Audible Bleeding

Audible Bleeding Editor and vascular surgery fellow Richa Kalsi (@KalsiMD) is joined by James Martinson,  practicing general surgeon with an interest in vascular surgery currently serving as the ship's surgeon for the USS Harry S Truman aircraft carrier and Langford Green (@langfordgreen_), research fellow at the Center for Vascular Research at the University of Maryland currently applying to medical school, JVS editor Dr. Audra Duncan (@ADuncanVasc), and JVS-VI editor Dr. Anahita Dua (@AnahitaDua) to discuss two great articles in the JVS family of journals.
Articles:
Part 1: Open bypass versus endovascular therapy in chronic limb-threatening ischemia patients with prior endovascular attempts (Hamouda & Malas)

Part 2: Retrospective review of 3126 patients with chronic lower extremity wounds treated with intermittent topical oxygen therapy (Lohr & Dua)

Show Guests 
Dr. Mohammed Hamouda was a postdoctoral research fellow at UC San Diego, Division of Vascular & Endovascular Surgery, and an incoming integrated vascular surgery resident at the Houston Methodist Hospital (LinkedIn)

Dr. Mahmoud Malas is the chief of vascular and endovascular surgery at UC San Diego, and the vice chair of surgery for clinical research at UC San Diego School of Medicine (@malas_mahmoud)

Dr. JoAnn Lohr is a vascular surgeon with her own practice in Cincinnati, OH, and has also worked in the VA system of Columbia, SC (LinkedIn)

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Welcome back to the Audible Bleeding Series: Landmark Papers in Vascular Surgery. In this episode, Audible Bleeding editor John Culhane and co-host Dr. Jesse Columbo are joined by our guests, Dr. David Stone, Dr. Salvatore Scali, and Dr. Anders Wanhainen to unpack one of the longest-running debates in aortic surgery: when (and whether) to repair an abdominal aortic aneurysm.
We'll start our episode with the open-repair era and the two trials that set the basis for the 5.5 cm threshold—UKSAT and ADAM—then move into the early EVAR years with PIVOTAL and CAESAR, which asked whether fixing smaller aneurysms with endovascular technology could do better. Finally, we'll look at how modern screening programs, improved medical therapy, and current guidelines have reshaped the practical decisions we make for these patients every day.
 
Links to Papers Discussed:
Open Surgery Era
1.    UKSAT (1998)
2.    ADAM (2002) 
 
Endovascular Era
1.    PIVOTAL (2010)
2.    CAESAR (2012) 
 
Contemporary Results
1.    Oliver-Williams/NHS NAAASP 
2.    Rokosh/SVS Guidelines
3.    ESVS 2026 Guidelines
 
Guests:
Dr. David Stone, MD (@DHStoneMD); Dartmouth
Dr. Salvatore Scali, MD (@UFVascular); University of Florida
Dr. Anders Wanhainen, MD, PhD (@AWanhainen); Uppsala University, Sweden
 
Hosts:
John Culhane, MD (@JohnCulhaneMD); Vascular Surgery Fellow, Montefiore
Dr. Jesse Columbo, MD; Dartmouth
 
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Learn more about us at https://www.audiblebleeding.com/about-1/ and provide us with your feedback with our listener survey.
*Gore is a financial sponsor of this podcast, which has been independently developed by the presenters and does not constitute medical advice from Gore. Always consult the Instructions for Use (IFU) prior to using any medical device.

In this episode, we spotlight editorials and abstracts from the Journal of Vascular Surgery Cases, Innovations, and Techniques (JVS-CIT). Editorials and Abstracts are read by Authors as well as members of the SVS Social Media Ambassadors.
 
Guests: 
Isabel Banks, MS4, SLU 
Best of 2025 - rare, high-risk, and unforgettable vascular cases

Best of 2025: Venous disease 

Hemodynamic and patient-level considerations in inferior mesenteric artery aneurysm management

Reply

Ultra-distal bypass remains a valuable option for tibial disease with tissue loss

Stewart Treves syndrome as a catastrophic sequela of chronic lymphedema: Clinical spectrum, management challenges, and outcomes

The best of 2025 - peripheral and splanchnic aneurysms and mesenteric vascular disease

Hosts:
John Culhane (@JohnCulhaneMD)
 
Follow us @audiblebleeding, @JVS-CIT
Learn more about us at https://www.audiblebleeding.com/about-1/ and provide us with your feedback with our listener survey.
 
