This transcript has been edited for clarity.
Kaniksha Desai, MD: Welcome back to the Thyroid Stimulating Podcast. This podcast was created in partnership with the American Thyroid Association to discuss up-to-date diagnosis and management of a wide array of thyroid diseases.
I’m your host, Dr Kaniksha Desai, and today we’re diving into a newer topic that many endocrinologists and primary care clinicians are starting to hear more about, ask more questions about, and encounter more frequently, which is thyroid artery embolization, or TAE.
For years, our management options for symptomatic benign thyroid disease have largely lived at the extremes, observation on one end and surgery or radioactive iodine on the other. More recently, thermal ablation techniques, such as RFA and microwave and laser ablation, have expanded that middle ground.
Despite these advances, we still see many patients who are not ideal surgical candidates who want to avoid general anesthesia or who fall into these gray zones, where none of our traditional options are a perfect fit for them. That’s where TAE enters the conversation.
In today’s episode, it’s going to be designed specifically for clinicians who are ordering, referring, and counseling patients. What we’ll focus on is the practical questions that come up in real-world care. Who is eligible for TAE and who is not? How does it compare with surgery, radioactive iodine, or thermal ablation? What should we be telling our patients about expectations, safety, and follow-up after TAE procedures?
To guide our conversation, we’re honored to be joined by Dr Juan Camacho, a board-certified vascular interventional radiologist with deep expertise in complex image-guided procedures, and a pioneer voice in the emerging field of TAE. Dr Camacho completed an advanced fellowship training in vascular and interventional radiology and body imaging and currently practices at Radiology Associates of Florida at Sarasota Memorial Healthcare System in Florida.
He also served as clinical associate professor at Florida State University College of Medicine, where he’s led translational research and helped develop clinical applications of percutaneous and endovascular thyroid intervention that are now being adopted more broadly and used by interventionalists worldwide.
Dr Camacho brings a unique, valuable perspective, not only as a proceduralist but as someone deeply engaged in defining patient selection, outcomes, and how TAE can be thoughtfully integrated into a multidisciplinary approach for thyroid care alongside endocrinologists as well as referring clinicians.
Whether you have a patient that’s asking about TAE or you’re just starting to see it mentioned at conferences or in the literature, today’s episode will give you a clear, practical framework for understanding what TAE is, when to consider it, and how it fits into modern thyroid management.
Thank you for joining us, Dr Camacho.
Juan C. Camacho, MD: Thank you very much for the invitation. I’ve been looking for spaces to actually share the experiences and be able to educate our peers. This is a great platform and I really appreciate it.
Desai: For clinicians who are new to TAE, how do you explain what TAE is and a little bit about the history of the procedure and how it came about?
Camacho: TAE, contrary to what many people think, it’s actually been around for many years. The first case report was in 1994. It came out of Poland, and it was about a patient that was in thyrotoxicosis, they ran out of medical options, and they thought that treating noninvasively could have potentially been an alternative. That was the first case report back in 1994.
The way we think about it, or the way I explain it to my colleagues, is that embolization in general implies blocking off the blood vessels to an organ. What we’re doing with TAE is blocking off the blood supply to the thyroid in order to generate a controlled infarct. The materials that we use, even though they’re permanent, they’re technically resorbable. You create an ischemia that’s not permanent, it’s transitory, and that whole process lasts around a few weeks for the vessel to get recanalized.
That’s probably the reason why the tissue doesn’t die off completely. In summary, it’s just a technique to block off the blood supply to the thyroid in order to induce a controlled infarct that will ultimately end in decreasing the gland volume and improving the thyroid function in some scenarios.
Desai: Who does this procedure? Is it mainly interventional radiologists or is this something that can be done by endocrinologists or surgeons?
Camacho: This is an interventional radiology procedure. This is an endovascular intervention that requires deep expertise in management of catheterization, catheters and wires, and deep expertise in the anatomy of the head and neck and also of the collaterals that the head and neck has. Definitely it’s a procedure that needs to be performed by an expert. The experts in vascular and endovascular procedures are definitely interventional radiologists.
Desai: Is it an outpatient procedure or does it require hospitalization?
Camacho: There’s been history around it, right? At the beginning, when I first got involved doing the procedures and we were gaining experience, we were actually admitting our patients under telemetry. We were cautious about the possibility of our patients developing symptomatic hyperthyroidism. Over the course of our experience and as we started doing cases, we figured out that that was not necessary anymore.
We do these procedures completely outpatient. Our patients are in the hospital probably around 2 or 3 hours, and then they go home on medications. There’s obviously a protocol that we follow to prevent manifestations of hyperthyroidism in the post-procedural period.
