At the VEITH Symposium, which I attended briefly last week, while I foraged for lunch and sought out friends, I wandered into a crab trap (diagram above). Or more specifically, the WL Gore exhibit hall (below).
The coffee and bevarages featured all day, and the steak buffet at lunch, draws people in, like the smell of chicken to a crab, and once you have a plate of food, you then are kind of committed to moving forward into the conference room where they have a video feed of aortic symposium and tables to gobble your lunch.
Like a hand reaching into a crab trap to retrieve the catch, the reps wander in and chat you up, but thankfully only if they know you, which is fine because any hard sales tactic would trigger a fight or flight reflex that would ruin the generally chill atmosphere. There are exits to the left because, you know, fire codes, but they are small, and going out the way you came in risked bumping people juggling plates of their lunch, cups of their coffee. So you go in, sit down, and nibble, watch someone you vaguely know up on the big screen who just decided to go full head shave bald (why is that a thing?), check your phone and find out your friends are in another trap on the other side of the center. And their doors are closed, invitation only. Silly crabs.
Median arcuate ligament syndrom (MALS), also known as celiac axis compression syndrome (CACS) and its eponym Dunbar Syndrome, is manifest as epigastric abdominal pain and a compendium of symptoms, arising from chronic compression and inflammation resulting from compression of the celiac plexus between the median arcuate ligament and the celiac axis.
Graphic showing the pathoanatomy of neurogenic MALS (from ref 1). The repeated trauma to the celiac plexus results in inflammation and nerve injury with transmission of pain and neuropathic sensations.
The diaphragm muscle descends from the neck during development (the phrenic nerve originates from C3-C5 nerve roots), and in perhaps up to 25 percent of individuals, drapes across the origin of the celiac axis, and sometimes anchors further down impinging on the SMA or renal artery origins.
While a significant number of patients have this coverage of the celiac axis origin, not everyone has pain. Some whose celiac axis is compressed develop post-stenotic dilatation. For some of these, there is damage to the celiac axis resulting in intimal injury, dissections, thromboses, webs. Turbulent flow causing post-stenotic dilatation in the celiac axis can proceed to aneurysm formation. Downstream in the splenic and hepatic artery and its branches, turbulent flow can engender tortuosity (lengthening) and aneurysms (widening). This disease subset of celiac axis compression should be termed aMALS (arterial median arcuate ligament syndrome).
A question was asked at this year’s VEITH Symposium as to whether post-stenotic dilatation due to median arcuate ligament compression could be considered an aneurysm. The answer given was no, but I think it would be yes in the above example.
Both arterial and neurogenic manifestations of celiac axis compression are under the same ICD code of I77.4, referring to both celiac axis compression syndrome and median arcuate ligament syndrome. While I would never suggest more ICD codes, there should be a differentiation similar to the other compression syndrome, thoracic outlet syndrome (TOS). The pain-based syndrome, which is more common, should be termed neurogenic MALS, or nMALS, and the arterial disease secondary to celiac axis compression should be termed arterial MALS or aMALS. The treatment of nMALS is surgical ablation of the celiac plexus along with median arcuate ligament release, done via open, laparoscopic, and robotic techniques. The treatment of aMALS is the treatment of the arterial complications of celiac axis compression and should involve median arcuate release and treatment of the arterial pathology with either open or endovascular techniques.
Case Presentation
The patient is a middle-aged man with several months of right sided abdominal pain, mostly in the right midaxillary line at the costal margin, right upper quadrant abdominal pain, and right sub-scapular pain. He did not have gallstones, and had no gastrointestinal complaints. He is hypertensive and was on a single agent which he took in the mornings. His pain began during the day and crescendoed in the evening. His prior visits to the emergency room had revealed a hepatic artery aneurysm and celiac axis aneurysm. In the ED, his examination was significant for pain and mild tenderness in the right upper quadrant of his abdomen. He underwent a CT scan.
