Zebras, not horses: popliteal artery entrapment syndrome

mega mushroom
Adding a vascular surgeon to a hospital is like eating one of these. It turns Mario into Mega Mario. Vascular surgeons turn community hospitals into tertiary care centers.

Recalling the medical school adage, “when you hear hoofbeats, it’s probably horses, not zebras,” it is critical to think about rarities down on the differential list whenever you come across a patient. Vascular diseases suffer from inadvertent obscurantism arising from its absence from medical school curricula such that common disorders like mesenteric ischemia and critical limb threatening ischemia are frequently missed by even experienced medical practitioners. Vascular zebras are even harder to pin down because many experienced vascular specialists practice for years before they encounter, for example, adventitial cystic disease or dysphagia lusoria with a Kommerell’s diverticulum. Even so, real patients have these disorders, and we are all subject to inexperience bias -the feeling that something does not exist until you see it. You may completely miss something staring at you in the face or worse, deny its existence.

The patient is a middle aged man in his 50’s who aside from mild hypertension had no real risk factors. One day, at work, his right leg stopped working. He developed a severe calf cramp and the forefoot was numb and cool. He went to his local hospital and the doctors there appreciated the lack of pulses in the right leg and got a CTA, of which I only had the report which found a right popliteal artery occlusion.

The next morning, as he had signals and was not having rest pain, his doctors discharged the patient on clopidogrel and scheduled for angiography and stenting, per patient. As his debilitating claudication did not go away over the weekend, he came to our emergency room. While he had no rest pain, he did have minimal walking distance before his calf muscles seized up. On exam, his right foot was cool and cyanotic, with intact motor function and sensation. There was a weak monophasic posterior tibial artery signal. Bedside point of care photoplethysmography showed dampened waveforms (below).

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Look at the blue line. The waveforms are dampened in the ischemic foot.

Because he did not bring his CT, I repeated the study. I have written extensively on the need to be able to share CTA studies without barriers. After his study, I brought it up on 3D reconstruction software.

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It clearly showed a Type II Popliteal Artery Entrapment affecting both legs (CTA images in series above). Stenting it would have failed.  I spoke with the patient about operating the next day. The plan was popliteal artery exploration and thromboendartectomy with myotomy of the congenitally errant medial head of the gastrocnemius muscle. The patient was agreeable and I took him to the operating room for a myotomy and popliteal thrombendarterectomy in the prone position. The medial head of the gastrocnemius muscle went over the  popliteal artery and inserted laterally onto the femur.

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Endofibrosis, cut medial head of gastrocnemius muscle to right of distal clsmp

The artery was opened and while there was fresh clot, the artery showed signs of chronic injury as evidence by endofibrosis which pealed off. Pathology showed to be fibrotic in nature.

04-SP-19-4119 Trichorme stain showing fibrous tissue as green
Trichrome stain showing chronic endofibrosis

The artery was repaired with a pericardial patch and flow restored to the tibials, not all of which were completely patent.

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The patient was discharged after about a week and will be scheduling repair of his contralateral popliteal artery entrapment.

The vascular surgeon has a vital role in a hospital’s medical ecosystem. One time, I heard hospital administrator say that with the advance of endovascular technologies, the vascular surgeon would become an expensive, redundant luxury easily replaced by the overlapping skillset of radiologists, cardiologists, general surgeons, trauma surgeons, cardiac surgeons, nephrologists, neurosurgeons, neurologists, podiatrists, infectious disease, and wound care specialists. When I identify these zebras, these rare diagnoses, I am neither replacing all those aforementioned specialties, nor having special insight unavailable to the uninitiated. I am keeping my eyes open. In a non-smoking, active, otherwise healthy and employed middle aged man with no cardiac history, it is very strange to have isolated popliteal occlusion with otherwise pristine arteries throughout the rest of the CT scan. That is a statistical outlier. People who occlude blood vessels in this fashion usually have more comorbidities, usually are older, and usually have more atherosclerotic disease burden. While not quite like the teenager who presented last year with the same diagnosis (after a month of misdiagnosis and delayed treatment), the cleanliness of the arteries elsewhere in the body was disturbing to me. This puts me on a zebra hunt and not the usual horse roundup.

