Categories
MALS May Thurner's Syndrome median arcuate ligament syndrome Nutcracker Syndrome SMAS superior mesenteric artery syndrome techniques

Arterial Median Arcuate Ligament Syndrome (aMALS)

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

  1. 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.
  2. 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.
Categories
AIOD aortoiliac occlusive disease (AIOD) clti hybrid technique techniques

hybrid AUI-Fem-Fem technique

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.

Categories
AIOD aortoiliac occlusive disease (AIOD) techniques

Aortoiliac Endarterectomy: Removing Occluded Stents Is Possible

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.

Categories
Carotid techniques

Brain Claudication -is it a thing?

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.

Categories
AIOD aortoiliac occlusive disease (AIOD) bypass hybrid technique Practice techniques

Good Surgeons Copy, Great Surgeons Adapt: Cribbing the Open Hybrid Renal Artery Angioplasty and Stenting During Aortic Reconstruction

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

  1. renal endarterectomy as part of aortic thromboendarterectomy
  2. renal artery bypass from the aortic graft
  3. reimplantation of renal artery
  4. 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.

Categories
aortoiliac occlusive disease (AIOD) bypass chronic limb threatening ischemia Practice techniques

Durability is the Gift that Keeps Giving

The patient was a 50 something year old man who I took care of in 2016 before I left for Abu Dhabi. He had a background of hypertension, hypercholesterolemia, and IDDM with chronic immunosuppression for rheumatoid arthritis. For several weeks he had rest pain in his feet and impending gangrene of his left great toe. More worrisome was the development of punched out ulcers on his groin crease resulting in weeping wounds after a bout of cellulitis. He had no palpable femoral pulses. Pulse volume recordings showed flat lines from the thigh to the feet.

CTA of the abdomen and pelvis with runoff showed aortic occlusion due to heavily calcified plaque with reconstitution of the external iliac arteries via the internal iliac arteries. The common femoral arteries were only mildly diseased and there was patent runoff.

Centerline up right femoral into aorta shows occluded aorto-iliac segment and diseased external iliac artery.
Centerline up left femoral into aorta shows mirror image of disease on left side

He was one of the rare instances of chronic limb threatening ischemia due to aortoiliac occlusive disease, AKA Leriche syndrome. The added background of autoimmunity made him vulnerable to the ulcers in the groin crease, and the infections there made access challenging.

Leriche Syndrome

The choices were endovascular versus open surgical repair. The groins were a problem with recent cellulitis, immunosuppression and open wounds, but with careful prep, and coverage with Ioban, access was possible, even for stent grafting. The problem was the aortic bifurcation was heavily calcified, and manipulating this likely thrombotic material with an end stump of aorta can cause renal embolism. There was a small risk of rupture at the bifurcation and of renal failure.

Standard aortobifemoral bypass graft was out of the question because of the lack of a safely clampable aorta -there was circumferential aortic plaque below and above the renal arteries and the infections in the groins would jeopardize any prosthetic graft. You have to respect unclampable aortas but like anything else, there are ways around it (link).

Regarding the groins, during fellowship, Dr. Thomas Bower used to take the distal anastomoses to the external iliac arteries which could be exposed via short lower abdominal incisions if not through the midline incision itself, avoiding groin incisions in hazardous groins.


I performed an aorto-bi-iliac bypass using the balloon in the infrarenal technique after obtaining supraceliac control described in my technical post (link).

A small aortotomy can be controlled with a finger and a foley easily slipped in -just remember to clamp it
This typically provides adequate hemostasis and space to perform a proximal anastomosis

I was able to endarterectomize a nice segment of aorta and anastomose end to side -always end to side as it preserves endovascular options. The distal anastomoses was to the external iliac arteries. He did well in the immediate postoperative period but I soon left for Abu Dhabi.

In the five years since the operation, he has needed an SMA stent and has devloped worsening CKD and autoimmune diseases. But one of the gratifying things is he healed his wounds on this groins and thighs and the left hallux, and pain has never recurred. He had a contrast CT at the 5 year point (figure) showing a widely patent graft, and he sought me out when he heard that I was back in Cleveland.

His PVRs remain normal (figure).