Desai: Can you talk a little bit more about what the procedure entails at a higher level, so if you’re explaining this to your patient as a clinician? I know you talked about how we’re going to basically block an artery to cause an infarct, and if the organ doesn’t have a blood flow, then it should — in theory — shrink. It’s a couple hours in the hospital, you come in, and then you just do the procedure?
Camacho: This is how I explain it to our patients. I tell them this is a procedure in which we’re going to use a very small catheter to access the inferior thyroid artery. Normally, the blood supply to the thyroid is comprised of four vessels, two superior thyroid arteries on each side and two inferior thyroid arteries on each side.
Now, the superior thyroid artery originates in the carotid artery, which is the artery that goes into your brain. The inferior thyroid artery originates in the subclavian artery, which is artery that goes into your hand. The way we approach it is we put a tiny little catheter to select either the inferior thyroid artery or the superior thyroid artery according to your particular condition.
Figure 1. Large toxic thyroid nodule measuring 115 mL, 14.6 mL on follow up, corresponding to 87.3% volume reduction rate (VRR). Single embolization of the left inferior thyroid artery. Left: Pre-procedural CT. Right: Post-procedural CT.
This is where things start becoming a little bit more complicated, because not every patient requires embolization of the four vessels. We only promote embolization of the four vessels when you are suspecting a diffuse process of the gland, ie, Graves disease.
Most processes, when it comes to goiters or nodules, and actually in our series, 45% of the procedures were unilateral, because you’re targeting a specific condition. Autonomously functioning nodules can be unilateral, or you have a dominant nodule that is the one that is causing disturbances that is unilateral, or sometimes you have unilateral nodules or goiters. There’s no need to treat the contralateral side. You just treat the one that is causing symptoms.
Now, if you have a very large cervical goiter or goiter that is extending into the mediastinum that is bilateral, that is multinodular, that is causing compression of the airway or the esophagus, then you will treat bilaterally, and at that point you will recommend treating the four vessels.
Now, that is with the traditional technique. With the technique that I described, which is pressure-enabled TAE, where we use a special catheter that allows us to leverage the intrathyroidal collaterals. What that means is that I do not need to access the carotid circulation. I did not need to access the superior thyroid artery. We just access the inferior thyroid arteries, we park the catheter as distal as possible, and we can invert the flow of blood inside the thyroid itself to leverage these intrathyroidal collaterals, and we’re able to completely embolize a load of the thyroid by only embolizing one vessel.
That’s why I was saying earlier that that’s where things get a little messy and a little bit complicated. When I explain it to my patients, I said like, “Listen. There’s two vessels on top, two vessels below. The way I do things is I only intervene in the artery that originates in the subclavian artery, which is the inferior thyroid artery. That’s how we perform the procedure.”
I do want to make a point here that you can only leverage the intrathyroidal collaterals — and this is what we’ve published in our experience — when you have two situations. Number one, when patients have not undergone RFA before the procedure. The reason for that is because radiofrequency burns the small capillaries and severs the collaterals inside the gland.
Figure 2. Diffuse cervical goiter measuring 468 mL, 95 mL on follow up, corresponding to 80.8 % VRR. Single embolization of the bilateral inferior thyroid arteries. Left: Pre-procedural CT. Right: Post-procedural CT.
Number two, you can only do this in multinodular goiters, because there is a diffuse hyperplastic process that is happening throughout the gland. When you have a dominant nodule, then it could be a hit or miss. A hit or miss means that there’s usually one vessel that dominates over the other one.
You can get supply either from the superior thyroid artery or from the inferior thyroid artery. The way you determine that is in the preprocedural phase when you do a CT scan of the neck, and then you are able to determine which vessels are enlarged, and that’s how you determine your targets.
I thought that it was important to make clarity of the different techniques. Traditional TAE implies embolizing three out of the four or four out of the four arteries according to the process that you have. Pressure-enabled TAE implies embolizing only one artery, okay, only the inferior heart artery and either the right side or the left side. If you have a diffuse process, then you do both inferior thyroid arteries. Now, if you only have a solitary nodule, you have to evaluate which artery is supplying that particular nodule, because it could be either superior thyroid artery or the inferior thyroid artery.
Desai: You can obviously treat benign thyroid nodules. You can treat a goiter, which is bilateral or unilateral. You can treat a toxic adenomatous process unilaterally or bilaterally. Graves we’re going to treat bilaterally. Do we ever treat thyroid cancer?
Camacho: Funny enough, the way I started initially in this space is I used to work in a cancer center in New York City. Some of our patients, unfortunately, because it was a large referral center, we used to receive a fair amount of consultations with aggressive forms of cancer that have limited options, essentially anaplastic thyroid cancer. With anaplastic, some patients do not get surgery or they’re too sick, or they have too much compression, or they have refractory hemoptysis or stuff like that, that is typical of these very aggressive and advanced cancer.