A hospital needs vascular surgeons in the way that America need the US Marine Corps. Every decade, there is some congressional movement to see how the USMC, which has fighter jets, tanks, planes, aircraft carriers, helicopters, and riflemen, can be phased out because it seems to duplicate the services of the Navy, Air Force, and Army, and every generation a conflict proves these arguments wrong. Individuals who know things broadly and deeply, who can do many things across specialty lines, work from head to toe, and whose specialty is to customize solutions to complex problems is the special quality that is the difference between tertiary hospitals and quaternary hospitals. While these qualities are goals within Vascular Surgery, it is a generalizable goal for anyone working in healthcare. My favorite professor in medical school was Dr. Harold Neu, chair of infectious diseases at P&S. He knew everything and was interested in everything and took every moment in the hospital to increase his knowledge a little more. That’s how and why I diagnosed a case of schistosomiasis earlier this year -the upper abdominal pain was not from a coincidental aortic aneurysm, but the fellow did swim in the Nile.

I texted Dr. Sean Lyden, my former boss and partner at the Cleveland Clinic main campus, if there was any situation where an asymptomatic popliteal entrapment who had gone over 50 years of life without complications could just be watched -it was a question from the patient actually. Dr. Lyden treats popliteal entrapment weekly and maintains a clinic specializing in popliteal artery entrapment (link). One of advantages of working in vascular is that the community is small and highly accessible, and I have a group of living textbooks on speed dial (that term pegs me as antique). There is an active social network of vascular specialists and the SVS maintains SVS Connect (link) for posting and discussing difficult questions. Despite the horrible hour that he received the text (“What’s the matter? Are you in trouble?” he asked) because of the time differences between Abu Dhabi and Cleveland, he answered, “no.” Sorry, Sean, for texting you at 4 in the morning.

When you look for four leaf clovers, and you have never seen one in your life, the moment you find one must be transformative. I have never found one, but I keep my eyes open, lest I trod on one.

 

Arterial Restoration in CLTI with Remote Endarterectomy (EndoRE).

preop PVR

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.

aortogram

R SFA arteriogram

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. endore-graphic.jpg

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).

preinterventionpost kissing stents

Afterword, the CFA was opened and endarterectomized, and the SFA was remote endarterectomized (below).

EndoRE setupEndoRE

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):

EndoRE plaqueplaque in toto

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.

Endpoint managementbefore and after endoRE

His pulse volume recording done after intervention reflects the improved flows (below).

PVR before and after

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.”

postop duplex at 2 months

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.

References:

  1. Eur J Vasc Endovasc Surg 2009;37: 68-76

  2. J Vasc Surg 2012;56:1598-605.

When You Pay Your Own Way, You Chose Value

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The patient is an active man in his 60’s with a history of hypertension who had known about a right common iliac artery aneurysm for several years and had come for an opinion. He was asymptomatic of pain. He had a prior splenic artery aneurysm embolization about a decade prior to presentation.. CT scan showed a large eccentric aneurysm arising from a retrograde chronic dissection dilating the right common iliac artery to over 4cm. This is typically iatrogenic, but impossible to know for sure. The left common iliac artery was ectatic to 2cm as was the aorta to 3 cm and all were “wavy.” This sort of tortuosity is the result of remodeling in the axis of flow resulting in lengthening of the artery and is found in those with the substrate for aneurysmal degeneration (footnote). He did not smoke and he could climb stairs without dyspnea or chest pain.