Common Hepatic Artery Aneurysm, 2.4cm with celiac axis ectasia to 14mm, median arcuate ligament compression of celiac axis
The CTA showed compression of the first centimeter of the celiac axis by the median arcuate ligament of the diaphragm and mild post-stenotic dilatation to 14mm. At the terminus of the common hepatic artery, where the hepatic bifurcated was a 2.4cm aneurysm with mural thrombus. With blood pressure control, his pain remitted.
The trainees and I had a lively discussion as to indications for repair and whether this constituted a symptomatic aneurysm. As I have stated in past posts, all pain has a nerve and a mechanism for pain. Abdominal pain and its points of referral are well known going back to the 19th century and encapsulated in Cope’s Early Diagnosis of the Acute Abdomen, whose most recent steward, Dr. William Silen just passed this September. Processes involving the gallbladder and nearby hepatic artery refer to the right upper quadrant abdomen, right chest, right shoulder and scapula which was where the patient’s pain was. And it improved with controlling his hypertension. There was no question to me the aneurysm was symptomatic, likely from strain on the aneurysm.
The question then devolves to whether this is to be done endovascularly or open. While it seems straightforward for me, I have realized at large meetings there will always be some endovascularist proposing something. For me, to exclude pressure from the aneurysm and avoid rupture, the aneurysm had to be isolated from the blood flow and pressure. Ideally, this would be done with tiny covered stents. There are no 7mm x 4mm stents bifurcation stents.
Hypothetical bifurcated small stent system -does not exist, would not work.
Embolization of the hepatic aneurysm, which is done for the splenic, offers hazard of hepatic ischemia. Despite what is written in the textbooks about the portal venous system providing most of the perfusion of the liver, you have to remember there is only portal flow when there is food. Acutely losing one of the hepatics, even clamping it for a time, reverberates as a spike in the LFTs, along with attendant systemic inflammatory response. While the liver, like spleen, can recover and regrow, you mess with it at your great peril. Based on the CTA, closing the hepatic artery with coils and plugs will likely be tolerated as hepatic flow would continue via the gastroduodenal artery which is not small, but there is no guarantee that the aneurysm wouldn’t be pressurized yet by the prominent GDA (if you disagree please feel free to comment).
He was prepared for surgery with echocardiography (normal) and lab testing (normal LFT’s, CBC, BMP, INR), and taken to the OR. A chevron incision was made to broadly expose the area. The median arcuate ligament was exposed and released -there was dense tissues proximal to the dilated celiac axis. The aneurysm was dissected out and the small branches were carefully dissected out and controlled. It is easy to injure the branch hepatic arteries which can constrict on dissection.
A suitable length of saphenous vein was harvested and prepared. The three vessels diagrammed above did not present themselves suitable for a single Carrel patch so I sewed end to end to a patch incorporating the right hepatic and gastroduodenal arteries, and performed a sequential side to end anastomosis to the left gastric artery.
The patient recovered well and was discharged home on POD#5, and in followup had no further symptoms.
Discussion:
The differentiation of arterial and neurogenic manifestations of MALS is an important refinement of our understanding of this disease, which I believe to be a byproduct of our bipedal lifestyle. The lordotic curvature of the spine, necessary to balance our upper torso on a vertical spine, pushes the spine forward and applies tension to the median arcuate ligament, along with other structures such as the duodenum and left renal vein in superior mesenteric artery syndrome and nutcracker syndrome, and the left iliac vein in May-Thurner Syndrome.
This compression is not only enough to narrow the celiac, but injure the artery by crushing. Stenting here does not do well because of the external compression and even after release, the artery may be damaged and require repair.
The chevron exposure heals well and is well tolerated and offers perfect exposure. While I was doing it, it occurred to me that a laparoscopic bypass is technically possible, and may be preferred to the long incision. Recent multi-institution study of MALS treatment would suggest laparoscopic approach offers a lower complication rate compared to open surgery (ref 2.)