In that particular scenario, you can manage palliatively the symptoms with TAE just to decrease the size and control the bleeding complications. Obviously, it’s not something that we advertise as a primary therapy for cancer.
I do have a case that’s anecdotal. It’s a case that I presented in our national meeting, and I hope to get it published soon. I anecdotally obtained complete pathologic necrosis of a patient with papillary thyroid cancer, following TAE. It was a planned TAE in the pre-surgical setting, because it was a very large lesion in a patient with many comorbidities, which is another indication.
We did the embolization first with the objective of taking out the cancer safely 48 hours after the fact. At 48 hours, when there was the explant of the thyroid gland, there was complete pathologic necrosis of the lesion. I guess that what I’m saying is, in the future, if a rigorous study is performed, then potentially TAE can be considered as a therapeutic alternative. But right now, we only use it in palliative settings and that’s how it’s being reported.
Desai: When we’re thinking about treatment options, we’re looking at treatment of the actual conditions such as thyroid function control in Graves’ disease versus more palliative approach. For things like goiter, we’re not going to make the thyroid gland disappear, but we’re going to hopefully improve the compressive symptoms, the tracheal deviation and compression. Those are kind of the two categories to think about, am I reading that correctly?
Camacho: A good way of understanding this procedure is, as you pointed out at the beginning of this conversation, there’s a spectrum of options for these patients, right?
On one side of the spectrum, you have observation. The other side of the spectrum, you have the most aggressive, which will be surgery. In between, you have things like radioactive iodine, which we know that the problems of radioactive iodine are about 50% of patients become hypothyroid long term. The volume reduction rate is probably around 30% when you take a look at the literature, so it’s not that great.
Then you have the percutaneous ablative techniques, and there’s a whole array of those, right? You have radiofrequency, microwave, laser, cryoablation, nanosecond pulsed electric fields ablation, and high-intensity focused ultrasound.
Out of those six, in general, they’re indicated for when your target volume is less than 30 mL if we’re talking about benign disease. If we’re talking about autonomously functioning nodules, your target should be around 15 mL. We know that out of the North American experience and the Korean experiences that the volume reduction rates are not great when you exceed those sizes, and your failures are also higher at one year.
What I tell my patients is that it’s not that it’s not entirely not indicated, it’s just that most likely you’re going to recur within 1 year. Most likely, if that happens, that means that you’re going to require multiple percutaneous ablation sessions.
When you don’t fall within those guidelines, then you have embolization as an alternative. We reserve embolization for hard nodules that are greater than 30 mL and for multinodular goiters that are greater than 50 mL. Actually, it’s the only series, but there was a paper published at the end of last year that compared radiofrequency ablation (RFA) and TAE head to head in large volume of disease, greater than 50 mL.
The conclusion is that it was not only safer, but TAE was more effective and the failure rates were less, as well as the risk of complications. We know that when patients require more sessions and more treatments, then the possibility of getting complications such as nodule ruptures is higher. That’s where I put it in the paradigm.
Desai: Just to clarify for our listeners, this is a one-time only procedure, right?
Camacho: It’s a one-time only procedure. I so far haven’t had the need of retreating any of my patients. Can you retreat patients safely? I do think you can.
We’ve done it in other organs, so embolization and internal ischemia is not a novel concept. We use it in other organs, like when people have uterine fibroids, we use it for fibroid embolization. When people have lower urinary tract symptoms because of benign prostatic hyperplasia, we use it for enlarged prostates.
We use it for the treatment of primary cancers in the liver, for example. It’s not a novel concept, and we know that those patients can be retreated safely. I wouldn’t necessarily say that it’s once in a lifetime. In my experience, it’s been once in a lifetime, but that doesn’t necessarily mean that patients cannot be retreated.
I think, more importantly, when you think about the natural history of disease, we know that goiters grow very slowly. Because of that, the probability of them requiring a second treatment throughout their lifetime is going to be low. We know that if they start growing at an accelerated pace, that’s an alarm sign that there’s something else happening.
That’s why I think that it’s probably a one encounter kind of deal is the way to go with TAE.
Desai: When you’re considering your ideal candidate, I know it would be patients who are not necessarily great surgical candidates or patients who are having progressive growth, so their observation isn’t great. Then you talked about how the volume has to be greater than things such as RFA or thermal ablation. Who would you consider your ideal candidate?
Camacho: It depends. As you point out, it depends on the indication. I think that in terms of diffuse processes, Graves’ patients that haven’t had the desired effect on hypothyroid drugs after two years, I think that those are good candidates. We know that, after two years, the risk of bad things happening with hypothyroid medications, and all of these bad side effects are higher. That is one population.