The PVRs and ABI’s remain robustly normal even after 5 years

I’m not saying that iliac stents from the iliac bifurcation to the renal arteries was a bad option, but there is a particular sadness and weariness when I have to take care of occluded stents. As an engineer, what is worse than ballooning an occluded stent and placing another stent inside? Knowing what I know about cell biology, what is worse than lasering, drilling, cutting, that cicatricial scar tissue that is neointimal hyperplasia in terms of what you leave behind. This man still has decades left to live and he will have his bypass graft far longer than any stent. This durability, a byproduct of the technique, is a worthy virtue.

When I operated, he was in his mid fifties and despite his comorbidities, was able to undergo a big operation. Now he is in his sixties and his autoimmune issues have progressed to where he is suffering from stiff person syndrome with difficulty walking. His renal function is poor and overall he is a terrible open surgical candidate. If I had done interventions at that time, which I was tempted to, he could today be facing amputations in the setting of cytotoxic immunosuppression having run out of endovascular options.

We have lost too much to innovation. The fact is, aortic surgery for critical limb ischemia was once and it still is a thing, because it works.

Categories
Carotid Commentary complications techniques training ultrasound vascular lab

Mind the size of your patch or you’ll make an aneurysm

The patient is a man in his 80’s who presented with left sided weakness and dysarthria. Over 25 years before, he had undergone a carotid endarterectomy after a stroke, and had remained stroke free since. Per protocol, he received systemic thrombolysis and underwent CT angiography which revealed a right sided patch pseudoaneurysm.

Patch pseudoaneurysm with irregularities in lumenal wall of mural thrombus in right carotid bulb

This was seen dramatically on carotid duplex below.

Mural thrombus at carotid bifurcation compresses the right IJ vein

He stabilized and regained much of his function on the left arm and leg, while having a residual paresthesia of the left leg. His dysarthria resolved. His left carotid system was affected by a severe stenosis confirmed on MRA.

Duplex confirmed a tight stenosis of the left ICA with biphasic flows in the ECA.

MRI confirmed a right hemispheric infarction and operation was planned.

Right sided embolic stroke in MCA distribution

One of the great thing about working in a group ours is that we can bounce ideas off of each other and the consensus was for repair of the right carotid aneurysm. No mention was made of stent grafting which would have meant sacrificing the external carotid artery. I feel that the ECA provides some degree of long term insurance much like a good profunda femoral artery does for the common femoral. Shunting was considered a good idea because of the contralateral severe disease.

For me, the technical issue was the size mismatch between the common carotid artery which was around 8mm and the internal carotid which was about 4mm. Sizing for the CCA would leave a step down in lumen size that would result in increased velocities in the smaller ICA, potentially resulting in shear/turbulence/injury. Re-implanting the ECA on a 7mm PTFE graft would draw off some of that flow, but then you might end up with accumulation of mural thrombus on the graft beyond the ECA takeoff -the original problem to begin with. Looking on the shelf, I saw a 4-7mm tapered PTFE graft which was appropriately sized on both ends and would avoid the mentioned issues.

The aneurysm remained thankfully intact during its dissection

The aneurysm remained thankfully intact during its dissection, but to make sure I had control, the CCA at the base of the neck was controlled much as in a TCAR. The next step was in finding the ICA over the hump of the aneurysm and getting a vessel loop doubly around it. The ECA was easily found and controlled. I left the aneurysm alone to avoid perturbing the clot until I had the ICA clamped.

To perform the graft implantation while on shunt, I did the old trick of placing the shunt through the graft. The carotids were clamped and the aneurysm opened. The shunt was inserted into the ICA and CCA and shunt flow started. The ICA anastomosis was done first and the fit was perfect.

Stretch and unstretch, the 4mm end was tapered for the anastomosis on the ICA

The second anastomosis was end to side ECA to graft. The last anastomosis was the proximal to the CCA and it was completed loosely to allow the shunt to be removed then closed after flushing.

After completing the repair, the aneurysm was explored by my chief resident Dr. Shashank Sharma, who will continue his training in vascular surgery at Houston Methodist next year, and the patch was retrieved. It was sterile.

