The patient is a man over 70 years of age who came to the hospital with severe pain of his right foot and leg with walking short distances and at night while recumbent. He had a history of hypertension, diabetes, and coronary artery disease, and several years ago had his left common iliac artery stented. On examination, he had no lesions of his foot, and his pulses were only palpable (barely) in the femoral arteries only. He did have strong monophasic signals in the anterior tibial arteries bilaterally.
Initial vascular lab testing showed only mildly depressed ankle brachial (above), with dampened waveforms consistent with inflow and femoropopliteal disease on the right. He underwent arteriography by our vascular medicine specialist and cardiologist Dr. Faisal Hasan, and it showed bilateral common iliac stenoses, a severely calcified and nearly occlusive plaque in the right common femoral artery, and a long segment occlusion in the superficial femoral artery with diffuse calcified plaque extending into the popliteal artery. There was diseased but patent 3 vessel tibial runoff.
To Act As A Unit are the Cleveland Clinic’s words and it shows the Clinic’s roots as an US Army field hospital on the vasty fields of World War I France a little over a century ago, and we take it seriously. It may come as a surprise to some that a cardiologist referred me this patient after mutually deciding that the common femoral disease and the TASC D SFA occlusive disease, but we both decided that a surgical approach was the best one. The question then is how much more flow?
I ordered a CTA (CT angiogram) particularly for endarterectomies as I find it imperative to know the actual end point of plaque. Arteriography only hints at it, and while a 5mm lumen may look large and patent, it may be a channel in a 10mm wide plaque that when a stent terminates within it, breaks and becomes biologically active as intimal hyperplasia at best or embolizes at worst. CTA shown below revealed the plaque where contrast angio showed only the lumena of the vessels.
The 3D reconstruction function also allowed me to see and plan the operative approach and predict the lack of saphenous vein confirmed on duplex ultrasound.
For the students reading this, ischemic rest pain is often simpler to treat because it requires only a little more blood flow. There is a neurologic ischemia component that is not well studied, particularly in diabetics, as ischemia may result in anesthesia in someone who has underlying diabetic neuropathy, but that is not an indication for revascularization while rest pain is, and someone should investigate this. This little more blood flow in the form of treating inflow disease only may be sufficient in relieving rest pain while avoiding interventions on the superficial femoral, popliteal and tibial arteries which have limited longevity.
The common femoral artery on the other hand is the throttle of inflow and as a principle, inflow can be considered as the infrarenal aorta to profunda femoral artery, and repairing the common femoral necessitates an operation. There is no durable or laudable endovascular procedure for occlusive disease of the common femoral artery, a feature shared with the subclavian artery at the thoracic outlet and the celiac axis at the median arcuate ligament. All three are externally compressed by hard structures and revascularization must be ever mindful of the inguinal ligament, the thoracic outlet, and median arcuate ligament. The only exception to the “you must operate” rule of the CFA is calcified atherosclerotic disease in high risk individuals, and I make careful exception here with rotational atherectomy devices.
Claudication is another thing entirely. Claudication limits lifestyle and can be corrected by changing lifestyle -either with more exercise or limiting exercise. The thing is, when a patient has reached a certain age, that lifestyle may be walking slowly from chair to commode, and if that activity is limited, no amount of haranguing may be able to induce that person to embark on an ambitious exercise program. Sometimes, you have to be realistic about telling a frail old man to go for a 60 minute walk. But if that person has difficulty getting to the bathroom because of leg cramps, then either they have to get assistance or more bloodflow, and ironically, a little more blood flow represented by improving inflow, may not be enough.
That was what I was thinking when I was planning this operation. Improve the inflow with stents to the common iliacs and a right CFA endarterectomy, but use the opportunity of surgical exposure to extend the endarterectomy to the distal external iliac and through the entire SFA.
My fondness of remote endarterectomy is well known from my many blog posts on it (link). It is a modern update on a very old procedure -the ring endarterectomy, done since the middle of the last century when bypass grafts were unavailable. The occlusive plaque is removed, and an end-point reached and cut with a scissor like device (available from LeMaitre). It is the ultimate hybrid operation (below) requiring open and endovascular skills. I tell prospective trainees to judge training programs by how facile are the surgeons and how many are the procedures with and involving a hybrid approach, because any program can have few (getting fewer) old surgeons doing only open surgery and a lot of young surgeons doing only endovascular procedures, but a rare few will do a lot of hybrid procedures.
I chose to add femoral EndoRE. This would bring the extra blood flow needed to kickstart any walking program, barring cardiopulmonary limitations.
