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 itThis 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.
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
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.
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.
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:
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).
Bypass with PTFE
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’sRetained 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
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.
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.
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.
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.
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:
Ligate, debride, obturator bypass
In situ bypass with femoral vein +/- sartorius flap
Rifampin soaked graft or crypreserved allograft
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.
One of the greatest surgical texts, Cope’s Early Diagnosis of the Acute Abdomen, is something every surgical resident, vascular or general, should read. The mid-century edition which I owned during my residency, has since been updated, but the central message of the book is this: every complaint or pain the patient has comes from a nerve, either peripheral or visceral, and understanding the nature of the pain, you narrow the diagnosis to only a few possibilities. Irritation of the psoas muscle results in a characteristic pain that years of diagnosing appendicitis the old fashioned way -by exam, then operation, makes it easy to recognize, like Marilyn Manson showing up as your substitute teacher (I would have said Alice Cooper, but that completely dates me). When the psoas muscle is irritated, by a hematoma, injury, inflammation, or abscess, the muscle relays intense pain localized to the retroperitoneum. Stretching the muscle worsens the pain, and the patient is often seen with the ipsilateral hip flexed. The genitofemoral nerve which rides on top of the psoas, is triggered and there is pain referred to the groin and proximal anterior thigh. Seeing this, and fitting the story allows for a diagnosis, before imaging. Without this insight, there is no swift vector to treatment and resolution.
Patient with inability to straighten left hip after iliac stent placement
The patient, a middle aged man, had undergone a redo-iliac angioplasty and stent for left iliac in-stent restenosis. He relayed that on the table, he felt immediate left lower quadrant abdominal pain and the desire to flex his left hip. He was restrained, sedated, and the procedure finished -a covered stent had been placed. When he came to my office a month after his initial procedure done elsewhere, he was in wheel chair, unable to straighten his leg. He claimed before coming to see me, he had gone to another hospital, where he had a CT scan and was told nothing was wrong (will have to confirm). He was having subjective fevers at home.
On examination, he sat on the exam table with left hip flexed. His pedal pulses were easily palpable. He had furuncles in his groins which he relayed he had had all of his life. I sent him for CTA and subsequently admitted him for surgery.
left iliopsoas abscess
The CT showed a large collection around the left iliac artery and stents and on the psoas muscle, an abscess. The blood cultures on admission were positive for Staphylococcus lugadensis sensitive to penicillin.
Putting the story together after the fact is much easier than when you are in the moment, but being aware of the location and type of pain should give you a clue. Very likely, he had a brief rupture on the angiosuite table resulting in his sudden pain, drowned out by the sedatives typically given in response to a patient moving when a stent is deployed. Inflating a balloon in an artery typically causes some discomfort -as the vessels are lined with visceral nerve fibers which are quite sensitive but less localizable than say a pin poking on the index finger. If you ever had bloating with gas, that general discomfort localizable to the mid abdomen, that nausea and discomfort is from stretched visceral pain fibers. If you have ever had dull aching pain of distended spider veins, that is visceral pain. It’s there, but you would not be able to pinpoint it exactly. That is not what this patient had when he flexed his hip on the angio suite table. While the covered stent was deploying, he likely briefly ruptured causing both somatic and visceral pain around his left common iliac artery and iliopsoas muscle. Additionally, if the sheath had been entered through an area of a skin abscess, likely the sheath, wires, and gloves were contaminated. Any handling of the balloon expandable stent graft, which I highly discourage, would have contaminated it, resulting in a device infection, which was made more likely due to his diabetes. As the hematoma got infected, it resulted in the worsening symptoms he was having of left lower quadrant abdominal pain, groin pain, thigh pain, and inability to straighten his hip without pain.