The critical thing is having more surgeons recognize the compression that occurs in the abdomen and manifests in disparate and unconventional ways. The key is tying pain to a lesion, a mechanism, a nerve, just the way Cope’s does.
References
Weber JM, Boules M, Fong K, Abraham B, Bena J, El-Hayek K, Kroh M, Park WM. Median Arcuate Ligament Syndrome Is Not a Vascular Disease. Ann Vasc Surg. 2016 Jan;30:22-7. doi: 10.1016/j.avsg.2015.07.013. Epub 2015 Sep 10. PMID: 26365109.
DeCarlo C, Woo K, van Petersen AS, Geelkerken R, Chen AJ, Yeh SL, Kim GY, Henke PK, Tracci MC, Schneck MB, Grotemeyer D, Meyer B, DeMartino RR, Wilkins PB, Iranmanesh S, Rastogi V, Aulivola B, Korepta LM, Shutze WP, Jett KG, Sorber R, Abularrage CJ, Long GW, Bove PG, Davies MG, Miserlis D, Shih M, Yi J, Gupta R, Loa J, Robinson DA, Gombert A, Doukas P, de Caridi G, Benedetto F, Wittgen CM, Smeds MR, Sumpio BE, Harris S, Szeberin Z, Pomozi E, Stilo F, Montelione N, Mouawad NJ, Lawrence P, Dua A. Factors Associated With Successful Median Arcuate Ligament Release in an International, Multi-Institutional Cohort. J Vasc Surg. 2022 Oct 25:S0741-5214(22)02443-0. doi: 10.1016/j.jvs.2022.10.022. Epub ahead of print. PMID: 36306935.
In no particular order, I list these problematic situations that are outsized in their ability to take a case sideways.
Ischemia syndromes in the unconscious. The unconscious tell you nothing about their pain and follow no commands. Therefore, vigilance and a low threshold for operating are what will save the patient if they are salvageable. Objective evidence of flow -examination, handheld pulse Doppler, duplex ultrasound, CT angiogram, exploration and visual inspection, must be obtained. The typical scenarios are dissections of the ascending thoracic aorta, polytrauma patients, and patients on ECMO. By the time the dissection is repaired and the patient is off pump, they may be long past the 6 hour threshold for irreversible ischemia for gut or muscles. The patient involved in a rollover MVA who had their femur fracture reduced after ten hours waiting on the add on schedule should have their compartments assessed visually through fasciotomies. Patients on ECMO via femoral access must by practice have distal perfusion cannulation. Assessment for ischemia need to start at admission for the unconscious patient with assessments of flow and function. Waiting until markers of cell death are apparent on blood tests is not the right approach unless the patient is DNR.
Operations in redo or irradiated fields. Preparation and coordination is key. Most vascular surgeons have a plan for controlling arteries and veins in these settings, but a common scenario is in trauma or oncologic surgery. I don’t know if anyone has done this, but the idea comes to me that if there is concern for oncologic invasion of a major artery -an aorta or iliac, it would be reasonable to place a wire, balloon, or stent graft across that area with solid seal zones to allow for free dissection and resection of any involved artery.
Central venous rupture during venoplasty for hemodialysis access with an open fistula. Instead of venous pressures, with a fistula attached, arterial pressure is driving the leak. A leak of an SVC can lead to a fatal cardiac tamponade. Because the heart fails to fill, CPR is futile. The only thing can be done once this has occurred is to be prepared to a. ligate the fistula, b. Drain the pericardium either with needle pericardiocentesis or left anterior thoracotomy. Better still is preparing for SVC venoplasty by balloon occluding the fistula prior to inflating the balloon in the SVC.
Rapidly progressing skin infections. It is amazing how fast necrotizing infections can progress. I’ve seen simple infections of a finger spread to the whole arm over the course of an hour or two in the waiting room of an emergency room. There are forgotten anecdotes of medical students dying after nicking their hands in gross anatomy. I saw a concert pianist lose her arm after getting a thorn from her rose garden. The image below is of a forequarter amputation I had to perform on a young man with a fulminant infection of the muscles of the left upper extremity undergoing a forequarter amputation after an overnight of misdiagnosis as a cellulitis at an outside facility. It grew among other things Candida auris, a terribly frightening organism and spread to his chest wall and ribs, resulting in death.