The patient was brought to our hybrid operating theatre and prepped from nipples to toes. The right common femoral artery was exposed for endarterectomy, and accessed then with a sheath along with a left femoral sheath for kissing balloon angioplasty and stenting of the common iliac artery stenoses (below).
Afterword, the CFA was opened and endarterectomized, and the SFA was remote endarterectomized (below).
The endpoint was chosen in the above knee popliteal artery to avoid having to stent the dissected end point plaque well into the popliteal artery. If I wanted to go all the way to the below knee popliteal artery, I would have to open it to manage the plaque and artery at the so-called trifurcation, typically with a patch angioplasty. The plaque came out in one piece (below):
The terminus of the plaque in the POP where it was cut has to be managed with a stent, unless you open and complete the endarterectomy and patch the artery. I was able to cross the dissection (no small feat) and plaque a stent. The artery was widely patent and even the small branches off the previously occluded SFA were now reopened.
His pulse volume recording done after intervention reflects the improved flows (below).
His rest pain resolved, but more gratifyingly, he has regained the confidence to walk and exercise, which he now does without limitation up to 45 minutes a day. In two month followup, we performed a duplex which showed his right SFA to be basically normal (below), including an intimal stripe and media. This is not an anomaly. When I took a punch out of restored artery to perform an anastomosis (from this case link), I sent it. Previously it had been an artery that was obstructed for nearly a decade, but after EndoRE, had become an elastic, compliant vessel. The pathology returned as “normal artery.”
When these fail, they typically do so a random points on the endarterectomized vessel and on the stent. While stent grafting may have better outcomes with regard to restenosis, doing so covers collateral vessels and PTFE grafts behave poorly by embolizing while clotting off, and PTFE stent grafts are no different. Data from over a decade ago suggests that EndoRE of the SFA while inferior in patency to vein grafts, are equivalent to PTFE [reference 1] and superior to endovascular revascularization [reference 2] in terms of primary patency. When they occlude, they achieve a “soft landing” without the furious acute ischemia and embolization seen with PTFE bypasses.
I think these handful of cases I performed here in the UAE represent the first in the region. The main difference here is that the arteries tend to be smaller by about 20%, and in one instance, the smallest Vollmer ring was too large for the vessel in a case where I abandoned the SFA revascularization -the profunda and inflow revascularization proved sufficient in reversing rest pain. The intriguing property of endarterectomy is something that we all try to do with surgery but rarely achieve -a restoration to an earlier time. I believe this patient’s right femoral artery is now back to a youthful state.
A body floating in space, a fetus in the womb, a dad lounging in his favorite chair, share the feature of weightlessness and represent the absolute neutral position (figure above) of the human which is the position of a relaxed supine quadruped -a dead mouse. Anything else is a stress position, including standing. Repeating motions outside of this relaxed pose or holding those positions away from this absolute neutral for long periods of time is a nidus for injury and pain. That is why most land animals sleep flat on the ground.
The Pain Operations
Operations to relieve pain are often the most gratifying to both patient and surgeon to perform successfully. This circumstance applies to the commonly performed procedures such as spine surgery, endometrial ablations, and varicose vein resections. When the pain is due to a rare set of circumstances, things are not so easy. Typically for rarer pain syndromes, two things need to coincide for the successful operation to happen. First is the patient must suffer while more common and potentially life threatening diseases are ruled out and even treated if these are found. This may take months or years. The second necessary condition is finding a physician who has seen the particular pain syndrome before and understand how to test for it and treat it. That meant the majority of people never get treated, or are shunted into the circle of shame as malingering, drug seeking, and mentally unstable. The opioid epidemic creates double jeopardy for these patients -they can become addicts as their pain is never successfully diagnosed and treated and they get labeled as drug seeking.
All pain syndromes that can be successfully treated share common features that give you a degree of surety about the diagnosis, but at the end, there is a leap of faith on the part of both patient and practitioner because many of these operations have a failure rate ranging from 5-20 percent. First, the symptoms must be associated with sensory nerves, somatic or visceral. Second, there is a physical mechanism for that nerve to be inflamed from compression, swelling, or irritation that can be accounted for through history, physical examination, and imaging studies. Third, though not a constant, a major nerve trunk will be associated with a blood vessel, typically and artery, that is also affected by compression. Fourth, when swollen veins are the cause of pain, it has to be recognized that at an end stage the organ that the veins drain can also be affected.
