many different factors. We’re mixing up TR grading, and we know that grading is unreliable. We have all seen patients with full-fledged TR, and after we put them on Lasix (furosemide, Sanofi), 3 days later they have mild TR. So the same patient with no treatment becomes let’s say a “Dreyfus indication,” and then suddenly in 3 days the patient doesn’t need surgery. At any further stage of his life this patient can experience severe TR again; tricuspid annuloplasty will prevent that from happening.
Moderate TR according to the common definition does not exist. If you look at the reports in echocardiography and if you ask any cardiologist, everything between no TR and severe TR is considered moderate. We have proposed a new staging system for evaluating FTR that uses three factors: TR severity; annular dilatation; and extent of tethering, or mode of leaflet coaptation (J Am Coll Cardiol. 2015;65:2331-6).
Dr. Dreyfus is director of the medical and surgical team at the Cardiothoracic Centre of Monaco in Monte Carlo and professor of cardiothoracic surgery at Paris V University and the Imperial College of London. He disclosed receiving speaker fees from Edwards Lifesciences, LivaNova, and Medtronic.
No, few FTR patients at risk after MVR (Hartzell Schaff, MD)
Echocardiography can provide a great deal of information about when concomitant repair for TR is indicated during MVR. We’ve found that if the patient has no right-sided signs, has normal right atrial pressure, and has mild or mild/moderate TR at the time of repair to the journey mitral valve, the chance of him returning for a tricuspid valve procedure is near zero.
A few patients do return after MVR. They develop atrial fibrillation and may need a pacemaker, but we see very few patients return for tricuspid surgery.
It’s fair to say we cannot demonstrate any benefit of correcting functional mitral regurgitation. Why would we think there’s a benefit of correcting FTR? We can say we’re going to look at grade of TR down the road, or we could look at some other endpoint, but think about it this way: If we cannot prove that correcting functional mitral regurgitation is helpful, why is correcting FTR going to help?
Dr. Schaff is a cardiothoracic surgeon at Mayo Clinic Foundation, Rochester, Minn. He reported no financial relationships.
AT THE AATS MITRAL CONCLAVE 2017
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
Open vs. endovascular for chronic mesenteric ischemia
Chronic mesenteric ischemia is best treated in an open operation.
Chronic mesenteric ischemia is a rare disorder accounting for about 1 out of 100,000 admissions.1 Because of the rarity of this disease, diagnosis is often delayed. Patients are often evaluated for other gastrointestinal diseases and/or malignancies, which in turn contributes to significant delays in diagnosis. Additionally, there are no prospective, randomized trials on which to base decisions regarding treatment; and it is unlikely that such studies will ever be undertaken.
Chronic mesenteric ischemia develops when two or more of the mesenteric vessels (celiac, superior mesenteric [SMA], or inferior mesenteric [IMA]) become occluded or develop severe stenosis. In my experience, patients most often develop occlusion (as opposed to stenosis) of their mesenteric vessels. The atherosclerotic plaque responsible for the disease originates within the aorta and the stenosis/occlusion develops at the vessel origin.
As a whole, these comorbidities would suggest that a more minimally invasive approach would be preferred. Yet, an open operation for chronic mesenteric ischemia should not be discarded as an initial operation.
Endovascular treatment of mesenteric ischemia is not without risk. As in all endovascular procedures there are complications associated with the access vessels. The orientation of the mesenteric vessels as they arise from the aorta often favors an approach from the left arm. The brachial artery is smaller than the femoral artery, and it is more difficult to apply pressure to the brachial artery to control the puncture site. This leads to a higher rate of access site complications including hemorrhage, pseudoaneurysm and thrombosis of the vessel. Bleeding or hematoma formation within the brachial neurovascular sheath can result in significant neurologic dysfunction of the arm and hand. There is risk of stroke, especially when the access vessel is the brachial artery. There are also complications directly related to the endovascular procedure.
Atheroembolism of plaque can result in occlusion of small mesenteric vessels and focal areas of bowel necrosis. Dissection of the mesenteric vessel can occur. Oderich has advocated for the use of a covered stent.2 A covered stent could cover proximal branches, and thus, in theory, the treatment itself could cause bowel ischemia or infarction. Many series that have compared open and endovascular surgery show no difference in early outcomes, but demonstrate early restenosis, decreased primary patency, and decreased assisted primary patency with endovascular treatment as compared with open operations.3-5
Another concern regarding the treatment of mesenteric ischemia is the status of the end organ, the bowel. Successful treatment of mesenteric ischemia cannot only assess the atherosclerotic lesion, but requires the surgeon to be cognizant of the condition of the bowel.
This concern is especially true for acute mesenteric ischemia,6 but the status of the bowel must also be kept in mind for chronic mesenteric ischemia. Unlike the lower extremity where the results of treatment are easily observed by inspection (color, evidence of atheroembolization), palpation (temperature, pulse), and physiologic testing (ABI), the bowel is not accessible. There are no highly accurate tests to determine if the patient has on-going bowel ischemia or has developed infarction. Should a complication occur, physical examination findings and laboratory changes often become apparent late in the course of the disease. As previously noted, these patients are often physiologically compromised and have little reserve and may not survive such complications. An open operation allows visualization of the bowel, before and after revascularization.
Traditional teaching for the surgical treatment of chronic mesenteric ischemia has emphasized that two mesenteric vessels, usually the celiac and SMA, should be revascularized.7,8 Various approaches to revascularization have been suggested including transaortic endarterectomy and an antegrade bifurcated bypass originating from the supraceliac aorta. These operations are effective in restoring flow to the mesenteric circulation, but both of these approaches involve aortic cross-clamping and are physiologically challenging for patients.
There are alternatives for open revascularization of the mesenteric vessels. The infrarenal aorta, iliac vessels, and even renal arteries can be, and have been used as the inflow source. It has been my experience that a bypass graft using an iliac artery (common or external) as the inflow source is well tolerated by patients. I have preferentially used either great saphenous vein or femoral-popliteal vein as the conduit. In many cases, the distal anastomosis is simply the SMA. However, both the celiac and SMA can be revascularized by creating a side-side anastomosis to the SMA and an end-side anastomosis to the common or proper hepatic artery. Such procedures have been durable, providing relief of symptoms and allowing patients to regain weight.9
In reality, I believe that an endovascular approach for the treatment of chronic mesenteric ischemia has a role. Vascular surgeons are uniquely positioned to carefully evaluate each patient and recommend what they feel is most appropriate. I tend to feel that an endovascular approach is less likely to be successful for patients with occluded vessels, especially those with a flush occlusion, and so will preferentially recommend an open operation for these patients. On the other hand, in my practice, I have used an endovascular approach for patients with severe stenosis, and as Dr. Harris states, know that a bypass is always an option should this be unsuccessful or ultimately fail.
References
1. Ann Vasc Surg. 1991;5:403-6
2. J Vasc Surg. 2013;58:1316-23
3. Ann Vasc Surg. 2015:29;934-40
4. World J Gastroenerol. 2013;19:1333-7
5. J Vasc Surg. 2007;45:1162-71
6. J Vasc Surg. 2015;62:767-72
7. J Vasc Surg. 2002:35:853-9
8. Surgery. 1981;90:940-6
9. J Vasc Surg. 2000;32:37-47
Eric Endean, MD, is the director of the aortic center, Gordon L. Hyde Endowed Professor and Chair, and vascular surgery section head, vascular and endovascular surgery at UK HealthCare, University of Kentucky, Lexington. He had no relevant disclosures.
Presenting the case for endovascular intervention
Chronic mesenteric ischemia (CMI) is an uncommon, but lethal, problem when left untreated. Before the endovascular era, the only option was open revascularization, which is challenging in this chronically ill, malnourished population with diffuse, systemic, atherosclerotic disease. Morbidity and mortality was relatively high because of the comorbid conditions and chronically ill status of the patients. The first mesenteric bypass was performed in 1958 by Maynard and Shaw.1
Options for open repair include transaortic endarterectomy, antegrade bypass from the supraceliac aorta or distal thoracic aorta, or retrograde bypass from the iliac artery, all of which are major abdominal procedures. Endovascular interventions are now the most commonly performed procedures for CMI in the United States based on national studies.2
Technical success with endovascular interventions can be achieved in well over 90% of patients, and multiple vessels can be treated simultaneously from either a femoral or brachial approach. The primary concern with endovascular interventions has been long-term patency, with restenosis from intimal hyperplasia or thrombosis causing recurrent symptoms in up to 30%-50% at 3-5 years.5-7 However, these rates are based on use of bare metal stents, rather than covered stents. Recent studies8 suggest that stent grafts have markedly improved outcomes over bare metal stents for ostial lesions, decreasing recurrence. Oderich found that freedom from recurrence was 92% with stent grafts as compared with 53% for bare metal stents, with primary patency rates of 92%, at 3 years8, comparable to even the best open bypass results. Schoch first reported the use of covered stents in the mesenteric circulation, and found that no patients developed recurrent stenosis at 2 years.9 Other concerns with endovascular intervention include embolization and dissection, which have not been frequently reported.
Mortality from open surgery ranges from 5% to 15%, with morbidity of 30%-40%.4 Mortality from endovascular intervention is markedly lower, in the range of 3.56% vs. 7.23%.5 Long-term survival is not different between endovascular vs. open repair (69% vs. 65%),4 with the majority of deaths related to cardiac, pulmonary, or malignancy issues. Moghadamyeghaneh, in a review of the Nationwide Inpatient Sample database, found that open surgery was one of the major predictors for higher morbidity (odds ratio, 5.07) and mortality (OR, 5.13), despite the fact that endovascular patients were older (another risk factor for adverse outcomes) and had more comorbidities in this nonrandomized, real-world study.2
Further, if one considers cost as a metric for decision making, a Markov clinical decision model by Hogendoorn et al suggests an endovascular first approach is preferred, despite the presumed higher rate of recurrence expected with use of bare metal stents, rather than covered stents, utilized for this analysis.10 Clearly, the financial advantage would be even greater for endovascular with the lower rates of recurrence with covered stents more recently reported.
If a patient develops recurrent stenosis after endovascular intervention, open bypass may be considered as an alternate to repeat endovascular intervention, dependent on the nutritional status, life expectancy, and initial intervention undertaken. Alternately, patients who undergo open repair are not immune to restenosis, with a recurrence rate of 10%-20%.11,12 Oderich found that there was a 22% mortality in those treated with repeat open interventions, with a 47% complication rate. Endovascular interventions, however, had a significantly lower rate of complications, 16%, and mortality. For patients with recurrent disease after open revascularization for CMI, the endovascular approach should also be the preferred approach.
Any lesion which is anatomically suitable for endovascular repair should first have an attempt made via this approach, utilizing covered stents. While there is a role for open revascularization, endovascular interventions can be safely performed, with minimal morbidity and mortality, and good long-term patency, even in the sickest patients. Endovascular intervention should be the procedure of choice for chronic mesenteric ischemia and recurrent chronic mesenteric ischemia.
References
1. NEJM. 1958;258:874-8
2. Am Surg. 2015;81:1149-56
3. Cardiovasc Intervent Radiol. 1980;3:43-4
4. Ann Vasc Surg. 2009;23:700-12
5. Ann Vasc Surg. 2013;27:113-22
6. J Vasc Surg. 2011;54:1422-29
7. J Vasc Surg. 2010;51:140-7
8. J Vasc Surg. 2013;58:1316-24
9. JACS. 2001;212:668-75
10. J Vasc Surg. 2014;60;715-25
11. J Vasc Surg. 200;49:1472-9
12. J Vasc Surg. 2007;45:1162-71
Linda Harris, MD, is professor of surgery; chief, division of vascular surgery; program director, vascular surgery residency & fellowship at the State University of New York at Buffalo; and an associate medical editor for Vascular Specialist. She had no relevant disclosures.
Chronic mesenteric ischemia is best treated in an open operation.
Chronic mesenteric ischemia is a rare disorder accounting for about 1 out of 100,000 admissions.1 Because of the rarity of this disease, diagnosis is often delayed. Patients are often evaluated for other gastrointestinal diseases and/or malignancies, which in turn contributes to significant delays in diagnosis. Additionally, there are no prospective, randomized trials on which to base decisions regarding treatment; and it is unlikely that such studies will ever be undertaken.
Chronic mesenteric ischemia develops when two or more of the mesenteric vessels (celiac, superior mesenteric [SMA], or inferior mesenteric [IMA]) become occluded or develop severe stenosis. In my experience, patients most often develop occlusion (as opposed to stenosis) of their mesenteric vessels. The atherosclerotic plaque responsible for the disease originates within the aorta and the stenosis/occlusion develops at the vessel origin.
As a whole, these comorbidities would suggest that a more minimally invasive approach would be preferred. Yet, an open operation for chronic mesenteric ischemia should not be discarded as an initial operation.
