A Surgeon's Notesgolfist
October Journal Club (October 21, 2014) is approaching. The papers chosen by the presenters are linked below. Please refer to the club format and rules, also attached.
Presenters/Papers:
D. Hardy – Endovascular Repair of Type B Aortic Dissection
H. El Arousy – EVAR v Open
D. Virvilis – evarsurveillance3years
The patient had undergone an uneventful EVAR, but in followup had developed AAA sac growth. Pictured above are the post deployment CT’s from 1 month and 6 months. Reviewing the original aortogram, you can see that there was flow into the sac very late via an iliolumbar collateral.
Plan was made for arteriography and intervention. As discussed in an earlier post, 3D VR was very helpful in planning access to the type II endoleak, particularly in plotting C-arm angles and access vessels.
The 3D-VR image view on Aquarius Intuition (TeraRecon) predicts a camera angle of 50 degree LAO to see the branch leaking to the lumbar vessel causing the leak.
Initial aortography confirms the absence of a type I or III leak in early phase.
Later in the phase, the endoleak can be well seen, corresponding to the CTA.
I do an intraoperative transabdominal duplex of the aorta. I have submitted this technique for presentation and eventual publication, but briefly, using an abdominal probe on the abdomen, the sac and endoleak can be readily visualized, and the source of the leak confirmed.
The inferior mesenteric artery which is so often involved is not in this case, and can be easily seen with duplex in patients who are NPO and under general anesthesia. I perform these studies myself, as they are far less challenging than when a patient is awake.
Selection of the branch vessel is straightforward as the CTA well illustrates the course of the source iliolumbar vessel. The CTA even showed the loop that was challenging to traverse. The sequence of access involved IIA, branch access with a glide catheter, placing a Rosen wire for anchorage, and pushing the sheath over the glide catheter into the branch vessel, giving stability. Further access into and across the loop was then possible with superselective catheters based on an 0.18 wire system.
Once access into the AAA sac was achieved, coil embolization of the leak cavity chased by glue (NBCA) allowed for obliteration of the endoleak.
Duplex ultrasound confirmed effective closure, with absence of perigraft flow.
Using duplex in this fashion adds another dimension to the treatment imaging and has the potential for reducing radiation dose and contrast volume.
The patient in followup has shown sac shrinkage. The other treatment options are: direct lumbar puncture, open surgery with sac marsupialization and oversewing of leaks, and laparoscopic ligation of lumbar arteries. I have tried all of these, but this went as easy as could be expected and I credit the ability to visualize the entry path in 3 dimensional virtual reality. The toughest part was negotiating the loop, but a shaped 0.18 glide wire simplified this.
In 2006, Sheehan et al [J Vasc Surg 2006;43:657-61] reviewed an 7 year experience from 5 academic centers. 1909 patients had EVAR with various endografts, and there was an overall 15% rate of type II endoleak. Most resolved within the first year. No significant variation by endograft design appeared to correlate with type II endoleak, which makes sense, although TALENT graft had the highest rate. Spontaneous resolution was common. Late endoleaks were frequent. No conversions were due to type II endoleak. Higashiura, Greenberg et al [J Vasc Interv Radiol 2007;18:975-981] reviewed the CCF experience with the Zenith graft and type II leaks. Of 204 patients with suitable followup, there was a 17% rate of early type II endoleak. Of these, only a 7 of 18 patients with persistent leak developed sac enlargement. Most type II endoleaks spontaneously resolved in followup. No variables could predict persistence of type II endoleak. Treatment prevented sac enlargement.
Silverberg, Marin et al [J Vasc Surg 2006;44:453-59] found similar rates of type II endoleaks -16%, in a study group of 965. Spontaneous resolution occurred in 36% in a mean time of 14.5 months. Treatment was reserved for sac enlargement. 8.4% of those with type II endoleaks experienced sac enlargement greater than 5mm. The vast majority of patients had a benign course. Regression analysis revealed cancer, CAD, COPD were associated with earlier spontaneous closure of type II endoleaks.
Ruptures can occur with persistent type II endoleak [Jones, Cambria et al. J Vasc Surg 2007;46:1-8]. Selective treatment of those with persistent leak and sac growth >5mm seems to be a safe and cost effective approach [Steinmetz, Sicard et al. J Vasc Surg 2004;39:306-13].