The Pain Must Have a Testable Anatomic Basis
The somatic sensory nerves in the periphery are well mapped out and known since even classical times. The described pain should be consistent with a nerve. The best and easiest example is a neuroma that forms in an amputation stump. It triggers pain in its former distribution. It is palpable as a nodular mass. It is visible under ultrasound or cross sectional imaging. And it is easy to turn off temporarily with an injection of lidocaine, either under palpation or image guidance. If you can turn off the nerve and relieve the pain, it is likely that ablating or relieving the nerve of irritation will also relieve the pain. Such is the case in median arcuate ligament syndrome (figure below). The celiac plexus is caught under the median arcuate ligament and compressed. It causes a neuropathy that is felt in its visceral sensory distribution and the brain interprets these signals in the typical ways irritation of the stomach is interpreted -as pain, burning, nausea, sensations of bloating, and general malaise. These nerves can be turned off with a celiac plexus block and the effects tested by giving the patient a sandwich. When it works, the patient will say they will have had relief for the first time in years and operation to relieve the ligament compression and ablate the nerve can proceed. Same for many of the diseases listed.
Tight Spaces Impinging Nerves, Arteries, and Veins
Many of the tight spaces involving the nerves have accompanying arteries that are compressed. This results in injury to the artery in the form of intimal hyperplasia, post stenotic dilatation, aneurysm formation, and thromboembolism. Shared tight spaces that cause problems for nerves and arteries have the common features of fixed ligaments, adjacent bones and muscles, inflammation, and motion. These include the thoracic outlet, antecubital fossa, cubital canal, diaphragmatic hiatus at median arcuate ligament, inguinal ligament, popliteal fossa, carpal tunnel, obturator canal, mediastinum, retroperitoneum -basically anywhere nerve, compression, and motion occur. In some instances of median arcuate ligament syndrome, postures and breathing trigger the pain. Holding a child in an arm may trigger pain in neurogenic thoracic outlet. Or sitting while wearing tight jeans may trigger a burning pain in meralgia paresthetica. It is not uncommon to find damaged arteries in median arcuate ligament syndrome, thoracic outlet syndrome, and popliteal entrapment or thrombosed veins in nutcracker syndrome, May-Thurner Syndrome, and Paget-von Schroetter Syndrome. Because nerves are typically difficult to visualize, their compression may only be inferred by testing for compression in their adjacent arteries.
Dilated Veins and Swollen Organs and Visceral Pain
Venous hypertension is most commonly conceived of as varicose and spider veins of the legs and offer a model of pain when applied to other pain caused by venous dissension. The visceral sensory fibers veins and arteries trigger a very intense pain that localizes to the trigger. I have often witnessed this when I manipulate a blood vessel during local anesthesia cases. Visceral pain from swelling has a dull achiness that is localizable to my spider veins after a long day standing like a bruise (below). The swelling from varicoceles which I have also had feel nothing less than feeling the aftereffects of getting a kick in the balls -not the immediate sharp pain but imagine about 5 minutes after with the mild nausea, abdominal discomfort and desire not to move too much, and even a little flank pain. Imagine this occurring low in the pelvis with ovarian vein varices in pelvic congestion syndrome. This kind of swollen gonad pain afflicts many women whose pain is so frequently dismissed by male physicians because they have no context -well imagine getting kicked in the balls hard, wait about 5 minutes and that moment stretch it out to whenever you stand for a long period of time (below).
When a limb is swollen from a thrombosis, the veins hurt and is similar to a bone pain from a fracture or a pulled muscle -that is how the brain processes the pain, but when the muscles and skin get tight from edema, the pain is sharp and dire. This is the same kind for pain from a distended left kidney from nutcracker syndrome or a spleen from a splenic vein thrombosis. These conditions can be modeled and predicted based on history and correct differential and confirmed with proper imaging -always.
Build a theory of the pain based on a testable proposition and set of nerves
That is the final message. These pain syndrome require some imagination and empathy to map and model. Predictive tests then can be performed on physical examination, functional testing, or imaging. Often, the adjacent artery is the only thing that can be reliably visualized and tested, knowing that it is the nerve that is compressed. Turning off the offending nerve with a block and relieving the pain is the most powerful argument for operating. It is building the argument for an operation that requires these objective data, but at the end, it does require some experience and faith. You have to believe in your patient and the science and when they coincide, you have to act.
I taught myself to draw during medical school when I couldn’t figure out the three dimensional relations of structures. I discovered that if you just draw the shading of an object, it pops out in three dimensions. Over the years, I took to carrying little notebooks to sketch out anatomy and proposed operations for patients through this medium. While I found this to be a handy tool that I used only occasionally, since moving to Abu Dhabi, where much of my communicating is done through an interpreter, my drawings carry a much greater weight as direct communication of my thoughts and intentions.
Drawing helps the patient and family understand the unseeable. It gives form to words that are often confused like blood vessel, graft, stent, artery, and vein.
What is informed consent when patient’s cannot describe their problems to their friends and relatives what the problem is and what is going to be done about it?