The other population is autonomously functioning nodules exceeding 15 mL because we know that the likelihood of them being resolved by a single session RFA is going to be very low, number one. Number two, you can just put it again in the balance against radioactive iodine and you know that there’s the risk of hyperthyroidism as well as that the volume reduction rate is not going to be that great.
Number three, if you have a solitary nodule that exceeds 30 mL. Again, you can have a direct conversation with a patient and tell them, hey, listen, your failure rate is going to be higher. You may require multiple ablation sessions, and if the patient is willing to go through multiple ablation sessions, I don’t think that there’s anything wrong about offering them an ablation, but this is an alternative in case the patient just wants to get one procedure and get it over with. This is probably an alternative in that scenario.
The multinodular goiters that exceed 50 mL, or more importantly, that will require aggressive surgeries to get them resected. For example, those that are going into the thoracic inlet or with extension into the mediastinum or extending into the posterior mediastinum in which those patients will require a manubriotomy, a sternotomy, or a thoracotomy in order to get these benign procedures out. I think that’s probably the best indication that this is really a good alternative.
Figure 3. Large mediastinal goiter measuring 670 mL, 112 mL on follow up, corresponding to 84.3% VRR. Single embolization of the right inferior thyroid artery. Left: Pre-procedural CT. Right: Post-procedural CT.
Finally, the last indication is the presurgical indication. It’s not that when patients undergo surgery, they’re going to bleed out. We know that is not true. However, when you are performing minimally invasive thyroid surgery, for example, transoral thyroidectomy or transaxillary thyroidectomies, the main reason why surgeons convert to an open surgery is because of bleeding in the field.
They cannot identify recurrent laryngeal nerves, or they cannot identify the parathyroids. Essentially, it’s because the gland is so vascular that when you’re moving the goiter around, there’s just bleeding from the goiter itself. It’s not uncontrolled bleeding from a necrotic artery or something like that. The goiter just bleeds too much with manipulation. I think that’s a great indication.
There are a couple of papers that were published in the presurgical scenario that demonstrated significant decreases in blood loss and decreased complications in the postsurgical period, like neck hematomas and whatnot.
Just to clarify again, the scenarios are diffuse disease, Graves refractory to conventional therapy; autonomously functional nodules greater than 15 mL; solitary nodules greater than 30 mL; multinodular goiters greater than 50 mL with extension into the thoracic inlet or mediastinum; as well as in the presurgical scenario in those patients in which they have very large glands that are at risk of bleeding, or obese patients, that will benefit from pre-procedural blood flow supply control.
Desai: These are our inclusion criteria. Do we have any exclusion criteria on who would not be a good candidate, even if they met this?
Camacho: Absolutely. Obviously, pregnancy is a big problem because we do this under X-ray guidance. If you cannot have X-rays, such as in pregnancy, you cannot have the procedure. The other one that is very important is, if you have any renal impairment, we have to administer an iron IV contrast in order to see the blood vessels and to see the anatomy.
Obviously, if you have malignancies. All of our patients have to have Bethesda II or Bethesda III category cytology. If they have Bethesda III, at least in our protocol, we’re mandating molecular testing to verify that these are indeed low probability or low malignancy risk processes. I think those are the main contraindications.
Desai: A significant portion of patients could have this option done.
Camacho: Correct. One of the things that we talked about earlier — that is not necessarily a contraindication, but is just that something the interventionalist should be aware of — is that you need to know if the patient has undergone a prior RFA or microwave ablation or any other thyroid procedure.
If you’re performing pressure-enabled delivery and you’re trying to leverage those intrathyroidal collaterals, you’re not going to be able to do it, number one. Number two, when you’re inducing necrosis by performing percutaneous ablation, the thyroid is going to obtain blood supply from other sources, from other vessels in the vicinity. You need to be aware of that to make sure that you can map out adequately those collateral vessels during your angiogram.
It’s not a contraindication. I will just say it’s potentially a relative contraindication or just a word of caution for the interventionalists to be aware of. Hey, this patient has had prior procedures in the head and neck.
Desai: You go through the hand, right? Are there any physical contraindications? What about a history of having a stroke, because there may be an increased risk of stroke, theoretically, right?
Camacho: There are two things. The procedure itself carries a risk of stroke secondary to non-target embolization, and that’s a completely different animal. You are right in the sense that radial access poses a risk of stroke; however, this has only been reported in the cardiology literature, and I think it’s probably because of the nature of the work.
The bulk of their work is not elective, right? It’s patients that are undergoing myocardial infarction, where they need an emergent angiogram somehow. They don’t necessarily take the precautions that we in interventional radiology take.