5. Iliocaval venous injury, particularly small tributaries going under aorta or around its branches. While not pressurized, they have tremendous flow like a hole in a plastic bag holding a goldfish, and without precise control, you are as likely to widen the hole or make more holes as you try to suture the holes. I’ve had some success using the Park clamp (link). You can’t buy one but you are free to have one made by your local smith. Otherwise, you need to keep your finger on the hole while you call in help, usually in the form of more vascular surgeons to get exposure and the vein properly clamped for repair.
I had posted the above picture from over 15 years ago during my time in Iowa of my hybrid AUI-Fem-Fem (under unclampable 2, link). This technique came back to me as I was strategizing the upcoming aortic revascularization of a patient with iliac occlusions with the added complexity of an ileal conduit in the right abdomen. He had multiple failed prior iliac stents and failed femorofemoral bypasses -his right CIA and EIA were occluded while the left EIA had become occluded resulting in ischemic rest pain. While the picture alone is sufficient for me, it was brought to my attention by Dr. Joedd Biggs, fellow alum of the Mayo Clinic, on faculty at University of Kansas Hospital, that more detail was needed. So while resting my tired dogs, I got on my tablet and drew it out. Joedd, I present you my technique for a hybrid AUI-Fem-Fem bypass of the aorta.
This technique is made easier if one of the iliac arteries are patent. It is not a necessary condition.
The image above shows the necessary incisions for the femorofemoral bypass and the retroperitoneal pelvic (transplant) exposure of the left iliac bifurcation. I nearly always make oblique rather than vertical skin incisions in the groin to avoid wound complications from incising the inguinal crease orthagonally.
The transplant exposure facilitates a retropubic tunneling of the femorofemoral bypass which is performed first.
A left lower quadrant retroperitoneal exposure of the pelvis is performed -this is a standard renal “transplant exposure.” The two groin incisions are made and the common femoral arteries are exposed. Endarterectomy may be performed, although if the orifices of the SFA and PFA are patent, I don’t. The bypass graft is tunneled retropublicly and this is facilitated by the transplant incision. I generally use a 7mm ringed PTFE graft. Once done, the common iliac artery is divided above its bifurcation and the bifurcation is oversewn or stapled. A 12mm bypass graft is then sewn end to end to the common iliac artery (below).
The secret sauce in this technique is the end-to-end anastomosis of a 12mm bypass graft to the common iliac artery.
Through the conduit, a suitably chosen iliac limb of an EVAR system is brought through to the aorta and deployed with its end across the anastomosis into the conduit. A Gore Excluder 12mm ending iliac limb is ideal as its proximal end is appropriately sized for the diseased abdominal aorta. The limb is then aggressively ballooned to profile, particularly in the 12mm graft (below).
The Excluder 12mm limb works nicely and will seal against the 12mm bypass graft with sufficient overlap. It is then aggressively ballooned to profile from inflow to end.
The 12mm conduit graft is then sewn end to side to the femorofemoral bypass (below), completing the AUI-Fem-Fem.
I believe there are hemodynamic advantages to this over reintervening on native aortoiliac segment. First, size does matter, and until a suitable aortoiliac occlusive disease stent graft system is engineered, this represents an optimum. The Gore excluder graft limb is 16mm proximally and this is usually more than enough to diameter for the diseased abdominal aorta. The end diameter of 12 or 14.5mm will seal nicely in a 12mm conduit. I have not used a 16mm conduit only because I prefer not rupturing the aortic bifurcation with the “aggressive ballooning” mentioned above. The 12mm diameter is the boundary above the “small aorta syndrome” diameter of 10mm.