I took him to the operating room and drained his abscess, assisted by Dr. Andrew Tang, chief resident headed to CT Surgery fellowship here at the Clinic, and Dr. Jenny Chang, PGY 2 Surgery. I gave Dr. Chang a copy of Cope’s with the admonition to read it soon and pass it on, as most of the current generation claim no knowledge of this important text. While I am not against interventional drainage, it takes time to drain the collection through a tube whereas sticking your hand in, sampling the collection, observing the injury, and breaking up collections and washing out with brown-bubbly -a mix of betadine/peroxide diluted in saline, I believe speeds the recovery from the infection. His drainage was done through a retroperitoneal approach from the left side and notably, his psoas muscle while viable, did not retract to cautery energy, suggesting some degree of rhabdomyolysis. The iliac artery was an indurated, thickened, and hard from the calcium and plaque that was the original problem affecting his distal aorta and iliac arteries (see left arteriogram centerline). I placed a pair of JP drains, removed one that wasn’t draining much on POD #3, and the other about a week after discharge on POD#5. His WBC elevation which was never high promptly resolved. I kept him on oxacillin with consultation from ID, and waited. After 3 weeks, I repeated his CTA.
His right iliac centerline showed patent stent with diffuse plaque and calcium starting in mid infrarenal aorta.
His abscess had significantly resolved and his pain was gone. He was ambulating again.
Before and after abscess drainage
The choices at this point were the following
Continue treatment of patient with supressing antibiotics for life
Resection of left iliac stent graft which is presumed to be infected
If resection chosen, the options for repair that I considered included:
NAIS (ref 1). Neoaortoiliac System graft using femoral vein
Aortoiliac homograft
Rifampin soaked gelatin coated graft (ref 2)
Extra-anatomic bypass with axillofemoral bypass or femorofemoral bypass.
Aortoiliac endarterectomy and repair with bovine pericardial patch and graft
The choice of replacement is becoming clearer in that while rifampin soaked grafts offer immediacy and expedience, all grafts seem to be prone to reinfection at a higher rate than autologous material (ref 3). The NAIS bypass is a great option, but is hampered by the addition of several hours invested in harvest of the femoral veins. While it can be staged with mobilization done one day and harvest another, those added hours add complications. We often forget that the simple metric of procedure time is the most important determinant of complication rate. Any operation going over 2 hours risks wound infection for example simply from ambient colonization of the open wounds from the rain of dead skin from the surgeon’s face, aerosolized fecal flora from flatii (prohibited in my ORs). The microenvironment of the open wound is also room temperature and not 37, having an impact on organ function and hemostasis. The homograft is the original aortic graft -before Arthur Voorhees invented the cloth vascular graft as a resident at Columbia P&S (my medical school alma mater, ref 4), major hospitals had tissue banks of aortic homografts harvested from the recently deceased. Having homografts is now an outsourced function, but does require having proper refrigeration for the cyropreserved grafts and generally can’t be ordered with short notice.
Rifampin soaked grafts work well, especially wrapped in omental flap, in the short and medium term but suffer a reinfection rate that is higher than seen with autologous tissues, and prosthetic grafts without rifampin, such as PTFE for extraanatomic bypass, have the highest rates of reinfection (3), despite being the board answer decades ago.
Endarterectomy allows for use of native tissues for repair. The adventitia around plaque and stents, while thin, can support physiologic pressures, even when they have been occluded for years. And while practice of aortoiliac endarterectomy is a bit of a lost art, it has both a long history stretching back nearly a century and a modern track record with carotid and femoral endarterectomy. It is merely a matter of scale. Pinch and zoom in on a femoral endarterectomy at the bifurcation and you have the same case as with an aortic one.
The question is, is bovine pericardium more autologous than prosthetic? It is a decellularized sheet of collagen from a cow’s pericardium, used in heart valves and vascular patches, but only recently applied as a graft (ref 5-7). I have long used bovine pericardium as a patch with some caution, but the rule of thumb is are there well vascularized tissues around it? A layer of Scarpa’s fascia and fat in a groin wound are not sufficient to protect a bovine patch, but a sartorius flap is. For me, once the infected stent graft is out, knowing if the surrounding tissues bleeds well is an important one.
I chose to do aortoiliac endarterectomy. The patch and graft would be made with bovine pericardium, unless I found the left iliac segment to be devitalized and foul with anaerobic vapors, then, I would close and go NAIS or extra-anatomic. The key point is that choices have to be on the table and constantly rearranged during the conduct of the operation.