Those precautions are that, when we’re doing radial artery access, we always measure the radial artery. If we have an artery under 1.6 mm, in theory, you should avoid radial artery access, because the rates of occlusion are going to be much higher.
Number two, we always do, in interventional radiology, a modified Barbeau test, which is we put a pulse oximeter on the index of the hand that we’re going to be accessing. We compress both the radial and ulnar arteries until we lose the pulse ox plethysmography, and then we release the compression on the ulnar.
If you have a patent palmar arch, you should have return of the waveform within 2 minutes, and there’s a classification for it, but essentially, if the waveform doesn’t come back after 2 minutes after you release the compression of the ulnar, then that means you’re at a high risk of hand ischemia and therefore you should not access the hand. That’s part of the physical examination that an interventional radiologist would do to determine if you are a candidate to have radial access versus femoral access.
Now, there’s also the possibility of a stroke. A stroke when you’re performing angiography in the head and neck vasculature is a risk. It doesn’t have anything to do with the embolization itself. It’s just because you’re manipulating catheters in the supra-aortic vessels. When you’re doing that, then you’re always going to have the possibility of a small bubble of air migrating north, a small clot migrating north, or while you are manipulating the catheters, then there’s a possibility of you dislodging plaque.
There is a philosophical approach to this, which is my approach in the sense that, if you’re a patient with benign thyroid disease and you really don’t have any other issues except your thyroid issues, and I’m doing an intervention that has a potential risk of stroke, you should try to do everything you can to minimize that risk. Theoretically, when you access the femoral vessels, which is the way we do conventional angiography, if you’re going into the right side of the thyroid, for example, you have to cross the supra-aortic vessels.
In other words, you have to go from the aorta, cross the left subclavian, cross the left carotid, and then go into the right carotid circulation. You’re putting a catheter across all of those vessels, which could potentially impair flow. That doesn’t mean that it’s not safe because it’s absolutely safe, okay?
The possibility of you developing a stroke because of this is minimal, but it’s just a philosophical conception that, if you have a risk factor or something that could potentially increase the risk, then you should avoid it. That’s why I choose radial access.
If you’re doing radial access and you measured the artery correctly, you do your Barbeau test, and you anticoagulate your patients. When we do the procedures, we put the patients on blood thinners throughout the procedure only, not permanently. It’s just throughout the procedure so there’s no clot formation and we can ensure patency of the vessels. Then it is a very safe procedure.
Desai: Can you talk to me about what other complications may occur? I think you alluded that hypothyroidism is not necessarily going to happen?
Camacho: Correct. Let’s talk about the elephant in the room when it comes to TAE, which is, in my opinion, two things: non-target embolization and hypothyroidism and hypoparathyroidism.
To my knowledge, there’s only been one case reported of hypoparathyroidism. It was simply because after doing the embolizations, people were measuring calcium routinely. There was only one patient who developed hypocalcemia, but he was asymptomatic and then resolved, so it wasn’t a permanent hypoparathyroidism.
To my knowledge, there hasn’t been a single case reported of hypothyroidism in primary disease. The only cases that have been reported of hypothyroidism following TAE are when embolizing drop goiters.
A drop goiter is essentially when you have a very large gland, the patient underwent surgery, and some cells remained in the surgical bed. Those cells were hyperplastic, so there’s regrowth of the goiter. I have had a couple of patients that developed drop goiters that were deep into the mediastinum. They were causing compressing symptoms, and in order to remove them, those patients require a manubriotomy, thoracotomy, or sternotomy.
They chose TAE, and both patients actually developed hypothyroidism. I think this is a very particular scenario. It didn’t imply treating the primary gland, it was just treating hyperplastic tissue. Hyperplastic tissue, we know, is very sensitive to ischemia, so it will die completely, and that’s the reason why actually on CT, after you do a TAE, you can see the defects of the nodules completely dead, but the normal parenchyma is actually viable. That’s why you don’t develop hypothyroidism.
The other elephant in the room is non-target embolization. I feel that non-target embolization is rare. It’s extremely rare. If we go by the guidelines of the Society of Neurointerventional Radiology, when you’re embolizing structures in the head and neck, they actually have a threshold of up to 10% of ischemic stroke.
Keep in mind that this is all head and neck embolizations, right? Obviously, if you’re operating close to the base of the skull, then your risk of non-target embolization to the brain is going to be higher, versus if you’re gonna operate closer to the clavicle, in which the risk is going to be far lower.
In the literature, at least in what I’ve been able to gather, there have only been six strokes reported and only one death. Theoretically, they attribute it to the stroke itself following a hemorrhagic transformation, which is something that can happen with a small stroke. These are extremely rare circumstances, I feel, and I think that it is reasonable to quote a risk of about 1%-3% of stroke to a patient.