I usually draw with the pen in my shirt pocket and some copier paper, but sitting down and doing a proper sketch is soothing and very helpful for me as the surgeon to previsualize the goals that I have to reach during an operation to take the patient across the finish line. During meetings and conferences, I sketch into one of those fancy bound notebooks that I collect.
While pencil and markers do a fine job, the real magic is in using tablet based sketching software, using layers, to build serial images of the steps of an operation.
I am increasingly tempted to use these images as my operative note, but understanding that words are needeed for billing, I comply. Even so, I find it helpful to put these illustrations on my EMR notes, because it allows everyone to see and understand what I saw and what I did. I leave you with some of my illustrations with attached comments.
Innovating Our Way Out of Not Having Enough Vascular Surgeons
This year’s SVS meeting featured a sobering assessment about the vascular manpower deficit affecting North America at the E. Stanley Crawford Critical Issues Forum, moderated by Dr. Michel Makaroun, MD, president-elect of the SVS. 35-45% of practicing vascular surgeons plan on retiring in the next decade by conservative estimates. We are not attracting enough candidates for the training programs. The solutions, including decreasing the length of training, public relations campaigns, and incentivizing retention have had mixed results, but we have yet to see a sustainable rise in vascular surgeon numbers.
Burnout driven by lack of work-life balance, the advent of electronic medical records optimized for billing, the passing of the private practice era, and the constant need to adapt to new techniques, create a persistent downdraft on staffing. So as some hospital face the reality of having to contract services, little attention is given to delivering best care with the staffing that we have. Changing how we practice is the only viable solution.
There are an estimated 3000 active vascular surgeons in the US. Imagine if all the cheese needs of this country could only be met by 3000 artisanal cheesemakers who make cheeses one at a time and want to live in places with international airports, BMW dealerships, and major league sports teams, and must have 3-4 partners to share cheese call. If you are a rural hospital in dire need of vascular surgery services and your one vascular surgeon is retiring, you are probably SOL.
When I was training, vascular surgery was oft touted as a primary care specialty. And that is how many of us still practice, managing risk factors, monitoring mild disease, as well as planning and performing interventions and operations. As much as I enjoy that kind of interaction, the half hour to an hour visit for a head to toe cardiovascular survey and discussion, educating patients and families about pipes and pumps, is incredibly inefficient. A healthcare system, a hospital, facing a staffing shortfall, has to do everything possible keep that vascular surgeon in the OR during work hours.
What is the core function of a vascular surgeon? Making good decisions and executing plans well. Decisions require data. What is this data? We laud the history and physical examination, but this is a throwback to another era. If you look at the diagnosis of myocardial infarction, it is not standard practice for a cardiologist to come and get a history, examine the patient, and declare that the patient is having a heart attack based solely on history and physical examination. It is a triage nurse in the ED who draws labs and orders an EKG which is read by a machine. These data points will tell you if heart muscle is being damaged. A process is started which triggers a team to come and take care of this patient. The hospitals focused on this actually drill their cath lab teams like pit crews. A stopwatch starts with the goal of revascularization under an hour.
Not so with peripheral vascular disease. The ischemic foot might have only a few hours depending on its presentation before it is irretrievably lost, but no matter -they sit in the ED until a vascular surgeon comes to speak to the patient and family, examine them, and then order tests, admission, consults, and operating room -typically all by themselves. Getting these patients into the operating room is in many places hampered by the lack of dedicated OR staffing, radiology techs, anesthesiologists, space, equipment, and critical care capacity. During work hours, there are scheduled cases that have to be delayed or canceled for another time, which takes time to do. After hours, the patient may have too many comorbidities to handle safely with the available staff. The vascular surgeon may have to bargain and cajole, to align several factions whose attention is demanded by many equally important concerns. If you decide to hold a lavish dinner party of twenty important guests -reserving space, calling caterers, inviting guests, arranging transportation – on short notice, you might pull it off once, but if you do this regularly, you are a masochist of the first order.
In the heart attack model, the history and physical examination is relegated to a series of yes/no or how long questions, and positive responses trigger a series of coordinated actions of a system -a reflex. In the leg attack model, there is no such system. I have to blame the vascular surgeons for preserving the current model. Vascular surgeons are organized as a guild. Guilds are protective of their monopolies on skills and markets and fiercely resist change. Most vascular surgeons are terrified by loss of control, and cling to the notion of being misunderstood and unappreciated saviors. We can do better.