The patch, retrieved floating in the lateral part of the pseudoaneurysm, appears to have been cut from its original configuration

Back in the 90’s, when I was a resident at Roosevelt Hospital in New York,  I scrubbed in on a carotid operation. Dr. Eric Moore, among the first generation of general surgeons to train in a vascular surgery fellowship, was operating. The patient was billed as having a rare carotid aneurysm but in fact had a patch pseudoaneurysm. What was lost on me at the time as we dissected out the dilated bloated artery and replaced it with a graft was the complication was a consequence of the choices made at the carotid endarterectomy done years past. The aneurysm would not have been possible if a saphenous vein patch hadn’t been placed. After resecting the aneurysmal carotid artery, we cut it open. It was lined with the yellow and green mush outside a layer of hard brown laminate thrombus, a kind of AAA in miniature. Dr. Moore muttered, “we should write this up,” and I thought about it briefly, but couldn’t get excited. Now a quarter century later, I am interested because it is poorly studied. 

When you open an artery, you eventually have to close it (figure1).

A longitudinal arteriotomy

If the arteriotomy is in a transverse orientation, you can simply close it because all the sutures can be placed in the axis of flow. This is an important concept when sewing anastomoses -the sutures at the heel and toe need to be placed aligned with the longitudinal axis of the artery. This may shorten the artery but never narrows it. Any suture placed with a bite length of x with an angle θ away from the direction of flow narrows the artery by 2x(sine(θ)). The problem with primary closure, particularly of a small artery is that it narrows the vessel, decreasing the circumference by x, the length of the bite.

Primary closure narrows the artery…unless the adventitia stretches after endarterectomy.

You can sometimes get away with it because after endarterectomy, the adventitia may stretch and accomodate the bites without loss of circumference. To avoid this, since time immemorial, we have been taught that a patch should be applied.

Appropriately sized patch prevents narrowing, but also prevents excess widening

If the suture’s bite is 1mm on both patch and arterial wall, to have no effect on the artery in terms of narrowing or excessively widening the vesssel, the patch theoretically needs to be no wider than 2mm. For the purposes of handling, a wider patch is desired, so let’s say the ideal patch should about 5mm wide. Unfortunately, the precut carotid patches, both bovine pericardium and Dacron, are in the box pre-cut up to 8mm in width. A slim 5mm patch is available in Dacron but who sews in Dacron patches?

Is 8mm too wide? In some patients I believe it is.

Sometimes, the precut patch that is 8mm wide is too big, adding up to 50% to the circumference on a small artery, therefore 50% to the diameter, making the artery aneurysmal. If you see this, you should correct it.

When an 8mm wide patch is sewn on to an ICA at the carotid bifurcation which is 6mm wide, about 6mm is added to the circumference, which results in adding 2mm to the diameter, or 33%. 133% is close to the 150% which is the definition of an aneurysm. There are animal models of aortic aneurysm which involve sewing on a large bovine pericardial patch. While reading carotid ultrasounds, it is not uncommon to come across patient’s after carotid endarterectomy whose patched segments are lined with thrombus, the identifying marker of an aneurysm (picture below).

Patient post carotid endarterectomy over a decade ago now has clot lining a carotid patch aneurysm

The image above is a late presentation in a patient who is asymptomatic of stroke -am observing for now as I have just performed an eversion endarterectomy on the other side. Reading many ultrasounds, on occasion, I will see thrombus-like material accumulating on a patched artery early. And every once in a while, you come across an awkward, oversized patch such as this:

This patch is oversized but also ends where the left ICA makes a sharp turn, something you see more often on the left than on the right. This CT was taken after the patient had a postop TIA and may have formed emboli in the cul-de-sac created by the patch. DAPT was started.

I am not advocating primary closure. It is well established that primary closure of carotid arteries is associated with increased rates of stroke and restenosis in multiple studies and meta-analyses (ref 1), but there are surgeons who still close primarily.

Dr. Matthew Menard (ref 2) et alia found, along with the primary finding greenlighting bovine pericardial patch for the rest of us, that patch pseudoaneurysms are exceedingly rare. I do wonder if each of the ultrasounds were checked for the development of mural thrombus in the followup period. And what do you do about it?