If the iliac is occluded, a wire can be driven through it from above and the conduit sewn over it. The iliac limb can be delivered after some pre-dilatation then followed by the “aggressive ballooning” of the iliac limb. The deployment into the conduit creates a stable “endo-anastomosis.”
Patients like my upcoming patient usually fail intervention due to the lumen size issues. An 8mm fem-fem bypass fed by a diseased series of iliac stents with at most 7mm lumen diameter is a recipe for the development of mural thrombosis and occlusion. The lower half of the body are fed by the diseased conduit of the donor EIA. This way, true aortic inflow is created.
I recently had lunch with Dr. PJ O’Hara, emeritus professor, and former partner of mine from the Cleveland Clinic. We hadn’t met since 2018 at the VAM in Boston, while I was still in Abu Dhabi. It was a recent case I did that caused me to reach out. I won’t be posting that recent case in detail today -it was a patient who had had multiple aortoiliac interventions for aortic bifurcation disease, but who closed up their stents within a few months of intervention. Rather than subject that patient to another round of interventions, I chose aortoiliac endarterectomy because the prior interventions failed to address the basic problem of the undersized aorta and iliac arteries.
The last case that Dr. O’Hara did before retiring was an aortoiliac endarterectomy which I assisted with, nearly a decade ago. During that case, Dr. O’Hara mentioned a video he had put together for an SVS meeting. He was kind enough to give me a copy share.
Aortoiliac endarterectomy -forget thee not!
The modern application of this technique is in the removal of occluded aortoiliac stents. The aorta and iliac arteries are restored, and yes, stents can go back in if needed.
A quick survey of some of my contacts at major centers reveals that this technique is rapidly becoming forgotten as its practitioner retire or revert to teaching the technically easier aortobifemoral bypass (ABF) graft. I hope to revive this because I know there are many patients who have challenging anatomy for ABF but potentially could undergo plaque and stent removal and restoration of their aorta and iliac arteries.
CTA tends to overread stenoses which was in the 60-79% range on duplex
The patient is a middle aged executive who complains of bouts of aphasia triggered by intense conversations and business meetings. It first occurred while driving to Dubai on a conference call. Since then, they occurred several times a week, typically triggered during meetings where he needs to think and speak. Casual conversation and cognition does not seem to trigger this. Workup revealed a heterogeneous plaque affecting the left ICA with velocities in the 60-79% range. CTA confirmed this plaque. MRI failed to show any stroke or other lesions. Neurology evaluation showed normal exam. The patient underwent endarterectomy, and had a normal recovery. In followup, he denied any further episodes of aphasia.
Standard endarterectomy with patch
Aphasia, the loss of function in the language centers, typically of the left brain, although in a minority, it may live in the right hemisphere, is terrifying manifestation of stroke. This case, if examined superficially, is nothing special in that TIA’s associated with a reasonable culprit lesion went away after elimination of that culprit lesion. To me, it was fascinating because it represents a possible case of brain claudication.
The human brain is believed to have evolved to its large size in conjunction with bipedalism, social hunting and gathering, and climate change in the Great Rift Valley favoring a savannah over forests, that created heat stresses on the brain, favoring the development of sweating and redundancies in brain tissue. The advent of fire and cooking enhanced available calories to feed this enlarged brain’s metabolic needs. When the metabolism isn’t supported through adequate blood supply, the brain tissue dies. Rarely, it blinkers on and off, and even more rarely, this occurs in the motor strip triggering today a neurologic evaluation including a carotid duplex that brings these patients to our attention. The fascinating question for me is, does increased metabolic demand in the form of complex thinking result in a supply-demand mismatch much as seen in exercise induced angina or claudication? If it can, can we test for it?
The tests we have available are hemodynamically based. At its simplest, after carotid angiography, an occluding balloon can be inflated to test for symptoms. This is an archaic test and I do not do it. There are nuclear medicine, PET CT, and MRI tests that use pharmacologic agents to induce hypotension, but again, for this patient, it wouldn’t apply. This patient needed the equivalent of a treadmill in the MRI machine. Maybe having him read a dry, technical treatise on neurobiology taped to the MRI tube?