The patient was preoperatively vein mapped and had suitable deep femoral vein for bypass conduit, having robust duplicated systems that would impact the patient minimally. The patient was placed in a supine position and via a midline laparotomy, the infrarenal aorta and the common iliac arteries beyond the short iliac stents exposed. I chose this limited exposure as any further into the phlegmon on the left risk injury to ureter and vein. The aorta had a palpable demarcation between plaque and mildly diseased proximal segment, predicted by the CTA to be at the IMA. A longitudinal arteriotomy was created on the right side from mid aorta to mid right iliac, and the left side had a separate arteriotomy to release the stent. The plaque came out in a single specimen (image).
The exposed stent is the left iliac stent holding within a stent graft.
The left iliac artery was destroyed by the infection but the tissues around it bled avidly and were not foul or infected. I avoided excess debridement here as the iliac vein was intimate with the phlegmon. There was a 3cm gap. Again, I thought briefly about taking femoral vein, but proceeded to make a graft from the bovine pericardium. This was sewn around the rod portion of a renal vein retractor from the OMNI set. The finished product resembled Voorhees’ graft. It was sewn into the orifice of the iliac from inside the aorta and end to end to the freshened iliac stump. Unfortunately, the omentum was atropic across the transverse colon, but the tissues around the resected artery and stent graft bled well, indicating good penetration of antibiotic. The retroperitoneum was closed after hemostasis obtained. Dr. Shashank Sharma, our chief resident headed to a vascular surgery fellowship at the renown Houston Methodist next year got to see what is unfortunately a rare occurrence -an aortoiliac endarterectomy, which through me puts him three degrees of separation from Cid Dos Santos (ref 8). Dr. D’Andre Williams, PGY-2 Vascular Surgery Resident, got important lessons on sewing the aorta. She’s part of a fortunate cohort that get exposed to open aortic surgery at our main campus which is unfortunately rare throughout the world.
The pericardium was soaked in rifampin, but probably did not bond to the collagen.
The final graphic shows the operative end result.
The patient recovered well and was discharged within the week with another month of IV antibiotics planned.
Before and After
Conclusion: The operation was started at 8 in the morning and was done by lunch time. For aortic cases, this is a crucial metric, as when the clock winds past the surgeon’s comfort, the patient suffers even more. Adding the femoral vein for a NAIS may have been the textbook thing to do, but we don’t do extra-anatomic bypasses that much either. I don’t believe that adding two more hours for retrieving the femoral vein would have enhanced the procedure, and would have served to add potential areas for complication. Technically, the aorta closes much as with a carotid or femoral endarterectomy, but the adventia is thin and really should be sewn with 5-0 or 6-0 Prolene. The larger needles such as the SH size creates unnecessary bleeding unless sewn with a line of felt which could become infected. Despite the thinness, it will hold pressure if it is not infected. Clamps that bend out of the “airspace” above the laparotomy, such as the Cherry Supraceliac Clamp and Wiley Hypogastric Clamp, prevent limiting the operative space with long clamps such as aortic Fogarty or DeBakey clamps, while being stronger than the Zenker.
A final comment for Staphyloccocus lugudensis. This is the second major vascular graft infection with this organism I encountered this year. The other was an infected aortic stent graft. Lugudensis means from Lyons. I do not know why that is, but it is so far not the nasty player that is S. aureus. I am sure it will share some plasmids, and become resistant one day, but in the earlier case in Abu Dhabi and now this, it is sensitive to penicillin, and came from the skin at the femoral puncture site, and for this we are fortunate. Major vascular infections are one of the few areas that still demand open surgical skills, and we foresake them at great peril. It’s critical to remember all the collective memory of surgery from the past, or we will become mere technicians fixing whatever comes out of the radiologist’s report with whatever knowledge obtained from a Zoom meeting for the latest, greatest device.
Acknowledgement
Gratefully, the patient gave his permission, as with all patient, for use of his case for educational purposes.