Endovascular treatment of mesenteric ischemia is not without risk. As in all endovascular procedures there are complications associated with the access vessels. The orientation of the mesenteric vessels as they arise from the aorta often favors an approach from the left arm. The brachial artery is smaller than the femoral artery, and it is more difficult to apply pressure to the brachial artery to control the puncture site. This leads to a higher rate of access site complications including hemorrhage, pseudoaneurysm and thrombosis of the vessel. Bleeding or hematoma formation within the brachial neurovascular sheath can result in significant neurologic dysfunction of the arm and hand. There is risk of stroke, especially when the access vessel is the brachial artery. There are also complications directly related to the endovascular procedure.
Atheroembolism of plaque can result in occlusion of small mesenteric vessels and focal areas of bowel necrosis. Dissection of the mesenteric vessel can occur. Oderich has advocated for the use of a covered stent.2 A covered stent could cover proximal branches, and thus, in theory, the treatment itself could cause bowel ischemia or infarction. Many series that have compared open and endovascular surgery show no difference in early outcomes, but demonstrate early restenosis, decreased primary patency, and decreased assisted primary patency with endovascular treatment as compared with open operations.3-5
Another concern regarding the treatment of mesenteric ischemia is the status of the end organ, the bowel. Successful treatment of mesenteric ischemia cannot only assess the atherosclerotic lesion, but requires the surgeon to be cognizant of the condition of the bowel.
This concern is especially true for acute mesenteric ischemia,6 but the status of the bowel must also be kept in mind for chronic mesenteric ischemia. Unlike the lower extremity where the results of treatment are easily observed by inspection (color, evidence of atheroembolization), palpation (temperature, pulse), and physiologic testing (ABI), the bowel is not accessible. There are no highly accurate tests to determine if the patient has on-going bowel ischemia or has developed infarction. Should a complication occur, physical examination findings and laboratory changes often become apparent late in the course of the disease. As previously noted, these patients are often physiologically compromised and have little reserve and may not survive such complications. An open operation allows visualization of the bowel, before and after revascularization.
Traditional teaching for the surgical treatment of chronic mesenteric ischemia has emphasized that two mesenteric vessels, usually the celiac and SMA, should be revascularized.7,8 Various approaches to revascularization have been suggested including transaortic endarterectomy and an antegrade bifurcated bypass originating from the supraceliac aorta. These operations are effective in restoring flow to the mesenteric circulation, but both of these approaches involve aortic cross-clamping and are physiologically challenging for patients.
There are alternatives for open revascularization of the mesenteric vessels. The infrarenal aorta, iliac vessels, and even renal arteries can be, and have been used as the inflow source. It has been my experience that a bypass graft using an iliac artery (common or external) as the inflow source is well tolerated by patients. I have preferentially used either great saphenous vein or femoral-popliteal vein as the conduit. In many cases, the distal anastomosis is simply the SMA. However, both the celiac and SMA can be revascularized by creating a side-side anastomosis to the SMA and an end-side anastomosis to the common or proper hepatic artery. Such procedures have been durable, providing relief of symptoms and allowing patients to regain weight.9
In reality, I believe that an endovascular approach for the treatment of chronic mesenteric ischemia has a role. Vascular surgeons are uniquely positioned to carefully evaluate each patient and recommend what they feel is most appropriate. I tend to feel that an endovascular approach is less likely to be successful for patients with occluded vessels, especially those with a flush occlusion, and so will preferentially recommend an open operation for these patients. On the other hand, in my practice, I have used an endovascular approach for patients with severe stenosis, and as Dr. Harris states, know that a bypass is always an option should this be unsuccessful or ultimately fail.
References
1. Ann Vasc Surg. 1991;5:403-6
2. J Vasc Surg. 2013;58:1316-23
3. Ann Vasc Surg. 2015:29;934-40
4. World J Gastroenerol. 2013;19:1333-7
5. J Vasc Surg. 2007;45:1162-71
6. J Vasc Surg. 2015;62:767-72
7. J Vasc Surg. 2002:35:853-9
8. Surgery. 1981;90:940-6
9. J Vasc Surg. 2000;32:37-47
Eric Endean, MD, is the director of the aortic center, Gordon L. Hyde Endowed Professor and Chair, and vascular surgery section head, vascular and endovascular surgery at UK HealthCare, University of Kentucky, Lexington. He had no relevant disclosures.
Presenting the case for endovascular intervention
Chronic mesenteric ischemia (CMI) is an uncommon, but lethal, problem when left untreated. Before the endovascular era, the only option was open revascularization, which is challenging in this chronically ill, malnourished population with diffuse, systemic, atherosclerotic disease. Morbidity and mortality was relatively high because of the comorbid conditions and chronically ill status of the patients. The first mesenteric bypass was performed in 1958 by Maynard and Shaw.1
Options for open repair include transaortic endarterectomy, antegrade bypass from the supraceliac aorta or distal thoracic aorta, or retrograde bypass from the iliac artery, all of which are major abdominal procedures. Endovascular interventions are now the most commonly performed procedures for CMI in the United States based on national studies.2
Technical success with endovascular interventions can be achieved in well over 90% of patients, and multiple vessels can be treated simultaneously from either a femoral or brachial approach. The primary concern with endovascular interventions has been long-term patency, with restenosis from intimal hyperplasia or thrombosis causing recurrent symptoms in up to 30%-50% at 3-5 years.5-7 However, these rates are based on use of bare metal stents, rather than covered stents. Recent studies8 suggest that stent grafts have markedly improved outcomes over bare metal stents for ostial lesions, decreasing recurrence. Oderich found that freedom from recurrence was 92% with stent grafts as compared with 53% for bare metal stents, with primary patency rates of 92%, at 3 years8, comparable to even the best open bypass results. Schoch first reported the use of covered stents in the mesenteric circulation, and found that no patients developed recurrent stenosis at 2 years.9 Other concerns with endovascular intervention include embolization and dissection, which have not been frequently reported.
Mortality from open surgery ranges from 5% to 15%, with morbidity of 30%-40%.4 Mortality from endovascular intervention is markedly lower, in the range of 3.56% vs. 7.23%.5 Long-term survival is not different between endovascular vs. open repair (69% vs. 65%),4 with the majority of deaths related to cardiac, pulmonary, or malignancy issues. Moghadamyeghaneh, in a review of the Nationwide Inpatient Sample database, found that open surgery was one of the major predictors for higher morbidity (odds ratio, 5.07) and mortality (OR, 5.13), despite the fact that endovascular patients were older (another risk factor for adverse outcomes) and had more comorbidities in this nonrandomized, real-world study.2
Further, if one considers cost as a metric for decision making, a Markov clinical decision model by Hogendoorn et al suggests an endovascular first approach is preferred, despite the presumed higher rate of recurrence expected with use of bare metal stents, rather than covered stents, utilized for this analysis.10 Clearly, the financial advantage would be even greater for endovascular with the lower rates of recurrence with covered stents more recently reported.
If a patient develops recurrent stenosis after endovascular intervention, open bypass may be considered as an alternate to repeat endovascular intervention, dependent on the nutritional status, life expectancy, and initial intervention undertaken. Alternately, patients who undergo open repair are not immune to restenosis, with a recurrence rate of 10%-20%.11,12 Oderich found that there was a 22% mortality in those treated with repeat open interventions, with a 47% complication rate. Endovascular interventions, however, had a significantly lower rate of complications, 16%, and mortality. For patients with recurrent disease after open revascularization for CMI, the endovascular approach should also be the preferred approach.
Any lesion which is anatomically suitable for endovascular repair should first have an attempt made via this approach, utilizing covered stents. While there is a role for open revascularization, endovascular interventions can be safely performed, with minimal morbidity and mortality, and good long-term patency, even in the sickest patients. Endovascular intervention should be the procedure of choice for chronic mesenteric ischemia and recurrent chronic mesenteric ischemia.
References
1. NEJM. 1958;258:874-8
2. Am Surg. 2015;81:1149-56
3. Cardiovasc Intervent Radiol. 1980;3:43-4
4. Ann Vasc Surg. 2009;23:700-12
5. Ann Vasc Surg. 2013;27:113-22
6. J Vasc Surg. 2011;54:1422-29
7. J Vasc Surg. 2010;51:140-7
8. J Vasc Surg. 2013;58:1316-24
9. JACS. 2001;212:668-75
10. J Vasc Surg. 2014;60;715-25
11. J Vasc Surg. 200;49:1472-9
12. J Vasc Surg. 2007;45:1162-71
Linda Harris, MD, is professor of surgery; chief, division of vascular surgery; program director, vascular surgery residency & fellowship at the State University of New York at Buffalo; and an associate medical editor for Vascular Specialist. She had no relevant disclosures.
Chronic mesenteric ischemia is best treated in an open operation.
Chronic mesenteric ischemia is a rare disorder accounting for about 1 out of 100,000 admissions.1 Because of the rarity of this disease, diagnosis is often delayed. Patients are often evaluated for other gastrointestinal diseases and/or malignancies, which in turn contributes to significant delays in diagnosis. Additionally, there are no prospective, randomized trials on which to base decisions regarding treatment; and it is unlikely that such studies will ever be undertaken.
Chronic mesenteric ischemia develops when two or more of the mesenteric vessels (celiac, superior mesenteric [SMA], or inferior mesenteric [IMA]) become occluded or develop severe stenosis. In my experience, patients most often develop occlusion (as opposed to stenosis) of their mesenteric vessels. The atherosclerotic plaque responsible for the disease originates within the aorta and the stenosis/occlusion develops at the vessel origin.
As a whole, these comorbidities would suggest that a more minimally invasive approach would be preferred. Yet, an open operation for chronic mesenteric ischemia should not be discarded as an initial operation.
Endovascular treatment of mesenteric ischemia is not without risk. As in all endovascular procedures there are complications associated with the access vessels. The orientation of the mesenteric vessels as they arise from the aorta often favors an approach from the left arm. The brachial artery is smaller than the femoral artery, and it is more difficult to apply pressure to the brachial artery to control the puncture site. This leads to a higher rate of access site complications including hemorrhage, pseudoaneurysm and thrombosis of the vessel. Bleeding or hematoma formation within the brachial neurovascular sheath can result in significant neurologic dysfunction of the arm and hand. There is risk of stroke, especially when the access vessel is the brachial artery. There are also complications directly related to the endovascular procedure.
Atheroembolism of plaque can result in occlusion of small mesenteric vessels and focal areas of bowel necrosis. Dissection of the mesenteric vessel can occur. Oderich has advocated for the use of a covered stent.2 A covered stent could cover proximal branches, and thus, in theory, the treatment itself could cause bowel ischemia or infarction. Many series that have compared open and endovascular surgery show no difference in early outcomes, but demonstrate early restenosis, decreased primary patency, and decreased assisted primary patency with endovascular treatment as compared with open operations.3-5
Another concern regarding the treatment of mesenteric ischemia is the status of the end organ, the bowel. Successful treatment of mesenteric ischemia cannot only assess the atherosclerotic lesion, but requires the surgeon to be cognizant of the condition of the bowel.
This concern is especially true for acute mesenteric ischemia,6 but the status of the bowel must also be kept in mind for chronic mesenteric ischemia. Unlike the lower extremity where the results of treatment are easily observed by inspection (color, evidence of atheroembolization), palpation (temperature, pulse), and physiologic testing (ABI), the bowel is not accessible. There are no highly accurate tests to determine if the patient has on-going bowel ischemia or has developed infarction. Should a complication occur, physical examination findings and laboratory changes often become apparent late in the course of the disease. As previously noted, these patients are often physiologically compromised and have little reserve and may not survive such complications. An open operation allows visualization of the bowel, before and after revascularization.
Traditional teaching for the surgical treatment of chronic mesenteric ischemia has emphasized that two mesenteric vessels, usually the celiac and SMA, should be revascularized.7,8 Various approaches to revascularization have been suggested including transaortic endarterectomy and an antegrade bifurcated bypass originating from the supraceliac aorta. These operations are effective in restoring flow to the mesenteric circulation, but both of these approaches involve aortic cross-clamping and are physiologically challenging for patients.
There are alternatives for open revascularization of the mesenteric vessels. The infrarenal aorta, iliac vessels, and even renal arteries can be, and have been used as the inflow source. It has been my experience that a bypass graft using an iliac artery (common or external) as the inflow source is well tolerated by patients. I have preferentially used either great saphenous vein or femoral-popliteal vein as the conduit. In many cases, the distal anastomosis is simply the SMA. However, both the celiac and SMA can be revascularized by creating a side-side anastomosis to the SMA and an end-side anastomosis to the common or proper hepatic artery. Such procedures have been durable, providing relief of symptoms and allowing patients to regain weight.9
In reality, I believe that an endovascular approach for the treatment of chronic mesenteric ischemia has a role. Vascular surgeons are uniquely positioned to carefully evaluate each patient and recommend what they feel is most appropriate. I tend to feel that an endovascular approach is less likely to be successful for patients with occluded vessels, especially those with a flush occlusion, and so will preferentially recommend an open operation for these patients. On the other hand, in my practice, I have used an endovascular approach for patients with severe stenosis, and as Dr. Harris states, know that a bypass is always an option should this be unsuccessful or ultimately fail.