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On examination, he was a fit middle aged man with a slight paunch. His abdomen was soft and his peripheral pulses were present and normal. Laboratory results were normal, including creatinine. EKG and echocardiogram were also normal.Treatment options were discussed in detail. The patient was paying for the operation himself and wanted to understand in detail the possible options. These included

1. Open aortobi-iliac bypass with a jump bypass to the right internal iliac artery
2. Open aortobi-iliac bypass with ligation of right internal iliac artery
3. EVAR with right external iliac extension after embolization of right internal iliac artery
4. EVAR with parallel grafts to right external and internal iliac artery (off label)
5. EVAR with iliac branched graft to right internal and external iliac artery (off label)

People are known to react with emotions and to decide typically for near term gain over far term benefits. The offer of an operation involving laparotomy and a possible weeklong hospitalization with all the attendant risks of death, heart attack, stroke, ileus, wound infection, pneumonia, organ failure and so on provides a stark contrast to the appeal of endovascular repair which can be done percutaneously, with local anesthesia, and with a short hospital stay. The lifelong CT scans are in the murky future compared to the present which is sharply in focus. This is why few people save for retirement, why profligate grasshoppers far outnumber industrious ants. In the same vein, the offer of an “advanced minimally invasive” solution plays to several cognitive biases that exists in the mind of not only the patient but the health-care provider. These include this preference for short term gain over long term gain, but also viewing all innovation as being necessarily better than what was available.

After going over the operation in great detail, the patient cut me off when I mentioned the need for lifelong followup CT scanning. Because he lives in several countries, typically, he has to pay for his healthcare out of pocket and he balked at the notion of paying for an annual CT scan. He was also disdainful of the possibility of reintervention (quoted at 10%) and having to pay for it. Also, the stent grafts, which he would have to pay for, end up being as costly as a new luxury sedan based on local pricing.

We chose open surgical repair via a midline laparotomy. An aortobi-iliac bypass was performed from proximal aorta to right internal iliac artery and left common iliac artery bifurcation with a jump bypass from the right graft branch to the right external iliac artery. Technically, this sequence was chosen for ease of access to the internal iliac artery with the external clear of graft. Operative time was 3 hours. He was in the ICU for one night. He went home after 10 days after contracting a UTI. In followup three weeks after discharge, because he had fevers, a CT scan was performed (figure). He was treated for an upper respiratory infection which cleared, and he has been doing well since. We are both happy that he will never need a followup CT scan.

Before and After

The literature supports this stance. The long term followup of the EVAR-1 Trial (Reference 1) is an example. This was the late followup of the prospective randomized study looking at open surgery versus EVAR in 1252 patients. The initial EVAR 1 findings are well known and put into question the long term benefits of EVAR as the initial mortality benefit of EVAR is lost within a few years of treatment. At a mean of 12.7 years of followup, there were more deaths from aortic aneurysm rupture and aneurysm related death in the EVAR group compared OPEN surgery (adjusted HR 5.82, p=.0064), with 13 AAA ruptures. I have mentioned before that the failure of a handful of pacemakers drove the Guidant company to recall over 20,000 of their devices. Plus, the cost of annual CT scans in the treatment group and cost of devices and cost of reintervention have driven the UK’s NICE Guidelines recommending against EVAR in elective AAA repair. The meta-analysis of EVAR-1, DREAM, OVER, and ACE trials comprising 2783 patients is confirmatory, that aneurysm related mortality was significantly higher after the initial mortality benefit of EVAR fades away, and that patients of marginal fitness gain no advantage from EVAR, particularly those with heart or renal disease, and those with PAD had lower mortality in the period of 6 months to 4 years (reference 2).

I post this case, because despite a complications, in this case UTI and URI, the patient did fine. So why is open aortic surgery considered a dying art? Why is there such pushback against the UK NICE Guidelines?During my residency in the 1990’s, in the heyday of open surgery, I observed a lot of mediocre vascular surgeons and a very few great ones. The average vascular surgeon would take 6-8 hours to perform open aortic surgery, and the patient would come out with a typical picture of oliguria, third spacing, SIRS, that would generate a 1-2 week stay that would even be described as the normal and expected course for AAA repair in surgical and critical care textbooks. The best surgeons back in the day did these operations under 3 hours with 100mL blood loss and the patients would spend a day in the ICU (often not needing it), and 3-7 days in the hospital, but they were the exception.A higher percentage of surgeons today can do EVAR well than surgeons 25 years ago could perform competent open aortic surgery. Most surgeons graduating from training rarely see or do open aortic surgery compared to the multitude of interventions. Capable open surgery basically is not available outside of a few centers, and most surgeons admit to not having equipoise to start a new trial with modern devices. Open aortic surgery is a lost art, like growing your own vegetables, dressing your own game, reading cursive script, and dialing a rotary telephone.