I went to the OR with the indication of TIAs associated with a >50% lesion, but I did tell the patient that it was possible his thinking-induced aphasia would not remit. Thankfully it did.
Every time someone on Seinfeld went to the hospital, a stock scene (above) would play. It’s the old ER of Roosevelt Hospital on 9th Ave before the renovations moved it to current 59th street entrance. I was a surgery resident there in the 90’s and watched each Seinfeld episode for the upper West Side stuff that would pop up. The soup Na2i was a few blocks over. Not seen on this pic is the Sym’s operating theater designed by Dr. Charles McBurney which is a designated landmark and currently a private school for “gifted but difficult” children (link). I used to round on patients in the red building -they would be ten in a room separated, if lucky, by rolling privacy screens. My sister was born here. John Lennon died here. All that gone, because hospital buildings are like dressings on a city’s wounds and need to be changed every generation. In fact, it’s not even called Roosevelt Hospital any more.
Roosevelt Hospital’s name was changed to Mount Sinai West, and its sister hospital, St. Luke’s, was changed to Mount Sinai Morningside. I would like to imagine that it was vengeance a century in the making, for pearl clutching slights originating from the gilded age, of blue bloods v. upstart Jews. Because no matter how far you are from the shtetl, there is always another golden door closed to you in New York City. So it seemed for me, an immigrant who had worked hard to get to Harvard College, and Columbia P&S, to look with squinted eyes at my letter on match day and see St. Luke’s/Roosevelt Hospital Center, my last choice that I listed out of a general interest to avoid not matching.
When I landed on St. Luke’s-Roosevelt for my general surgery training, the house officers were quartered in the older parts of the hospital, some rooms dating back to the 19th century, unchanged like unearthed chambers from Pompeii. Both hospitals still had the open wards for the “ward” patients with segregation of the private patients up in the towers. For a time, they still had seamstresses to mend your white coat and cafeterias that still cooked their foods fresh. The resident’s lounge at St. Luke’s was like a frat house common room from the thirties, with a scratched-up pool table, a broken piano, pedastaled hotel ashtrays, and card tables. An old handprinted sign (which I regret not taking) listed the house officer’s rules and entitlements which included two beers or a shot of whiskey per night on call.
After my intern year, both hospitals started sorely needed renovations. The surgery office had to be cleaned out, and behind an antique cabinet, wooden boxes of chromic cat-gut suture were found, still in their glass tubes and preserving fluids, little brown skeins of suture floating like preserved fetuses, a strange message from a faraway time. I ran into Walter Wichern, chairman emeritus, who showed up randomly to the hospital in blue blazer and bow tie. I had just stained my dress shirt pocket with my soon-to-be-lost Mont Blanc fountain pen, and he launched into a story about how he repaired a ruptured aortic aneurysm back in 60’s by cutting his new polyester dress shirt into a tube and sewing a graft out of it down in the laundry, after hearing a talk from Arthur Vorhees at P&S. And he was smiling an enigmatic little smile, recalling how that patient on being discharged gifted him annually with ten new dress shirts every year. I later found out that Dr. Wichern was famously taciturn, and I had somehow unlocked an achievement -getting a story out of an old surgeon. It was around then that I had started to feel that it wasn’t all a big mistake.
When I recently changed hospitals from the Cleveland Clinic to University Hospitals, I had to submit documents for privileging, and I get a testy email. “Where did you do your residency?” The administrator couldn’t find St. Luke’s/Roosevelt anywhere on the ACGME website, or even on Google. When I offered the new names, the reply came back, “They only have records going back to when they took over in 2008.” I briefly contemplated retiring, then asked if sending pictures of my framed degrees would be sufficient. Only partly, was the reply. She wanted witnesses.