That’s what I tell my patients. I tell them, listen, non-target embolization is definitely a risk. It’s definitely something that can happen. I do a very judicious mapping of the inferior thyroid artery and of its collaterals. I want to make sure that there is no communication with the vertebral artery, that we don’t have any reflux, and actually, I have a very high threshold to abort. Again, I’m doing this for a benign process. It’s not like I’m treating a cancer or someone that is dying or that requires an emergency embolization because they’re bleeding to death.
This is something that is a benign process, so I think it’s definitely our responsibility to make sure that we do everything we can to avoid these potential complications. The techniques have now been polished significantly to the point that we know exactly where to part the catheters and how deep into the gland we need to go. I think that all of these things matter when it comes to making a stroke a minimal risk.
Desai: Dr Camacho, for Graves disease, do we get hypothyroidism following treatment with TAE?
Camacho: In my experience, we have not seen any cases of hypothyroidism. To my knowledge, it has not been reported in the literature. There’s actually good pathologic evidence of what happens after Graves disease, and we’ve seen glandular fibrosis with decrease of the hyperplasia as well as decrease in blood of endothelial growth factors and other things that are implied in Graves physiopathology. That tells you that the ischemia does help.
More importantly, what we see is that about 70% of the patients will normalize their thyroid function at six months, and those patients who do not respond to TAE do see a decrease in the dosages of the antithyroid medications that they’re on. That also applied for the benign or the other causes of hyperthyroidism.
Let’s say that you have a diffuse autonomously functioning goiter or something like that. Sometimes those patients do not respond to the therapy. We know that around 80% of the patients with hyperthyroidism will respond, but that remaining 20% will decrease the amount of medications that they require.
Desai: In this aspect, this treatment is a little bit better than surgery, which is 100% hypothyroidism, and even radioactive iodine, which has a significantly high rate of hypothyroidism as well. This is a little flipped, as far as hypothyroidism is concerned.
Camacho: Correct. As I said, there are no reports to my knowledge of hypothyroidism, but more importantly, even if you fail, you may gain a good clinical outcome, which is decreasing the dose of the medications that you have to get your patients on because of the primary process they have.
Desai: I think you mentioned earlier that you can use it perioperatively, but is this a contraindication to surgery later? Say you didn’t get off the antithyroid medicines that you really wanted to get off, so now you want to go to surgery. Is that a contraindication?
Camacho: Not really. The other side of the experience is that the surgeons that I’ve interacted with, in which we do a staged TAE followed by resection, they’ve told me that this is the best resection that they’ve ever done.
Essentially, they’re manipulating the goiter and it doesn’t bleed. It’s like doing bloodless surgery. They really appreciate that because they can identify the parathyroids easily and they can also identify the recurrent laryngeal nerve, especially when these goiters are very big where you have to manipulate them quite a bit to get them out.
Desai: It doesn’t cause the same fibrosis that radioactive iodine would cause?
Camacho: Maybe I’m being misinterpreted. When we do presurgical embolization, we do it 48-72 hours after a procedure so there’s not enough time for this to settle. I haven’t had yet the first case where you do, let’s say an embolization because you have a goiter going into the mediastinum and you just want to shrink it, downstage it, and then take it out at a future encounter. I have not encountered that scenario yet.
Desai: Are there any other side effects or complications that you counsel your patients on?
Camacho: More than side effects, it’s what I expect. This is something that we see in interventional radiology all the time, again, because we do embolization throughout the body of multiple different pathologies. We frequently see something that is called post-embolization syndrome. We put it under this generic umbrella, and it’s essentially a consequence of when you generate ischemia, you generate inflammation. There’s release of inflammatory factors into the bloodstream, which can essentially generate weakness, fatigue, and malaise, kind of a flu-like process.
Some patients develop low-grade fevers. Some patients develop mild pain or discomfort. Some patients can have non-target embolizations to very small tracheoesophageal branches so they can have some mild discomfort when they swallow or a little bit of a sore throat. Those are things that I expect that can happen.
Basically, we treat them medically. We give the patients anti-inflammatories, a small course of steroids to control the inflammation, and we also, very importantly, beta-block all of our patients because every single one of our patients will develop most likely subclinical hyperthyroidism or they can become symptomatic.
We start with a small dose of propranolol, about 20 mg a day, and we titrate it. We start 7 days prior to the procedure, and then we continue it one month after the procedure just to prevent arrhythmias and also to prevent peripheral conversion of T4 into T3 with propranolol.
Desai: Then you’re on your blood thinner that you start beforehand?
Camacho: You’re not permanently on the blood thinner.
Desai: You do it for a month.
Camacho: No, it’s actually only during the procedure for the hour or so that the procedure lasts.