The area that needs streamlining is at the point of referral. The majority of time of a vascular surgeon is spent working up normal blood vessels, varicose and spider veins, leg edema and pain, and mild and moderate arterial atherosclerosis. This work initially does not require a vascular surgeon but rather a focused set of policies and initial diagnostic studies that can be administered or ordered by any caregiver. Reducing the need for vascular surgeons at this point in vascular care will go a long way in extending the vascular work force at hand.
Point of Care Blood Flow Evaluation
Finding and declaring blood vessels to be normal is challenging and too often time consuming. Streamlining this will go a long way in freeing vascular surgeons to take care of disease.
The average caregiver is an inconsistent pulse taker. The palpable pulses are not always easy to find. Asking over the phone or as policy for someone to examine pedal pulses -the posterior tibial artery and dorsalis pedis artery pulses, is challenging. A positive is just as likely to be true or false as a negative. No cardiologist would ask a similarly detailed and technical question about an MI. In fact, they can’t ask, “Is there a pulse in the LAD?” Cardiologists make do with tests easy to obtain and interpret with certainty -the plasma troponin level and the EKG. The EKG is read by an algorithm so established and so tested, that it should stand as an example of early machine intelligence taking over a human job -but I digress.
What is our EKG? It is not the ABI -the ankle brachial index, because it is terrible at identifying disease, and is difficult to obtain reliably without practice. The closest thing to an EKG we have in terms of simplicity and accuracy is the pulse volume recording, the PVR (figure below). A FloLab machine, the machine used to obtain PVRs, will basically run itself once the cuffs are correctly applied on the leg, and the tracings are very easy to interpret. Unlike an EKG, there are no electrodes whose locations you must memorize. If the closest vascular surgeon is an hour away by ambulance, the transfer of a patient with flat waveforms and ischemic foot does not require a consultation on site. The patient would go to the vascular surgeon with no time wasted and no kidneys injured by CTA’s that too often fail to travel with the patient. Unlike an EKG which can be performed by many caregivers, a PVR requires both the equipment and a vascular technologist. A vascular technologist is not available 24-7 in most hospitals, and FloLab machines purchased for vascular labs are not meant to be dragged around the hospital.
So let’s think out of the box about another box in every triage nurse’s cell, every ER and ICU bed, and on every hospital nursing floor. These are pulse oximeters with a digital tracing, and bonus points, some come with strip printers! Placing a pulse oximeter probe on the second toe and comparing to an erstwhile normal wave signal such as on an index finger can provide qualitative information about normality and disease. Normal waveforms and abnormal ones can be easily discerned. A flat line is another obvious finding when in comparison, a finger or an ear on the same patient has normal signals.
How much better would a vascular surgeon feel about a transfer call that has this information, “digital waveforms are flat in this patient with rest pain and a bruised toe.” How much better would a vascular surgeon feel about a call about a patient with “digital wave forms are normal in this patient with toe pain and a bruised toe. We got an x-ray and there was a fracture.” The communication can be quite detailed and refined. For example: “The patient had no pulses, we think. Digital wave forms were dampened but pulsatile in a patient with a bruised toe, we’ll send to vascular clinic in the morning.”
A study comparing pulse oximetry signals and ABI in type 2 Diabetes Mellitus found the following results (link).[i]
These data suggests pulse oximetry signal is equal to and somewhat better than ABI. Why is this important? Cost. This information is better than asking unsure people, “Is there a pulse?” A vascular technologist need not be on call 24/7. Extra FloLabs for ED, ICU, and floors need not be purchased. The pulse oximeter with waveform tracing is nearly ubiquitous wherever patient’s oxygenation needs to be assessed in most hospitals. While not perfect, it has great potential for serving as vascular surgery’s EKG machine for critical limb ischemia. Policies and algorithms can be built out in collaboration with Emergency Departments and nursing departments that can effectively determine if blood flow is normal or abnormal at point of care. Effective emergency responses to critical limb ischemia can be authored triggered by abnormal findings. Acute limb ischemia protocols based on time sensitive responses can be initiated. All of these can flow from referring entities being able to determine objectively normal or abnormal blood flow.
The vascular clinic is a sorting process where patients are determined to be normal or have mild, moderate, or severe disease. The vast majority of the time spent in clinic can be spent in triage by trained nurses and testing by technologists. Clear pathways and guidelines can dictate the ordering of vascular laboratory tests obviating the need for vascular consultation at this stage. Patients with normal blood vessels and vascular function are sent back to their physicians with the normal report. Patients with mild disease and moderate disease are sent to a physician with specialization in cardiovascular medicine for management of risk factors and periodic surveillance. At any point in the process, a vascular surgeon can be called to provide guidance and direct patients to different tests and consultations. The patients needing operations, based on correct indications and imaging are sent to a focused clinic where the surgeon and interventional team can review films, determine the urgency of indications balanced against risk, and plan and schedule procedures. Currently, vascular surgeons do all of this by themselves, as well as make hospital rounds, perform procedures, and interpret vascular laboratory studies, seeing one patient at a time.