References
1. Ann Vasc Surg. 1991;5:403-6
2. J Vasc Surg. 2013;58:1316-23
3. Ann Vasc Surg. 2015:29;934-40
4. World J Gastroenerol. 2013;19:1333-7
5. J Vasc Surg. 2007;45:1162-71
6. J Vasc Surg. 2015;62:767-72
7. J Vasc Surg. 2002:35:853-9
8. Surgery. 1981;90:940-6
9. J Vasc Surg. 2000;32:37-47
Eric Endean, MD, is the director of the aortic center, Gordon L. Hyde Endowed Professor and Chair, and vascular surgery section head, vascular and endovascular surgery at UK HealthCare, University of Kentucky, Lexington. He had no relevant disclosures.
Presenting the case for endovascular intervention
Chronic mesenteric ischemia (CMI) is an uncommon, but lethal, problem when left untreated. Before the endovascular era, the only option was open revascularization, which is challenging in this chronically ill, malnourished population with diffuse, systemic, atherosclerotic disease. Morbidity and mortality was relatively high because of the comorbid conditions and chronically ill status of the patients. The first mesenteric bypass was performed in 1958 by Maynard and Shaw.1
Options for open repair include transaortic endarterectomy, antegrade bypass from the supraceliac aorta or distal thoracic aorta, or retrograde bypass from the iliac artery, all of which are major abdominal procedures. Endovascular interventions are now the most commonly performed procedures for CMI in the United States based on national studies.2
Technical success with endovascular interventions can be achieved in well over 90% of patients, and multiple vessels can be treated simultaneously from either a femoral or brachial approach. The primary concern with endovascular interventions has been long-term patency, with restenosis from intimal hyperplasia or thrombosis causing recurrent symptoms in up to 30%-50% at 3-5 years.5-7 However, these rates are based on use of bare metal stents, rather than covered stents. Recent studies8 suggest that stent grafts have markedly improved outcomes over bare metal stents for ostial lesions, decreasing recurrence. Oderich found that freedom from recurrence was 92% with stent grafts as compared with 53% for bare metal stents, with primary patency rates of 92%, at 3 years8, comparable to even the best open bypass results. Schoch first reported the use of covered stents in the mesenteric circulation, and found that no patients developed recurrent stenosis at 2 years.9 Other concerns with endovascular intervention include embolization and dissection, which have not been frequently reported.
Mortality from open surgery ranges from 5% to 15%, with morbidity of 30%-40%.4 Mortality from endovascular intervention is markedly lower, in the range of 3.56% vs. 7.23%.5 Long-term survival is not different between endovascular vs. open repair (69% vs. 65%),4 with the majority of deaths related to cardiac, pulmonary, or malignancy issues. Moghadamyeghaneh, in a review of the Nationwide Inpatient Sample database, found that open surgery was one of the major predictors for higher morbidity (odds ratio, 5.07) and mortality (OR, 5.13), despite the fact that endovascular patients were older (another risk factor for adverse outcomes) and had more comorbidities in this nonrandomized, real-world study.2
Further, if one considers cost as a metric for decision making, a Markov clinical decision model by Hogendoorn et al suggests an endovascular first approach is preferred, despite the presumed higher rate of recurrence expected with use of bare metal stents, rather than covered stents, utilized for this analysis.10 Clearly, the financial advantage would be even greater for endovascular with the lower rates of recurrence with covered stents more recently reported.
If a patient develops recurrent stenosis after endovascular intervention, open bypass may be considered as an alternate to repeat endovascular intervention, dependent on the nutritional status, life expectancy, and initial intervention undertaken. Alternately, patients who undergo open repair are not immune to restenosis, with a recurrence rate of 10%-20%.11,12 Oderich found that there was a 22% mortality in those treated with repeat open interventions, with a 47% complication rate. Endovascular interventions, however, had a significantly lower rate of complications, 16%, and mortality. For patients with recurrent disease after open revascularization for CMI, the endovascular approach should also be the preferred approach.
Any lesion which is anatomically suitable for endovascular repair should first have an attempt made via this approach, utilizing covered stents. While there is a role for open revascularization, endovascular interventions can be safely performed, with minimal morbidity and mortality, and good long-term patency, even in the sickest patients. Endovascular intervention should be the procedure of choice for chronic mesenteric ischemia and recurrent chronic mesenteric ischemia.
References
1. NEJM. 1958;258:874-8
2. Am Surg. 2015;81:1149-56
3. Cardiovasc Intervent Radiol. 1980;3:43-4
4. Ann Vasc Surg. 2009;23:700-12
5. Ann Vasc Surg. 2013;27:113-22
6. J Vasc Surg. 2011;54:1422-29
7. J Vasc Surg. 2010;51:140-7
8. J Vasc Surg. 2013;58:1316-24
9. JACS. 2001;212:668-75
10. J Vasc Surg. 2014;60;715-25
11. J Vasc Surg. 200;49:1472-9
12. J Vasc Surg. 2007;45:1162-71
Linda Harris, MD, is professor of surgery; chief, division of vascular surgery; program director, vascular surgery residency & fellowship at the State University of New York at Buffalo; and an associate medical editor for Vascular Specialist. She had no relevant disclosures.
Point/Counterpoint: Is limb salvage always best in diabetes?
Salvage limbs at all costs
Aggressive limb salvage in people with diabetes leads to an overall reduction in cost not only economically, but also from the patient’s perspective. The vast majority of diabetic patients with critical ischemia are actually good candidates for limb salvage. Tragically, many of these patients are never referred for evaluation for limb salvage because of misconceptions about the pathophysiology of the disease.
An argument against limb salvage is that primary amputation prevents or shortens the course of wound care and enables patients to become ambulatory, albeit with a prosthesis, faster. However, in the modern era of vascular surgery, revascularization can be performed successfully with minimal mortality and excellent rates of limb salvage, especially when it’s done within a team-based approach.
The mortality in primary amputation is shockingly high, anywhere from 5% to 23% higher than revascularization alone, and the major complication rate of amputation associated with diabetes is also unacceptably high – up to 37%. This is in contrast to a 17% rate in major nonamputation vascular surgery and 1%-5% in endovascular procedures (BMC Nephrol. 2005;6:3).
We can’t ignore the economic burden this places on the country. In 2014, primary amputations cost the health care system $11 billion annually, and that is expected to grow to more than $25 billion in the next several years, according to the SAGE Group. It’s important to keep in mind that Medicare covers over 80% of this cost.
A number of studies have shown that conservative management with wound care and amputation is more cost effective than primary amputation in ambulatory, independent adults. Data can be difficult to interpret because of different recording strategies for all the costs associated with amputation, but a single-institution study concluded that revascularization costs almost $5,280 more than expectant management, but $33,900 less than primary amputation alone (Cardiovasc Surg. 1999;7;62-9).
We must also consider the costs of revision after primary amputation; above-the-knee amputation has a 12% in-hospital revision rate, and below-the-knee amputation about 20%. Endovascular interventions, on the other hand, have a 1%-9% in-hospital revision rate, and only 2%-4% of these patients will go on to require an amputation during the same admission (Eur J Vasc Endovasc Surg. 2006;32:484-90; Arch Phys Med Rehabil. 2005;86:480-6).This does not include the costs of those complications as well as other indirect costs of amputation, such as nursing home care and living situation modification (Int J Behav Med. 2016;23:714-21; Pak J Med Sci. 2014; 30:1044-9). They quickly add up to that $25 billion.
The proponents of primary amputation tell us that it leads to quicker recovery time and an earlier time to ambulation. However, only 47% of patients will actually ambulate after amputation, in contrast to 97% who will ambulate after limb salvage as a primary procedure. In a nonambulatory cohort, 21% of those patients go on to regain functional status that was lost prior to surgery (J Vasc Surg. 1997;25;287-95).
Many question if our success with vascular surgery over the past few decades can translate to helping the most difficult subset of patients. An Italian study reported on a cohort of diabetic vs. nondiabetic patients and determined both groups have similar amputation-free rates after infrainguinal arterial reconstruction for critical limb ischemia, with excellent primary and secondary patency rates and a limb salvage rate of 88% at 5 years (J Vasc Surg. 2014;59:708-19). This tells us that we do have the skill set necessary to save these limbs.
A multidisciplinary limb preservation team is paramount to the success of any limb salvage program. A revascularization team should be in place which uses early intervention to achieve the highest limb salvage rates possible. Wound care needs to be an integrated part of it. Advanced podiatric reconstructive surgery also is key because this can provide complex foot reconstructions and help ambulatory patients return home.
Dr. Trissa A. Babrowski is an assistant professor of surgery, specializing in vascular surgery and endovascular therapy, at the University of Chicago Heart and Vascular Center. She had no financial relationships to disclose.
Primary amputation can be OK
I am not an amputationalist. I do practice limb salvage. In fact I’m probably the most aggressive limb salvage surgeon in my hospital. But primary amputation is a completely acceptable option for a selected group of patients with diabetes. We should not try to do limb salvage “at all costs.”
I do not find this to be a contradictory position. In fact, I think it adds credence to my support of limb salvage that I think primary amputation can be OK. In all honesty, there are very few things in life that should be done at all costs.
A study out of Loma Linda University involving patients with CLI compared primary amputation vs. revascularization; 43% of patients had a primary amputation (Ann Vasc Surg. 2007;21:458-63). A multivariate analysis showed that patients with major tissue loss, end-stage renal disease (ESRD), diabetes and nonambulatory status were more likely to undergo primary amputation rather than revascularization.
While major tissue loss (Rutherford category 6) is certainly an indication for primary amputation, ambulatory status can represent a gray area in determining the best course. ESRD and diabetes are much more nonspecific factors; probably more than 10% of the patients that we see with CLI have ESRD. Also, 50%-70% of these patients with CLI, and in some series even higher percentages, have diabetes. Thus, these factors by themselves do not assist us in determining which patients potentially should be offered primary amputation vs. revascularization.
In general, we know that we can get good results in limb bypass or revascularization in patients with CLI: The PREVENT III multicenter trial, with the use of the vein as the conduit, showed 1-year limb salvage rates of 88% in these high-risk patients (J Vasc Surg. 2006;43:742-51). However, one of the major risk factors that adversely affected outcome was ESRD.
We know that ESRD is a significant predictor of lowering our chances of saving a limb successfully. Knowing the cost of multiple continued episodes of revascularization in these patients prior to proceeding with an amputation, it’s intuitive that these patients would benefit from a more precise process in their treatment from the beginning. A number of papers have concluded that a primary amputation may be the preferred approach in patients with ESRD.
Can we preoperatively predict which patients with CLI will fail operative revascularization? Data from the New England Vascular Quality Initiative identified eight variables associated with failure of revascularization, among them age younger than 59, ESRD, diabetes, CLI, conduit requiring venovenostomy, tarsal target, and nursing home residence (Ann Vasc Surg. 2010;24:57-68). The presence of three or more risk factors has a 27.7% risk of limb loss and/or graft thrombosis within 1 year.
Postponing amputation is a major cost issue. Direct costs of bypass for critical limb ischemia were $3.6 billion in 2004 (J Vasc Surg. 2011;54:1021-31), and we know that a functional outcome can be problematic in this patient group. Factors associated with a poor functional outcome include dementia, dependent-living situation preoperatively and nonambulatory status.
Unfortunately, there are not a lot of data that deal with quality of life outcomes for patients with CLI who have undergone bypass. Using a point system comprised of dialysis (4 points), tissue loss (3 points), age above 75 (2 points), hematocrit less than or equal to 30 (2 points), and coronary artery disease (1 point), a follow-up study of patients in the PREVENT III trial found that a high-risk group (greater than or equal to 8 points) had an amputation-free survival of only 45% (J Vasc Surg. 2009;50:769-75). Again, these results do not justify the effort and costs of limb salvage in this high-risk patient group.
We should consider the following options carefully in selecting a cost-effective patient-focused approach in patients with CLI: wound care, primary amputation, bypass revascularization, or endovascular revascularization. I would argue that the vascular surgeon who is qualified as an expert in all of the above is best positioned to select an appropriate plan of treatment based upon the patient’s risk factors, wound factors, ambulatory ability, pattern of disease, severity of ischemia, and living status.
Thus, upon presentation, a patient with CLI should undergo confirmatory tests and optimize his or her risk factors. The vascular surgeon then has the option, in discussion with the patient and family, to pursue an appropriate treatment plan inclusive of primary amputation – not one of limb salvage “at all costs.”