*Gore is a financial sponsor of this podcast, which has been independently developed by the presenters and does not constitute medical advice from Gore. Always consult the Instructions for Use (IFU) prior to using any medical device.

CORE RESOURCES:
Rutherford's Vascular and Endovascular Therapy 10th Edition, Chapters 88, 89, 91, and 94

Atlas of Vascular Surgery and Endovascular Therapy 2nd Edition, Chapter 9

ADDITIONAL RESOURCES:
Audible Bleeding Episodes
Holding Pressure - Carotid Endarterectomy: https://www.audiblebleeding.com/2024/02/27/holding-pressure-carotid-endarterectomy/

Holding Pressure Case Prep - Endovascular Basics: https://www.audiblebleeding.com/2023/04/23/holding-pressure-case-prep-endovascular-basics/

Videos
TCAR Technical Video: https://jnis.bmj.com/content/14/8/842

Articles
Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovascular disease:  https://www.jvascsurg.org/article/S0741-5214%2821%2900893-4/fulltext

Technical aspects of transcarotid artery revascularization using the ENROUTE transcarotid neuroprotection and stent system: https://www.jvascsurg.org/action/showPdf?pii=S0741-5214%2816%2931862-6

Referenced Studies
ROADSTER-1

https://pubmed.ncbi.nlm.nih.gov/30611582/

ROADSTER-2

https://pubmed.ncbi.nlm.nih.gov/32811386/

https://pubmed.ncbi.nlm.nih.gov/35381327/

TCAR Surveillance Project

https://jamanetwork.com/journals/jama/fullarticle/2757579?utm_source=openevidence&utm_medium=referral

https://pubmed.ncbi.nlm.nih.gov/36172943/

 
OUTLINE:
 
CAROTID ARTERY DISEASE
1. Pathophysiology/etiology
Carotid artery disease is primarily driven by atherosclerotic plaque deposition. 

Risk factors: hypertension, hyperlipidemia, diabetes, smoking, and advanced age.

Nonatherosclerotic etiologies: fibromuscular dysplasia, carotid dissection, vasculitic disease, carotid webs, and trauma.

When the endothelium is damaged, monocytes migrate to the site and differentiate into macrophages that take up oxidized LDL particles to become foam cells. Meanwhile, an inflammatory response occurs where activated platelets release thromboxane A2, platelet derived growth factor, and inflammatory cytokines that promote further platelet aggregation and vascular inflammation. Smooth muscle cells migrate and proliferate, forming the structural framework of the atheroma. 

Within the lesion, necrotic debris and lipid accumulate, creating a vulnerable plaque. Plaque rupture exposes this material to the bloodstream, serving as a nidus for thrombus formation which can lead to ischemic events.

Carotid bifurcation is particularly prone to plaque formation due to turbulent blood flow. Embolization of plaque from this area can result in TIA or ischemic stroke. 

2. Presentation
Patients are often asymptomatic and stenosis is incidentally found on imaging. 

Symptomatic patients present with neurologic symptoms including unilateral motor and sensory loss, aphasia (difficulty finding words), dysarthria (difficulty speaking), amaurosis fugax (temporary monocular vision loss due to embolus to the ophthalmic artery), transient ischemic attacks

Physical exam findings may be notable for auscultation of a carotid bruit. Patients may also have evidence of retinal artery embolization on fundoscopic examination (Hollenhorst plaque) or asymptomatic cerebral infarction. 

3. Diagnosis
USPTF recommends against screening for asymptomatic carotid artery stenosis. 

In patients with no risk factors, SVS recommends against screening for asymptomatic carotid artery stenosis. However, they do recommend screening for asymptomatic clinically significant carotid bifurcation in certain groups of patients with multiple risk factors. 

These risk factors include patients with clinically significant peripheral vascular disease, patients 65 and older with history of CAD, smoking, hypercholesterolemia, and patients prior to coronary artery bypass. 

Relevant findings on physical exam or imaging findings may warrant screening, but screening is not recommended for the presence of neck bruit alone without other risk factors, as this finding has a low sensitivity and specificity for detecting clinically significant carotid artery stenosis. 