In introductory computer sciences courses, search algorithms are taught to be brute force if you look at one item at a time for the thing you want, and to be efficient if you have presorted those items because every time you look, you can exclude part of the data set, ever shrinking the pool in which you search, making the search shorter and faster
The shortfalls in vascular surgeon numbers have as much to do with this dependence on the star chef cooking up one meal at a time, rather than a team working off recipes, with the chef directing the flow and occasionally jumping by the fire to make the most difficult of dishes. The first restaurant can seat three parties. The latter, easily ten times the number. Everyone gets fed.
Only asking how many vascular surgeons you need misses the big picture because there are many equally important questions. How many vascular technologists do you need? An accredited laboratory provides the critical diagnostics upon which decisions are made, and the surgeon should oversee but not be directly involved in the initial screening. Nurses trained to triage and order vascular laboratory tests and even perform the simpler ones is the second need. Third, is the cardiovascular medicine physician who manages those patients discovered to have mild to moderate disease, and depending on symptoms, refers severely symptomatic moderate disease and severe disease to a scheduling clinic. The scheduling clinic is composed of both interventionalists and vascular surgeons who plan interventions and operations.
Surgeons must be in the operating room to be effective. A well thought out and organized system, with interlocking teams, and well disseminated basic knowledge and awareness of vascular diseases reduces the need for a vascular surgeon to be present all the time in many places and ultimately increases the effectiveness of the vascular surgeons that are available by keeping them in the operating room. The system needs to be set up by the surgeon to allow clinic to be a setting mostly for consenting the patient for an operation or a discussion of treatment options.
Finally, vascular surgeons must be aligned with all the resources of the hospital including the considerable numbers of interventional cardiologists and radiologists, neurologists, and nephrologists. There is no reason someone should wait a month to get on the OR list for an iliac angioplasty and stent if an equally skilled and privileged cardiologist or radiologist has an opening the next day. The surgeon’s special talent should be open surgery and hybrid surgery -that which mixes open surgery and intervention in optimal measures which is not possible from a purely percutaneous approach. The key is frequent and easy communication between specialities and trust built by being in one shared cardiovascular institute.
There is a critical need of good operators. The acuity of disease and their solutions demand the continued presence and availability of open surgery. The fact is, many solutions are optimal in a hybrid fashion and for peripheral vascular disease, these options can only be offered via a vascular surgeon trained in both open surgery and peripheral interventions, or in a combined effort of open surgeon and interventionalist. And many disease categories can only be managed by open surgery.
The reality is that silos, economics, and practice patterns prevent this kind of combined effort. Market forces have pushed the training of vascular surgeons forcefully into the interventional realm at the cost of open surgical training. Some of the geographic maldisdribution of vascular surgeons has to do with younger vascular surgeons flocking to established practices where there are senior surgeons more comfortable in opening a belly or chest (or both). The trap they and hospital systems fall into is then allowing these new recruits to become the interventional specialist of that group, relegating the aging open surgeon to a narrow role, and then finding that the hospital has a problem when that surgeon announces retirement at 60. Every year, millennia of surgical experience retires to beaches and golf courses. The hospital systems should recognize this brain drain as a crisis and create work arounds that keep these skills going. The other opportunity lost is close coordination with interventional cardiologists, radiologists, and nephrologists who in many cases compete with vascular surgeons for the same patients but treat the patients based on their training and skill sets to the exclusion of potentially better operations offered by surgeons. This disjointed care creates both suboptimal outcomes for patients and high costs for hospital systems.
Commerce should never dictate the fate of a patient. A particular point is where competencies and privileging overlap, and guidelines recommend intervention over surgery as in the case of a TASC A or B iliac artery lesion. A patient should not be kept waiting weeks for a spot on a busy surgeon’s OR schedule when an open interventional cardiologist or radiologist slot is available for a iliac stent the next day. It should be a matter of practice that these cases are discussed and distributed, optimally in a shared indication clinic or rounds. Patients bumped off of a surgeon’s elective schedules for emergencies who could be cared for by an interventional partner without an added delay should be given that option. This kind of change requires a commitment to continual reorganization and optimization into a vascular institute.