References
Chung J, Clagett GP. Neoaortoiliac System (NAIS) procedure for the treatment of the infected aortic graft. Semin Vasc Surg. 2011 Dec;24(4):220-6. doi: 10.1053/j.semvascsurg.2011.10.012. PMID: 22230677.
Oderich GS, Bower TC, Hofer J, Kalra M, Duncan AA, Wilson JW, Cha S, Gloviczki P. In situ rifampin-soaked grafts with omental coverage and antibiotic suppression are durable with low reinfection rates in patients with aortic graft enteric erosion or fistula. J Vasc Surg. 2011 Jan;53(1):99-106, 107.e1-7; discussion 106-7. doi: 10.1016/j.jvs.2010.08.018. PMID: 21184932.
Smith RB 3rd. Arthur B. Voorhees, Jr.: pioneer vascular surgeon. J Vasc Surg. 1993 Sep;18(3):341-8. PMID: 8377227.
Almási-Sperling V, Heger D, Meyer A, Lang W, Rother U. Treatment of aortic and peripheral prosthetic graft infections with bovine pericardium. J Vasc Surg. 2020 Feb;71(2):592-598. doi: 10.1016/j.jvs.2019.04.485. Epub 2019 Jul 18. PMID: 31327614.
Lutz B, Reeps C, Biro G, Knappich C, Zimmermann A, Eckstein HH. Bovine Pericardium as New Technical Option for In Situ Reconstruction of Aortic Graft Infection. Ann Vasc Surg. 2017 May;41:118-126. doi: 10.1016/j.avsg.2016.07.098. Epub 2016 Nov 27. PMID: 27903471.
Belkorissat RA, Sadoul C, Bouziane Z, Saba C, Salomon C, Malikov S, Settembre N. Tubular Reconstruction with Bovine Pericardium Xenografts to Treat Native Aortic Infections. Ann Vasc Surg. 2020 Apr;64:27-32. doi: 10.1016/j.avsg.2019.10.104. Epub 2020 Jan 10. PMID: 31931127.
Barker WF. A history of endarterectomy. Perspectives in Vascular and Endovascular Therapy. 1991;4(1)1-12. doi:10.1177/153100359100400102
Our debranch first technique described by Dr. Niranjan Hiremath and was presented at CX Aortic in Vienna in October. Hoping to collect multicenter experience with this technique.
At CCAD, during my 4 years here as chief of vascular surgery, I had the privilege of working with excellent colleagues in a world class facility in an amazing and generous host nation. Over that time, our operative case volumes grew rapidly (figure below) as we proved our worth.
Our unique situation as both a main campus of Cleveland Clinic and a startup in 2015 with a fraction of the systems already in place at Cleveland made innovation a necessity. When making do became making great, we achieved the world class results as we were tasked to do. I count 5 off the top off my head in vascular, but there are many more that we do every day, contributed by all the team members. It is in the Cleveland Clinic’s DNA, from its origins century ago in the vasty fields of wartime France, this systemic mission to make things better. I think a lot of how our founders worked from necessity near the trenches in operating theaters within tents, sleeping on rough cots, thousands of miles from Cleveland. It is working in a startup hospital here, a stunning facility endowed by the Emirate of Abu Dhabi, that I realized that practical innovations were the lifeblood of hospitals in times past, and that it continues to have meaning when lives are saved. In a world where costs, not ideas, will, or skills, limit the availability of healthcare, cost innovation will play a large role in its salvation.
The thoracoabdominal aortic aneurysm (TAAA) is the most challenging operation to do either with open or endovascular approaches because of the complications associated with the procedure including bleeding, kidney failure, spinal cord ischemia, and death. You really can only get good by doing a lot of these regularly, as it brings with it precious experience for the OR, ICU, rehab, and floor staff. The patients with TAAA presenting to CCAD do not always have the opportunity to travel to one of the acknowledged aortic centers (with which each of the faculty here have close ties), and we must offer results that match those other centers. To me, the biggest hassle and source of complication with an open TAAA repair is the drying up of bleeding at the end of the case, the result of long visceral clamp times. Long procedure time prolongs the case and exposes the patient to a more turbulent and prolonged recovery and higher risk.