Primary amputation should be used in situations where there is dementia and nonambulatory status, and in patients who are poor candidates for revascularization because of high risk of failure and limited life expectancy. The recently developed WIfI (wound, ischemia, and foot infection) classification can also be utilized, as stage 4 WIfI classification is associated with high risk of limb loss – 38%-40% at 1 year.
Primary amputation is an option that can result in better care overall, and it is a cost-effective approach for a selected group of patients. We should not try to do limb salvage at all cost. Primary amputation, in selected patients, is OK.
Dr. Timothy J. Nypaver is head of vascular surgery at Henry Ford Hospital, Detroit. He had no financial relationships to disclose.
Salvage limbs at all costs
Aggressive limb salvage in people with diabetes leads to an overall reduction in cost not only economically, but also from the patient’s perspective. The vast majority of diabetic patients with critical ischemia are actually good candidates for limb salvage. Tragically, many of these patients are never referred for evaluation for limb salvage because of misconceptions about the pathophysiology of the disease.
An argument against limb salvage is that primary amputation prevents or shortens the course of wound care and enables patients to become ambulatory, albeit with a prosthesis, faster. However, in the modern era of vascular surgery, revascularization can be performed successfully with minimal mortality and excellent rates of limb salvage, especially when it’s done within a team-based approach.
The mortality in primary amputation is shockingly high, anywhere from 5% to 23% higher than revascularization alone, and the major complication rate of amputation associated with diabetes is also unacceptably high – up to 37%. This is in contrast to a 17% rate in major nonamputation vascular surgery and 1%-5% in endovascular procedures (BMC Nephrol. 2005;6:3).
We can’t ignore the economic burden this places on the country. In 2014, primary amputations cost the health care system $11 billion annually, and that is expected to grow to more than $25 billion in the next several years, according to the SAGE Group. It’s important to keep in mind that Medicare covers over 80% of this cost.
A number of studies have shown that conservative management with wound care and amputation is more cost effective than primary amputation in ambulatory, independent adults. Data can be difficult to interpret because of different recording strategies for all the costs associated with amputation, but a single-institution study concluded that revascularization costs almost $5,280 more than expectant management, but $33,900 less than primary amputation alone (Cardiovasc Surg. 1999;7;62-9).
We must also consider the costs of revision after primary amputation; above-the-knee amputation has a 12% in-hospital revision rate, and below-the-knee amputation about 20%. Endovascular interventions, on the other hand, have a 1%-9% in-hospital revision rate, and only 2%-4% of these patients will go on to require an amputation during the same admission (Eur J Vasc Endovasc Surg. 2006;32:484-90; Arch Phys Med Rehabil. 2005;86:480-6).This does not include the costs of those complications as well as other indirect costs of amputation, such as nursing home care and living situation modification (Int J Behav Med. 2016;23:714-21; Pak J Med Sci. 2014; 30:1044-9). They quickly add up to that $25 billion.
The proponents of primary amputation tell us that it leads to quicker recovery time and an earlier time to ambulation. However, only 47% of patients will actually ambulate after amputation, in contrast to 97% who will ambulate after limb salvage as a primary procedure. In a nonambulatory cohort, 21% of those patients go on to regain functional status that was lost prior to surgery (J Vasc Surg. 1997;25;287-95).
Many question if our success with vascular surgery over the past few decades can translate to helping the most difficult subset of patients. An Italian study reported on a cohort of diabetic vs. nondiabetic patients and determined both groups have similar amputation-free rates after infrainguinal arterial reconstruction for critical limb ischemia, with excellent primary and secondary patency rates and a limb salvage rate of 88% at 5 years (J Vasc Surg. 2014;59:708-19). This tells us that we do have the skill set necessary to save these limbs.
A multidisciplinary limb preservation team is paramount to the success of any limb salvage program. A revascularization team should be in place which uses early intervention to achieve the highest limb salvage rates possible. Wound care needs to be an integrated part of it. Advanced podiatric reconstructive surgery also is key because this can provide complex foot reconstructions and help ambulatory patients return home.
Dr. Trissa A. Babrowski is an assistant professor of surgery, specializing in vascular surgery and endovascular therapy, at the University of Chicago Heart and Vascular Center. She had no financial relationships to disclose.
Primary amputation can be OK
I am not an amputationalist. I do practice limb salvage. In fact I’m probably the most aggressive limb salvage surgeon in my hospital. But primary amputation is a completely acceptable option for a selected group of patients with diabetes. We should not try to do limb salvage “at all costs.”
I do not find this to be a contradictory position. In fact, I think it adds credence to my support of limb salvage that I think primary amputation can be OK. In all honesty, there are very few things in life that should be done at all costs.
A study out of Loma Linda University involving patients with CLI compared primary amputation vs. revascularization; 43% of patients had a primary amputation (Ann Vasc Surg. 2007;21:458-63). A multivariate analysis showed that patients with major tissue loss, end-stage renal disease (ESRD), diabetes and nonambulatory status were more likely to undergo primary amputation rather than revascularization.
While major tissue loss (Rutherford category 6) is certainly an indication for primary amputation, ambulatory status can represent a gray area in determining the best course. ESRD and diabetes are much more nonspecific factors; probably more than 10% of the patients that we see with CLI have ESRD. Also, 50%-70% of these patients with CLI, and in some series even higher percentages, have diabetes. Thus, these factors by themselves do not assist us in determining which patients potentially should be offered primary amputation vs. revascularization.
In general, we know that we can get good results in limb bypass or revascularization in patients with CLI: The PREVENT III multicenter trial, with the use of the vein as the conduit, showed 1-year limb salvage rates of 88% in these high-risk patients (J Vasc Surg. 2006;43:742-51). However, one of the major risk factors that adversely affected outcome was ESRD.
We know that ESRD is a significant predictor of lowering our chances of saving a limb successfully. Knowing the cost of multiple continued episodes of revascularization in these patients prior to proceeding with an amputation, it’s intuitive that these patients would benefit from a more precise process in their treatment from the beginning. A number of papers have concluded that a primary amputation may be the preferred approach in patients with ESRD.
Can we preoperatively predict which patients with CLI will fail operative revascularization? Data from the New England Vascular Quality Initiative identified eight variables associated with failure of revascularization, among them age younger than 59, ESRD, diabetes, CLI, conduit requiring venovenostomy, tarsal target, and nursing home residence (Ann Vasc Surg. 2010;24:57-68). The presence of three or more risk factors has a 27.7% risk of limb loss and/or graft thrombosis within 1 year.
Postponing amputation is a major cost issue. Direct costs of bypass for critical limb ischemia were $3.6 billion in 2004 (J Vasc Surg. 2011;54:1021-31), and we know that a functional outcome can be problematic in this patient group. Factors associated with a poor functional outcome include dementia, dependent-living situation preoperatively and nonambulatory status.
Unfortunately, there are not a lot of data that deal with quality of life outcomes for patients with CLI who have undergone bypass. Using a point system comprised of dialysis (4 points), tissue loss (3 points), age above 75 (2 points), hematocrit less than or equal to 30 (2 points), and coronary artery disease (1 point), a follow-up study of patients in the PREVENT III trial found that a high-risk group (greater than or equal to 8 points) had an amputation-free survival of only 45% (J Vasc Surg. 2009;50:769-75). Again, these results do not justify the effort and costs of limb salvage in this high-risk patient group.
We should consider the following options carefully in selecting a cost-effective patient-focused approach in patients with CLI: wound care, primary amputation, bypass revascularization, or endovascular revascularization. I would argue that the vascular surgeon who is qualified as an expert in all of the above is best positioned to select an appropriate plan of treatment based upon the patient’s risk factors, wound factors, ambulatory ability, pattern of disease, severity of ischemia, and living status.
Thus, upon presentation, a patient with CLI should undergo confirmatory tests and optimize his or her risk factors. The vascular surgeon then has the option, in discussion with the patient and family, to pursue an appropriate treatment plan inclusive of primary amputation – not one of limb salvage “at all costs.”
Primary amputation should be used in situations where there is dementia and nonambulatory status, and in patients who are poor candidates for revascularization because of high risk of failure and limited life expectancy. The recently developed WIfI (wound, ischemia, and foot infection) classification can also be utilized, as stage 4 WIfI classification is associated with high risk of limb loss – 38%-40% at 1 year.
Primary amputation is an option that can result in better care overall, and it is a cost-effective approach for a selected group of patients. We should not try to do limb salvage at all cost. Primary amputation, in selected patients, is OK.
Dr. Timothy J. Nypaver is head of vascular surgery at Henry Ford Hospital, Detroit. He had no financial relationships to disclose.
Salvage limbs at all costs
Aggressive limb salvage in people with diabetes leads to an overall reduction in cost not only economically, but also from the patient’s perspective. The vast majority of diabetic patients with critical ischemia are actually good candidates for limb salvage. Tragically, many of these patients are never referred for evaluation for limb salvage because of misconceptions about the pathophysiology of the disease.
An argument against limb salvage is that primary amputation prevents or shortens the course of wound care and enables patients to become ambulatory, albeit with a prosthesis, faster. However, in the modern era of vascular surgery, revascularization can be performed successfully with minimal mortality and excellent rates of limb salvage, especially when it’s done within a team-based approach.
The mortality in primary amputation is shockingly high, anywhere from 5% to 23% higher than revascularization alone, and the major complication rate of amputation associated with diabetes is also unacceptably high – up to 37%. This is in contrast to a 17% rate in major nonamputation vascular surgery and 1%-5% in endovascular procedures (BMC Nephrol. 2005;6:3).
We can’t ignore the economic burden this places on the country. In 2014, primary amputations cost the health care system $11 billion annually, and that is expected to grow to more than $25 billion in the next several years, according to the SAGE Group. It’s important to keep in mind that Medicare covers over 80% of this cost.
A number of studies have shown that conservative management with wound care and amputation is more cost effective than primary amputation in ambulatory, independent adults. Data can be difficult to interpret because of different recording strategies for all the costs associated with amputation, but a single-institution study concluded that revascularization costs almost $5,280 more than expectant management, but $33,900 less than primary amputation alone (Cardiovasc Surg. 1999;7;62-9).
We must also consider the costs of revision after primary amputation; above-the-knee amputation has a 12% in-hospital revision rate, and below-the-knee amputation about 20%. Endovascular interventions, on the other hand, have a 1%-9% in-hospital revision rate, and only 2%-4% of these patients will go on to require an amputation during the same admission (Eur J Vasc Endovasc Surg. 2006;32:484-90; Arch Phys Med Rehabil. 2005;86:480-6).This does not include the costs of those complications as well as other indirect costs of amputation, such as nursing home care and living situation modification (Int J Behav Med. 2016;23:714-21; Pak J Med Sci. 2014; 30:1044-9). They quickly add up to that $25 billion.
The proponents of primary amputation tell us that it leads to quicker recovery time and an earlier time to ambulation. However, only 47% of patients will actually ambulate after amputation, in contrast to 97% who will ambulate after limb salvage as a primary procedure. In a nonambulatory cohort, 21% of those patients go on to regain functional status that was lost prior to surgery (J Vasc Surg. 1997;25;287-95).
Many question if our success with vascular surgery over the past few decades can translate to helping the most difficult subset of patients. An Italian study reported on a cohort of diabetic vs. nondiabetic patients and determined both groups have similar amputation-free rates after infrainguinal arterial reconstruction for critical limb ischemia, with excellent primary and secondary patency rates and a limb salvage rate of 88% at 5 years (J Vasc Surg. 2014;59:708-19). This tells us that we do have the skill set necessary to save these limbs.
A multidisciplinary limb preservation team is paramount to the success of any limb salvage program. A revascularization team should be in place which uses early intervention to achieve the highest limb salvage rates possible. Wound care needs to be an integrated part of it. Advanced podiatric reconstructive surgery also is key because this can provide complex foot reconstructions and help ambulatory patients return home.
Dr. Trissa A. Babrowski is an assistant professor of surgery, specializing in vascular surgery and endovascular therapy, at the University of Chicago Heart and Vascular Center. She had no financial relationships to disclose.
Primary amputation can be OK
I am not an amputationalist. I do practice limb salvage. In fact I’m probably the most aggressive limb salvage surgeon in my hospital. But primary amputation is a completely acceptable option for a selected group of patients with diabetes. We should not try to do limb salvage “at all costs.”
I do not find this to be a contradictory position. In fact, I think it adds credence to my support of limb salvage that I think primary amputation can be OK. In all honesty, there are very few things in life that should be done at all costs.
A study out of Loma Linda University involving patients with CLI compared primary amputation vs. revascularization; 43% of patients had a primary amputation (Ann Vasc Surg. 2007;21:458-63). A multivariate analysis showed that patients with major tissue loss, end-stage renal disease (ESRD), diabetes and nonambulatory status were more likely to undergo primary amputation rather than revascularization.