Link to type II endoleak papers
Completion angiography fits into the range of things that many of us were taught to do because it might help avoid the problem of early graft failure. I remember a time in the nineties when vascular surgery was synonymous with terrifyingly long bypass operations that sometimes worked. Back in that preinternet era, all day bypass operations were capped at the end with a flat plate arteriogram. As with all things archaic and historic, I firmly believe that our trainees should feel comfortable with this type of on-table arteriography because not every place will have a corridor of rooms with robotic c-arms. I feel that each trainee should feel comfortable wheeling in a portable c-arm, assembling it, turning it on, put in patient information, and perform a study. But I digress. The completion arteriogram clearly has a role in bypass surgery, but I question its usage as a “I do it all the time” routine. When anything is written in stone, it immediately takes on a hallowed, sanctified aura, usually taken on during M&M’s when the person at the podium intones beatifically looking skyward, “the completion arteriogram showed no abnormalities.” Science is about questioning the status quo and backing up practice with evidence.
The purpose of the arteriogram is to evaluate the anatomy for treatable lesions. Screening for these lesions can be just as easily performed with handheld pulse Doppler and if needed, duplex ultrasound. In my experience, the triad of pink toes, palpable pedal pulses, and multiphasic signals in the distal anastomosis is more than enough evidence to start drying up and closing. In this particular case shown in the picture above, the anastomosis looked pristine, but the signals were weak and monophasic in the distal anastomosis despite palpable pulses. Arteriography reveals the reason below, but frankly, the arteriogram was dispensible even in this case (trainees –reason why?). In fact, arteriography takes care of the surgeon more than it does the patient. Tan et al [J Vasc Surg 2014;60:678-85] for the Vascular Study Group of New England, including my friend Dr. Alik Farber, reviewed the VSGNE database and found that a strategy of compulsive completion studies which included angiography or duplex ultrasonography, did not improve short term or 1 year graft patency.
I have used many different flavors of image post processing software including Osiris, Vitrea, and now Aquarius, aka TeraRecon. But I notice that outside of endovascular planning, people rarely use the virtual 3D reconstructed images (the pretty pictures) for anything other than posting images for publication in JVS, and even there I think we have reached saturation.
I have found 3D reconstruction to be especially useful for open surgical planning, and that is by doing two things. First, on viewing the 3DVR data, I reorient and center on the surgeon’s perspective, using left button to rotate the picture around the zero at the center of the screen, and the right mouse button to grab the whole image and recenter as necessary.
I then window-level in tissue density -this is done by pressing both the right and left mouse buttons, but you can choose this off the menu.
I can plan the incisions and exposures from any angle -in this case, I can see the saphenous vein and its relative proximity to the CFA to perform an in site bypass to the AK POP. And I see the loci of the tributaries that I may need to ligate.
This is a powerful tool that is often overlooked.
Median arcuate ligament syndrome has some disrepute among vascular surgeons because it does not make intrinsic sense that an isolated celiac axis stenosis, an intermittent one at that, would cause a regional mesenteric ischemia in a population that is in the literature, generally younger than the classic population seen for chronic mesenteric ischemia. And it shouldn’t, because no exceptions to the physiology and anatomy of mesenteric ischemia can be made.
The finding that some younger patients present with post prandial upper abdominal pain with associated compression of the celiac axis by the median arcuate ligament of the diaphragm dates to the 1960’s. These patients lose weight and find relief by leaning forward, standing, and crouching. They resort to small volume liquid diets in extreme cases, and more than 50 pounds of weight loss is seen.
During my fellowship, we treated these with operative release of the median arcuate ligament and there would be fibrosis and the celiac plexus, nerves mediating somatic pain from the foregut, would be ablated during the dissection. Inevitably, the celiac axis would undergo a patch or bypass because of the chronic scarring on the artery due to the compression. For the past two years, in collaboration with Drs. Matthew Kroh and Kevin El-Hayek (now in CCF Abu Dhabi), these releases have been performed laparoscopically, and celiac stents are hardly ever used.
John Weber, our vascular surgery chief resident, has prepared this data and we have submitted it to the PVSS for the meeting in February. Not thinking of this as a vascular disease, but rather a nerve compression disease, much like neurogenic thoracic outlet syndrome or carpel tunnel syndrome, the pathoanatomy and clinical presentation make far more sense. There is inflammation typically and nerves are ablated, and celiac plexus block, it turns out, is an excellent screening tool when the classic presentation is not present. It is analogous to using a scalene block in neurogenic thoracic outlet syndrome. Redo operation is feasible if the original procedure fails to relieve pain completely, if the celiac plexus block works to block the pain.