My first night on call was terrifying. I was on call with Bobby Borromeo -my fellow intern, Anil Hingorani -our PGY4, and Jesse Jean-Claude -our Chief Resident. All of us are now practicing vascular surgeons -Bobby (fellowship Yale), Anil (fellowship Montefiore), Jesse (fellowship UCSF), and myself (fellowship Mayo), embarked on a night of call that involved no sleep and little food. The single moment I recall was taking Bobby through a blood draw and filling the forms for processing the labs and performing EKGs with an antique strip recorder, cutting and pasting the strips onto a formatted sheet for the chart. Bobby didn’t know how because there were many people to do these things in his home hospital in the Phillipines. For myself, I knew the two hospitals from my rotations during medical school. I could draw blood and cut, sew and tie above my level from my time as a senior student at P&S. I got a bit too comfortable with my privilege, and I was still thinking I should have been somewhere else. Over breakfast, I absentmindedly voiced this out loud and was corrected in a way that is no longer possible in 2022. It was the tone that I remember, of being chewed out.
One of chiefs snapped at me,”You have no idea how big and important these hospitals are. They are older than all the other hospitals here in NY. McBurney did the first appy here. Halsted was chief at Roosevelt and invented cancer surgery and the surgical residency. Green invented the LIMA bypass at St. Luke’s. Our chiefs go to better fellowships year over year than any other hospital in Manhattan. You should be grateful to be allowed to round with us.”
Tie given out at graduation, designed by Howard Nay, MD (link), RIP. One of the few keepsakes of my time there. Dr. Skip Nay, was old school, and gave everyone nicknames. Learning surgery from him was like taking blues guitar lessons from Mr. Robert Leroy Johnson.
It was by my third year I got used to the 120 hours a week. It is only now a quarter century later, that I value it. I was expending my. youth living and breathing surgery in the latter days of St. Luke’s and Roosevelt Hospitals. I was missing my friend’s weddings, missing time with my wife, seeing New York during the glory of the 90’s through the dank recesses of a trauma bay. I was six figures in debt, but I could take out your appendix in twenty minutes. I had just signed on for a year of research with the peerless Dr. David Tilson and was not looking forward to telling my wife who found the original five year deal of residency interminable. Add to that, two years of fellowship. Walking out on the deck of the call room overlooking the Cathedral of St. John the Divine and Columbia’s campus, listening for the sirens, I really felt the spirit of the hospital.
It’s not the name of the place, neither its splendor nor its comforts, but the commitment of the people in the teams that you build, which allows you to do great things. And yet…
Summer 2022, in front of Mt. Sinai West, formerly and forever Roosevelt Hospital.
A New Day -created by @nightcafestudios AI upon my suggestion.
Ten years ago, I joined the Cleveland Clinic. I worked five years at the main campus as teaching faculty. I learned as much as I taught, as I got to apply the accumulated volume of experience and knowledge from the previous decades in New York, Rochester (MN), and Des Moines. Five years ago, I took myself and my family to Abu Dhabi, and started a vascular surgery program at CCAD (Cleveland Clinic Abu Dhabi). Last year, still in the middle of the second year of the pandemic, we returned, and I had the privilege of working at Cleveland Clinic Fairview and Cleveland Clinic Avon on Cleveland’s west side. This spring, I made the decision to join University Hospitals, where I will be starting this August. I crave these new days and am so grateful to have them. Thank you, Cleveland Clinic, for ten amazing years. Hello University Hospitals! I can be reached at docpark(at)golfism.org during this transition.
Steve Jobs is credited with popularizing the saying credited to Pablo Picasso, “good artists copy, great artists steal.” While its provenance may be apocryphal, it makes an excellent point about how we learn. Even in the lack of understanding, it is still possible to learn by copying. Toddlers do this. We, as land mammals, are hard wired to copy.
Take for example this patient below with Leriche syndrome with a triad of smoking, claudication, and impotence.
Aortoiliac occlusive disease with history of smoking, claudication, and impotence in a middle aged man = Leriche Syndrome
Because of his relative youth, being his 50’s, I felt the most appropriate procedure was an aortobifemoral bypass.