Technically speaking, I advocate developing a sense of beauty when looking at the final product of an endarterectomy. I am not advocating trimming the patch all the time, but I frequently do, but rather to purposely tailor the repair well to recreate the sizes and dimensions that the body originally intended to have.

Patch angioplasty, using bovine pericardium, full width accommodated from about the time the Menard paper came out, taken on an iPhone 3.

Or you can do an eversion endarterectomy and avoid the problem entirely. 

Postop 1 month post eversion endarterectomy duplex above shows a normal ICA with very little evidence I was ever there

References

  1. Counsell C, Salinas R, Warlow C, Naylor R. Patch angioplasty versus primary closure for carotid endarterectomy. Cochrane Database Syst Rev. 2000;(2):CD000160. doi: 10.1002/14651858.CD000160. Update in: Cochrane Database Syst Rev. 2004;(2):CD000160. PMID: 10796309.
  2. Ho KJ, Nguyen LL, Menard MT. Intermediate-term outcome of carotid endarterectomy with bovine pericardial patch closure compared with Dacron patch and primary closure. J Vasc Surg. 2012 Mar;55(3):708-14. doi: 10.1016/j.jvs.2011.10.007. Epub 2012 Jan 4. PMID: 22226180.
Categories
chronic limb threatening ischemia edema iliocaval venous interstitium lymphedema opinion Practice techniques

The Squeeze Play: Managing a Lymphedema Emergency

When I was a young attending at the Allen Pavilion of Columbia Presbyterian Hospital, I was called into an operating room for a stat consult on a patient about to undergo a cholecystectomy. During the case, the IV had infiltrated and a bag of saline had filled the patient’s hand and forearm with saline, causing the hand to look like an inflated glove. The fingers were cool and white and the edema was firm but yielded to touch.

I elevated the hand and firmly squeezed the edema out of each digit, then gently massaged the edema from the hand onto the forearm. From there, I pushed the edema onto the arm. I then wrapped the hand up in an Ace wrap, and suspended it from an IV pole and returned to my case. Later, I returned and the hand was restored, warm, and perfused.

The lymphatics serve to move extracellular fluid (link). They can be overwhelmed much as drainage from a house can be overwhelmed resulting in puddles and ponds (link). This extracellular space has been “discovered” to be a new organ, but vascular surgeons have known about it for some time. Ultrastructurally, it is very close to a sea sponge with lattices of structural protein connecting cells to form tissues. And like a sea sponge, the salty water can be squeezed out or drained using gravity.

In olden times in central Europe, if you had chronic leg ulcers, you went to abbeys that specialized in their care. There, nuns would milk the edema out of your leg swollen typically from parasites and dress the leg and ulcer in linen cloth soaked in special oils. This is how Dr. Paul Gerson Unna came up with his eponymous Unna’s Boot, substituting Zinc Oxide paste which created a bacteriostatic environment.

Professor Paul Gerson Unna

Every year or so, I will be consulted for what I term a lymphatic emergency. A subset of this is phlegmasia. Whatever color you find -alba (white) or cerulea (blue) is really no matter -who really knows which comes first? It is an emergency in that the time clock for arterial ischemia -minutes to an hour for nerves, an hour to 6 for skeletal muscles, 6-12 for skin and bone, are all in play. The instinct is to go right to fasciotomy, but what you are usually doing is releasing the extracellular space, and the muscles are typically fine, even though their compartment pressures were very high.

Take this patient who developed severe upper extremity edema in the recovery phase after a cardiac arrest.

The ICU staff noted the had discoloration about four hours after the arrest. There were no arterial pulses and the forearm and hand were rock hard, the finger tips ice cold. Compartment pressures measured using the arterial line and needle method didn’t drop after the initial flush of saline below 70mmHg. While I could have been justified in performing upper extremity fasciotomy and even trying thrombectomy in a critically ill, coagulopathic patient on multiple pressors, I could just as easily have been on solid ground for saying the life was more valuable than the dominant hand. Both would have been the wrong move.

I performed the nun’s milking maneuver mentioned at the beginning and lacking an Unna’s boot, I compressed and elevated the best I could with double gloving using a small sized glove and ACE wrap.

Notice the edema has segregated into the arm.