While major tissue loss (Rutherford category 6) is certainly an indication for primary amputation, ambulatory status can represent a gray area in determining the best course. ESRD and diabetes are much more nonspecific factors; probably more than 10% of the patients that we see with CLI have ESRD. Also, 50%-70% of these patients with CLI, and in some series even higher percentages, have diabetes. Thus, these factors by themselves do not assist us in determining which patients potentially should be offered primary amputation vs. revascularization.
In general, we know that we can get good results in limb bypass or revascularization in patients with CLI: The PREVENT III multicenter trial, with the use of the vein as the conduit, showed 1-year limb salvage rates of 88% in these high-risk patients (J Vasc Surg. 2006;43:742-51). However, one of the major risk factors that adversely affected outcome was ESRD.
We know that ESRD is a significant predictor of lowering our chances of saving a limb successfully. Knowing the cost of multiple continued episodes of revascularization in these patients prior to proceeding with an amputation, it’s intuitive that these patients would benefit from a more precise process in their treatment from the beginning. A number of papers have concluded that a primary amputation may be the preferred approach in patients with ESRD.
Can we preoperatively predict which patients with CLI will fail operative revascularization? Data from the New England Vascular Quality Initiative identified eight variables associated with failure of revascularization, among them age younger than 59, ESRD, diabetes, CLI, conduit requiring venovenostomy, tarsal target, and nursing home residence (Ann Vasc Surg. 2010;24:57-68). The presence of three or more risk factors has a 27.7% risk of limb loss and/or graft thrombosis within 1 year.
Postponing amputation is a major cost issue. Direct costs of bypass for critical limb ischemia were $3.6 billion in 2004 (J Vasc Surg. 2011;54:1021-31), and we know that a functional outcome can be problematic in this patient group. Factors associated with a poor functional outcome include dementia, dependent-living situation preoperatively and nonambulatory status.
Unfortunately, there are not a lot of data that deal with quality of life outcomes for patients with CLI who have undergone bypass. Using a point system comprised of dialysis (4 points), tissue loss (3 points), age above 75 (2 points), hematocrit less than or equal to 30 (2 points), and coronary artery disease (1 point), a follow-up study of patients in the PREVENT III trial found that a high-risk group (greater than or equal to 8 points) had an amputation-free survival of only 45% (J Vasc Surg. 2009;50:769-75). Again, these results do not justify the effort and costs of limb salvage in this high-risk patient group.
We should consider the following options carefully in selecting a cost-effective patient-focused approach in patients with CLI: wound care, primary amputation, bypass revascularization, or endovascular revascularization. I would argue that the vascular surgeon who is qualified as an expert in all of the above is best positioned to select an appropriate plan of treatment based upon the patient’s risk factors, wound factors, ambulatory ability, pattern of disease, severity of ischemia, and living status.
Thus, upon presentation, a patient with CLI should undergo confirmatory tests and optimize his or her risk factors. The vascular surgeon then has the option, in discussion with the patient and family, to pursue an appropriate treatment plan inclusive of primary amputation – not one of limb salvage “at all costs.”
Primary amputation should be used in situations where there is dementia and nonambulatory status, and in patients who are poor candidates for revascularization because of high risk of failure and limited life expectancy. The recently developed WIfI (wound, ischemia, and foot infection) classification can also be utilized, as stage 4 WIfI classification is associated with high risk of limb loss – 38%-40% at 1 year.
Primary amputation is an option that can result in better care overall, and it is a cost-effective approach for a selected group of patients. We should not try to do limb salvage at all cost. Primary amputation, in selected patients, is OK.
Dr. Timothy J. Nypaver is head of vascular surgery at Henry Ford Hospital, Detroit. He had no financial relationships to disclose.
Should clopidogrel be discontinued prior to open vascular procedures?
The continued use of perioperative clopidogrel is appropriate
Surgeons have always worried about bleeding risks for procedures we do. Complex vascular procedures are further complicated by the myriad of available antiplatelet agents designed to reduce ischemic events from cardiovascular disease burden at the expense of potential bleeding complications if antiplatelet medications are continued. Rather than relying on anecdotal reports by historical vignettes, let’s look at the evidence.
There probably is no other drug available in our vascular toolbox which has been studied more in the last 20 years than clopidogrel. Multiple randomized and double blinded studies such as CASPAR1 and CHARISMA2 have amplified what was known since the early CAPRIE trial in the 1990’s and that is that clopidogrel is safe when used as a single medication or as a dual agent with aspirin (duel antiplatelet therapy [DAPT]).
But not all our patients need DAPT. There is no level 1 evidence demonstrating the need for any antiplatelet therapy in the primary prevention of cardiovascular events for patients deemed at low or moderate risk of cardiovascular disease from a large meta-analysis review of six primary prevention trials encompassing over 95,000 patients.3
If our patients do present with vascular disease, current ACCP guidelines recommend single-agent antiplatelet medication (either ASA or clopidogrel) for symptomatic peripheral arterial disease (PAD) whether planning LE revascularization with bypass or via endovascular means with grade 1A evidence.4 This works fine for single-focus vascular disease and each antiplatelet agent have proponents but either works well.
That’s great, but what about all those sick cardiac patients we see the most of? First, CHARISMA subgroup analysis of patients with preexisting coronary and/or cerebrovascular disease demonstrate a 7.1% risk reduction in MI, cerebrovascular events, and cardiac ischemic deaths when continuing DAPT over aspirin alone, and similar risk reduction is found in PAD patients for endpoints of MI and ischemic cardiovascular events. Second, there was no significant difference in severe, fatal, or moderate bleeding in those receiving DAPT vs. aspirin alone with only minor bleeding increased using DAPT. Third, real-life practice echoes multiple trial experiences such as the Vascular Study Group of New England study group confirmed in reviewing 16 centers and 66 surgeons with more than 10,000 patients. Approximately 39% underwent major aortic or lower extremity bypass operations.
No statistical difference could be found for reoperation (P = .74), transfusion (P = .1) or operative type between DAPT or aspirin use alone.5 This is rediscovered once again by Saadeh and Sfeir in their prospective study of 647 major arterial procedures over 7 years finding no significant difference in reoperation for bleeding or bleeding mortality between DAPT vs. aspirin alone.6
So can we stop bashing clopidogrel as an evil agent of bleeding as Dr. Dalsing wishes to do? After all, he has been on record as stating, “I don’t know if our bleeding risk is worse or better … something we have to do to keep our grafts going.” Evidence tells us the benefits for continuing DAPT as seen in risk reduction in primary cardiovascular outcomes far outweigh the risk of minor bleeding associated with continued use.
Let the science dictate practice. Patients with low or moderate risk for cardiovascular disease need no antiplatelet medication unless undergoing PAD treatment where a single agent, either aspirin or clopidogrel alone, is sufficient. In those patients having a large cardiovascular burden of disease, combination of aspirin and clopidogrel improves survival benefit and reduces ischemic events without a significant risk of reoperation, transfusion, or bleeding-related mortality. As many of our patients require DAPT for drug eluting coronary stents, withholding clopidogrel preoperatively increases overall risk beyond acceptable limits. Improving surgical skills and paying attention to hemostasis during the operation will allow naysayers to achieve improved patient survival without fear of bleeding when continuing best medical therapy such as DAPT.
Gary Lemmon, MD, is professor of vascular surgery at Indiana University, Indianapolis, and chief, vascular surgery, Indianapolis VA Medical Center. He reported no relevant conflicts.
References
1. J Vasc Surg. 2010;52:825-33
2. Eur Heart J. 2009;30:192-201
3. Lancet. 2009;373:1849-604. Chest. 2012;141:e669s-90s
5. J Vasc Surg. 2011;54: 779-84
6. J Vasc Surg. 2013;58: 1586-92
The continued use of perioperative clopidogrel is debatable!
There are cases in which clopidogrel should not be discontinued for a needed vascular intervention. Delaying operation or maintaining clopidogrel during operation if your patient required a recent coronary stent is warranted unless you are willing to accept an acute coronary thrombosis.
However, in other cases, for example infrainguinal grafts, the risk of potential increased bleeding when adding clopidogrel to aspirin may outweigh potential improvements in graft patency. This is especially true of below-knee vein bypass grafts where data do not support improved patency. However, in the CASPAR trial, prosthetic graft patency did appear to be beneficial, but only in subgroup analysis.1
It is true that severe bleeding was not increased (intracranial hemorrhage, or hemodynamic compromise: 1 vs 2.7%, P = NS) but moderate bleeding (transfusion required: 0.7 vs 3.7%, P = .012) and mild bleeding (5.4 vs 12.1%, P = .004) was increased when this agent was used especially in vein graft surgery. This risk of bleeding was present even when clopidogrel was begun 2 or more days after surgery.1
To complicate this decision, a Cochrane review did not consider subgroup analysis as statistically valid and so the authors considered infrainguinal graft patency as not improved with clopidogrel but bleeding risk was increased. One might even question the use of acetylsalicylic acid (ASA) for vein graft bypasses based on the results of this metanalysis.2 Carotid endarterectomy is a common vascular surgery procedure in which antiplatelet use has been evaluated in the real-world situation and with large cohorts. As is always the case when dealing with patient issues, the addition of one agent does not tell the entire story and patient demographics can have a significant influence on the outcome. A report from the Vascular Quality Initiative (VQI) database controlled for patient differences by propensity matching with more than 4,500 patients in each of the two groups; ASA vs. ASA + clopidogrel; demonstrated that major bleeding, defined as return to the OR for bleeding, was statistically more common with dual therapy (1.3% vs. 0.7%, P = .004).3
The addition of clopidogrel did statistically decrease the risk of ipsilateral TIA or stroke (0.8% vs. 1.2%, P = .02) but not the risk of death (0.2% vs. 0.3%, P = .3) or postoperative MI (1% vs. 0.8%, P = .4). Reoperation for bleeding is not inconsequential since in patients requiring this intervention, there is a significantly worse outcome in regard to stroke (3.7% vs. 0.8%, P = .001), MI (6.2% vs. 0.8%, P = .001), and death (2.5% vs. 0.2%,P = .001). Further drill down involving propensity score–matched analysis stratified by symptom status (asymptomatic vs. symptomatic) was quite interesting in that in only asymptomatic patients did the addition of clopidogrel actually demonstrate a statistically significant reduction in TIA or stroke, any stroke, or composite stroke/death. Symptomatic patients taking dual therapy demonstrated a slight reduction in TIA or stroke (1.4% vs. 1.7%, P = .6), any stroke (1.1% vs. 1.2%, P = .9) and composite stroke/death (1.2% vs. 1.5%, P = .5) but in no instance was statistical significance reached. The use of protamine did help to decrease the risk of bleeding.
Regarding the use of dual therapy during open aortic operations, an earlier report of the VQI database demonstrated no significant difference in bleeding risk statistically, but if one delves deeper the data indicate something different. In the majority of cases, vascular surgeons do not feel comfortable preforming this extensive dissection on dual therapy. Of the cases reported, 1,074 were preformed either free of either drug or only on ASA while 42 were on dual therapy and only 12 on clopidogrel only. In fact, in the conclusions, the authors note that they do not believe that conclusions regarding clopidogrel use in patient undergoing open abdominal aortic aneurysm repair can be drawn based on their results since the potential for a type II error was too great.4
It may be that our current level of sophistication is not sufficiently mature to determine the actual effect that clopidogrel is having on our patients. Clopidogrel, a thienopyridine, inhibits platelet activation by blocking the ADP-binding site for the P2Y12 receptor. Over 85% of ingested drug is metabolized into inactive metabolites while 15% is metabolized by the liver via a two-step oxidative process into the active thiol metabolite. Inter-individual variability in the antiplatelet response to thienopyridines is noted and partially caused by genetic mutations in the CP isoenzymes. Platelet reactivity testing is possible but most of the work has been conducted for those patients requiring coronary artery revascularization. Results of tailoring intervention to maximize therapeutic benefit and decrease the risk of bleeding have been inconsistent but, in some studies, appear to be promising.5 This approach may ultimately be found superior to determining how effective clopidogrel actually is in a particular case with some insight into the bleeding risk as well. With this determination, whether or not to hold clopidogrel perioperatively can be made with some science behind the decision.
Clearly, a blanket statement that the risk of bleeding should be accepted or ignored because of the demonstrated benefits of clopidogrel in patients requiring vascular surgery is not accurate. In some cases, there is no clear benefit, so eliminating the bleeding risk may well be the appropriate decision. The astute vascular surgeon understands the details of the written word in order to make an educated decision and understands that new information such as determining platelet reactivity may provide more clarity to such decisions in the future.
Michael C. Dalsing, MD, is chief of vascular surgery at Indiana University, Indianapolis. He reported no relevant conflicts.