Desai: Is there anything else medication-wise that you have to take in the recovery period? How long are we looking at? A month for the recovery period?
Camacho: Actually, patients recover quite quickly. I used to think that patients were messing with me when some of my patients used to tell me in the recovery area, “Doc, I really feel better.” I was like, “Listen, you’re absolutely crazy. I just did this for you. There’s no way you can tell me that.”
Then I started seeing the pattern, and some of the patients that really have compression, they very rapidly recoup. I think it’s because of a phenomenon that we see in other organs, and it’s that the gland becomes more compliant. As you generate the infarct, it’s like going from something that is rock solid to a balloon full of water. The gland becomes more compliant, so the compression symptoms go away really quickly.
Actually, the volume reduction also happens very quickly. Within 3 months, you have the bulk of the volume reduction. Our mean volume reduction that we reported is about 73%, and we’re talking about large glands. We’re talking about glands above 150 to 200 mL. This is fairly impressive, and it’s even quicker for smaller processes.
I do expect everybody to get some degree of post-embolization syndrome. For that reason, we give them a Medrol dose pack, a short course of steroids. We discharge them with just anti-inflammatory medications. I give them opioids just for rescue, but I can tell you that 95% of the patients do not use the opioids. It’s a very small minority that struggle with pain. Truly, that’s about it.
Then we just manage the symptoms. If some patients develop nausea and vomiting, you can do a prescription for that. If you’re going to take the opioid, then we give them a stool softener. The most important thing is for them to take the beta-blocker for about a month throughout the procedure. Usually, patients are back to being themselves within a period of 7-10 days.
Desai: The recovery’s pretty fast.
Camacho: Yeah.
Desai: When we’re comparing it to surgery, surgery will be like, you have compressive symptoms and they’re gone in like 5 minutes because we take out the thyroid gland. Then you have the radioactive iodine, which we’re looking at maybe years. Then we have the RFA, which is months to a year. This is more on the surgical aspect, just to clarify?
Camacho: I think it’s days to months if you’re going to put it like that. I think that the bulk of the improvement does happen in the first 3 months. I see my patients at 2 weeks following the procedure just to make sure that they’re doing fine.
I used to take labs at 2 weeks, but then I realized that I was wasting my time because I knew exactly what was happening. Every patient presented with lab abnormalities, and they don’t necessarily correlate with any symptoms. I stopped doing that, and now I just follow them at 2 weeks for symptoms.
I check to make sure that they’re not tachycardic, that they’re not feeling fatigue, or that they don’t have any other symptoms related to hypothyroidism or hyperthyroidism. To this day, I haven’t had to prescribe any antithyroid medications like methimazole. I haven’t had the need to prescribe cholestyramine, because somebody is in thyrotoxicosis. As long as you start the beta-blocker ahead of time, I think that it’s very safe to perform the procedure.
Desai: You mentioned labs, so we’re just talking about thyroid function labs, right? A TSH and T4?
Camacho: Correct.
Desai: If you’re not getting them at 2 weeks, do you recommend getting them ever after the procedure, and when do you recommend that?
Camacho: Yes, absolutely. I get them at 3 months and at 6 months. I know at 2 weeks, everybody’s going to be hyperthyroid. With every endocrinologist that I have interacted with, they were freaking out because they were like, this TSH is suppressed and now the T4 is through the roof, what’s going on? I’m like, don’t worry about it. This is completely normal.
It’s what we see in other organs. If you measure ALT and AST after a liver embolization, you’re going to see them in the thousand. It is not something that is completely unexpected. That’s the reason why I stopped doing it and I only obtain labs if the patients are completely symptomatic.
Obviously, I have a baseline prior to the procedure, and then I compare against that at 3 months. We know that it takes about 4-6 weeks for the labs to change, so I think that the 3-month mark is a good measure to compare pre- and post-procedure.
Then I’ll take labs at 6 months with a CT so I can do a CT volumetry. I think that ultrasound severely underestimates the volume of the gland. I can tell you that sometimes I’ve had glands that, by ultrasound, appear to be 50-60 mL. Then I do a CT and I do a very judicious contouring of the gland and a volume segmentation, and the value grows from 50 to 70, 80, 90, or 100 mL.
It’s because it’s hard to measure the gland, especially when they’re going into the mediastinum or into the posterior cervical spine. It’s complicated to address the whole volume. I like to get CTs so I can get a comprehensive measurement. Also, pre-procedure, I get the CT because it allows me to take a look at the vasculature to see if there’s anatomical variance and which are the dominant vessels.
Desai: For our listeners, compared to radioactive iodine or thermal ablation techniques, what is the volume reduction? It seems like this has more volume reduction, but I just wanted to clarify.