In the morning, taking down the dressing, and re-compressing, there was now a radial artery signal and the fingers were a much improved color. The pulse-oximeter waveform was near normal. As an aside -the pulse oximeter uses the same technology as the digital photoplethysmography for generating toe waveforms in the vascular lab -ie. a vascular lab at every bedside! We have collected and are analyzing the data on this for publication.

The pulse oximetry waveform is the same tech as digital photoplethysmography. Cotton cast padding (Webril) and Coban wrap is a good method of compression that avoids the problems with ACE wrapping.

It’s a hard thing to not run off to the operating room in most cases because that is how we are trained, but understanding how a patient got to that point is crucial in deciding if compression alone will work. If they call you from the ER about a patient with a swollen cold foot with diminished signals, you have to figure out the mechanism. Was it arterial occlusion, rest pain, and chronic dependency of the foot that resulted in this? Typically the swelling appears late. Was it heart failure and inability to walk, resulting in the patient sitting all day in a chair that is the cause? Was it pregnancy with a DVT? Was it the deadly sin of sloth? Only in arterial occlusion in a chronic presentation would compression be contraindicate. In this ICU case, the lack of arterial signal is secondary to the swelling, not the cause of it.

Elevation alone does not manage edema well. Only hanging upside down or being in water up to your neck…

Compression is a necessary component of treating lymphedema emergencies because elevation alone may be insufficient, particularly in the leg.

Wrapping a leg is a critically, undertaught skill. Also, never cover the knee cap.

Elastic compression is ubiquitously available as the ACE wrap, but they can shift and move and roll, causing zones of excess and not enough compression. TED hose and compression stockings are definitely helpful in long term management, but with legs, compression needs to go up to the knee joint, or up to the groin, never halfway or the edema will create a line of ischemia at the end of the stocking that blisters when the stocking is removed, and can progress to full thickness necrosis. Cotton cast padding and Coban, or an Unna’s Boot may be the safest in terms of avoiding skin injury.

ACE wrapping is never taught adequately, and for it to work well and avoid injury to the skin, the wrapping has to be reapplied several times a day. It should be a prerequisite for nursing and medical student certification, as edema is the most common vascular disease.

Moving into our new home after four years out of country, I welcome an old friend from storage, but also unfortunately a health hazard, only mitigated by being fully reclinable.
Categories
acute limb ischemia bypass chronic limb threatening ischemia cli clti cost innovation hybrid technique limb salvage Practice techniques vascular lab

MacGyvering as tactical innovation -set your mind free.

The patient is a 70 year old man with risk factors of cigarette smoking, type II diabetes mellitus, hypertension, and hypercholesterolemia who presents with rest pain and gangrene of the tip of his left great toe. Several weeks prior to this, he went to his pharmacy and received a flu vaccination and picked up over the counter topical medication for an ingrown toenail. who developed pain from an ingrown toenail. Several weeks later, the tip of his toe blackened and the pain became unbearable and he came to the hospital.

No pulses, dry gangrene of tip of toe

Physical examination was notable for the dry gangrene affecting the distal phalanx of the left hallux. There was a left femoral pulse, but nothing was palpable below. His forefoot was cool and painful and this pain was relieved with dependency.

Pulse volume recording showed a drop in flow across the left knee and flate waveforms at the ankle, foot, and digits. The ABI was zero. WIfI 2 3 2, Stage 4, potential benefit of revascularization high (reference 1). CTA was performed and revealed patent aortoiliac segment, patent common femoral and profunda femoral arteries, with occlusion of the mid to distal SFA, reconstitution of the above knee popliteal artery with 2 vessel runoff via a patent posterior tibial and peroneal arteries.

CTA VR Reconstruction Shows Reconstitution of AK POP and 2V Runoff via PT and Peroneal Arteries

The centerline reconstructions, adapted from aortic planning, lets me determine the character of the arteries for size, calcification, stiffness, collateralization, and length of occlusion. This was had low density and given the timecourse of the events -from claudication to gangrene, and the lack of collaterization implying an acute process possibly on a chronic lesion, I felt there was likely to be some thrombus burden over a chronic plaque across Hunter’s Canal with occlusion of the geniculate arteries. Usually, when the occlusion is chronic, femoropopliteal occlusions of this type come with an ABI of 0.5-0.7, not 0.