Carotid duplex ultrasound: first-line imaging modality for both screening and initial evaluation of stenosis, noninvasive, low-cost

CTA: rapid, high-resolution, three-dimensional imaging of vascular anatomy, risk of contrast and radiation exposure

MRA: high-quality, three-dimensional imaging without radiation or contrast, expensive with longer acquisition time, can overestimate stenosis in severe disease

DSA/angiography: gold standard, expensive, invasive, not generally recommended for routine diagnostic evaluation or screening

4. Classification
Carotid artery stenosis is classified by degree of luminal narrowing.

NASCET method: standard in current practice. Compares the minimal residual lumen at the point of greatest stenosis to the diameter of the normal distal internal carotid artery. 

Classification of stenosis:
Mild: Moderate: 50-69% narrowing

Severe: ≥70% narrowing


 
TRANSCAROTID ARTERY REVASCULARIZATION (TCAR)
5. Relevant Trials
ROADSTER-1 trial: prospective, multicenter, single-arm study evaluating TCAR with dynamic flow reversal in patients at high risk for carotid endarterectomy (CEA), including both symptomatic (≥50% stenosis) and asymptomatic (≥80% stenosis) patients. 
30-day stroke rate of 1.4% and a combined stroke/death/MI rate of 3.5%, with technical success in 99% of cases

At 1 year, the ipsilateral stroke rate was 0.6%, indicating excellent durability in a high-risk population

Limitations: highly controlled environment with a select group of experienced operators, which raised concerns about the generalizability, especially among physicians new to TCAR. Additionally, ROADSTER-1 was a single-arm study without a comparison group.


ROADSTER-2: prospective, multicenter, post-approval registry format. Addressed limitations of ROADSTER-1 by enrolling a larger and more diverse group of operators, the majority of whom were TCAR-naïve. 
The per-protocol population had a 30-day stroke rate of 0.6% and a combined stroke/death rate of 0.6%, with technical success in 99.7% of cases. These results confirmed the low perioperative stroke and death rates seen in ROADSTER-1, even with less experienced operators. 


TCAR Surveillance Project: ongoing study that provides real-world, comparative data using the VQI registry. 
In propensity-matched analyses, TCAR had similar in-hospital stroke/death rates to CEA (1.6% vs 1.6%) and significantly lower rates than transfemoral carotid artery stenting (TF-CAS, 2.9%). 

TCAR was also associated with significantly lower cranial nerve injury and myocardial infarction rates compared to CEA (0.7 vs 2.4%, and 0.5 vs 0.9%, respectively). 

At 1 year, stroke/death rates remained similar between TCAR and CEA (5.1-6.4% vs 5.2-6.6%, respectively), but TCAR outperformed TF-CAS (5.1-6.4% vs 9.6-9.7%).


 
6. Indications for Surgery
All patients with carotid artery stenosis benefit from best medical therapy (BMT): antiplatelet, high-intensity statin, aggressive risk factor control, and lifestyle modification. 

Asymptomatic patients: ≥70% stenosis, provided the anticipated perioperative risk for stroke, MI, or death is Symptomatic patients: >50% stenosis, benefit of revascularization increases with higher degrees of stenosis. 
Carotid intervention for symptomatic patients should be performed 2-14 days after stroke. 


TCAR anatomic criteria:
Internal carotid artery diameter 4-9mm

Clavicle-carotid bifurcation distance ≥ 5cm

Common carotid artery (CCA) diameter ≥ 6mm

No or mild puncture site plaque


TCAR may be more favorable than CEA in patients who have a high lesion at or above C2 vertebral level, high carotid bifurcation, "hostile neck" (restenosis post-CEA, cervical spine immobility, history of neck irradiation or radical neck dissection)

Contraindications: 100% occlusion, or patients with severe comorbidities or life expectancy 3, unsuitable anatomy or an inability to tolerate flow reversal

 
7. Surgery
Preop
DAPT at least 3 days and statin for 5 days to reduce periprocedural risk of stroke and mortality.

Anesthesia: general anesthesia or MAC

Positioning: supine position with the head extended and turned to the contralateral side. The neck and contralateral groin are prepped and draped in sterile fashion. 


Steps to the procedure and relevant anatomy

Common carotid artery exposure
Identify the triangle created by the sternal and clavicular heads of the sternocleidomastoid muscle (SCM) and the superior edge of the clavicle. 

Create a 2- to 4-cm longitudinal or transverse incision between the two heads. 

Electrocautery is used to divide through the subcutaneous tissue and platysma. 

The SCM is retracted laterally to access the carotid sheath. 

The carotid sheath contains three critical structures. From medial to lateral we have the common carotid artery, vagus nerve, and internal jugular vein. 

The internal jugular vein is dissected and retracted. 