It’s Dr. Eagleton’s birthday. So in celebration, I recommend you read his authored or co-authored papers from this year. Link to MJE 2014 papers.
By Max Wohlauer, MD, fellow in vascular surgery at Cleveland Clinic Foundation
As a rugby player in high school and college, I found strength and camaraderie through hard work, blood, and sweat. Like rugby, vascular surgery is a team sport, and not for the faint of heart.
My father was diagnosed with stage IV prostate cancer while I was a first year medical student. I was his cheerleader and coach as he fought against the illness that eventually took his life, and learned that healing becomes the most important when a cure is out of reach. At this point I had established that continuity of care was important to me, but I was not satisfied with the role of cheerleader or coach, however. I was intent on being captain – a team leader in the center of the action – and surgery called to me. Where could I find a specialty that combined traditional surgery and cutting edge procedures to provide optimal patient care, while at the same time maintain the ability to care for patients with a chronic disease over time?
Dr. Ben Starnes at the University of Washington, who combined an explosive technical skill with a genuine concern for each patient’s well being provided a definitive answer. I learned that open arterial or endovascular repair could immediately and consistently improve quality of life. The patient could have a body worn-out by seven or eight decades of systemic illness with a life or limb threatening lesion, or at the other end of the scale, have a youthful body facing similar threats from blunt or penetrating trauma. The results were equally inspiring to me. In clinic and on the wards, Dr. Starnes made a connection with each of the patients, celebrating their unique lives and personalities. He set an example inside and out of the operating room, which I strive to emulate to this day.
At the University of Colorado, Dr. Mark Nehler created an environment for success and has shown me how a vascular surgeon displays leadership outside of the operating room. He stepped into Dr. Rutherford’s large shoes to build the department, launch the careers of several young vascular surgeons, and has made several important contributions to vascular literature. He has given me myriad opportunities for growth inside and outside the operating room. I have learned from Dr. Nehler more about the importance of interpersonal relationships between myself and my colleagues as well as with my patients. These teachings have made me a better surgeon.
Then, working with Dr. Ernest Moore as a Trauma Research Fellow, I was inspired by a man committed to science, surgical practice, training the next generation of academic surgeons, and administration; a bona fide quadruple-threat. His accomplishments and mentoring ability are equally phenomenal. He is a role model that I strive to emulate.
It would be selfish to have the advantage of excellent training without contributing new information. During my two laboratory years, I had the opportunity to explore post-injury coagulation derangements, which I continue to study while on the clinical services. I have also traveled to many conferences to present research throughout the US and in Europe. I continue to write, publish and present during my clinical years, and feel that this is only the beginning. I know that I have a genuine ability to become a leader in the field of vascular surgery.
Thank you for consideration of my application.
There are several areas yet to be satisfactorily traversed by endovascular technology and the common femoral artery is one area. While not completely a no stent zone, stents and interventions in the CFA do poorly compared to the open surgical alternative. As vascular surgeons we know that the key to inflow problems is the produnda femoris arteria and she does not tolerate being ignored, stented across, or ballooned too much. I have tabulated some areas that are still in the purview of open surgery in no particular order :
1: systemic infection
2: failure of stent grafts
3: rupture/hemorrhage/trauma
4: thoracic outlet obstructions
5: cancer
6: SVC syndrome after failure of interventions
7: MALS
8: popliteal entrapment
9: hypothenar hammer syndrome
10: very large thoracoabdominal or juxtarenal aortic aneurysms (until we get FDA approved off the shelf devices)
11: dialysis access
12: extreme limb salvage
13: severe aortic occlusive disease
14: CKD on the cusp of dialysis
15: congenital vascular disease
17: trauma/contaminated fields
18: low risk patients
19: common femoral artery
20: subclavian artery/innominate artery
21: carotid endarterectomy -for now
The list is open ended and you may add in the comments below, but the list in some parts is esoteric. The data is sobering if you read “Predicted shortfall in open aneurysm experience for vascular surgery trainees,” by Dua et al in the 10/2014 JVS. When I trained, I graduated with about 50 open AAA under my belt. Dua et al are predicting 10 per trainee in 2015, and 5 per trainee by 2020.
Who will do my open AAA?
Percutaneous access for EVAR and TEVAR does several things. First, the procedure becomes shorter by an hour or two, and (don’t discount not having nursing count instruments because the case was percutaneous). Second, the patients experience far less discomfort and it is easier to discharge them the next day when they have a bandaid versus an incision. And this leads to the third thing: not having an incision means it is far less likely that a groin infection will occur, especially in the obese.