Endovascular repair with branched or fenestrated stent grafts offers one solution in avoiding the thoracoabdominal exposure and long procedure times. Unfortunately, a significant minority of patients do not have the anatomy for endovascular approaches. We have the skills, staffing, and facilities to offer both approaches, but are handicapped by low volume. Review of our volumes show that aortic aneurysm disease is dwarfed by diabetic circulatory problems. So to offer these patients the same results with open aortic surgery as the patients I had at main campus in Cleveland, I had to cheat a bit by rearranging the deck. How so? By turning the highwire act of thoracoabdominal aortic aneurysm surgery and turning into a deliberate walk on a low balance beam. By debranching the visceral branches from the graft one by one, the visceral ischemia time is minimized (video) or largely eliminated.
I discussed this with Dr. Niranjen Hiremath, our aortic trained clinical associate and like all things in medicine, a similar concept was applied by his mentor, Dr. Matalanis in Australia, to the aortic arch. We have performed two of these and both patients survived and are doing well, including the most recent one with a hybrid extant 2 repair. We published the technique after the first case in Journal of Thoracic and Cardiovascular Surgery (figure below, reference 1). I also presented the first case on this blog (link). More gratifying are the reports of adoption of this technique around the world. The patients come out of the operation without the torrent of coagulopathic bleeding seen with the traditional technique.
Innovation #2, The Vascular Lab in Every Patient’s Room
One of the things that happened early in my tenure was realizing how limited the tools available for vascular assessment were for non vascular caregivers. Both the physical examination with pulse palpation and pulse Doppler examination are challenging to master and usually fail to answer the simple question: is there enough perfusion? The absence of a pulse or Doppler signal in the hands of a non-vascular caregiver is an inconstant thing, and various projects have been undertaken that do not specifically address the triage gap that vascular surgery has compared to cardiology for chest pain. Not all chest pains are referred to cardiology. Only those those patients who pass the screening test of EKG and serum troponin levels are referred. My first inclination was to budget for pulse volume recording machines to be located in the ED and ICU’s of the hospital, but it was not a simple solution and would require stretching the limited vascular lab staff. Then it dawned on me that the toe waveforms offered a solution. On the PVR machines, the toe waveforms are captured by transmitting red laser light through the nail of the toe. A receptor captures a waveform (figure below) that is reflects the passage of blood that absorbs that red light.
This is in fact the identical technology in a pulse oximeter which has extra circuitry to calculate an oxygen saturation. I was not interested in the saturation, but rather the waveform. It turns out, for all practical purposes, the waveform given by pulse oximeter units is qualitatively the same as that given by the pulse volume recorder’s digital plethysmograph (figure below).
So now, when I get a phone call from the ED that a patient has no DP or PT pulse, I ask the caller to place a pulse oximeter with a waveform trace on the patient’s second toe (or nearest extant toe). I then ask, is there a waveform? The presence of a waveform, no matter how dampened, means the patient does not face acute ischemia, and can safely wait until the morning, avoiding a drive in the middle of the night (figure below, severely dampened waveforms).
an abnormal DPPG captured with a hospital ICU pulse oximeter
We are validating this with a study that has completed data collection and hope to present this simple test to a broad audience. This is something akin to having a point of care vascular lab study that can answer a simple question: is there blood flow at the level of the toes? The finer points of “how much blood flow” can be answered by formal testing but that keen absence of broad vascular assessment skills among healthcare providers and absence of a simple test like an EKG for MI will feel less sharp, particularly because of the near universal availability of a pulse oximeter with waveform display throughout most hospitals.