References
1. J Vasc Surg. 2010;52:825-33
2. Cochrane Database Syst Rev. 2015, Issue 2. Art. No.: CD000535
The continued use of perioperative clopidogrel is appropriate
Surgeons have always worried about bleeding risks for procedures we do. Complex vascular procedures are further complicated by the myriad of available antiplatelet agents designed to reduce ischemic events from cardiovascular disease burden at the expense of potential bleeding complications if antiplatelet medications are continued. Rather than relying on anecdotal reports by historical vignettes, let’s look at the evidence.
There probably is no other drug available in our vascular toolbox which has been studied more in the last 20 years than clopidogrel. Multiple randomized and double blinded studies such as CASPAR1 and CHARISMA2 have amplified what was known since the early CAPRIE trial in the 1990’s and that is that clopidogrel is safe when used as a single medication or as a dual agent with aspirin (duel antiplatelet therapy [DAPT]).
But not all our patients need DAPT. There is no level 1 evidence demonstrating the need for any antiplatelet therapy in the primary prevention of cardiovascular events for patients deemed at low or moderate risk of cardiovascular disease from a large meta-analysis review of six primary prevention trials encompassing over 95,000 patients.3
If our patients do present with vascular disease, current ACCP guidelines recommend single-agent antiplatelet medication (either ASA or clopidogrel) for symptomatic peripheral arterial disease (PAD) whether planning LE revascularization with bypass or via endovascular means with grade 1A evidence.4 This works fine for single-focus vascular disease and each antiplatelet agent have proponents but either works well.
That’s great, but what about all those sick cardiac patients we see the most of? First, CHARISMA subgroup analysis of patients with preexisting coronary and/or cerebrovascular disease demonstrate a 7.1% risk reduction in MI, cerebrovascular events, and cardiac ischemic deaths when continuing DAPT over aspirin alone, and similar risk reduction is found in PAD patients for endpoints of MI and ischemic cardiovascular events. Second, there was no significant difference in severe, fatal, or moderate bleeding in those receiving DAPT vs. aspirin alone with only minor bleeding increased using DAPT. Third, real-life practice echoes multiple trial experiences such as the Vascular Study Group of New England study group confirmed in reviewing 16 centers and 66 surgeons with more than 10,000 patients. Approximately 39% underwent major aortic or lower extremity bypass operations.
No statistical difference could be found for reoperation (P = .74), transfusion (P = .1) or operative type between DAPT or aspirin use alone.5 This is rediscovered once again by Saadeh and Sfeir in their prospective study of 647 major arterial procedures over 7 years finding no significant difference in reoperation for bleeding or bleeding mortality between DAPT vs. aspirin alone.6
So can we stop bashing clopidogrel as an evil agent of bleeding as Dr. Dalsing wishes to do? After all, he has been on record as stating, “I don’t know if our bleeding risk is worse or better … something we have to do to keep our grafts going.” Evidence tells us the benefits for continuing DAPT as seen in risk reduction in primary cardiovascular outcomes far outweigh the risk of minor bleeding associated with continued use.
Let the science dictate practice. Patients with low or moderate risk for cardiovascular disease need no antiplatelet medication unless undergoing PAD treatment where a single agent, either aspirin or clopidogrel alone, is sufficient. In those patients having a large cardiovascular burden of disease, combination of aspirin and clopidogrel improves survival benefit and reduces ischemic events without a significant risk of reoperation, transfusion, or bleeding-related mortality. As many of our patients require DAPT for drug eluting coronary stents, withholding clopidogrel preoperatively increases overall risk beyond acceptable limits. Improving surgical skills and paying attention to hemostasis during the operation will allow naysayers to achieve improved patient survival without fear of bleeding when continuing best medical therapy such as DAPT.
Gary Lemmon, MD, is professor of vascular surgery at Indiana University, Indianapolis, and chief, vascular surgery, Indianapolis VA Medical Center. He reported no relevant conflicts.
References
1. J Vasc Surg. 2010;52:825-33
2. Eur Heart J. 2009;30:192-201
3. Lancet. 2009;373:1849-604. Chest. 2012;141:e669s-90s
5. J Vasc Surg. 2011;54: 779-84
6. J Vasc Surg. 2013;58: 1586-92
The continued use of perioperative clopidogrel is debatable!
There are cases in which clopidogrel should not be discontinued for a needed vascular intervention. Delaying operation or maintaining clopidogrel during operation if your patient required a recent coronary stent is warranted unless you are willing to accept an acute coronary thrombosis.
However, in other cases, for example infrainguinal grafts, the risk of potential increased bleeding when adding clopidogrel to aspirin may outweigh potential improvements in graft patency. This is especially true of below-knee vein bypass grafts where data do not support improved patency. However, in the CASPAR trial, prosthetic graft patency did appear to be beneficial, but only in subgroup analysis.1
It is true that severe bleeding was not increased (intracranial hemorrhage, or hemodynamic compromise: 1 vs 2.7%, P = NS) but moderate bleeding (transfusion required: 0.7 vs 3.7%, P = .012) and mild bleeding (5.4 vs 12.1%, P = .004) was increased when this agent was used especially in vein graft surgery. This risk of bleeding was present even when clopidogrel was begun 2 or more days after surgery.1
To complicate this decision, a Cochrane review did not consider subgroup analysis as statistically valid and so the authors considered infrainguinal graft patency as not improved with clopidogrel but bleeding risk was increased. One might even question the use of acetylsalicylic acid (ASA) for vein graft bypasses based on the results of this metanalysis.2 Carotid endarterectomy is a common vascular surgery procedure in which antiplatelet use has been evaluated in the real-world situation and with large cohorts. As is always the case when dealing with patient issues, the addition of one agent does not tell the entire story and patient demographics can have a significant influence on the outcome. A report from the Vascular Quality Initiative (VQI) database controlled for patient differences by propensity matching with more than 4,500 patients in each of the two groups; ASA vs. ASA + clopidogrel; demonstrated that major bleeding, defined as return to the OR for bleeding, was statistically more common with dual therapy (1.3% vs. 0.7%, P = .004).3
The addition of clopidogrel did statistically decrease the risk of ipsilateral TIA or stroke (0.8% vs. 1.2%, P = .02) but not the risk of death (0.2% vs. 0.3%, P = .3) or postoperative MI (1% vs. 0.8%, P = .4). Reoperation for bleeding is not inconsequential since in patients requiring this intervention, there is a significantly worse outcome in regard to stroke (3.7% vs. 0.8%, P = .001), MI (6.2% vs. 0.8%, P = .001), and death (2.5% vs. 0.2%,P = .001). Further drill down involving propensity score–matched analysis stratified by symptom status (asymptomatic vs. symptomatic) was quite interesting in that in only asymptomatic patients did the addition of clopidogrel actually demonstrate a statistically significant reduction in TIA or stroke, any stroke, or composite stroke/death. Symptomatic patients taking dual therapy demonstrated a slight reduction in TIA or stroke (1.4% vs. 1.7%, P = .6), any stroke (1.1% vs. 1.2%, P = .9) and composite stroke/death (1.2% vs. 1.5%, P = .5) but in no instance was statistical significance reached. The use of protamine did help to decrease the risk of bleeding.
Regarding the use of dual therapy during open aortic operations, an earlier report of the VQI database demonstrated no significant difference in bleeding risk statistically, but if one delves deeper the data indicate something different. In the majority of cases, vascular surgeons do not feel comfortable preforming this extensive dissection on dual therapy. Of the cases reported, 1,074 were preformed either free of either drug or only on ASA while 42 were on dual therapy and only 12 on clopidogrel only. In fact, in the conclusions, the authors note that they do not believe that conclusions regarding clopidogrel use in patient undergoing open abdominal aortic aneurysm repair can be drawn based on their results since the potential for a type II error was too great.4
It may be that our current level of sophistication is not sufficiently mature to determine the actual effect that clopidogrel is having on our patients. Clopidogrel, a thienopyridine, inhibits platelet activation by blocking the ADP-binding site for the P2Y12 receptor. Over 85% of ingested drug is metabolized into inactive metabolites while 15% is metabolized by the liver via a two-step oxidative process into the active thiol metabolite. Inter-individual variability in the antiplatelet response to thienopyridines is noted and partially caused by genetic mutations in the CP isoenzymes. Platelet reactivity testing is possible but most of the work has been conducted for those patients requiring coronary artery revascularization. Results of tailoring intervention to maximize therapeutic benefit and decrease the risk of bleeding have been inconsistent but, in some studies, appear to be promising.5 This approach may ultimately be found superior to determining how effective clopidogrel actually is in a particular case with some insight into the bleeding risk as well. With this determination, whether or not to hold clopidogrel perioperatively can be made with some science behind the decision.
Clearly, a blanket statement that the risk of bleeding should be accepted or ignored because of the demonstrated benefits of clopidogrel in patients requiring vascular surgery is not accurate. In some cases, there is no clear benefit, so eliminating the bleeding risk may well be the appropriate decision. The astute vascular surgeon understands the details of the written word in order to make an educated decision and understands that new information such as determining platelet reactivity may provide more clarity to such decisions in the future.
Michael C. Dalsing, MD, is chief of vascular surgery at Indiana University, Indianapolis. He reported no relevant conflicts.
References
1. J Vasc Surg. 2010;52:825-33
2. Cochrane Database Syst Rev. 2015, Issue 2. Art. No.: CD000535
The continued use of perioperative clopidogrel is appropriate
Surgeons have always worried about bleeding risks for procedures we do. Complex vascular procedures are further complicated by the myriad of available antiplatelet agents designed to reduce ischemic events from cardiovascular disease burden at the expense of potential bleeding complications if antiplatelet medications are continued. Rather than relying on anecdotal reports by historical vignettes, let’s look at the evidence.
There probably is no other drug available in our vascular toolbox which has been studied more in the last 20 years than clopidogrel. Multiple randomized and double blinded studies such as CASPAR1 and CHARISMA2 have amplified what was known since the early CAPRIE trial in the 1990’s and that is that clopidogrel is safe when used as a single medication or as a dual agent with aspirin (duel antiplatelet therapy [DAPT]).
But not all our patients need DAPT. There is no level 1 evidence demonstrating the need for any antiplatelet therapy in the primary prevention of cardiovascular events for patients deemed at low or moderate risk of cardiovascular disease from a large meta-analysis review of six primary prevention trials encompassing over 95,000 patients.3
If our patients do present with vascular disease, current ACCP guidelines recommend single-agent antiplatelet medication (either ASA or clopidogrel) for symptomatic peripheral arterial disease (PAD) whether planning LE revascularization with bypass or via endovascular means with grade 1A evidence.4 This works fine for single-focus vascular disease and each antiplatelet agent have proponents but either works well.
That’s great, but what about all those sick cardiac patients we see the most of? First, CHARISMA subgroup analysis of patients with preexisting coronary and/or cerebrovascular disease demonstrate a 7.1% risk reduction in MI, cerebrovascular events, and cardiac ischemic deaths when continuing DAPT over aspirin alone, and similar risk reduction is found in PAD patients for endpoints of MI and ischemic cardiovascular events. Second, there was no significant difference in severe, fatal, or moderate bleeding in those receiving DAPT vs. aspirin alone with only minor bleeding increased using DAPT. Third, real-life practice echoes multiple trial experiences such as the Vascular Study Group of New England study group confirmed in reviewing 16 centers and 66 surgeons with more than 10,000 patients. Approximately 39% underwent major aortic or lower extremity bypass operations.
No statistical difference could be found for reoperation (P = .74), transfusion (P = .1) or operative type between DAPT or aspirin use alone.5 This is rediscovered once again by Saadeh and Sfeir in their prospective study of 647 major arterial procedures over 7 years finding no significant difference in reoperation for bleeding or bleeding mortality between DAPT vs. aspirin alone.6
So can we stop bashing clopidogrel as an evil agent of bleeding as Dr. Dalsing wishes to do? After all, he has been on record as stating, “I don’t know if our bleeding risk is worse or better … something we have to do to keep our grafts going.” Evidence tells us the benefits for continuing DAPT as seen in risk reduction in primary cardiovascular outcomes far outweigh the risk of minor bleeding associated with continued use.
Let the science dictate practice. Patients with low or moderate risk for cardiovascular disease need no antiplatelet medication unless undergoing PAD treatment where a single agent, either aspirin or clopidogrel alone, is sufficient. In those patients having a large cardiovascular burden of disease, combination of aspirin and clopidogrel improves survival benefit and reduces ischemic events without a significant risk of reoperation, transfusion, or bleeding-related mortality. As many of our patients require DAPT for drug eluting coronary stents, withholding clopidogrel preoperatively increases overall risk beyond acceptable limits. Improving surgical skills and paying attention to hemostasis during the operation will allow naysayers to achieve improved patient survival without fear of bleeding when continuing best medical therapy such as DAPT.
Gary Lemmon, MD, is professor of vascular surgery at Indiana University, Indianapolis, and chief, vascular surgery, Indianapolis VA Medical Center. He reported no relevant conflicts.