There are three things which you must do before undertaking pEVAR. First, you have to become comfortable with using the Perclose S device in 6F-8F access -about 5 to 10 successful closures will do. You should become facile with the deployment of the sutures and closure of the access point. Avoid small arteries or heavily calcified arteries. This leads to the second point -all of your groin access should be ultrasound guided -this has been shown to improve results in pEVAR (Ref 1). I am a firm believer that the source of groin access complications starts with the initial needle stick. The 18g needle is basically a short 11 blade rolled up into a cylinder, and during groin access without ultrasound imaging, one can shear branch arteries, skewer arteries, dissect plaque, and access too proximally or distally, or into the profunda femoris.
The third need is access to 3D reconstruction software and multislice CTA. This gives you powerful ability to predict which patients are more suitable for a percutaneous approach, and which should have a cut down, and with 3D virtual reality reconstructions, you can plan where the incisions will be. In the skinny patient, this is not a pressing issue, but in the merely obese and the frankly obese, and the super obese, choosing to go percutaneous and avoiding a groin complication, which may be the one thing that debilitates the patient far more than a stent graft deployment, becomes an easy decision with experience.
As you build your 6-8F Perclose experience, you may notice that having too tight and subcutaneous tract can result in the suture catching on SQ fat, and not closing, or that bleeding won’t surface properly and create a hematoma under Scarpa’s fascia, often after the patient gets to the recovery room. Expanding on this principle, as you leap to 12F access and preclosure, I recommend you try this -make a 10mm incision, and using a tonsil clamp, pop through Scarpa’s fascia and seat the tips of the clamp under ultrasound on top of the soft part of the CFA that you intend to access. Gently spreading creates the space that you need to deploy the sutures and ensure that any bleeding will exit the skin and not dive under the fascia. It amounts to an ultrasound guided dissection of the common femoral artery. Before you remove the tonsil, you gently maneuver a micropuncture (always) access needle between the tines of the tonsil clamp until it gets to the artery -this keeps the eventual wire going through the tunnel you just made.
12F can usually close with a single Perclose, but start practicing by placing two Perclose sutures in a 10 oclock and 2 oclock orientation. Once the sutures are in, I make sure the two ends of the suture are pulled out and the end loop of the suture is on the artery and I clamp these sutures to the drapes medially and laterally depending on how I deploy the two sutures. This also helps avoid catching the suture and driving it into the aorta.
After performing EVAR or TEVAR, I remove the sheath, leaving a wire -typically the stiff wire originally supporting the sheath and deploy one of the sutures. This first suture should cinch down onto the artery and substantially decrease the bleeding coming from the access site. I then deploy the second suture, and if the bleeding has stopped or is a steady dribble, I remove the wire. If pulsatile bleeding persists, I recinch the sutures using the knot pushers. If this decreases flow, I remove the wire, otherwise, I place a dilator, stop the bleeding and cut down. Cutting down after SQ dissection means merely dividing skin and tissues over the dilator, and the artery is easily visible for suture placement. If I remove the wire and there is still some bleeding, and usually there is, I place Gel-Foam soaked in diluted thrombin into the tract, reverse heparin, and hold pressure for 10-20minutes. It is very rare to have to convert after this is done.
The skin is closed with an absorbable 4-0 monofilament suture, and skin glue. I usually use the micropuncture needle to give an ilioinguinal field block with Marcaine. This gives 24hrs of pain relief.
A note about incisions. Usually, with 3D VR imaging of CTA, the CFA and its quality (size and absence of plaque), and location relative to the inguinal crease can be ascertained. I try to make the access point at the inguinal crease or distally, as this goes under the subpannus of groin fat rather than through it.
I sincerely believe sheath size is not the limiting factor to percutaneous access. Rather, it is the common femoral and iliac artery. Zakko et al at the University of Florida just published their experience on the obese with percutaneous TEVAR (ref 2), and found that while the arteries were deeper, the technical success rate of staying percutaneous (over 90%) was no different between their obese patients non-obese patients. The predictors of failure were poor access artery quality and size. I believe that you can select for patients most likely to succeed and greatly reduce failure. In this population, groin complications are potentially life threatening, and avoiding an open groin exposure is valuable.
References
1. J Vasc Surg 2012;55:1554-61 (ultrasound guided access)
2. J Vasc Surg 2014;60:921-928 (p-TEVAR and obesity)
A Surgeon's Notes 