GLASS FP:3, IP: 0 Stage II: Intermediate complexity disease

Global Limb Anatomical Staging System (GLASS) Classification of CLTI (reference 2) through the easy to use SVS calculator came out Stage II: Intermediate Complexity. I had the good fortune of being in the audience when GLASS was presented to a rapt audience in Lyons, France, by Dr. John White in 2017, at the ESVS meeting. I include it because Dr. Devin Zarkowsky on a tweet that generated this post wanted WIfI and GLASS. WIfI I find helpful. GLASS I am still figuring out, because it tends to tell me what I already know: this is a lesion of intermediate complexity that could go either way to open or endovascular.

Treatment options include:

  1. Endovascular -starting with POBA and escalating to various additional therapies such as stents, covered stents, DCB, drug coated stents, atherectomy, thrombectomy, thrombolysis (then any of the previously mentioned).
  2. Bypass with PTFE
  3. Bypass with vein
White Arrows Show the Excellent GSV

The data tells us so far that open or endovascular is broadly equivalent, but experience guides me. For rest pain, any incremental increase of flow will do, and it does not necessarily have to be in-line. For healing major tissue loss, there really can’t be enough flow. Bypasses with good runoff deliver a lot of flow. Bypasses with vein have great longevity and the shorter they are, the longer they last.

So is long patency important? Numerous studies have shown that patency does not impact limb salvage or amputation free survival, going to BASIL Trial (reference 3), but even stretching back to Dr. Frank Veith’s advocacy of PTFE bypass to infrageniculate targets (reference 4), patency does not add to limb salvage beyond the initial wound healing. The patency of a PTFE bypass to a tibial target is less than 20% at 5 years, but the limb salvage rate is a laudable 80% plus, and this is repeated in numerous evaluations of POBA, stents, and every new technology that has accrued in the nearly 4 decades since that paper.

What does patency buy you? Less reinterventions. There is nothing worse to me than having to reintervene within a year or two of an intervention. When a bypass works well, the patients just come for a hello-how-do-you-do for years. The BASIL trial concluded that bypass operations were more expensive, and I dispute this. In 2021, operations were far less expensive than the latest energy weapon, their box you have to purchase, and the catheters you use once and throw away. The argument given by interventionalists is that bypass operations are disfiguring and ridden with complications and that argument holds water as there are many points where vascular surgeons fail or have largely stopped work on investigating and optimizing open surgery. What if bypass surgery could be brought to the level of dialysis access surgery in terms of invasiveness? What if groin complications could be minimized? What if long filleting-type incisions of the thigh and leg could be eliminated entirely? What if edema could be prevented or minimized postoperatively to prevent serous drainage and infections? If you focus on the art of bypass surgery and choose patients well, you can get a quick, minimally invasive bypass with the overall physiologic impact of a Brescia-Cimino AV fistula. After considering endovascular, I chose bypass.

This patient had on mapping excellent saphenous vein between 3-5mm in diameter. He had excellent skin and was not obese. A vertical groin incision could be avoided by making a skin line incision over the saphenofemoral junction and transposing it to the adjacent SFA which was patent. Skin line oblique incisions in the groin heal much better than the standard vertical incisions, and it is possible to mobilize and expose the saphenous vein using an appendiceal retractor and clipping the generous proximal thigh tributary. In this patient, the most proximal incision was well away from the inguinal crease, the generator of wound infections in the groin. Essentially, if there is no groin incision there can be no groin complication.

The distal vein is mobilized first before dropping on the above knee popliteal artery which is exposed through a separate incision. This is because the AK POP space is best exposed over the sartorius, and the vein in this patient was well below (posterior) to the sartorius. The vein was tunneled under the sartorius to the AK POP. With the in-situ technique, the proximal anastomosis is completed, then the valves lysed with a retrograde LeMaitre valvulotome. Doing, after two or three passes, the pulse was strong, and the flow strong enough to fling the blood beyond the foot -a key step. If there is no such flow, if there is a weak pulse, or poor blood flight, I do one more pass of the valvulotome then duplex for any large diverting tributaries and tie them off one by one until good flow is achieved.