A branch off of the internal jugular vein that we commonly encounter is the facial vein. This can be safely ligated when encountered. 

In most patients, the vagus nerve lies lateral and posterior to the common carotid artery and care should be taken to avoid injury to it, especially in the later steps when we get to clamping the artery. 

Other critical structures: 
Hypoglossal nerve: crosses the carotid artery transversely approximately 2-3 cm above the carotid bifurcation

Ansa cervicalis: encountered in the carotid sheath as it branches from the hypoglossal nerve as it crosses the internal carotid artery

Carotid body: at the base of the carotid bifurcation

Marginal mandibular branch of the facial nerve: encountered at higher incisions, though this is not as common as with carotid endarterectomies


Once the common carotid artery is dissected and exposed, a vessel loop or umbilical tape is placed to facilitate manipulation of the vessel during carotid artery access. 

A purse string or U-stitch 5-0 polyproline suture is placed on the common carotid for the closure of the arterial puncture site at the end of the procedure. 

 
Femoral vein access
Femoral triangle anatomy:
Borders
Superior: inguinal ligament

Lateral: medial border of the sartorius muscle

Medial: lateral border of the adductor longus muscle


Contents
Lateral to medial: femoral nerve, femoral artery, femoral vein, empty space/femoral canal, and lymphatics

Mnemonic - NAVEL: nerve, artery, vein, empty space, lymphatics



Using ultrasound guidance, the femoral vein contralateral to the common carotid artery we just exposed is visualized. 

The common femoral vein is typically accessed 1-2 cm below the inguinal ligament and is around 2-4 cm deep to the skin in most adults. We access the vein with a micropuncture system via Seldinger technique. 

The TCAR venous return sheath is advanced over a 0.035-inch guidewire. Blood is aspirated from the flow line and the sheath is flushed with heparinized saline to ensure proper access. 

Secure the venous return sheath with suture. 

The contralateral femoral vein is accessed to facilitate optimal circuit setup and minimize interference with arterial access and other steps. 

 
Common carotid artery access and sheath placement
Heparin should be given prior to obtaining arterial access. An activated clotting time, also known as ACT, between 250-300 should be achieved. 

Obtain micropuncture access of the common carotid at the site where we previously placed the suture. A 21-gauge micropuncture needle is slowly advanced into the anterior wall of the common carotid artery and a 0.018-inch micropuncture wire is advanced 3 cm into the common carotid artery. A micropuncture sheath and dilator are advanced 2-3 cm into the common carotid. 

After removal of the dilator and micropuncture wire, brisk and pulsatile backbleeding confirms correct positioning. 

Angiogram is obtained to delineate the carotid bifurcation and where the lesion is located. 

A 0.035-inch ENROUTE J wire is positioned in the CCA, the micropuncture sheath is removed, and the arterial sheath and dilator are inserted (stop short technique). 

The arterial access sheath is advanced to the 2.5-cm marker, predetermined by the sheath stopper. 

The sheath position should be checked using angiography in two projections after removal of the dilator to ensure the sheath tip is placed coaxially within the common carotid. 

Secure the sheath to the patient at 3 points using 2-0 silk stitches. The side ports are burped and a control run confirms no evidence of dissection or vessel injury. 

 
Initiation of dynamic flow reversal
The flow controller is connected to the arterial access sheath. The column should be held upward and arterial blood should fill the column. 

Once it fills to the line on the controller, connect the system to the venous return sheath. You have now established an extracorporeal AV shunt. 

The integrity of the circuit is verified by flushing the venous sheath with hep saline and confirming rapid blood flow through the circuit. 

Perform a TCAR time out, confirming systolic blood pressure 140–160 mmHg, heart rate >70 bpm, and ACT >250 seconds to optimize cerebral perfusion and minimize thrombotic risk.

Clamp the carotid artery just proximal to the arterial sheath to establish active flow reversal. 

Flow controller settings:
Low setting

High setting

Flow-stop button: allows for temporary cessation of flow (used when we inject contrast). 


Confirm flow reversal via two different ways: 

The first way is to stop flow to the venous return sheath with the stopcock, clearing the line with hep saline injection, and then opening the stopcock and seeing the blood returning to the controller in a reverse fashion.

The second way is to perform an angiogram with a small amount of contrast injection while holding the flow-stop button. Using the angio we want to make sure that contrast is flowing retrograde in the cervical ICA thereby confirming flow reversal. 