I frequently use these diagrams to illustrate for the patient.
The only real complexity to manage was the severe stenosis he had in his left renal artery.
A severe stenosis of left renal artery
The options included
renal endarterectomy as part of aortic thromboendarterectomy
renal artery bypass from the aortic graft
reimplantation of renal artery
something else
Something Else: The complexity of renal revascularization creates risk. An antegrade endarterectomy of the renal artery would be done below a suprarenal clamp, adding to clamp time. A bypass would require the kidney to bide its time during the proximal aortic anastomosis, and the anastomosis for a jump graft, then the anastomosis to the left renal artery. This renal ischemia time can be extended by cooling the kidneys with cold (5 degree) LR, but why risk it? A renal endarterectomy can devolve into a visceral segment endarterectomy. After an hour, a nephrectomy.
That’s where this whole copying concept comes into play. Back in 2012, I worked with Dr. Jeanwan Kang, who had just come out of training with Dr. Richard Cambria. We were doing a type IV thoracoabdominal aortic aneurysm, and the right renal artery had a ostial stenosis. While I was figuring out the best way to manage this, Dr. Kang asked for a 6x18mm renal stent and an insufflator. She stuck the stent into the renal orifice and deployed the stent, opening the orifice. I had to find my jaw which had dropped to the floor.
Now, ten years on, that’s how I managed this patient’s ostial renal artery stenosis.
The patient’s thrombotic plaque went up to the renal origins and needed to be endarterectomized, but embarking on a renal endarterectomy adds potentially harmful renal ischemia time. Therefore, through the vertical aortotomy, I was able to get a clean end point to the aortic thromboendarterectomy and position a stent in the renal orifice and deploy it.
After thromboendarterectomy of the aortic plaque, the left renal ostium is treated with a balloon expandable stent. The aorta then is partially closed primarily to move the clamp below the renal arteries
Once the stent was deployed, the aorta was partially closed primarily to allow the clamp to be moved below the renal arteries. This all took less than ten minutes of ischemia time. The aortic graft was then sewn end to side to the remaining aortotomy.
The patient recovered and was discharged on POD#6 with normal renal function. In followup, his CTA showed excellent graft and stent patency.
A followup CTA shows a patent 14x7mm aortobifemoral bypass. I choose the bypass based on avoiding excess size mismatching distally as I find that patients who get 20x10mm grafts run into problem with mural thrombus because of limited flows into smaller femoral vessels. The renal stent is patent.
The centerline view of the renal stent shows it to be widely patent.
Patent stent with avoidance of the pitfalls of a renal endarterectomy
The patient is walking well without limitations and has improved blood pressure control, achieving normotensions at times.
If you are curious about the results from MGH, I refer you to their paper on 67 patients treated with open hybrid revascularization of the renal artery during complex aortic reconstructions (reference). At a mean followup of a year, they reported a 98% stent patency.
There is a comfort in sticking to what you know. The extreme example of this is the practitioner who graduates with a skill set from training and never expands on it. Yet there is an opportunity cost to blind devotion to sticking what you know and that is never growing. I recall this in the panel discussions during the VEITH Symposia I used to sneak into as a resident in the 90’s where great authorities pooh-poohed or condemned anything endovascular.
It’s a sign of a nimble mind that Dr. Cambria, after learning endovascular techniques mid-career, adapted these skills to his open surgical toolkit. His trainee, Dr. Kang, soon after, taught me.
Or was I just looking over her shoulders taking notes?
Reference:
Patel R, Conrad MF, Paruchuri V, Kwolek CJ, Cambria RP. Balloon expandable stents facilitate right renal artery reconstruction during complex open aortic aneurysm repair. J Vasc Surg. 2010 Feb;51(2):310-5. doi: 10.1016/j.jvs.2009.04.079. Epub 2009 Oct 22. PMID: 19853403.
A Surgeon's Notes 