It is not for a lack of desire. I have several younger colleagues I have met or interacted with via social media who have an intense interest in gaining open vascular skills. They have organized open skills courses at major European vascular meetings, but I believe that is not enough.The need for exovascular fellowship, the running topic of conversation of older surgeons through the 2000’s, is never as critical as it is now as we see milennia of surgeon-years of experience retiring to golf courses and cottages. The recommendation for preferring open surgery in the younger and fitter patients is sadly out of reach for most patients and surgeons. The same passion in disseminating endovascular knowledge needs to be applied to repair the damage to vascular education by over-relying on and over-prescribing endovascular approaches.

Finally, and sadly, this patient is the exception. When given clear options and outcomes and costs, this patient made a rational decision, choosing value over convenience.

Reference
1. Lancet 2016;388: 2366-2374.
2. BJS 2017;104:166-178

Footnote:

Pearls for finding AAA:
1. Tortuosity of the internal carotid arteries including loops and hairpin turns found in patients particularly smokers implies the present of a AAA until proved otherwise
2. Palpating bounding popliteal or pedal pulses in an older smoker implies the presence of a AAA until proved otherwise. Especially if the medical student can feel these pulses.
3. African-American Females with Diabetes almost never get AAA.
4. Palpate their abdomen

The Pain Operations

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Absolute Neutral Position is suprisingly universal

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.

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A random list of conditions that cause pain that should be on the mind after the usual things are ruled out. Also, vasculitis, autoimmune disorders, and foreign body reactions

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).Screen Shot 2019-03-03 at 5.34.02 PM.png 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).my spider vein 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).

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Actual Slide From Midwest Vascular Surgery Traveling Fellowship talk 2017, Chicago, IL, USA

 

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.

A lot of people can put in a stent graft, unfortunately only a few can take them out.

 

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Drs. Roy Miler and Xiao Yi Teng performing anastomosis on open coversion of an aortic stent graft, now graduated and in practice. A significant part of their open aortic experience is in addressing failing stent grafts.

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.

IMG_8144

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.

IMG_8151

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.

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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).

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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.

References

  1. Lancet 2005;365:2187–92.
  2. J Vasc Surg. 2009 Mar;49(3):589-95.
  3. J Vasc Surg. 2016 Feb;63(2):332-40.
  4. J Vasc Surg. 2013 Aug;58(2):371-9.
  5. Lancet 2005;365:2179–86.

Exovascularist’s Dilemma: Where Is Our LIMA to LAD

During our daily morning huddles, peopled by cardiologists and cardiac surgeons, one thing impresses me more than anything else. The assembled interventional cardiologists, world class and renown, they who can place a stent in any part of the body, will defer to the unassailable superiority of the LIMA to LAD bypass over any existing intervention. I am always a little sad that the analog for this, the vein bypass in the leg does not get the same love. The open surgical bypass of the leg is the great straw man at international symposia. It is fast becoming a diminishing and curious habit of a fading generation.

The acknowledged superior hemodynamics and patency of the bypass is diminished in the literature by pooling patency loss with other factors such as amputation, heart attacks, and death. Some vascular surgeons dogmatically cling to habits learned in training that favor complications, making themselves their own worst enemies both in the literature and in the marketplace. These bad habits involve long incision length, closure techniques that do not anticipate edema, and wound orientation that makes failure more likely.

Operations require far more support and resources to succeed than do interventions that soon go home. Brilliant operations alone will not heal the patient. It is pathways and postoperative care infrastructure and staff that prevent these secondary complications -the very complications that keep the leg vein bypass from being as respected, if not loved, as the LIMA to LAD.