References
1. J Vasc Surg. 2010;52:825-33
2. Eur Heart J. 2009;30:192-201
3. Lancet. 2009;373:1849-604. Chest. 2012;141:e669s-90s
5. J Vasc Surg. 2011;54: 779-84
6. J Vasc Surg. 2013;58: 1586-92
The continued use of perioperative clopidogrel is debatable!
There are cases in which clopidogrel should not be discontinued for a needed vascular intervention. Delaying operation or maintaining clopidogrel during operation if your patient required a recent coronary stent is warranted unless you are willing to accept an acute coronary thrombosis.
However, in other cases, for example infrainguinal grafts, the risk of potential increased bleeding when adding clopidogrel to aspirin may outweigh potential improvements in graft patency. This is especially true of below-knee vein bypass grafts where data do not support improved patency. However, in the CASPAR trial, prosthetic graft patency did appear to be beneficial, but only in subgroup analysis.1
It is true that severe bleeding was not increased (intracranial hemorrhage, or hemodynamic compromise: 1 vs 2.7%, P = NS) but moderate bleeding (transfusion required: 0.7 vs 3.7%, P = .012) and mild bleeding (5.4 vs 12.1%, P = .004) was increased when this agent was used especially in vein graft surgery. This risk of bleeding was present even when clopidogrel was begun 2 or more days after surgery.1
To complicate this decision, a Cochrane review did not consider subgroup analysis as statistically valid and so the authors considered infrainguinal graft patency as not improved with clopidogrel but bleeding risk was increased. One might even question the use of acetylsalicylic acid (ASA) for vein graft bypasses based on the results of this metanalysis.2 Carotid endarterectomy is a common vascular surgery procedure in which antiplatelet use has been evaluated in the real-world situation and with large cohorts. As is always the case when dealing with patient issues, the addition of one agent does not tell the entire story and patient demographics can have a significant influence on the outcome. A report from the Vascular Quality Initiative (VQI) database controlled for patient differences by propensity matching with more than 4,500 patients in each of the two groups; ASA vs. ASA + clopidogrel; demonstrated that major bleeding, defined as return to the OR for bleeding, was statistically more common with dual therapy (1.3% vs. 0.7%, P = .004).3
The addition of clopidogrel did statistically decrease the risk of ipsilateral TIA or stroke (0.8% vs. 1.2%, P = .02) but not the risk of death (0.2% vs. 0.3%, P = .3) or postoperative MI (1% vs. 0.8%, P = .4). Reoperation for bleeding is not inconsequential since in patients requiring this intervention, there is a significantly worse outcome in regard to stroke (3.7% vs. 0.8%, P = .001), MI (6.2% vs. 0.8%, P = .001), and death (2.5% vs. 0.2%,P = .001). Further drill down involving propensity score–matched analysis stratified by symptom status (asymptomatic vs. symptomatic) was quite interesting in that in only asymptomatic patients did the addition of clopidogrel actually demonstrate a statistically significant reduction in TIA or stroke, any stroke, or composite stroke/death. Symptomatic patients taking dual therapy demonstrated a slight reduction in TIA or stroke (1.4% vs. 1.7%, P = .6), any stroke (1.1% vs. 1.2%, P = .9) and composite stroke/death (1.2% vs. 1.5%, P = .5) but in no instance was statistical significance reached. The use of protamine did help to decrease the risk of bleeding.
Regarding the use of dual therapy during open aortic operations, an earlier report of the VQI database demonstrated no significant difference in bleeding risk statistically, but if one delves deeper the data indicate something different. In the majority of cases, vascular surgeons do not feel comfortable preforming this extensive dissection on dual therapy. Of the cases reported, 1,074 were preformed either free of either drug or only on ASA while 42 were on dual therapy and only 12 on clopidogrel only. In fact, in the conclusions, the authors note that they do not believe that conclusions regarding clopidogrel use in patient undergoing open abdominal aortic aneurysm repair can be drawn based on their results since the potential for a type II error was too great.4
It may be that our current level of sophistication is not sufficiently mature to determine the actual effect that clopidogrel is having on our patients. Clopidogrel, a thienopyridine, inhibits platelet activation by blocking the ADP-binding site for the P2Y12 receptor. Over 85% of ingested drug is metabolized into inactive metabolites while 15% is metabolized by the liver via a two-step oxidative process into the active thiol metabolite. Inter-individual variability in the antiplatelet response to thienopyridines is noted and partially caused by genetic mutations in the CP isoenzymes. Platelet reactivity testing is possible but most of the work has been conducted for those patients requiring coronary artery revascularization. Results of tailoring intervention to maximize therapeutic benefit and decrease the risk of bleeding have been inconsistent but, in some studies, appear to be promising.5 This approach may ultimately be found superior to determining how effective clopidogrel actually is in a particular case with some insight into the bleeding risk as well. With this determination, whether or not to hold clopidogrel perioperatively can be made with some science behind the decision.
Clearly, a blanket statement that the risk of bleeding should be accepted or ignored because of the demonstrated benefits of clopidogrel in patients requiring vascular surgery is not accurate. In some cases, there is no clear benefit, so eliminating the bleeding risk may well be the appropriate decision. The astute vascular surgeon understands the details of the written word in order to make an educated decision and understands that new information such as determining platelet reactivity may provide more clarity to such decisions in the future.
Michael C. Dalsing, MD, is chief of vascular surgery at Indiana University, Indianapolis. He reported no relevant conflicts.
References
1. J Vasc Surg. 2010;52:825-33
2. Cochrane Database Syst Rev. 2015, Issue 2. Art. No.: CD000535
Angiosome revascularization improves limb salvage
YES: The importance of the concept is established.
An angiosome is a three-dimensional anatomic unit of tissue fed by a single-source artery. The angiosome theory was first investigated in the plastic surgical literature by Taylor in the British Journal of Plastic Surgery in 1987,1 describing 40 angiosomes throughout the body. In the lower extremity, six distinct angiosomes have been defined; one arising from the anterior tibial artery (dorsalis pedis), two from the peroneal artery (the lateral calcaneal branch and the anterior perforating branch), and three from the posterior tibial artery (the calcaneal branch, the medial plantar branch, and the lateral plantar branch).2 Indirect connections known as choke vessels exist to enhance perfusion between angiosomes.
The question arises as to whether angiosome-specific revascularization enhances the healing of ischemic tissue loss of the lower extremity. Is direct revascularization of the appropriate angiosome an important part of the planning process for such revascularization efforts? Personal experience with 60 consecutive bypasses for ischemic lower extremity wounds left little doubt that angiosome-specific revascularization enhanced healing. Direct revascularization obtained 91% healing, compared with 62% when revascularization was performed to an artery which indirectly perfused the angiosome where the wound was located.3 There was also a trend for faster healing with direct angiosome revascularization. Other investigators have reported similar findings. Kret and colleagues found similar results for bypass, reporting complete healing in 78% of 106 limbs with direct revascularization with only 46% healing after bypass resulting in indirect angiosome revascularization. These authors noted that a “significant predictor for wound healing and reduced healing time was angiosome revascularization.”4
Consideration of the appropriate angiosome may be even more important for endovascular techniques in determining the target artery for revascularization. Iida et al investigated 200 ischemic ulcers, showing that healing was greatly enhanced by direct revascularization of the angiosome in which the wound was located.5 Kabra examined a mixed cohort of bypass and endovascular procedures and documented increased healing with angiosome revascularization for both modalities in treating critical limb ischemia, therefore, advising that angiosomes should be considered whenever possible.6 This is also an important concept for those diabetic ulcers in need of robust perfusion for healing. Alexandrescu demonstrated improved healing for diabetic ischemic ulcers after endovascular therapy with direct angiosome revascularization, concluding, “an angiosome model of perfusion helps the treatment of diabetic foot ulcers.”7 The group in Helsinki documented statistically significant better healing with endovascular revascularization of the appropriate angiosome in more than 250 patients with ischemic diabetic ulcers, surmising that the angiosome model is important for ulcer healing in diabetic patients.8
Given the many series, from around the world, confirming the impact of direct revascularization of the appropriate angiosome for a wound or non-healing ulcer to enhance healing, the importance of this concept in planning lower extremity revascularization has been established. There are certainly many considerations in planning revascularization such as patient presentation, arterial anatomy, and conduit or device selection. However, as revascularization of the appropriate wound angiosome results in more complete and rapid healing, it is irrefutable that the angiosome concept should be a consideration in planning revascularization for healing and limb preservation.
Dr. Neville is the Sara and Arnold P. Friedman and Carol and Eugene A. Ludwig Chief of Vascular Surgery Professor, Department of Surgery, and the Director, Limb Preservation Center, George Washington University, Washington.
References
1. Br J Plast Surg. 1987 Mar;40:113-41.
2. Plast Reconstr Surg. 2006 Jun;117;261S-293S.
3. Ann Vasc Surg. 2009;23:367-73.
4. J Vasc Surg. 2014 Jan;59:121-8.
5. Endovascular Today. 2010;9;96-100.
6. J Vasc Surg. 2013 Jan;57:44-49.
7. J Endovasc Ther. 2008 Oct;15:580-83.
8. J Vasc Surg. 2013 Feb;57:427-35.
NO: Only a guide, not an absolute.
Despite an aggressive approach to revascularization, amputation rates of up to 20% can occur despite a patent bypass.1 This has led to enthusiasm for an angiosome-based revascularization strategy for the management of ischemic foot lesions.2-4 There is no question that clinicians would opt to revascularize a blood vessel that directly feeds an involved angiosome if the vessel is easily accessible, is of good quality, and has good run-off. The issue arises if the target vessel does not meet that criteria and the surgeon is forced to intervene on an alternative feeding vessel (indirect revascularization).
There have been several studies which compare outcomes after direct and indirect revascularization strategies and they conclude that direct revascularization has better limb salvage rates.2 However, most of the studies were retrospective and details on the status and quality of the pedal arch were not consistently evaluated. Rashid et al studied the impact of direct angiosome revascularization on the healing of the foot and reported that healing and time to healing of foot tissue loss were significantly influenced by the quality of the pedal arch rather than the angiosome revascularized.3
Because of variations in the arterial anatomy of the foot,5 inconsistencies in the extent of an angiosome and the collateral connections between angiosomes are frequent, suggesting that the angiosome that needs to be revascularized may not be perfused by the predicted artery. This helps explain why technical success may not always equate directly with clinical success, as corroborated by indocyanine green (ICG) imaging and white-light tissue spectrophotometry.6 It is also important to emphasize that in their initial publication, Taylor and Palmer emphasized that the basis of their proposed angiosome concept was on the structural anatomy of the feeder vessel territory. They did not and could not assess the perfusion levels and extent of the feeder vessel with their corresponding choke vessels.
Forefoot procedures, such as trans-metatarsal amputations, frequently interrupt this foot arch. Likewise, a large proportion of patients with renal insufficiency and/or diabetes mellitus present with extensive foot wounds with deep infection that may result in compartmentalization within the foot. In one series, only one third of patients had a single angiosome involved in the tissue loss, 45% of patients had two angiosomes involved and more than 20% of patients had three angiosomes involved.7 Patients with more than one angiosome affected by extensive tissue loss are not easily analyzed using the angiosome-oriented concept and so attempts at classifying the intervention as being direct or indirect is problematic.
Studies analyzing the utility of the angiosome concept need to be careful in analyzing the extent of the territories encompassed by the wounds. More importantly, many interventionalists equate tibial or peroneal revascularization with angiosomal revascularization. This may not be the case if the terminal branches are diseased and pedal loop interventions may still be necessary.
In summary, the angiosome model should not be used as an absolute strategy for interventions on critical limb ischemia patients but should be a guide to assist with a patient-specific strategy for revascularization. Further well-structured prospective studies are needed to assess the value of integrating the interangiosome concept, the status of the pedal arch, and the anatomic-physiologic perfusion angiosome model.
Dr. Sumpio is a professor of surgery and radiology, Yale University, New Haven, Conn.
References
1. J Vasc Surg. 2010 Jun;51:1419-24.
2. J Vasc Surg. 2013 Sep;58:814-26.
3. J Vasc Surg. 2013 May;57:1219-26.
4. J Vasc Surg. 2013 Jan;57:44-9.
5. Am J Surg. 1993 Aug;166:130-5.
YES: The importance of the concept is established.
An angiosome is a three-dimensional anatomic unit of tissue fed by a single-source artery. The angiosome theory was first investigated in the plastic surgical literature by Taylor in the British Journal of Plastic Surgery in 1987,1 describing 40 angiosomes throughout the body. In the lower extremity, six distinct angiosomes have been defined; one arising from the anterior tibial artery (dorsalis pedis), two from the peroneal artery (the lateral calcaneal branch and the anterior perforating branch), and three from the posterior tibial artery (the calcaneal branch, the medial plantar branch, and the lateral plantar branch).2 Indirect connections known as choke vessels exist to enhance perfusion between angiosomes.