Innovation #3: Assessing for Visceral Malperfusion before Surgery for Aortic Dissection
The typical scenario for a sad ending is this: a patient undergoes emergency surgery for an ascending aortic dissection. The operation ends in the middle of the night. The morning labs show a lactate of 10 which had been rising since the end of the operation from a high borderline level of 2. The urine output also dropped to zero. The patient remains intubated and has palpable femoral pulses, but now has a distended abdomen full of bowel gas, and is unable to report pain. The decision is made to get a CTA on top of the ones the patient received preoperatively which nearly guarantees permanent renal failure and need for hemodialysis. The descending aortic portion of the dissection is noted to be causing a malperfusion of the SMA and left renal artery, and there is pneumatosis of the small bowel through transverse colon which are resected after revascularization. The patient recovers with a jejunostopy and lifelong TPN and hemodialysis. This sad scenario is what I thought about when I was asked to assess a patient intraoperatively without a femoral pulses after an aortic dissection for possible visceral malperfusion. The question was if CT with contrast was indicated. Having an RVT credential (I’m old), I frequently do my own scans, and have found under general anesthesia, the abdomen is easy to scan well. The patient is typically prepped from neck to toes for the operation, so sliding in with an abdominal probe was simple. It is possible to get excellent windows on the visceral segment abdominal aorta with long axis and short axis views of the celiac axis, SMA, renal arteries, and iiac and lower extremity arteries (figure below).
At CCAD, the patients also get a TEE, and the arch and descending thoracic aorta is well visualized. That first patient underwent a femorofemoral bypass for the lower extremity malperfusion, and I found that the left renal artery had obstruction, but the right did not. The patient was reassessed at the end of the case and good visceral perfusion was seen at that point. I realized I was onto something, and whenever possible now for ascending aortic dissections, myself or the vascular tech is called to evaluate the visceral and lower extremity arteries at the beginning of the case, avoiding contrast studies. We are submitting the experience as an abstract for the STS conference.
Innovation #4: Retrograde tibial artery distal perfusion cannulas for ECMO
This past year, ECMO has been lifesaving for many patients facing cardiovascular collapse from COVID and other conditions. Once the cannulas go in, a hypoxic patient in heart failure has a chance at recovery. The drama of the moment causes the caregivers to overlook the fact that up to 10 percent of patients without a distal perfusion cannula will develop leg ischemia, and that after 6 hours, irreversible will occur leading in neuromuscular death and limb loss. This has happened for two patients transferred for care this year. The problem is that the skill of placing a antegrade femoral artery distal perfusion cannula in the proximal thigh is not always present, and the ability to judge perfusion is degraded with ECMO flow. While older patients on ECMO may have significant arterial disease, young patients generally do not, and I saw that as an opportunity for simplifying the distal perfusion cannula by placing a 5F micropuncture sheath into the dorsalis pedis artery (figure below).
The distal perfusion cannula is in the dorsalis pedis artery
This provided sufficient flow to avoid limb loss in a series of patients on which we published a technical article (reference 2) and presented. The retrograde access of these supericial vessels is within the technical envelope of most intensivists and cardiologists, those who most frequently place emergency ECMO cannulae. It was gratifying to catch up with one of my first patients who walked in with both legs, having undergone a heart transplant while bridged with ECMO.
Innovation #5: Park Clamp Used in Thoracoscopic and Laparoscopic Surgery
The Park Clamp (link) is a circular compressor that is intended to compress bleeding tissues allowing for suturing within the circle. I invented this while at main campus, and missing it sorely, had two custom made at the prototyping facility at Cleveland Clinic and shipped into CCAD. It is particularly useful in venous bleeding during spinal exposures, redo groins around the profunda, and retroperitoneal tumor resection. Dr. Redha Souilamas, chief of thoracic surgery (image above) found it particularly useful in thoracoscopic pneumonectomies, when staple line bleeding is encountered on the pulmonary artery (image below).
Pulmonary artery staple line bleeding controlled, ready for suturing.
In laparoscopic surgery, it is possible to introduce the compressor via a small incision and this will allow for laparoscopic suturing of a vascular injury in a bloodless field. I was able to resect an IVC tumor thrombus with Dr. Waleed Hassen using this device to achieve hemostasis. The critical feature of the Park Clamp, lacking a manufacturer, is that we made it ourselves in our own hospital.