I do not mobilize the entire vein (and tie off every collateral) unless I cannot do an in-situ technique. It defeats the purpose of this beautiful minimally invasive procedure.

Femoral artery to above knee popliteal bypass with in-situ vein

He recovered rapidly and was discharged home after a partial hallux amputation by podiatry. In followup, he was feeling better. All of his surgical wounds had healed. Duplex and ABI did find this:

Retained valve, very hard to see but present on B-mode, causing a hemodynamically significant stenosis, with ABI of 0.57

I took him to the angiosuite for repair of this retained valve. Rarely, retained valves occur after in-situ bypasses, but require generally unsatisfactory solutions involving either open valvulectomy and patch venoplasty or stenting of a virgin vein. Valvulotomy is possible, but generally described as an open procedure as well, but I had other plans.

Downstream of this retained valve were tributaries which could be seen on duplex, and therefore accessible with a micropuncture needle. This would then allow for placement of a 4F sheath, through which the LeMaitre valvulotome would pass unhindered, allowing for valvulotomy. I would use this session in the angiosuite to deliver embolization coils to the diverting tributaries as well.

Arteriography reveals a retained valve and diverting AVF’s
Retained valve catches the catheter sent up and over from the other side

LeMaitre is a unique company in that it focuses on vascular surgical operations and arises from the original product and reason for the company the eponymous valvulotome. Because it comes sheathed in a low profile catheter, it is immediately familiar to modern surgeons even though it was made in another century.

Cutting of retained valve with LeMaitre valvulotome​ using ultrasound guidance​

Cutting the valves involved passing the valvulotome several under fluoroscopy through a 4F sheath placed through the tributary seen above. After the valvulotomy, the diverting tributaries, only one of which drained quickly into a deep vein, were coiled. At the end of the procedure, a manual cuff was found and an ABI checked. It was now 1.05.

Diverting tributaries coiled

In 2015, the Oxford English Dictionary added McGyver as a verb -“Make or repair (an object) in an improvised or inventive way, making use of whatever items are at hand.” A television show from the 80’s and early 90’s, the main character, McGyver, was able to make useful tools out of what was available, allowing him to come out victorious, but usually just survive. It is a useful concept that is a must have in managing complex and dynamic situations. Just because it hasn’t been done before to your knowledge doesn’t mean that it isn’t a simple solution. I have only one ask that LeMaitre flip their blades around and design an ante grade valvulotome. Those who know what I’m getting at know what I am getting at.

The LeMaitre valvulotome allows for in-situ saphenous vein bypass, a prototypical hybrid vascular procedure from the 80’s that portended the endovascular revolution that followed. It is meant to be used intraoperatively, but because of its low profile, it can be applied.

I will allow that this second procedure likely makes any argument to cost moot, but numerous incisions and extra time in the OR is avoided. The patient now has a vein bypass that could last many years which diminishes the need for follow up procedures to maintain assisted patency.

We will be arguing this point for years even after BEST-CLI is presented. BASIL-2 just closed enrollment. Hopefully we will get some clarity.

Reference

  1. Mills JL Sr, Conte MS, Armstrong DG, Pomposelli FB, Schanzer A, Sidawy AN, Andros G; Society for Vascular Surgery Lower Extremity Guidelines Committee. The Society for Vascular Surgery Lower Extremity Threatened Limb Classification System: risk stratification based on wound, ischemia, and foot infection (WIfI). J Vasc Surg. 2014 Jan;59(1):220-34.e1-2. doi: 10.1016/j.jvs.2013.08.003. Epub 2013 Oct 12. PMID: 24126108.
  2. Conte MS, Bradbury AW, Kolh P, White JV, Dick F, Fitridge R, Mills JL, Ricco JB, Suresh KR, Murad MH; GVG Writing Group. Global vascular guidelines on the management of chronic limb-threatening ischemia. J Vasc Surg. 2019 Jun;69(6S):3S-125S.e40. doi: 10.1016/j.jvs.2019.02.016. Epub 2019 May 28. Erratum in: J Vasc Surg. 2019 Aug;70(2):662. PMID: 31159978; PMCID: PMC8365864.
  3. Adam DJ, Beard JD, Cleveland T, Bell J, Bradbury AW, Forbes JF, Fowkes FG, Gillepsie I, Ruckley CV, Raab G, Storkey H; BASIL trial participants. Bypass versus angioplasty in severe ischaemia of the leg (BASIL): multicentre, randomised controlled trial. Lancet. 2005 Dec 3;366(9501):1925-34. doi: 10.1016/S0140-6736(05)67704-5. PMID: 16325694.
  4. Veith FJ, Gupta SK, Ascer E, White-Flores S, Samson RH, Scher LA, Towne JB, Bernhard VM, Bonier P, Flinn WR, et al. Six-year prospective multicenter randomized comparison of autologous saphenous vein and expanded polytetrafluoroethylene grafts in infrainguinal arterial reconstructions. J Vasc Surg. 1986 Jan;3(1):104-14. doi: 10.1067/mva.1986.avs0030104. PMID: 3510323.