The question arises as to whether angiosome-specific revascularization enhances the healing of ischemic tissue loss of the lower extremity. Is direct revascularization of the appropriate angiosome an important part of the planning process for such revascularization efforts? Personal experience with 60 consecutive bypasses for ischemic lower extremity wounds left little doubt that angiosome-specific revascularization enhanced healing. Direct revascularization obtained 91% healing, compared with 62% when revascularization was performed to an artery which indirectly perfused the angiosome where the wound was located.3 There was also a trend for faster healing with direct angiosome revascularization. Other investigators have reported similar findings. Kret and colleagues found similar results for bypass, reporting complete healing in 78% of 106 limbs with direct revascularization with only 46% healing after bypass resulting in indirect angiosome revascularization. These authors noted that a “significant predictor for wound healing and reduced healing time was angiosome revascularization.”4
Consideration of the appropriate angiosome may be even more important for endovascular techniques in determining the target artery for revascularization. Iida et al investigated 200 ischemic ulcers, showing that healing was greatly enhanced by direct revascularization of the angiosome in which the wound was located.5 Kabra examined a mixed cohort of bypass and endovascular procedures and documented increased healing with angiosome revascularization for both modalities in treating critical limb ischemia, therefore, advising that angiosomes should be considered whenever possible.6 This is also an important concept for those diabetic ulcers in need of robust perfusion for healing. Alexandrescu demonstrated improved healing for diabetic ischemic ulcers after endovascular therapy with direct angiosome revascularization, concluding, “an angiosome model of perfusion helps the treatment of diabetic foot ulcers.”7 The group in Helsinki documented statistically significant better healing with endovascular revascularization of the appropriate angiosome in more than 250 patients with ischemic diabetic ulcers, surmising that the angiosome model is important for ulcer healing in diabetic patients.8
Given the many series, from around the world, confirming the impact of direct revascularization of the appropriate angiosome for a wound or non-healing ulcer to enhance healing, the importance of this concept in planning lower extremity revascularization has been established. There are certainly many considerations in planning revascularization such as patient presentation, arterial anatomy, and conduit or device selection. However, as revascularization of the appropriate wound angiosome results in more complete and rapid healing, it is irrefutable that the angiosome concept should be a consideration in planning revascularization for healing and limb preservation.
Dr. Neville is the Sara and Arnold P. Friedman and Carol and Eugene A. Ludwig Chief of Vascular Surgery Professor, Department of Surgery, and the Director, Limb Preservation Center, George Washington University, Washington.
References
1. Br J Plast Surg. 1987 Mar;40:113-41.
2. Plast Reconstr Surg. 2006 Jun;117;261S-293S.
3. Ann Vasc Surg. 2009;23:367-73.
4. J Vasc Surg. 2014 Jan;59:121-8.
5. Endovascular Today. 2010;9;96-100.
6. J Vasc Surg. 2013 Jan;57:44-49.
7. J Endovasc Ther. 2008 Oct;15:580-83.
8. J Vasc Surg. 2013 Feb;57:427-35.
NO: Only a guide, not an absolute.
Despite an aggressive approach to revascularization, amputation rates of up to 20% can occur despite a patent bypass.1 This has led to enthusiasm for an angiosome-based revascularization strategy for the management of ischemic foot lesions.2-4 There is no question that clinicians would opt to revascularize a blood vessel that directly feeds an involved angiosome if the vessel is easily accessible, is of good quality, and has good run-off. The issue arises if the target vessel does not meet that criteria and the surgeon is forced to intervene on an alternative feeding vessel (indirect revascularization).
There have been several studies which compare outcomes after direct and indirect revascularization strategies and they conclude that direct revascularization has better limb salvage rates.2 However, most of the studies were retrospective and details on the status and quality of the pedal arch were not consistently evaluated. Rashid et al studied the impact of direct angiosome revascularization on the healing of the foot and reported that healing and time to healing of foot tissue loss were significantly influenced by the quality of the pedal arch rather than the angiosome revascularized.3
Because of variations in the arterial anatomy of the foot,5 inconsistencies in the extent of an angiosome and the collateral connections between angiosomes are frequent, suggesting that the angiosome that needs to be revascularized may not be perfused by the predicted artery. This helps explain why technical success may not always equate directly with clinical success, as corroborated by indocyanine green (ICG) imaging and white-light tissue spectrophotometry.6 It is also important to emphasize that in their initial publication, Taylor and Palmer emphasized that the basis of their proposed angiosome concept was on the structural anatomy of the feeder vessel territory. They did not and could not assess the perfusion levels and extent of the feeder vessel with their corresponding choke vessels.
Forefoot procedures, such as trans-metatarsal amputations, frequently interrupt this foot arch. Likewise, a large proportion of patients with renal insufficiency and/or diabetes mellitus present with extensive foot wounds with deep infection that may result in compartmentalization within the foot. In one series, only one third of patients had a single angiosome involved in the tissue loss, 45% of patients had two angiosomes involved and more than 20% of patients had three angiosomes involved.7 Patients with more than one angiosome affected by extensive tissue loss are not easily analyzed using the angiosome-oriented concept and so attempts at classifying the intervention as being direct or indirect is problematic.
Studies analyzing the utility of the angiosome concept need to be careful in analyzing the extent of the territories encompassed by the wounds. More importantly, many interventionalists equate tibial or peroneal revascularization with angiosomal revascularization. This may not be the case if the terminal branches are diseased and pedal loop interventions may still be necessary.
In summary, the angiosome model should not be used as an absolute strategy for interventions on critical limb ischemia patients but should be a guide to assist with a patient-specific strategy for revascularization. Further well-structured prospective studies are needed to assess the value of integrating the interangiosome concept, the status of the pedal arch, and the anatomic-physiologic perfusion angiosome model.
Dr. Sumpio is a professor of surgery and radiology, Yale University, New Haven, Conn.
References
1. J Vasc Surg. 2010 Jun;51:1419-24.
2. J Vasc Surg. 2013 Sep;58:814-26.
3. J Vasc Surg. 2013 May;57:1219-26.
4. J Vasc Surg. 2013 Jan;57:44-9.
5. Am J Surg. 1993 Aug;166:130-5.
YES: The importance of the concept is established.
An angiosome is a three-dimensional anatomic unit of tissue fed by a single-source artery. The angiosome theory was first investigated in the plastic surgical literature by Taylor in the British Journal of Plastic Surgery in 1987,1 describing 40 angiosomes throughout the body. In the lower extremity, six distinct angiosomes have been defined; one arising from the anterior tibial artery (dorsalis pedis), two from the peroneal artery (the lateral calcaneal branch and the anterior perforating branch), and three from the posterior tibial artery (the calcaneal branch, the medial plantar branch, and the lateral plantar branch).2 Indirect connections known as choke vessels exist to enhance perfusion between angiosomes.
The question arises as to whether angiosome-specific revascularization enhances the healing of ischemic tissue loss of the lower extremity. Is direct revascularization of the appropriate angiosome an important part of the planning process for such revascularization efforts? Personal experience with 60 consecutive bypasses for ischemic lower extremity wounds left little doubt that angiosome-specific revascularization enhanced healing. Direct revascularization obtained 91% healing, compared with 62% when revascularization was performed to an artery which indirectly perfused the angiosome where the wound was located.3 There was also a trend for faster healing with direct angiosome revascularization. Other investigators have reported similar findings. Kret and colleagues found similar results for bypass, reporting complete healing in 78% of 106 limbs with direct revascularization with only 46% healing after bypass resulting in indirect angiosome revascularization. These authors noted that a “significant predictor for wound healing and reduced healing time was angiosome revascularization.”4
Consideration of the appropriate angiosome may be even more important for endovascular techniques in determining the target artery for revascularization. Iida et al investigated 200 ischemic ulcers, showing that healing was greatly enhanced by direct revascularization of the angiosome in which the wound was located.5 Kabra examined a mixed cohort of bypass and endovascular procedures and documented increased healing with angiosome revascularization for both modalities in treating critical limb ischemia, therefore, advising that angiosomes should be considered whenever possible.6 This is also an important concept for those diabetic ulcers in need of robust perfusion for healing. Alexandrescu demonstrated improved healing for diabetic ischemic ulcers after endovascular therapy with direct angiosome revascularization, concluding, “an angiosome model of perfusion helps the treatment of diabetic foot ulcers.”7 The group in Helsinki documented statistically significant better healing with endovascular revascularization of the appropriate angiosome in more than 250 patients with ischemic diabetic ulcers, surmising that the angiosome model is important for ulcer healing in diabetic patients.8
Given the many series, from around the world, confirming the impact of direct revascularization of the appropriate angiosome for a wound or non-healing ulcer to enhance healing, the importance of this concept in planning lower extremity revascularization has been established. There are certainly many considerations in planning revascularization such as patient presentation, arterial anatomy, and conduit or device selection. However, as revascularization of the appropriate wound angiosome results in more complete and rapid healing, it is irrefutable that the angiosome concept should be a consideration in planning revascularization for healing and limb preservation.
Dr. Neville is the Sara and Arnold P. Friedman and Carol and Eugene A. Ludwig Chief of Vascular Surgery Professor, Department of Surgery, and the Director, Limb Preservation Center, George Washington University, Washington.
References
1. Br J Plast Surg. 1987 Mar;40:113-41.
2. Plast Reconstr Surg. 2006 Jun;117;261S-293S.
3. Ann Vasc Surg. 2009;23:367-73.
4. J Vasc Surg. 2014 Jan;59:121-8.
5. Endovascular Today. 2010;9;96-100.
6. J Vasc Surg. 2013 Jan;57:44-49.
7. J Endovasc Ther. 2008 Oct;15:580-83.
8. J Vasc Surg. 2013 Feb;57:427-35.
NO: Only a guide, not an absolute.
Despite an aggressive approach to revascularization, amputation rates of up to 20% can occur despite a patent bypass.1 This has led to enthusiasm for an angiosome-based revascularization strategy for the management of ischemic foot lesions.2-4 There is no question that clinicians would opt to revascularize a blood vessel that directly feeds an involved angiosome if the vessel is easily accessible, is of good quality, and has good run-off. The issue arises if the target vessel does not meet that criteria and the surgeon is forced to intervene on an alternative feeding vessel (indirect revascularization).
There have been several studies which compare outcomes after direct and indirect revascularization strategies and they conclude that direct revascularization has better limb salvage rates.2 However, most of the studies were retrospective and details on the status and quality of the pedal arch were not consistently evaluated. Rashid et al studied the impact of direct angiosome revascularization on the healing of the foot and reported that healing and time to healing of foot tissue loss were significantly influenced by the quality of the pedal arch rather than the angiosome revascularized.3
Because of variations in the arterial anatomy of the foot,5 inconsistencies in the extent of an angiosome and the collateral connections between angiosomes are frequent, suggesting that the angiosome that needs to be revascularized may not be perfused by the predicted artery. This helps explain why technical success may not always equate directly with clinical success, as corroborated by indocyanine green (ICG) imaging and white-light tissue spectrophotometry.6 It is also important to emphasize that in their initial publication, Taylor and Palmer emphasized that the basis of their proposed angiosome concept was on the structural anatomy of the feeder vessel territory. They did not and could not assess the perfusion levels and extent of the feeder vessel with their corresponding choke vessels.
Forefoot procedures, such as trans-metatarsal amputations, frequently interrupt this foot arch. Likewise, a large proportion of patients with renal insufficiency and/or diabetes mellitus present with extensive foot wounds with deep infection that may result in compartmentalization within the foot. In one series, only one third of patients had a single angiosome involved in the tissue loss, 45% of patients had two angiosomes involved and more than 20% of patients had three angiosomes involved.7 Patients with more than one angiosome affected by extensive tissue loss are not easily analyzed using the angiosome-oriented concept and so attempts at classifying the intervention as being direct or indirect is problematic.
Studies analyzing the utility of the angiosome concept need to be careful in analyzing the extent of the territories encompassed by the wounds. More importantly, many interventionalists equate tibial or peroneal revascularization with angiosomal revascularization. This may not be the case if the terminal branches are diseased and pedal loop interventions may still be necessary.
In summary, the angiosome model should not be used as an absolute strategy for interventions on critical limb ischemia patients but should be a guide to assist with a patient-specific strategy for revascularization. Further well-structured prospective studies are needed to assess the value of integrating the interangiosome concept, the status of the pedal arch, and the anatomic-physiologic perfusion angiosome model.
Dr. Sumpio is a professor of surgery and radiology, Yale University, New Haven, Conn.
References
1. J Vasc Surg. 2010 Jun;51:1419-24.
2. J Vasc Surg. 2013 Sep;58:814-26.
3. J Vasc Surg. 2013 May;57:1219-26.
4. J Vasc Surg. 2013 Jan;57:44-9.
5. Am J Surg. 1993 Aug;166:130-5.