 
Carotid artery stenting, balloon angioplasty, and completion angiogram
At this point, a standard carotid angioplasty and stenting procedure is performed.

ENROUTE transcarotid Neuroprotection System device: 
inner diameter of 8F and an outer diameter of 10F

Has its own carotid artery stent system but is also compatible with all FDA-approved carotid stents. 


Final angiogram is performed to confirm stent position, vessel patency, and absence of complications including vasospasm at the distal end of the stent and filling defects from protrusion of atheromatous material through the stent 

 
Cessation of flow reversal and sheath removal
Allow the flow reversal to run for a few minutes after the final balloon angioplasty to clear any debris. 

Antegrade flow is restored by releasing the carotid clamp and closing the stopcocks on the neuroprotection system. 

The patient is auto-transfused the blood from the flow line back to the venous system. 

As the arterial access system is removed and the puncture site is closed with the U-stitch. 

IV protamine is administered to reverse the heparin.

Standard closure is performed at the incision site. Meanwhile, hemostasis is achieved after removal of the femoral vein sheath with brief manual compression. 




Postop care/complications
Postop care
All patients after a TCAR should be monitored in the ICU setting for 24 hours, as an embolic stroke, hypotension with or without bradycardia, or hypertension can occur. 
Should a TIA or stroke be observed, a carotid duplex scan and CT angiogram should be immediately obtained to assess the stent site and the presence of an embolic or thrombotic filling defect, dissection, or occlusion. 


Dual antiplatelet therapy: continue for 45 days to 12 months

Aspirin and statin therapy: continued indefinitely

Surveillance duplex imaging: 4 weeks, 6 months, and 12 months, and annually thereafter.


Postop complications
Hematoma

Stroke

Myocardial infarction

Cerebral hyperperfusion syndrome
Sudden and excessive increase in cerebral blood flow to previously hypoperfused brain tissue is met with vasculature that cannot constrict appropriately from chronic vasodilation

Leads to breakthrough hyperperfusion. This results in cerebral edema, intracerebral hemorrhage, and neurological symptoms. 


Cranial nerve injury
Hypoglossal nerve (CN XII) injury: ipsilateral tongue deviation. It is the most commonly injured cranial nerve. 

Vagus nerve (CN X) injury: hoarseness and possible vocal cord paralysis. 

Glossopharyngeal nerve (CN IX) injury: soft palate dysfunction. 

Recurrent laryngeal nerve injury: voice hoarseness and inability to cough as it innervates all of the voice box muscles except for the cricothyroid muscle

Marginal mandibular nerve injury: ipsilateral lip droop, injury is rare in TCAR. 


Stent restenosis

Pseudoaneurysm

Access site infection

Welcome back to the Audible Bleeding series: Landmark Papers in Vascular Surgery. In this episode, co-hosts John and Dr. Jesse Columbo are joined by our guest, Dr. Caitlin Hicks, to discuss one of the most studied—and most debated—topics in vascular surgery: asymptomatic carotid stenosis.
 
In this episode, we'll trace that evolution through three pivotal trials: ACAS and ACST-1, which established carotid endarterectomy as the standard of care; and the newly published CREST-2, which challenges us to reconsider everything we thought we knew. Along the way, we'll explore how advances in statin therapy, blood pressure control, and antiplatelet agents have fundamentally changed the natural history of this disease—and what that means for our patients today."
 
Links to Landmark Papers: 
(ACAS) Endarterectomy for Asymptomatic Carotid Artery Stenosis

 
(ACST-1) 10-year stroke prevention after successful carotid endarterectomy for asymptomatic stenosis: a multicentre randomised trial 

 
(CREST-2) Medical Management and Revascularization for Asymptomatic Carotid Stenosis 

 
Guests:
Dr. Caitlin Hicks, MD (@CaitlinWHicks); Associate Fellowship Program Director, Vascular Surgery & Endovascular Therapy at Johns Hopkins and Director of Research
 
Hosts:
John Culhane, MD (@JohnCulhaneMD); General Surgery Resident, Abrazo Health
Dr. Jesse Columbo, MD; Assistant Professor of The Dartmouth Institute, Geisel School of Medicine, Dartmouth



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Learn more about us at https://www.audiblebleeding.com/about-1/ and provide us with your feedback with our listener survey.
*Gore is a financial sponsor of this podcast, which has been independently developed by the presenters and does not constitute medical advice from Gore. Always consult the Instructions for Use (IFU) prior to using any medical device.