Categories
bypass complications graft infection mycotic aneurysm open aneurysm surgery peripheral aneurysm pseudoaneurysm skunk works techniques

EIA pulldown transposition: another way to treat infected common femoral pseudoaneurysm

Patient with infected femoral pseudoaneurysm, skin necrosis, about to blow

A surgeon from Nepal posted a case of a ruptured common femoral pseudoaneurysm infected from IV drug abuse on LinkedIn. The comments centered around typical textbook responses which were:

  1. Ligate, debride, obturator bypass
  2. In situ bypass with femoral vein +/- sartorius flap
  3. Rifampin soaked graft or crypreserved allograft
  4. Ligate only

My preferred treatment is #2, in-situ bypass with harvest of adjacent deep femoral vein. I never liked that procedure because in general in these patients, everything bleeds. Then I had a thought -how about if you mobilize the external iliac artery in the pelvis over its entire length and pull it out from under the inguinal ligament to sew to the femoral bifurcation or SFA? That is, when you enter the pelvic retroperitoneum to gain proximal control:

The external iliac artery is usually redundant and elastic in young people

You mobilize the external iliac artery from the iliac bifurcation to the inguinal ligament, detaching the inferior epigastrics as a last step. And then you pull it out from under the inguinal ligament, and anastomose it to the femoral bifurcation or the SFA.

The mobilized external iliac artery is pulled down to reach normal femoral artery. The distance x is the length of CFA that needs replacing

This makes sense because in young people and those with AAA and minimal atherosclerosis, the external iliac artery is both redundant and elastic, making it suitable for a pull down transposition. But then, how do you know as you mobilize the artery in the pelvis that you have enough to pull down?

Pythagoras figured that out two an a half millenia ago. If you measure the straight line distance from iliac bifurcation to the takeoff of the inferior epigastric arteries, you get the straight line external iliac artery distance. The length of the common femoral artery which is the excess EIA length needed, is assigned the value x. Then the height of the stretched artery off the line between the iliac bifurcation and the inguinal ligament will determine how much extra artery you have.

Taking these values, I did some maths.

The solution for h, the height, is highlighted in yellow below. (note, the variable x in my notes is half the length of CFA, l is half the length of EIA, ie. 2x is CFA length).

Creating a spreadsheet for CFA lengths from 2 to 6cm and EIA straight distances of 5-10cm, the ratio of height H to CFA length varies from a minimum of 0.7 to maximum of 1.7 with an average of 1.1. That means the majority of the time, if you get 1.5x the length of CFA height off the pelvis, you should reach.

If you are short, you can detach the profunda and mobilize the SFA, pulling upwards, then reattach the PFA. Though this is entirely a thought experiment, there is no reason why it should not work. As with most things, I predict that it already has been done!

The advantages are using autologous tissues and leveraging the natural anatomy. There is a cost benefit in that OR time is shorter with less time for venous harvest and avoiding grafts, patches, and devices. The patient would avoid ischemia as would happen in the staged repair. The disadvantage is when you are short, but if you mobilize the appropriate amount (height off pelvis at least 1.5x the CFA length) you should be okay. The more curvature and tortuosity seen on 3DVR recontstruction and absence of significant atherosclerosis would predict feasibility.