The postoperative care of these patients devolves to management of leg edema. No medical or nursing school adequately teaches the basic science nor management of edema, which is the most common vascular condition

The incisions are too long in the classic vein bypass. When you create and then close an incision, the inflammation drives the accumulation of fluid in the extracellular space – creating edema. This postoperative edema, poorly managed, results in complications that leave the patient hobbled with time lost to healing wound complications, pain, and excess limb weight. Additionally, vein bypasses usually involve groin exposure and the delicate lymphatics that coalesce there are perturbed or destroyed during exposure. Postop, this damage and the inflammation rapidly overcomes the capacity of a lymphatic system. The traditional vein harvest also involves cutting through deep layers of fat. The fat is typically closed by broad sutures that create areas of fat necrosis -potential fodder for bacteria. The best ways the complications of long and deep incisions is to avoid them altogether. The calculus of the operative moment – “I must see the vein,” must include the vision of a patient losing months to wound therapies to heal a gaping, necrotic, infected wound. I recommend skip incisions or adopting in-situ bypass technique with endovascular management of fistulae. Or corral your cardiac PA to harvest the vein segment in the thigh after mobilizing the vein in the leg with the endoscope.

The incisions are often closed with Nylon sutures and skin clips which can become potential foci of infection. With edema, they create zones of ischemia around them, killing skin and creating entry points for skin flora as the skin expands under an unyielding clip or suture. Placed under a pannus, these sutures or clips fester in an anaerobic environment. Closure should adhere to anatomy. The body relies on connective tissue planes to keep itself together. In the groin, these are Scarpa’s layer and the dermis. They should be closed with absorbable monofilament in a buried interrupted fashion at the dermis with a final running subcuticular layer of 4-0 absorbable monofilament. Steristrips or glue at the skin finishes the job. If you use sutures, particularly at the distal anastomotic site, take care to realize that you have about 12 hours before the skin dies in the best of circumstances, and less with microangiopathy of diabetes and ESRD. Squeezing out the edema before closure with a sterile Esmarch or short counterincisions or even a large one to allow for tension free closure over an anastomosis will prevent wound complications over your graft.

The classic longitudinal groin incisions that cut across the inguinal crease divides a tension point -that crease is like a cord that supports the pannus that is slung over it and when divided and then closed with a stitch, that stitch then bears the weight of that pannus every time the patient sits up or stands. If you are observant, wound necrosis typically starts at the groin crease under a surgical clip or suture. Incisions in the groin should be obqlique and parallel to this crease, or if you can, even inside this crease. When these wounds are closed, the natural lines of tension are in line with the incision rather than orthogonal to it. The natural forces keep the wound shut.

This is only the first step. The next is keeping the wound clean and dry for at least 5 days. At the Mayo Clinic, where I trained, the nurses up on 5 Mary Brigh were trained to blow dry the groin wounds every few hours on cool setting and redressing the wound with dry gauze. You can get something close to it by ensuring the wounds painted with betadine, allowed to air dry, and dressed with dry gauze. If there is a constant leak of fluid, you have a serious problem as there is too much edema in the leg, or the wound isn’t closed, or there is a lymph leak. It needs to be actively dried out or you get a wet, macerated, infected wound like a grenade went off in the groin.

They don’t teach compression wrap techniques in medical or nursing school

The simplest thing to avoid lymph leaks is to not make them. Cutting near lymph nodes is hazardous, and once below Scarpa’s you have to orient your dissection directly over the femoral artery. Stray horizontally and you will undoubtedly cut one of the 4 to 10 invisible lymph channels.

They are invisible but detectable -after you break them, you will see a constant wetness in the wound. Think about injecting a cc or two of Lymphazurin (Isosulfan Blue, for those not allergic to Sulfa) into the intertriginous space on the same foot and you will see the lymph channel in bright blue, or stare carefully at the likely spots for a lymph leak and clip it, burn it, Ligasure or Harmonic scalpel it.

Lymph leak identified from saphenectomy incision (for CABG)

So how did we get to a rather dry discussion about edema? Wound complications are tremendously debilitating and offset any benefit from vein bypass operations. These long incisions become terrible big wounds if not prevented. It takes the concerted effort of a team and particularly nursing in actively managing edema. And at the end, the patient too must be included in this discussion. For the vein bypass of the leg to get the same respect and love as the LIMA to LAD bypass, surgical wound complications must become never events.

Water goes downhill