Camacho: The average volume reduction reported in the literature when you do conventional TAE, meaning what we discussed about embolizing three out of the four arteries, it’s been reported about 50%-60%.
In pressure-enabled delivery, we achieved the largest volume reduction reported in in the literature with TAE, and our median was 73%.
Desai: Compared to when we’re looking at radioactive iodine?
Camacho: The thing is that they’re not comparable in the sense that you’re treating different populations, but the estimated volume reduction with radioactive iodine is about 30%. The goal that you want to hit with RFA is 50% or more.
It’s different when we’re talking about a gland that is 100 mL and you go ahead and do RFA and you get a 30% or 40% volume reduction. That’s a significant chunk anyway. That’s what I mean that the percentile range, I don’t think, is comparable. We have to think of this as an alternative for a different population.
This is not for every patient that has a thyroid problem. It’s just like a step more within the progression of the treatments that you have. It’s just another tool, and this is for patients who are not eligible for percutaneous techniques and that they’re definitely refusing surgery or for patients that are ineligible for surgery.
Desai: What do you think is the most common misconception about TAE that’s out there?
Camacho: I think that people, probably because of lack of knowledge, will call it experimental. That is my first impression. I think that some other people will label it as a very dangerous procedure, which I don’t think is true.
I think that, in expert hands, the probability of complications is extremely low. Obviously, when you’re not familiar with the technique itself and with the outcomes, then you’re not going to be able to talk about it, and you’re probably going to dismiss it.
I can tell you that 100% of the patients that I see is because they have done their own research. I’m pretty sure that you’re familiar with this. Thyroid patients are probably the most educated patients that you can ever interact with. They’re very good about doing their own research. They want to go to a million different doctors, and some of them are stuck in their ways.
I think that what I want listeners to take out of this is that if you are seeing these patients, you really need to be familiar with all of these different alternatives and you have to build a multidisciplinary network so all of your patients can be informed and the patient can make the decision.
This is not about you or me saying that “I’m an interventional radiologist, I can do this,” or an ENT surgeon saying like, “Oh, you’re crazy. I can do it better because I can take it out.” I think that all of these procedures are perfectly indicated in the right scenario for the right patient, but there needs to be a multidisciplinary conversation.
Ultimately, the patient should make the decision. You should not pressure the patient to go one way or the other, unless it’s something that it’s like absolutely crazy and against regular guidelines. I think that’s important. If there’s a clinical takeaway about this conversation, this has to happen in a multidisciplinary fashion, and you have to educate your patient about all the different alternatives because ultimately if they don’t know and if they don’t trust you, they’re going to go to the next doctor because this is how thyroid patients are.
Desai: That was my hope for this podcast, too, to present a little bit of background about what it is, who the ideal candidate is, and then if your patient comes to you and asks you about the procedure, at least you know some information about how well does it work and what is the recovery going to look so you can counsel the patient and compare it to the traditional methods of surgery or radioactive iodine, or even the newer method of thermal ablation. If you had three takeaway points for our listeners, what would they be?
Camacho: Number one, TAE doesn’t compete with the other available minimally invasive techniques. It’s complementary and it has very precise scenarios.
Number two, I think that in expert hands, it’s not a dangerous procedure. I think it can be done safely if you know what you’re doing and if you’re a judicious interventional radiologist.
Number three, all of these decisions have to be made in a multidisciplinary fashion. You have to put the patient front and center. You have to present the options.
I think this is an option for, as I said, very particular scenarios. Just to recap them: Graves disease refractory to medical management, pre-surgical management for patients who are at high risk of bleeding or high risk of conversion from a minimally invasive laparoscopic surgery to an open surgery, autonomously functioning nodules greater than 15 mL, solid thyroid nodules greater than 30 mL, and multinodular goiter greater than 50 mL.
Desai: Thank you. As we wrap up today’s episode, I hope this conversation has given our listeners a clear, more practical framework for understanding TAE, which is TAE, who the ideal candidates are — which we just went through — and when to consider referral and how to kind of incorporate this in your tool for management for benign thyroid diseases.
Thank you, Dr Camacho, for joining us and sharing your expertise and insight in this area.
On our next episode, we’ll shift gears and tackle a topic that comes up constantly in both endocrine and primary care practice: how medications affect the thyroid gland. We’ll break down which drugs alter thyroid function tests, which ones cause true thyroid function, and how to interpret labs and medications, especially when using levothyroxine doses, which may need to be adjusted. Thank you for listening, and we’ll see you next month.
Image Credits (all images): Juan C. Camacho, MD, Sarasota Memorial Hospital, Florida
Cite this: Adding to the Toolbox: Thyroid Artery Embolization - Medscape - Feb 24, 2026.
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