Conclusion: a modest proposal or how cost innovation will save health care
Inventions and innovations exist in a vacuum unless they are implemented, and this requires the will to accept the possibility of a better way. You should never be satisfied with the status quo if there is harm to be reduced. There has to be buy in from everyone involved or you get the situation I had when I was a PGY-2 in 1995 in the ICU. Being the surgical ICU resident, I was called nearly hourly to change the dressing on a patient with HIV and necrotizing pancreatitis with an open abdomen. There was over a liter an hour of exudate soaking the dressings and pads, making it a nightmare for the nurses. After a third round of this and feeling it would interrupt lunch, I came upon a plan for covering the wound with lap pads, overlaying a chest tube, and sealing everything with an Ioban. With the chest tube to negative pressure via a Pleuravac, the calls to change the patient’s dressing ceased, and the nurses no longer hand to change the bedding hourly -bedding that was soaked with HIV positive exudate. I was very pleased about this until I was stat called to the director’s office. I was given the dressing down of my life -how dare I experiment on his patient and didn’t I think that placing a suction on the transverse colon would result in a fistula? I hung my head in shame and took down the dressing. Of course, readers will know that this preceded the VAC dressing by about a decade, and negative pressure wound therapy is now a multi-billion dollar industry. What it teaches me to this day is that progress only happens when success is actually seen by everyone, but also there has to be buy-in from the stakeholders -the people who bear responsibility for any bad outcomes -fistula and death in the case of this proto-VAC dressing. Without convincing everyone, there is no success, and the invention goes off to die.
The fact is, one time early in my tenure here at CCAD, we ran out of negative pressure pumps, and I placed this chest tube/Pleurevac dressing on a patient with a large groin wound that was leaking high volumes of exudate and lymph. After two days, when a VAC pump became available, the patient’s groin turned out to be clean and granulating and it came to me that the next great leap in innovation is low cost innovation.
Cost Innovation, to name it, is using what is available, sometimes repurposing, or at others, dialing back the clock, to replace costly things that threaten to break a hospital’s finances while maintaining quality. It was only a few generations ago when hospitals were self contained communities. Rather than use peel packs of disposable gowns and drapes, there were tailors, seamstresses, and launderers making and maintaining the same. The Mayo Clinic was making its own insulin after discovering it and gave away the recipe out of concern for ethics -out of believing it is wrong to profit from a life threatening condition. We have the technology and capacity to make low cost endoscopes and reprocess them -possibly undercutting current costs by a factor of a thousand. We slaughter millions of hogs and cows annually, but harvest no heparin from them in the US. Laser CNC cutters, 3D printers, and enthusiastic makers have proliferated and could make every item that we currently open from a peel pack, use once, and discard into landfills -one only has to look at the cottage industry of face shields and hand sanitizers that bloomed last year during the pandemic. Pharmacists are fully capable and trained to manufacture custom pills and compound salves and solutions by the gallons if only if they are allowed to, saving hospitals millions in cost of medications sold in blister packs and tiny tubes and bottles. Stents can be printed in-house, and stent grafts can be custom made (link). Every town or city has tradespeople who can work stainless steel, plastic, and glass, or make and program custom computers -it is a short jump to making medical equipment at scale in your hospital.
Cost innovation is the only way out for the inflationary cost cycle that has throttled healthcare throughout the world. We have become a world where healthcare is delivered out of peel packs and million dollar investments to perform single procedures is considered normal and desirable, almost to the point of thinking people as coming in disposable peel packs. When I watch shows about hospitals a century ago, such as The Knick, I don’t guffaw at the old-timey medical stuff. I see a fervent environment of innovation in purposeful communities of specialized workers within hospital walls. We need to return to such practicality if we are to break out of the plastic peel pack.
References
Hiremath N, Younes H, Aleinati T, Park WM. Open repair of extent-III thoracoabdominal aortic aneurysm using a modified branch-first technique. JTCVS Tech. 2021 Mar 13;7:29-31. doi: 10.1016/j.xjtc.2021.03.014. PMID: 34318197; PMCID: PMC8312144.
Göbölös L, Hogan M, Kakar V, Raposo N, Sänger S, Bhatnagar G, Park WM. Alternative option for limb reperfusion cannula placement for percutaneous femoral veno-arterial ECMO. Perfusion. 2021 Mar 26:2676591211003282. doi: 10.1177/02676591211003282. Epub ahead of print. PMID: 33765883.