The perfect vascular surgeon is a unicorn -well skilled, and experienced in open vascular surgery, but also versatile, innovative, and skillful in wielding a wire. I can name just a handful of unicorns. An apt analogy from the book Moneyball is the signing of superstars in baseball on the free agent market. The upshot of that book is that you can arbitrage for the valued metrics through signing several utility players with an aptitude for one thing or another which in sum equals or exceeds that superstar and get the final result -wins, in the same proportions as overspending on a superstar. Rather than searching for that unicorn, it is more important to set up the right system. Screening, testing, and management of mild vascular disease by a nurses and cardiovascular medicine physicians, while directing operations and interventions to vascular surgeons, cardiologists, and interventional radiologists should be the next step in the evolution of vascular care systems. There will never be enough vascular surgeons in the current system. The critical and rare competency is open vascular surgical skill. A surgeon who performs only interventions is not an “advanced minimally invasive practitioner” but rather someone equally privileged as an interventional cardiologist or radiologist, and therefore easily replaceable by an interventional cardiologist or radiologist specializing in peripheral vascular disease. A surgeon skilled in open vascular surgery is becoming rarer every year, but they are still out there, looking at brochures of real estate in sunny places. A team consisting of a cardiovascular medicine physician, many vascular technologists, nurses specializing in vascular diseases, several interventionalists, and a vascular surgeon skilled in open vascular surgery working as a single unit, is far more easy to assemble than finding and recruiting a herd of unicorns.
I recently had to remove a stent graft for infection and got to thinking about how the number of people who could comfortably and confidently manage that has thinned out in the world through the unintended consequence of the medical device market place. In every surgical specialty over the past twenty years, many open procedures were replaced with a minimally invasive option which generally involved adoption of new technology and large costs to the hospital. These newer procedures were touted as easier on the patient while being easier to perform for the average physician than the open procedure that they were replacing. That was the other selling point -that one could do several of these operations in the time it took one open procedure. In most cases, they were at best almost as good as the open procedure but at higher cost.
In the marketplace, minimally invasive always wins. In many specialties it became untenable to practice without marketing these “advanced minimally invasive” skills. Hence, the wide adoption of robotics in urology outside major academic centers -during those years of rapid adoption the surgeons would get flown to a course, work on an animal model, then for their first case a proctor would be flown out and voila -a minimally invasive specialist is born. The problem comes when learning these skills displaces the learning of traditional open surgical skills. In general surgery, it is not uncommon to hear of residents graduating without having ever having done an open cholecystectomy. It is also the case that many vascular trainees graduate with but a few if any open aortic cases. What happens when minimally invasive options run out? Who will do my carotid endarterectomy or open AAA repair?
The first case is an elderly man with an enlarging AAA sac despite having had EVAR about seven years prior. No endoleak was demonstrated but the proximal seal was short on CT. Also, it was a first generation graft which is prone to “peek a boo” endoleaks from graft junctions and stent anchoring sutures. On that last point, I use the analogy of a patio umbrella -after seven seasons, they can leak where cloth is sewn to the metal struts. It is very hard to demonstrate leak of this kind on CTA or duplex ultrasound because they are small. The patient had his EVAR because he was considered high risk for open repair at the time of his operation -moderate COPD, mild cardiac dysfunction. His sac had enlarged to over 6cm in a short time, and therefore open conversion was undertaken. No clinical signs of infection were present. A retroperitoneal approach was undertaken. After clamps were positioned, the sac was opened.
The picture does not show it, but a leak from the posterior proximal seal zone was seen with clamp off. The clamp was reapplied and the graft transected flush to the aortic neck. A bifurcated graft was sewn to this neck incorporating the main body stent graft and aortic neck in a generous running suture. The left iliac limb came out well and the new graft limb sewn to the iliac orifice, the right iliac limb was harder to clamp and therefore I clamped the stent graft and sewed the open graft to the stent graft.
The patient recovered well and went home within the week. He was relieved at no longer needing annual CT scans.
Who needs annual CT scans? Patients with metastatic cancer in remission.
The second patient was an older man referred for enlarging AAA sac without visible endoleak. The aneurysm had grown over 7cm and was causing discomfort with bending forward. He too had been deemed high risk for open repair prior to his EVAR. If he had had an early generation Excluder graft, the possibility of ultrafiltration would be more likely and relining the graft would be reasonable (link). This was again a cloth and metal stent graft which can develop intermittent bleeding from graft to stent sutures, and I don’t think relining will help.
The patient was taken for open repair (above), and on opening the AAA sac, bleeding could be seen coming from the flow divider. It stopped with pressure, but I replaced the graft in a limited fashion from the neck to the iliac limbs as in the first case. This patient did very well and was discharged home under a week.
The third patient was another fellow referred from outside who had an EVAR for a very short and angulated neck, and a secondary procedure with an aortic extension in an attempt to seal the leak had been done. This failed to seal the type Ia leak. This patient too was deemed too high risk for open surgery of what was basically a juxtarenal AAA with very tortuous anatomy.
The patient was taken for open repair, and the stent grafts slid out easily (below).
A tube graft was sewn to the short aortic neck and distally anastomosed to the main body of the stent graft -with pledgets because of the thin PTFE graft material in this particular graft. This patient did well and went home within a week.
All three cases are patients who were deemed originally too high risk for open repair, who underwent EVAR, then underwent explantation of their failing stent graft. Only one involved a patient whose graft was placed off the IFU (short angled neck), but the rationale was that he was too high risk.
What is high risk? In non-ruptured, non-infected explantation of failing stent graft, the mortality is 3% (ref 2) from an earlier series from Cleveland Clinic. With stent graft infection, the 30-day mortality of surgical management from a multi-institutional series was 11% (ref 3) when there was no rupture. From a Mayo Clinic series, stent graft resection for infection came with a 4% 30-day mortality (ref 4). These were nominally all high risk patients at the time of the original EVAR.
Real world risk is a range at the intersection of patient risk and the expertise of the operating room, critical care, and hospital floor teams. The constant factor is the surgeon.
Endografts for AAA disease (EVAR, endovascular aortic aneurysm repair), makes simple work of a traditionally complex operation, the open aortic aneurysm repair. The issue has been the cost and risks of long term followup as well as endograft failure and aneurysm rupture. The Instructions For Use on these devices recommend a preop, a followup 1 month, 6 month, and 12 month CTA (with contrast) and annual followup with CTA for life. These devices were meant to treat high risk patients but high risk patients with limited life spans do not benefit from EVAR (ref 1, EVAR-2 Trial). These have lead the NHS in the UK to propose that EVAR has no role in the elective repair of abdominal aortic aneurysms in their draft proposal for the NICE guidelines for management of AAA (link). While this is a critical discussion, it is a discussion that is coming at least ten years too late. A generation of surgeons have been brought up with endovascular repair, and to suddenly announce that they must become DeBakey’s, Wiley’s, Imperato’s, and Rutherford’s is wishful thinking at best or wilful rationing of services at worst.
In 2006, Guidant pacemakers were recalled because of a 1000 cases of possible capacitor failure out of 28,000 implants for a failure rate of 3.7% -there were 2 deaths for a fatality rate of 0.00007%. EVAR-1 Trial’s 8 year result (ref 5) reported 16 aneurysm related deaths out of 339 patients (1.3%) in the EVAR group compared to 3 aneurysm related deaths out of 333 patients (0.2%) in the OPEN group.
Academic medical centers, behemoths though they are, serve a critical function in that they are critical repositories of human capital. The elders of vascular surgery, that first and second generation of surgeons who trained and received board certification, are still there and serving a vital role in preserving open aortic surgery. My generation -the ones who trained in both open and endovascular, are still here, but market forces have pushed many of my colleagues into becoming pure endovascularists. The younger generation recognizes this and last year, I sat in on an open surgical technique course at the ESVS meeting in Lyons organized by Dr. Fernando Gallardo and colleagues. It was fully attended and wonderfully proctored by master surgeons. This is of critical importance and not a trivial matter. As in the 2000’s when endovascular training was offered as a postgraduate fellowship in centers of excellence, there is no doubt in my mind that today, exovascular fellowships need to be considered and planned and that current training must reinvigorate and reincorporate their open surgical components.
When I lecture to interventionalists (cough, cardiologists), I often end with some variation on the following:
1. The common femoral artery is the left main of the leg, so why would you ever leave a stent across the LCX?
2. Claudication is like stable angina, so is it okay to intervene on a long LAD CTO for stable angina?
3. Gangrene and ulceration are like STEMI and Non-STEMI, only you can’t take the dressing down on an infarcted heart three times a day and wash away the debris.
4. If a LIMA to LAD isn’t a failure and lasts many years beyond the best stents, how is a femoral to tibial bypass a failure?
5. Why is that [insert technology] is a failure in the coronary circulation but the latest and greatest thing in the peripheral circulation?
6. Reversible ischemia is well demonstrated in the foot by lifting it off the bed and watching the color change. It’s too bad for vascular surgeons we can’t build a giant white box around this test and have have the hospital build a center around it.
7. The ABI is a great test of cardiac risk, not so much for peripheral vascular disease.
8. Hybrid revascularization works for the legs in the same way it works for the heart -you maximize the hand that you are dealt.
9. The nitinol throne is not won without some cost.
10. One day, in the far future, someone will dig up an ancient human that is more nitinol, stainless, steel, and chromium, than bone, from the mitral valve out to the fingers and toes.