The patient is a young woman who presented with classic symptoms and findings of median arcuate ligament syndrome (MALS). She avoided food because eating triggered severe pain in her upper abdomen. Over a year, this resulted in 15 pounds of weight loss. As a result, she no longer had the energy to work or exercise. She had an extensive gastrointestinal workup including blood work (LFT’s, amylase, cholesterol panel), abdominal CT scan, and upper endoscopy which were normal except for the finding of narrowing of the celiac axis due to compression by the median arcuate ligament. Examination was notable for upper abdominal pain exacerbated by pressure and seated, hunched-over posture. Unfortunately, due to her health insurance, surgery was not covered and she did not want any. So I recommended she try the following.
Eat standing up with good posture, shoulder back, back arched, taking deep breaths and holding once food passes
Practice upward facing dog yoga pose (figure) 5 reps daily with deep inhalation breath holds. If this is difficult, do this standing up.
Improve the posture during seated work, never hunch over and pressed forward with “shrimp back,” periodically take a deep breath and hold with excellent posture.
Upward facing dog yoga pose -shoulders square, outward collar bone tension, with deep inhalation breath holds
Over the past several years, I’ve noted that most patients respond to this, even in acute MALS pain situations (yes, there is acute MALS like slipped discs, for another post). That patient came back a few weeks later reporting that she was able to eat more food, more frequently. She also acknowledged compliance with the exercise and postural adjustments at work. A month later she reported regaining her lost weight and only mild pain with sitting in a car for a long time. She was still eating standing up, and she was grateful for having been treated without surgery.
From reference below, a mechanism for celiac plexus compression, injury, fibrosis, and development of neuropathy
We have postulated that MALS is a nerve compression syndrome of the celiac plexus by the median arcuate ligament (reference). There are two consequences to MALS, neither of which is mesenteric ischemia. The first is this compression of the celiac plexus with injury resulting in inflammation and fibrosis, resulting in further compression and a neuropathy of the celiac plexus. This neuropathy triggers aberrant pain sensations in response to eating. The other consequence is remodeling and injury due to arterial compression. The celiac axis can develop post-stenotic dilatation, growing large enough to be considered aneurysmal. The compression can damage the intima resulting in dissection. The artery can be injured and a pseudoaneurysm can develop. Finally, the aneurysmal segments may develop thrombosis and be the source of thromboembolism, usually to the spleen. Even when the celiac axis clots off, unless there has been resectional surgery such as a Whipple or splenectomy, the stomach gets enough collateral flow that ischemia is rare when celiac axis occlusion occurs. So similarly to thoracic outlet syndrome (TOS), there is a neurogenic MALS and an arterial MALS.
The first line of therapy in neurogenic TOS is physical therapy. With symptomatic MALS, I wondered if there could be physical therapy as well. This young woman and others I have managed nonoperatively suggests good response in some, and partial response in most to exercises and maneuvers designed to address the compression.
Currently, in lieu of celiac plexus block, I have patients treat their MALS nonoperatively using the above protocol for 2-4 weeks, typically while they undergo further workup to rule out more common gastrointestinal etiologies of their abdominal pain, and many have been able to improve their circumstances with these measures alone. This patient chose not to have operation as she was able to live symptom free and regain lost weight with these recommendations alone.
Addendum
I received a comment from Ms. Suzanne Peek, president of the National MALS Foundation, who correctly pointed out not everyone presents in this way. I agree each patient undergoes a unique journey that is often marked by diagnostic delays because this is a rare condition. As I stated, not every patient responds to this regimen and after work up typically will undergo surgery to which in our published results 85% have a positive response to when diagnosed with MALS. Is certainly an area of further study to see if more people can respond to this non-operative approach. Our previous protocol which we instituted after the publication of our report was to use celiac plexus blockade as a diagnostic study and occasionally permanent blockade as therapy for those with prohibitive operative risk. A positive response to this regimen may signal a positive response to surgical celiac plexus ablation.
Reference
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.
A Surgeon's Notes 